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Pinessi</h1><div class="affiliations-container fake-truncate js-profile-affiliations"><div><a class="u-tcGrayDarker" href="https://unito.academia.edu/">Università degli Studi di Torino</a>, <a class="u-tcGrayDarker" href="https://unito.academia.edu/Departments/Neuroscience/Documents">Neuroscience</a>, <span class="u-tcGrayDarker">Faculty Member</span></div></div></div></div><div class="sidebar-cta-container"><button class="ds2-5-button hidden profile-cta-button grow js-profile-follow-button" data-broccoli-component="user-info.follow-button" data-click-track="profile-user-info-follow-button" data-follow-user-fname="L." data-follow-user-id="32055065" data-follow-user-source="profile_button" data-has-google="false"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">add</span>Follow</button><button class="ds2-5-button hidden profile-cta-button grow js-profile-unfollow-button" data-broccoli-component="user-info.unfollow-button" 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'//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/329751/137469/18260272/s200_prof.amjad.al-nasser.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://yu.academia.edu/AmjadAlNasser">Prof.Amjad Al-Nasser</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Yarmouk University</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://alicante.academia.edu/AngelBerenguer"><img class="profile-avatar u-positionAbsolute" alt="Angel Berenguer related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/464216/153653/178802/s200_angel.berenguer.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://alicante.academia.edu/AngelBerenguer">Angel Berenguer</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of Alicante / Universidad de Alicante</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://ehu.academia.edu/RobertoCortes"><img class="profile-avatar u-positionAbsolute" alt="Roberto Cortes related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/1166117/3418143/4019780/s200_roberto.cortes.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://ehu.academia.edu/RobertoCortes">Roberto Cortes</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of the Basque Country, Euskal Herriko Unibertsitatea</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://alicante.academia.edu/IsidroMart%C3%ADnezMira"><img class="profile-avatar u-positionAbsolute" alt="Isidro Martínez Mira related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/1742330/3622394/4248938/s200_isidro.mart_nez_mira.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://alicante.academia.edu/IsidroMart%C3%ADnezMira">Isidro Martínez Mira</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of Alicante / Universidad de Alicante</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://weillcornell.academia.edu/NicolasKarakatsanis"><img class="profile-avatar u-positionAbsolute" alt="Nicolas A Karakatsanis related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" src="https://gravatar.com/avatar/df326849047610f2799024acfcfb3334?s=200" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://weillcornell.academia.edu/NicolasKarakatsanis">Nicolas A Karakatsanis</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Weill Cornell Medicine</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://unipd.academia.edu/CarloSemenza"><img class="profile-avatar u-positionAbsolute" alt="Carlo Semenza related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/3886207/2825606/3297948/s200_carlo.semenza.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://unipd.academia.edu/CarloSemenza">Carlo Semenza</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Università degli Studi di Padova</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a data-nosnippet="" href="https://jhusom.academia.edu/santoshkbharti"><img class="profile-avatar u-positionAbsolute" alt="Santosh K. Bharti related author profile picture" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/7007633/2655169/3090580/s200_santosh.bharti.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://jhusom.academia.edu/santoshkbharti">Santosh K. Bharti</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Johns Hopkins University School of Medicine</p></div></div></ul></div><style type="text/css">.suggested-academics--header h3{font-size:16px;font-weight:500;line-height:20px}</style><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="32055065" href="https://www.academia.edu/Documents/in/Inorganic_Chemistry"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://unito.academia.edu/LPinessi","location":"/LPinessi","scheme":"https","host":"unito.academia.edu","port":null,"pathname":"/LPinessi","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Inorganic Chemistry"]}" data-trace="false" data-dom-id="Pill-react-component-a6509cc3-2528-46f5-af5f-8eec193469b6"></div> <div id="Pill-react-component-a6509cc3-2528-46f5-af5f-8eec193469b6"></div> </a><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="32055065" href="https://www.academia.edu/Documents/in/Neuroscience"><div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Neuroscience"]}" data-trace="false" data-dom-id="Pill-react-component-ca46ce3a-c8c8-4ddb-a742-dc36bbccd311"></div> <div id="Pill-react-component-ca46ce3a-c8c8-4ddb-a742-dc36bbccd311"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by L. Pinessi</h3></div><div class="js-work-strip profile--work_container" data-work-id="104613718"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613718/DOI_10_1007_s10194_007_0383_x_Association_between_the_G1246A_polymorphism_of_the_hypocretin_receptor_2_gene_and_cluster_headache_a_meta_analysis"><img alt="Research paper thumbnail of DOI 10.1007/s10194-007-0383-x Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">DOI 10.1007/s10194-007-0383-x Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis</div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The objective of this study was to investigate the associ-ation between polymorphisms of the hypo...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613718"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613718"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613718; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613718]").text(description); $(".js-view-count[data-work-id=104613718]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613718; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613718']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613718]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613718,"title":"DOI 10.1007/s10194-007-0383-x Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis","translated_title":"","metadata":{"abstract":"The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). 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Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%","internal_url":"https://www.academia.edu/104613718/DOI_10_1007_s10194_007_0383_x_Association_between_the_G1246A_polymorphism_of_the_hypocretin_receptor_2_gene_and_cluster_headache_a_meta_analysis","translated_internal_url":"","created_at":"2023-07-16T03:22:01.024-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"DOI_10_1007_s10194_007_0383_x_Association_between_the_G1246A_polymorphism_of_the_hypocretin_receptor_2_gene_and_cluster_headache_a_meta_analysis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":32913052,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.797.2637\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613717"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613717/Social_sense_and_occupational_neuroses"><img alt="Research paper thumbnail of Social sense' and occupational neuroses" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Social sense' and occupational neuroses</div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613717"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613717"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613717; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613717]").text(description); $(".js-view-count[data-work-id=104613717]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613717; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613717']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613717]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613717,"title":"Social sense' and occupational neuroses","translated_title":"","metadata":{"publication_date":{"day":null,"month":null,"year":1978,"errors":{}}},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613717/Social_sense_and_occupational_neuroses","translated_internal_url":"","created_at":"2023-07-16T03:22:00.897-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Social_sense_and_occupational_neuroses","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":221,"name":"Psychology","url":"https://www.academia.edu/Documents/in/Psychology"},{"id":1444349,"name":"Medicina Psicosomática","url":"https://www.academia.edu/Documents/in/Medicina_Psicosomatica"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613716"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism"><img alt="Research paper thumbnail of Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism" class="work-thumbnail" src="https://attachments.academia-assets.com/104295811/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism">Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism</a></div><div class="wp-workCard_item"><span>Neurotoxicity Research</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Objectives: We hypothesized that the IL-1β-511 C>T polymorphism could be associated with the deve...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Objectives: We hypothesized that the IL-1β-511 C>T polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C>T. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C>T gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C>T as genetic biomarkers to identify patients with higher risk to develop neurological deficits.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a0f7c6bc97a65c297d4ec370da9c3bb2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295811,"asset_id":104613716,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295811/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613716"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613716"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613716; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613716]").text(description); $(".js-view-count[data-work-id=104613716]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613716; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613716']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a0f7c6bc97a65c297d4ec370da9c3bb2" } } $('.js-work-strip[data-work-id=104613716]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613716,"title":"Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C\u003eT Polymorphism","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Objectives: We hypothesized that the IL-1β-511 C\u003eT polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C\u003eT. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C\u003eT gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C\u003eT as genetic biomarkers to identify patients with higher risk to develop neurological deficits.","publication_date":{"day":null,"month":null,"year":2016,"errors":{}},"publication_name":"Neurotoxicity Research","grobid_abstract_attachment_id":104295811},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism","translated_internal_url":"","created_at":"2023-07-16T03:22:00.678-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295811,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295811/thumbnails/1.jpg","file_name":"IL1b_ref_NTR_postprint_4aperto.pdf","download_url":"https://www.academia.edu/attachments/104295811/download_file","bulk_download_file_name":"Chemotherapy_Induced_Neurotoxicity_Evide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295811/IL1b_ref_NTR_postprint_4aperto-libre.pdf?1689510979=\u0026response-content-disposition=attachment%3B+filename%3DChemotherapy_Induced_Neurotoxicity_Evide.pdf\u0026Expires=1743102266\u0026Signature=ZiERAXXmVApRmqjlw8HyQsk3Dj3qqWMrKhGkazh8S--54pPC9v4cg2rWezw6qu-1HRRfMEGtSL0FQPREIcMEKFz7~gJ2PlRbund-giH51D7JrdVnNRqzlxhdoKQoG95nYrTMbRC-daxcdLfDgkmeqBPQCworc7sK4XQVLDQS3-SUEFMPnz~xUE-qdqJbCUAbM7sj4sqA57um0epF2~iCHWjINTR~q2wQu604pOHcssELN5Qa-B5EJ4Gsq4s6wW4A8EFxFXtHTzeKkizIjmZ--qZKKSO-IeH6lL5UtA1h-vzqYe0E6pIrrdbU70MRFhl0K77M3~Xk3g5p-UjU9AojlQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1β_Gene_511_C_T_Polymorphism","translated_slug":"","page_count":32,"language":"en","content_type":"Work","summary":"Objectives: We hypothesized that the IL-1β-511 C\u003eT polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C\u003eT. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C\u003eT gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C\u003eT as genetic biomarkers to identify patients with higher risk to develop neurological deficits.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":221,"name":"Psychology","url":"https://www.academia.edu/Documents/in/Psychology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":51566,"name":"Dopamine","url":"https://www.academia.edu/Documents/in/Dopamine"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":157726,"name":"Dopamine Receptors","url":"https://www.academia.edu/Documents/in/Dopamine_Receptors"},{"id":159958,"name":"Acetylcholine","url":"https://www.academia.edu/Documents/in/Acetylcholine"},{"id":2795557,"name":"Antipsychotic agents","url":"https://www.academia.edu/Documents/in/Antipsychotic_agents"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613714"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613714/_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_"><img alt="Research paper thumbnail of [Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]</div><div class="wp-workCard_item"><span>Minerva medica</span><span>, Jan 3, 1984</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In Parkinson&#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to mo...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In Parkinson&#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613714"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613714"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613714; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613714]").text(description); $(".js-view-count[data-work-id=104613714]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613714; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613714']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613714]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613714,"title":"[Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]","translated_title":"","metadata":{"abstract":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","publication_date":{"day":3,"month":1,"year":1984,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","internal_url":"https://www.academia.edu/104613714/_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_","translated_internal_url":"","created_at":"2023-07-16T03:22:00.424-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":161,"name":"Neuroscience","url":"https://www.academia.edu/Documents/in/Neuroscience"},{"id":2584,"name":"Neuromodulation","url":"https://www.academia.edu/Documents/in/Neuromodulation"},{"id":4670,"name":"Pathogenesis","url":"https://www.academia.edu/Documents/in/Pathogenesis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":51566,"name":"Dopamine","url":"https://www.academia.edu/Documents/in/Dopamine"},{"id":64657,"name":"Prolactin","url":"https://www.academia.edu/Documents/in/Prolactin"},{"id":157726,"name":"Dopamine Receptors","url":"https://www.academia.edu/Documents/in/Dopamine_Receptors"},{"id":176503,"name":"Synaptic Transmission","url":"https://www.academia.edu/Documents/in/Synaptic_Transmission"},{"id":208014,"name":"Levodopa","url":"https://www.academia.edu/Documents/in/Levodopa"},{"id":219680,"name":"Minerva Medica","url":"https://www.academia.edu/Documents/in/Minerva_Medica"},{"id":628485,"name":"Cholinergic Systems","url":"https://www.academia.edu/Documents/in/Cholinergic_Systems"},{"id":1134529,"name":"Parkinson´s Disease","url":"https://www.academia.edu/Documents/in/Parkinson_s_Disease"},{"id":1360928,"name":"Endorphins","url":"https://www.academia.edu/Documents/in/Endorphins"},{"id":1541077,"name":"Parkinson Disease","url":"https://www.academia.edu/Documents/in/Parkinson_Disease"},{"id":2483726,"name":"dopaminergic","url":"https://www.academia.edu/Documents/in/dopaminergic"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613713"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613713/_Preliminary_data_of_a_descriptive_epidemiologic_study_of_multiple_sclerosis_in_the_city_of_Turin_"><img alt="Research paper thumbnail of [Preliminary data of a descriptive epidemiologic study of multiple sclerosis in the city of Turin]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Preliminary data of a descriptive epidemiologic study of multiple sclerosis in the city of Turin]</div><div class="wp-workCard_item"><span>Minerva medica</span><span>, Jan 14, 1985</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-Ju...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613713"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613713"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613713; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613713]").text(description); $(".js-view-count[data-work-id=104613713]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613713; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613713']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613713]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613713,"title":"[Preliminary data of a descriptive epidemiologic study of multiple sclerosis in the city of Turin]","translated_title":"","metadata":{"abstract":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","publication_date":{"day":14,"month":1,"year":1985,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","internal_url":"https://www.academia.edu/104613713/_Preliminary_data_of_a_descriptive_epidemiologic_study_of_multiple_sclerosis_in_the_city_of_Turin_","translated_internal_url":"","created_at":"2023-07-16T03:22:00.300-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Preliminary_data_of_a_descriptive_epidemiologic_study_of_multiple_sclerosis_in_the_city_of_Turin_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":1085,"name":"Epidemiology","url":"https://www.academia.edu/Documents/in/Epidemiology"},{"id":3097,"name":"Multiple sclerosis","url":"https://www.academia.edu/Documents/in/Multiple_sclerosis"},{"id":5500,"name":"Incidence Geometry","url":"https://www.academia.edu/Documents/in/Incidence_Geometry"},{"id":22506,"name":"Adolescent","url":"https://www.academia.edu/Documents/in/Adolescent"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":85362,"name":"Descriptive Statistics","url":"https://www.academia.edu/Documents/in/Descriptive_Statistics"},{"id":219680,"name":"Minerva Medica","url":"https://www.academia.edu/Documents/in/Minerva_Medica"},{"id":570668,"name":"Urban Population","url":"https://www.academia.edu/Documents/in/Urban_Population"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613712"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine"><img alt="Research paper thumbnail of A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine" class="work-thumbnail" src="https://attachments.academia-assets.com/104295816/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine">A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine</a></div><div class="wp-workCard_item"><span>Journal of Headache and Pain</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The objective of this study was to assess patient satisfaction with acute treatment of migraine w...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. The study had a multicenter, randomized, double-blind, cross-over design, with treatment periods lasting\3 months. At the end of the study, patients assigned preference to one of the treatments using a questionnaire with a score from 0 to 5 (primary endpoint). Secondary endpoints were pain-free and pain relief episodes at 2 h, and recurrent and sustained pain-free episodes within 48 h. 104 of the 125 patients (83%, intentionto-treat population) expressed a preference for a triptan. The average preference score was not significantly different between frovatriptan (2.9 ± 1.3) and rizatriptan (3.2 ± 1.1). The rates of pain-free (33% frovatriptan vs. 39% rizatriptan) and pain relief (55 vs. 62%) episodes at 2 h were not significantly different between the two treatments. The rate of recurrent episodes was significantly (p \ 0.001) lower under frovatriptan (21 vs. 43% rizatriptan). No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="5ff2119ccfe204b954236f18c466ce18" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295816,"asset_id":104613712,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295816/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613712"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613712"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613712; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613712]").text(description); $(".js-view-count[data-work-id=104613712]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613712; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613712']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "5ff2119ccfe204b954236f18c466ce18" } } $('.js-work-strip[data-work-id=104613712]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613712,"title":"A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine","translated_title":"","metadata":{"grobid_abstract":"The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. The study had a multicenter, randomized, double-blind, cross-over design, with treatment periods lasting\\3 months. At the end of the study, patients assigned preference to one of the treatments using a questionnaire with a score from 0 to 5 (primary endpoint). Secondary endpoints were pain-free and pain relief episodes at 2 h, and recurrent and sustained pain-free episodes within 48 h. 104 of the 125 patients (83%, intentionto-treat population) expressed a preference for a triptan. The average preference score was not significantly different between frovatriptan (2.9 ± 1.3) and rizatriptan (3.2 ± 1.1). The rates of pain-free (33% frovatriptan vs. 39% rizatriptan) and pain relief (55 vs. 62%) episodes at 2 h were not significantly different between the two treatments. The rate of recurrent episodes was significantly (p \\ 0.001) lower under frovatriptan (21 vs. 43% rizatriptan). No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Journal of Headache and Pain","grobid_abstract_attachment_id":104295816},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine","translated_internal_url":"","created_at":"2023-07-16T03:22:00.161-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295816,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295816/thumbnails/1.jpg","file_name":"s10194-010-0243-y.pdf","download_url":"https://www.academia.edu/attachments/104295816/download_file","bulk_download_file_name":"A_double_blind_randomized_multicenter_It.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295816/s10194-010-0243-y-libre.pdf?1689510972=\u0026response-content-disposition=attachment%3B+filename%3DA_double_blind_randomized_multicenter_It.pdf\u0026Expires=1743102266\u0026Signature=K4fxv4Lw4jk~G0QSEHQBshzlYMiMwXJIVb494LS1S~VnApp5vrnoFBBkEJzEVwwt1u8W8jOAkpqG1K5Yr-RZP37JtMfOxtl8F9MYEyYVQtpbu1QxbFnzc9T37kv1O6mSYj6cP2ajnNcVvcbeMd7QuSQedgVxPvMIflDiNJyREcxALl66QXet2GHRBWD43NvPB01bE5oMiwTkKZG5AqwCLeENehDUHVvWUIa2DC1bjeLxkFAHPG99RpS6A62B7nJeZAmwQ9N~8hkwRXhxiAp~VF6ZiF8P23ADB8KeSBgSrSIm8i6TfjTPhAMBAWWAIRIMny-pLBsCo47m6rEySzgLOQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine","translated_slug":"","page_count":8,"language":"en","content_type":"Work","summary":"The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. The study had a multicenter, randomized, double-blind, cross-over design, with treatment periods lasting\\3 months. At the end of the study, patients assigned preference to one of the treatments using a questionnaire with a score from 0 to 5 (primary endpoint). Secondary endpoints were pain-free and pain relief episodes at 2 h, and recurrent and sustained pain-free episodes within 48 h. 104 of the 125 patients (83%, intentionto-treat population) expressed a preference for a triptan. The average preference score was not significantly different between frovatriptan (2.9 ± 1.3) and rizatriptan (3.2 ± 1.1). The rates of pain-free (33% frovatriptan vs. 39% rizatriptan) and pain relief (55 vs. 62%) episodes at 2 h were not significantly different between the two treatments. The rate of recurrent episodes was significantly (p \\ 0.001) lower under frovatriptan (21 vs. 43% rizatriptan). No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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The 1246 GϾA polymorphism of the gene was significantly different between cases and controls. Homozygosity for the G allele was associated with an increased disease risk (OR: 6.79, 95% CI, 2.25 to 22.99). The data suggest that the HCRTR2 gene or a linked locus significantly modulates the risk for cluster headache.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="03aad739205fe06168d1780001585cf8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295818,"asset_id":104613711,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295818/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613711"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613711"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613711; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613711]").text(description); $(".js-view-count[data-work-id=104613711]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613711; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613711']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "03aad739205fe06168d1780001585cf8" } } $('.js-work-strip[data-work-id=104613711]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613711,"title":"A polymorphism of the hypocretin receptor 2 gene is associated with cluster headache","translated_title":"","metadata":{"publisher":"Ovid Technologies (Wolters Kluwer Health)","ai_title_tag":"Hypocretin Receptor 2 Gene Polymorphism Linked to Cluster Headache","grobid_abstract":"Several polymorphisms of the hypocretin/orexin system genes were evaluated in 109 cluster headache patients and 211 controls. 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Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="adf87eea9862439d3e882e14904b33a1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295931,"asset_id":104613709,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295931/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613709"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613709"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613709; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613709]").text(description); $(".js-view-count[data-work-id=104613709]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613709; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613709']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "adf87eea9862439d3e882e14904b33a1" } } $('.js-work-strip[data-work-id=104613709]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613709,"title":"Association between tumor necrosis factor-alpha gene promoter polymorphism at position -308 and acne in Turkish patients","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Background: Tumor necrosis factor-alpha (TNF-α) is an important inflammatory cytokine that may play a role in controlling the progression of prostate cancer. Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Archives of Dermatological Research","grobid_abstract_attachment_id":104295931},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613709/Association_between_tumor_necrosis_factor_alpha_gene_promoter_polymorphism_at_position_308_and_acne_in_Turkish_patients","translated_internal_url":"","created_at":"2023-07-16T03:21:59.551-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295931,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295931/thumbnails/1.jpg","file_name":"1746-1596-9-74.pdf","download_url":"https://www.academia.edu/attachments/104295931/download_file","bulk_download_file_name":"Association_between_tumor_necrosis_facto.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295931/1746-1596-9-74-libre.pdf?1689510967=\u0026response-content-disposition=attachment%3B+filename%3DAssociation_between_tumor_necrosis_facto.pdf\u0026Expires=1743102266\u0026Signature=LWj-rtDxsU2Q9uwACtuLcax5tszEdvrKOxqsku6KbSGB~D7srzoVvTnPzkYwFBqzTUTqdHG6P6p1SIa1iKT10Sckc0ZeRPrfv5Oi22eCtYjSOcLcv~crszaJmZauMWqfW5of5NV6gN0PCSwF2~KBH2GvMvSzBlv-V1r~g34ZrZkwk5fdvhoKHWQ54CJim-PEoPt0q84g45n-JGVmG7K94LWtEDGCMbyCiRVzoAmaodWwAAcffUXkzF1nS34-CEky1nb2lw12cb4Q2TfFNGoHk96hpWtsoNTi27kcg8NrCpTkYACERrXvpibEeVROBnfwJ5EnGAE7Yjaf0Qf~rkn~2A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Association_between_tumor_necrosis_factor_alpha_gene_promoter_polymorphism_at_position_308_and_acne_in_Turkish_patients","translated_slug":"","page_count":11,"language":"en","content_type":"Work","summary":"Background: Tumor necrosis factor-alpha (TNF-α) is an important inflammatory cytokine that may play a role in controlling the progression of prostate cancer. Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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Recent epidemiological studies have shown the existence of a genetic etiology in some cases of Alzheimer&#39;s disease. Several pedigrees with an increased incidence of AD (familial Alzheimer&#39;s disease--FAD) have been described in the literature. Some of these contain sufficient numbers of affected individuals in multiple generations to provide a rigorous argument for an autosomal dominant inheritance of the AD phenotype. FAD pedigrees show several evidences of as phenotypic heterogeneity of the disease. Molecular genetic studies have shown a linkage between several polymorphic DNA markers specific for the pericentromeric region of chromosome 21 and early-onset FAD. In late-onset FAD pedigrees preliminary reports showed evidence for a linkage with chromosome 19 markers. Molecular genetic studies have clearly demonstrated the genetic heterogeneity of fami...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613656"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613656"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613656; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613656]").text(description); $(".js-view-count[data-work-id=104613656]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613656; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613656']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613656]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613656,"title":"[The genetics of Alzheimer's disease]","translated_title":"","metadata":{"abstract":"This paper examines recent epidemiological and molecular genetic studies on the genetic basis of Alzheimer\u0026#39;s disease (AD). 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Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198052,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.291.7948\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225807"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225807/Salvatore_Gentile"><img alt="Research paper thumbnail of Salvatore Gentile" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Salvatore Gentile</div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We report the case of a patient who developed typical cluster headache attacks and was diagnosed ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We report the case of a patient who developed typical cluster headache attacks and was diagnosed as having multiple scle-rosis (MS) at the same time. The headache attacks resolved after i.v. treatment with methylpred-nisolone. MR imaging showed a pontine demyelinating lesion involving the trigeminal nerve root inlet area, on the same side as the pain. The association between cluster headache and MS has been rarely described before. This case suggests that in patients with clus-ter headache neuroimaging is often useful in order to exclude structur-al lesions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225807"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225807"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225807; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225807]").text(description); $(".js-view-count[data-work-id=93225807]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225807; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225807']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225807]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225807,"title":"Salvatore Gentile","translated_title":"","metadata":{"abstract":"We report the case of a patient who developed typical cluster headache attacks and was diagnosed as having multiple scle-rosis (MS) at the same time. 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The association between cluster headache and MS has been rarely described before. This case suggests that in patients with clus-ter headache neuroimaging is often useful in order to exclude structur-al lesions.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198051,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.775.6094\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225806"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225806/DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply"><img alt="Research paper thumbnail of DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply</div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Ó The Author(s) 2011. This article is published with open access at Springerlink.com</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225806"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225806"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225806; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225806]").text(description); $(".js-view-count[data-work-id=93225806]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225806; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225806']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225806]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225806,"title":"DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply","translated_title":"","metadata":{"abstract":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","publication_date":{"day":null,"month":null,"year":2013,"errors":{}}},"translated_abstract":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","internal_url":"https://www.academia.edu/93225806/DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply","translated_internal_url":"","created_at":"2022-12-19T01:20:45.709-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198050,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.288.3445\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225805"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225805/Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone"><img alt="Research paper thumbnail of Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone</div><div class="wp-workCard_item"><span>Panminerva medica</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225805"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225805"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225805; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225805]").text(description); $(".js-view-count[data-work-id=93225805]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225805; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225805']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225805]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225805,"title":"Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone","translated_title":"","metadata":{"publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Panminerva medica"},"translated_abstract":null,"internal_url":"https://www.academia.edu/93225805/Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone","translated_internal_url":"","created_at":"2022-12-19T01:20:45.595-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":74780,"name":"Mutation","url":"https://www.academia.edu/Documents/in/Mutation"},{"id":901876,"name":"Sensitivity and Specificity","url":"https://www.academia.edu/Documents/in/Sensitivity_and_Specificity"},{"id":3647178,"name":"DNA Restriction Enzymes","url":"https://www.academia.edu/Documents/in/DNA_Restriction_Enzymes"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225803"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225803/_Neuroendocrinologic_aspects_of_epilepsy_"><img alt="Research paper thumbnail of [Neuroendocrinologic aspects of epilepsy]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Neuroendocrinologic aspects of epilepsy]</div><div class="wp-workCard_item"><span>Minerva medica</span><span>, Jan 3, 1984</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although the literature recognises the involvement of neuropeptide structures in the genesis of e...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225803"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225803]").text(description); $(".js-view-count[data-work-id=93225803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225803,"title":"[Neuroendocrinologic aspects of epilepsy]","translated_title":"","metadata":{"abstract":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","publication_date":{"day":3,"month":1,"year":1984,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","internal_url":"https://www.academia.edu/93225803/_Neuroendocrinologic_aspects_of_epilepsy_","translated_internal_url":"","created_at":"2022-12-19T01:20:45.343-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Neuroendocrinologic_aspects_of_epilepsy_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":161,"name":"Neuroscience","url":"https://www.academia.edu/Documents/in/Neuroscience"},{"id":7648,"name":"Epilepsy","url":"https://www.academia.edu/Documents/in/Epilepsy"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":57556,"name":"Hippocampus","url":"https://www.academia.edu/Documents/in/Hippocampus"},{"id":176503,"name":"Synaptic Transmission","url":"https://www.academia.edu/Documents/in/Synaptic_Transmission"},{"id":219680,"name":"Minerva Medica","url":"https://www.academia.edu/Documents/in/Minerva_Medica"},{"id":651604,"name":"Seizures","url":"https://www.academia.edu/Documents/in/Seizures"},{"id":1530411,"name":"Convulsion","url":"https://www.academia.edu/Documents/in/Convulsion"},{"id":1619808,"name":"Gamma-Aminobutyric Acid","url":"https://www.academia.edu/Documents/in/Gamma-Aminobutyric_Acid"},{"id":2558779,"name":"Gabaergic","url":"https://www.academia.edu/Documents/in/Gabaergic"},{"id":2583478,"name":"Neuropeptide","url":"https://www.academia.edu/Documents/in/Neuropeptide"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225802"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225802/Tumor_Necrosis_Factor_%CE%91_Gene_and_Cerebral_Aneurysms"><img alt="Research paper thumbnail of Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms</div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, im...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225802"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225802"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225802; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225802]").text(description); $(".js-view-count[data-work-id=93225802]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225802; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225802']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225802]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225802,"title":"Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms","translated_title":"","metadata":{"abstract":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Neurosurgery"},"translated_abstract":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","internal_url":"https://www.academia.edu/93225802/Tumor_Necrosis_Factor_%CE%91_Gene_and_Cerebral_Aneurysms","translated_internal_url":"","created_at":"2022-12-19T01:20:45.199-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Tumor_Necrosis_Factor_Α_Gene_and_Cerebral_Aneurysms","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":650,"name":"Neurosurgery","url":"https://www.academia.edu/Documents/in/Neurosurgery"},{"id":3855,"name":"Polymorphism","url":"https://www.academia.edu/Documents/in/Polymorphism"},{"id":4670,"name":"Pathogenesis","url":"https://www.academia.edu/Documents/in/Pathogenesis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":73153,"name":"Genetic Testing","url":"https://www.academia.edu/Documents/in/Genetic_Testing"},{"id":174502,"name":"Incidence","url":"https://www.academia.edu/Documents/in/Incidence"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":437772,"name":"Odds ratio","url":"https://www.academia.edu/Documents/in/Odds_ratio"},{"id":622589,"name":"Risk Assessment","url":"https://www.academia.edu/Documents/in/Risk_Assessment-2"},{"id":1004200,"name":"Allele","url":"https://www.academia.edu/Documents/in/Allele"},{"id":1159938,"name":"Cerebral Aneurysm","url":"https://www.academia.edu/Documents/in/Cerebral_Aneurysm"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":2482159,"name":"DNA mutational analysis","url":"https://www.academia.edu/Documents/in/DNA_mutational_analysis"},{"id":3208250,"name":"Intracranial aneurysm","url":"https://www.academia.edu/Documents/in/Intracranial_aneurysm"}],"urls":[{"id":27198049,"url":"https://journals.lww.com/00006123-200704000-00012"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225801"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225801/Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population"><img alt="Research paper thumbnail of Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population</div><div class="wp-workCard_item"><span>Journal of Neurology, Neurosurgery & Psychiatry</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Several lines of evidence indicate a role for inflammatory processes in the development of cerebr...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G&amp;gt;C and -572 G&amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G&amp;lt;C and the -572 G&amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225801"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225801"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225801; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225801]").text(description); $(".js-view-count[data-work-id=93225801]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225801; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225801']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225801]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225801,"title":"Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population","translated_title":"","metadata":{"abstract":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","publisher":"BMJ","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Journal of Neurology, Neurosurgery \u0026 Psychiatry"},"translated_abstract":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","internal_url":"https://www.academia.edu/93225801/Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population","translated_internal_url":"","created_at":"2022-12-19T01:20:45.096-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":67362,"name":"Italian","url":"https://www.academia.edu/Documents/in/Italian"},{"id":86952,"name":"Haplotypes","url":"https://www.academia.edu/Documents/in/Haplotypes"},{"id":99773,"name":"Disease","url":"https://www.academia.edu/Documents/in/Disease"},{"id":223022,"name":"Italiano","url":"https://www.academia.edu/Documents/in/Italiano"},{"id":289271,"name":"Aged","url":"https://www.academia.edu/Documents/in/Aged"},{"id":306990,"name":"Gene Polymorphism","url":"https://www.academia.edu/Documents/in/Gene_Polymorphism"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":1004200,"name":"Allele","url":"https://www.academia.edu/Documents/in/Allele"},{"id":1591688,"name":"Haplotype","url":"https://www.academia.edu/Documents/in/Haplotype"},{"id":1924712,"name":"Interleukin","url":"https://www.academia.edu/Documents/in/Interleukin"},{"id":3203621,"name":"Gene frequency","url":"https://www.academia.edu/Documents/in/Gene_frequency"},{"id":3208250,"name":"Intracranial aneurysm","url":"https://www.academia.edu/Documents/in/Intracranial_aneurysm"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225800"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225800/Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache"><img alt="Research paper thumbnail of Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache</div><div class="wp-workCard_item"><span>Headache: The Journal of Head and Face Pain</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P&amp;amp;amp;lt;0.01 and &amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225800"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225800"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225800; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225800]").text(description); $(".js-view-count[data-work-id=93225800]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225800; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225800']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225800]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225800,"title":"Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache","translated_title":"","metadata":{"abstract":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Headache: The Journal of Head and Face Pain"},"translated_abstract":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","internal_url":"https://www.academia.edu/93225800/Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache","translated_internal_url":"","created_at":"2022-12-19T01:20:44.967-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":154,"name":"Endocrinology","url":"https://www.academia.edu/Documents/in/Endocrinology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":52562,"name":"Growth Hormone","url":"https://www.academia.edu/Documents/in/Growth_Hormone"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":64657,"name":"Prolactin","url":"https://www.academia.edu/Documents/in/Prolactin"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":72938,"name":"Placebo","url":"https://www.academia.edu/Documents/in/Placebo"},{"id":97269,"name":"Chronic Disease","url":"https://www.academia.edu/Documents/in/Chronic_Disease"},{"id":103107,"name":"Migraine","url":"https://www.academia.edu/Documents/in/Migraine"},{"id":103108,"name":"Headache","url":"https://www.academia.edu/Documents/in/Headache"},{"id":161176,"name":"The","url":"https://www.academia.edu/Documents/in/The"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":312279,"name":"Serotonin Receptors","url":"https://www.academia.edu/Documents/in/Serotonin_Receptors"},{"id":612548,"name":"Tension-Type Headache","url":"https://www.academia.edu/Documents/in/Tension-Type_Headache"},{"id":1961440,"name":"Agonist","url":"https://www.academia.edu/Documents/in/Agonist"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225799"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease"><img alt="Research paper thumbnail of Autonomic responses and pain perception in Alzheimer’s disease" class="work-thumbnail" src="https://attachments.academia-assets.com/96021233/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease">Autonomic responses and pain perception in Alzheimer’s disease</a></div><div class="wp-workCard_item"><span>European Journal of Pain</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzh...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9da47f564d41fe3f358440b42dd88cc7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":96021233,"asset_id":93225799,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/96021233/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225799"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225799"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225799; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225799]").text(description); $(".js-view-count[data-work-id=93225799]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225799; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225799']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9da47f564d41fe3f358440b42dd88cc7" } } $('.js-work-strip[data-work-id=93225799]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225799,"title":"Autonomic responses and pain perception in Alzheimer’s disease","translated_title":"","metadata":{"publisher":"Wiley","ai_title_tag":"Autonomic Responses and Pain in Alzheimer’s Disease","grobid_abstract":"We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.","publication_date":{"day":null,"month":null,"year":2000,"errors":{}},"publication_name":"European Journal of Pain","grobid_abstract_attachment_id":96021233},"translated_abstract":null,"internal_url":"https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease","translated_internal_url":"","created_at":"2022-12-19T01:20:44.758-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":96021233,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/96021233/thumbnails/1.jpg","file_name":"eujp.2000.018520221219-1-wz36l9.pdf","download_url":"https://www.academia.edu/attachments/96021233/download_file","bulk_download_file_name":"Autonomic_responses_and_pain_perception.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/96021233/eujp.2000.018520221219-1-wz36l9-libre.pdf?1671447353=\u0026response-content-disposition=attachment%3B+filename%3DAutonomic_responses_and_pain_perception.pdf\u0026Expires=1743102266\u0026Signature=LV-ojb7w1hC6RJ32wX7MBhIstKNg2Z9RTkBCmVGdKCmZfq3zLQu3M3FmUFoFLoX0jiIYwrEpp3crpCVDrd-apQ4r-IYNImD6Lz~iWaDDy0O5t5Lgf31MWJ3NA4hEz8T194Hrn3pRYVrZ8SKuxATazejf~jogUsjpD5Gwdt9Iz~r5omLmZZtXJYBuL8PRVnSyiyetOWu-81GZ1C7JHQOhytqPDMTEC4J70B58jludJ0hoTzJIA9VCr4VwDTWgazVnkt3cOfSEgyFmLK6UAx8OZkZj6mfdL-IeaKP4XcLvvgCpz09WRk6fmoMr6dhDAgchb0QXobnLxAYS10FpXugdng__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease","translated_slug":"","page_count":8,"language":"en","content_type":"Work","summary":"We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613718"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613718"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613718; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613718]").text(description); $(".js-view-count[data-work-id=104613718]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613718; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613718']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613718]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613718,"title":"DOI 10.1007/s10194-007-0383-x Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis","translated_title":"","metadata":{"abstract":"The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%","publication_date":{"day":null,"month":null,"year":2007,"errors":{}}},"translated_abstract":"The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%","internal_url":"https://www.academia.edu/104613718/DOI_10_1007_s10194_007_0383_x_Association_between_the_G1246A_polymorphism_of_the_hypocretin_receptor_2_gene_and_cluster_headache_a_meta_analysis","translated_internal_url":"","created_at":"2023-07-16T03:22:01.024-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"DOI_10_1007_s10194_007_0383_x_Association_between_the_G1246A_polymorphism_of_the_hypocretin_receptor_2_gene_and_cluster_headache_a_meta_analysis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The objective of this study was to investigate the associ-ation between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymor-phisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymor-phism was significantly associated with CH (FE OR 1.58, CI 95%","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":32913052,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.797.2637\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613717"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613717/Social_sense_and_occupational_neuroses"><img alt="Research paper thumbnail of Social sense' and occupational neuroses" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Social sense' and occupational neuroses</div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613717"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613717"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613717; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613717]").text(description); $(".js-view-count[data-work-id=104613717]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613717; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613717']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613717]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613717,"title":"Social sense' and occupational neuroses","translated_title":"","metadata":{"publication_date":{"day":null,"month":null,"year":1978,"errors":{}}},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613717/Social_sense_and_occupational_neuroses","translated_internal_url":"","created_at":"2023-07-16T03:22:00.897-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Social_sense_and_occupational_neuroses","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":221,"name":"Psychology","url":"https://www.academia.edu/Documents/in/Psychology"},{"id":1444349,"name":"Medicina Psicosomática","url":"https://www.academia.edu/Documents/in/Medicina_Psicosomatica"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613716"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism"><img alt="Research paper thumbnail of Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism" class="work-thumbnail" src="https://attachments.academia-assets.com/104295811/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism">Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C>T Polymorphism</a></div><div class="wp-workCard_item"><span>Neurotoxicity Research</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Objectives: We hypothesized that the IL-1β-511 C>T polymorphism could be associated with the deve...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Objectives: We hypothesized that the IL-1β-511 C>T polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C>T. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C>T gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C>T as genetic biomarkers to identify patients with higher risk to develop neurological deficits.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a0f7c6bc97a65c297d4ec370da9c3bb2" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295811,"asset_id":104613716,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295811/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613716"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613716"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613716; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613716]").text(description); $(".js-view-count[data-work-id=104613716]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613716; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613716']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a0f7c6bc97a65c297d4ec370da9c3bb2" } } $('.js-work-strip[data-work-id=104613716]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613716,"title":"Chemotherapy-Induced Neurotoxicity: Evidence of a Protective Role of CC Homozygosis in the Interleukin-1β Gene-511 C\u003eT Polymorphism","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Objectives: We hypothesized that the IL-1β-511 C\u003eT polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C\u003eT. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C\u003eT gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C\u003eT as genetic biomarkers to identify patients with higher risk to develop neurological deficits.","publication_date":{"day":null,"month":null,"year":2016,"errors":{}},"publication_name":"Neurotoxicity Research","grobid_abstract_attachment_id":104295811},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613716/Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1%CE%B2_Gene_511_C_T_Polymorphism","translated_internal_url":"","created_at":"2023-07-16T03:22:00.678-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295811,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295811/thumbnails/1.jpg","file_name":"IL1b_ref_NTR_postprint_4aperto.pdf","download_url":"https://www.academia.edu/attachments/104295811/download_file","bulk_download_file_name":"Chemotherapy_Induced_Neurotoxicity_Evide.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295811/IL1b_ref_NTR_postprint_4aperto-libre.pdf?1689510979=\u0026response-content-disposition=attachment%3B+filename%3DChemotherapy_Induced_Neurotoxicity_Evide.pdf\u0026Expires=1743102266\u0026Signature=ZiERAXXmVApRmqjlw8HyQsk3Dj3qqWMrKhGkazh8S--54pPC9v4cg2rWezw6qu-1HRRfMEGtSL0FQPREIcMEKFz7~gJ2PlRbund-giH51D7JrdVnNRqzlxhdoKQoG95nYrTMbRC-daxcdLfDgkmeqBPQCworc7sK4XQVLDQS3-SUEFMPnz~xUE-qdqJbCUAbM7sj4sqA57um0epF2~iCHWjINTR~q2wQu604pOHcssELN5Qa-B5EJ4Gsq4s6wW4A8EFxFXtHTzeKkizIjmZ--qZKKSO-IeH6lL5UtA1h-vzqYe0E6pIrrdbU70MRFhl0K77M3~Xk3g5p-UjU9AojlQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Chemotherapy_Induced_Neurotoxicity_Evidence_of_a_Protective_Role_of_CC_Homozygosis_in_the_Interleukin_1β_Gene_511_C_T_Polymorphism","translated_slug":"","page_count":32,"language":"en","content_type":"Work","summary":"Objectives: We hypothesized that the IL-1β-511 C\u003eT polymorphism could be associated with the development of neurotoxicity and that it could be a possible biomarker to rate the risk of occurrence of neurotoxicity in cancer patients. Methods: Genomic DNA was extracted from 85 cancer patients: 49 received systemic chemotherapeutic treatment (CHT) and 36 patients did not receive it (No-CHT). All subjects were genotyped for the functionally active polymorphisms of IL-1β-511 C\u003eT. We estimated neurotoxicity with the evaluation of neurological deficits. Results: CHT patients showed erythrocytopenia, neurological deficit and a slight lowering of cognitive performance. The subgroup of patients carrying the CC genotype of the IL1β-511C\u003eT gene showed lesser neurological deficits. Conclusion: In the context of cancer treatment, we suggested the potential value of IL-1β-511 C\u003eT as genetic biomarkers to identify patients with higher risk to develop neurological deficits.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613715"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613715/_Current_status_of_our_knowledge_of_the_neurotropic_side_effects_of_neuroleptic_drugs_"><img alt="Research paper thumbnail of [Current status of our knowledge of the neurotropic side effects of neuroleptic drugs]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Current status of our knowledge of the neurotropic side effects of neuroleptic drugs]</div><div class="wp-workCard_item"><span>Minerva psichiatrica</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613715"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613715"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613715; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613715]").text(description); $(".js-view-count[data-work-id=104613715]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613715; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613715']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613715]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613715,"title":"[Current status of our knowledge of the neurotropic side effects of neuroleptic drugs]","translated_title":"","metadata":{"publication_name":"Minerva psichiatrica"},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613715/_Current_status_of_our_knowledge_of_the_neurotropic_side_effects_of_neuroleptic_drugs_","translated_internal_url":"","created_at":"2023-07-16T03:22:00.547-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Current_status_of_our_knowledge_of_the_neurotropic_side_effects_of_neuroleptic_drugs_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":221,"name":"Psychology","url":"https://www.academia.edu/Documents/in/Psychology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":51566,"name":"Dopamine","url":"https://www.academia.edu/Documents/in/Dopamine"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":157726,"name":"Dopamine Receptors","url":"https://www.academia.edu/Documents/in/Dopamine_Receptors"},{"id":159958,"name":"Acetylcholine","url":"https://www.academia.edu/Documents/in/Acetylcholine"},{"id":2795557,"name":"Antipsychotic agents","url":"https://www.academia.edu/Documents/in/Antipsychotic_agents"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613714"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/104613714/_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_"><img alt="Research paper thumbnail of [Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]</div><div class="wp-workCard_item"><span>Minerva medica</span><span>, Jan 3, 1984</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In Parkinson&#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to mo...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In Parkinson&#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613714"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613714"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613714; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613714]").text(description); $(".js-view-count[data-work-id=104613714]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613714; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613714']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613714]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613714,"title":"[Neuroendocrine correlations in the pathogenesis and pathology of Parkinson disease]","translated_title":"","metadata":{"abstract":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","publication_date":{"day":3,"month":1,"year":1984,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","internal_url":"https://www.academia.edu/104613714/_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_","translated_internal_url":"","created_at":"2023-07-16T03:22:00.424-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Neuroendocrine_correlations_in_the_pathogenesis_and_pathology_of_Parkinson_disease_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"In Parkinson\u0026#39;s disease the decrease of dopamine in the nigro-striatal pathway is allied to modifications of other neuromodulation systems. The biochemical disorder of cholinergic, gabaergic and epinephrinergic pathways is present. Moreover the alteration of certain neuropeptides such as endorphins or enkefalins have been found. The Authors analyse the functional repercussions of these important biochemical modifications in the T.I.D.A. tract. In particular the variation of PRL synthesis and secretion due to dopamine deficiency during basal conditions and after pharmacological treatment is discussed.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613713"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613713"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613713; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613713]").text(description); $(".js-view-count[data-work-id=104613713]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613713; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613713']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613713]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613713,"title":"[Preliminary data of a descriptive epidemiologic study of multiple sclerosis in the city of Turin]","translated_title":"","metadata":{"abstract":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","publication_date":{"day":14,"month":1,"year":1985,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","internal_url":"https://www.academia.edu/104613713/_Preliminary_data_of_a_descriptive_epidemiologic_study_of_multiple_sclerosis_in_the_city_of_Turin_","translated_internal_url":"","created_at":"2023-07-16T03:22:00.300-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Preliminary_data_of_a_descriptive_epidemiologic_study_of_multiple_sclerosis_in_the_city_of_Turin_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"A descriptive epidemiological survey conducted in Turin on a population of 1,065,304 in Jan. 1-June 30 1984, produced preliminary data on the incidence of MS. Given the restricted area and brief duration of the survey, such data are however purely indicative. Primarily clinical criteria supported by instrumental and laboratory tests (P., Ev., liquor) were uniformly adopted.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":1085,"name":"Epidemiology","url":"https://www.academia.edu/Documents/in/Epidemiology"},{"id":3097,"name":"Multiple sclerosis","url":"https://www.academia.edu/Documents/in/Multiple_sclerosis"},{"id":5500,"name":"Incidence Geometry","url":"https://www.academia.edu/Documents/in/Incidence_Geometry"},{"id":22506,"name":"Adolescent","url":"https://www.academia.edu/Documents/in/Adolescent"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":85362,"name":"Descriptive Statistics","url":"https://www.academia.edu/Documents/in/Descriptive_Statistics"},{"id":219680,"name":"Minerva Medica","url":"https://www.academia.edu/Documents/in/Minerva_Medica"},{"id":570668,"name":"Urban Population","url":"https://www.academia.edu/Documents/in/Urban_Population"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="104613712"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine"><img alt="Research paper thumbnail of A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine" class="work-thumbnail" src="https://attachments.academia-assets.com/104295816/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine">A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine</a></div><div class="wp-workCard_item"><span>Journal of Headache and Pain</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The objective of this study was to assess patient satisfaction with acute treatment of migraine w...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. The study had a multicenter, randomized, double-blind, cross-over design, with treatment periods lasting\3 months. At the end of the study, patients assigned preference to one of the treatments using a questionnaire with a score from 0 to 5 (primary endpoint). Secondary endpoints were pain-free and pain relief episodes at 2 h, and recurrent and sustained pain-free episodes within 48 h. 104 of the 125 patients (83%, intentionto-treat population) expressed a preference for a triptan. The average preference score was not significantly different between frovatriptan (2.9 ± 1.3) and rizatriptan (3.2 ± 1.1). The rates of pain-free (33% frovatriptan vs. 39% rizatriptan) and pain relief (55 vs. 62%) episodes at 2 h were not significantly different between the two treatments. The rate of recurrent episodes was significantly (p \ 0.001) lower under frovatriptan (21 vs. 43% rizatriptan). No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="5ff2119ccfe204b954236f18c466ce18" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295816,"asset_id":104613712,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295816/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613712"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613712"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613712; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613712]").text(description); $(".js-view-count[data-work-id=104613712]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613712; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613712']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "5ff2119ccfe204b954236f18c466ce18" } } $('.js-work-strip[data-work-id=104613712]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613712,"title":"A double-blind, randomized, multicenter, Italian study of frovatriptan versus rizatriptan for the acute treatment of migraine","translated_title":"","metadata":{"grobid_abstract":"The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. The study had a multicenter, randomized, double-blind, cross-over design, with treatment periods lasting\\3 months. At the end of the study, patients assigned preference to one of the treatments using a questionnaire with a score from 0 to 5 (primary endpoint). Secondary endpoints were pain-free and pain relief episodes at 2 h, and recurrent and sustained pain-free episodes within 48 h. 104 of the 125 patients (83%, intentionto-treat population) expressed a preference for a triptan. The average preference score was not significantly different between frovatriptan (2.9 ± 1.3) and rizatriptan (3.2 ± 1.1). The rates of pain-free (33% frovatriptan vs. 39% rizatriptan) and pain relief (55 vs. 62%) episodes at 2 h were not significantly different between the two treatments. The rate of recurrent episodes was significantly (p \\ 0.001) lower under frovatriptan (21 vs. 43% rizatriptan). No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Journal of Headache and Pain","grobid_abstract_attachment_id":104295816},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613712/A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine","translated_internal_url":"","created_at":"2023-07-16T03:22:00.161-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295816,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295816/thumbnails/1.jpg","file_name":"s10194-010-0243-y.pdf","download_url":"https://www.academia.edu/attachments/104295816/download_file","bulk_download_file_name":"A_double_blind_randomized_multicenter_It.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295816/s10194-010-0243-y-libre.pdf?1689510972=\u0026response-content-disposition=attachment%3B+filename%3DA_double_blind_randomized_multicenter_It.pdf\u0026Expires=1743102266\u0026Signature=K4fxv4Lw4jk~G0QSEHQBshzlYMiMwXJIVb494LS1S~VnApp5vrnoFBBkEJzEVwwt1u8W8jOAkpqG1K5Yr-RZP37JtMfOxtl8F9MYEyYVQtpbu1QxbFnzc9T37kv1O6mSYj6cP2ajnNcVvcbeMd7QuSQedgVxPvMIflDiNJyREcxALl66QXet2GHRBWD43NvPB01bE5oMiwTkKZG5AqwCLeENehDUHVvWUIa2DC1bjeLxkFAHPG99RpS6A62B7nJeZAmwQ9N~8hkwRXhxiAp~VF6ZiF8P23ADB8KeSBgSrSIm8i6TfjTPhAMBAWWAIRIMny-pLBsCo47m6rEySzgLOQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"A_double_blind_randomized_multicenter_Italian_study_of_frovatriptan_versus_rizatriptan_for_the_acute_treatment_of_migraine","translated_slug":"","page_count":8,"language":"en","content_type":"Work","summary":"The objective of this study was to assess patient satisfaction with acute treatment of migraine with frovatriptan or rizatriptan by preference questionnaire. 148 subjects with a history of migraine with or without aura (IHS 2004 criteria), with at least one migraine attack per month in the preceding 6 months, were enrolled and randomized to frovatriptan 2.5 mg or rizatriptan 10 mg treating 1-3 attacks. 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No significant differences were observed in sustained pain-free episodes (26% frovatriptan vs. 22% rizatriptan). The number of patients with adverse events was not significantly different between rizatriptan (34) and frovatriptan (25, p = NS). The results suggest that frovatriptan has a similar efficacy to rizatriptan, but a more prolonged duration of action.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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The 1246 GϾA polymorphism of the gene was significantly different between cases and controls. Homozygosity for the G allele was associated with an increased disease risk (OR: 6.79, 95% CI, 2.25 to 22.99). The data suggest that the HCRTR2 gene or a linked locus significantly modulates the risk for cluster headache.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="03aad739205fe06168d1780001585cf8" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295818,"asset_id":104613711,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295818/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613711"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613711"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613711; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613711]").text(description); $(".js-view-count[data-work-id=104613711]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613711; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613711']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "03aad739205fe06168d1780001585cf8" } } $('.js-work-strip[data-work-id=104613711]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613711,"title":"A polymorphism of the hypocretin receptor 2 gene is associated with cluster headache","translated_title":"","metadata":{"publisher":"Ovid Technologies (Wolters Kluwer Health)","ai_title_tag":"Hypocretin Receptor 2 Gene Polymorphism Linked to Cluster Headache","grobid_abstract":"Several polymorphisms of the hypocretin/orexin system genes were evaluated in 109 cluster headache patients and 211 controls. 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Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="adf87eea9862439d3e882e14904b33a1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":104295931,"asset_id":104613709,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/104295931/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613709"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613709"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613709; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613709]").text(description); $(".js-view-count[data-work-id=104613709]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613709; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613709']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "adf87eea9862439d3e882e14904b33a1" } } $('.js-work-strip[data-work-id=104613709]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613709,"title":"Association between tumor necrosis factor-alpha gene promoter polymorphism at position -308 and acne in Turkish patients","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"Background: Tumor necrosis factor-alpha (TNF-α) is an important inflammatory cytokine that may play a role in controlling the progression of prostate cancer. Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Archives of Dermatological Research","grobid_abstract_attachment_id":104295931},"translated_abstract":null,"internal_url":"https://www.academia.edu/104613709/Association_between_tumor_necrosis_factor_alpha_gene_promoter_polymorphism_at_position_308_and_acne_in_Turkish_patients","translated_internal_url":"","created_at":"2023-07-16T03:21:59.551-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":104295931,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/104295931/thumbnails/1.jpg","file_name":"1746-1596-9-74.pdf","download_url":"https://www.academia.edu/attachments/104295931/download_file","bulk_download_file_name":"Association_between_tumor_necrosis_facto.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/104295931/1746-1596-9-74-libre.pdf?1689510967=\u0026response-content-disposition=attachment%3B+filename%3DAssociation_between_tumor_necrosis_facto.pdf\u0026Expires=1743102266\u0026Signature=LWj-rtDxsU2Q9uwACtuLcax5tszEdvrKOxqsku6KbSGB~D7srzoVvTnPzkYwFBqzTUTqdHG6P6p1SIa1iKT10Sckc0ZeRPrfv5Oi22eCtYjSOcLcv~crszaJmZauMWqfW5of5NV6gN0PCSwF2~KBH2GvMvSzBlv-V1r~g34ZrZkwk5fdvhoKHWQ54CJim-PEoPt0q84g45n-JGVmG7K94LWtEDGCMbyCiRVzoAmaodWwAAcffUXkzF1nS34-CEky1nb2lw12cb4Q2TfFNGoHk96hpWtsoNTi27kcg8NrCpTkYACERrXvpibEeVROBnfwJ5EnGAE7Yjaf0Qf~rkn~2A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Association_between_tumor_necrosis_factor_alpha_gene_promoter_polymorphism_at_position_308_and_acne_in_Turkish_patients","translated_slug":"","page_count":11,"language":"en","content_type":"Work","summary":"Background: Tumor necrosis factor-alpha (TNF-α) is an important inflammatory cytokine that may play a role in controlling the progression of prostate cancer. Two common polymorphisms in the TNF-α gene, −308G/A and −238C/T, have been suggested to alter the risk for prostate cancer, but the results have been inconclusive so far. In order to obtain a better understanding of the effects of these two polymorphisms on prostate cancer risk, all available studies were considered in a meta-analysis. Methods: We conducted a comprehensive literature search in the Cochrane Library, PubMed, EMBASE, Chinese Biomedical Literature database (CBM), and the China National Knowledge Infrastructure (CNKI). The associations were evaluated by calculating the pooled odds ratio (OR) with 95% confidence interval (95% CI). Results: In this meta-analysis, we included 14 studies with 5,757 patients and 6,137 control subjects for the TNF-α-308G/A polymorphism and 1,967 patients and 2,004 control subjects for the TNF-α-238C/T polymorphism. A significantly increased prostate cancer risk was found to be associated with the TNF-α-308C/T polymorphism in studies with healthy volunteers (AA + AG vs. GG: OR = 1.531, 95% CI = 1.093-2.145; P = 0.013; AG vs. GG: OR = 1.477, 95% CI = 1.047-2.085; P = 0.026). No significant association was found between the TNF-α-238G/A polymorphism and prostate cancer risk in the overall or subgroup analyses. There was no risk of publication bias in this meta-analysis. Conclusions: Our results suggest that while the TNF-α-238G/A polymorphism may not be associated with prostate cancer the TNF-α-308C/T polymorphism may significantly contribute to prostate cancer susceptibility in healthy volunteers.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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Recent epidemiological studies have shown the existence of a genetic etiology in some cases of Alzheimer&#39;s disease. Several pedigrees with an increased incidence of AD (familial Alzheimer&#39;s disease--FAD) have been described in the literature. Some of these contain sufficient numbers of affected individuals in multiple generations to provide a rigorous argument for an autosomal dominant inheritance of the AD phenotype. FAD pedigrees show several evidences of as phenotypic heterogeneity of the disease. Molecular genetic studies have shown a linkage between several polymorphic DNA markers specific for the pericentromeric region of chromosome 21 and early-onset FAD. In late-onset FAD pedigrees preliminary reports showed evidence for a linkage with chromosome 19 markers. Molecular genetic studies have clearly demonstrated the genetic heterogeneity of fami...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="104613656"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="104613656"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 104613656; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=104613656]").text(description); $(".js-view-count[data-work-id=104613656]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 104613656; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='104613656']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=104613656]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":104613656,"title":"[The genetics of Alzheimer's disease]","translated_title":"","metadata":{"abstract":"This paper examines recent epidemiological and molecular genetic studies on the genetic basis of Alzheimer\u0026#39;s disease (AD). 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Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198052,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.291.7948\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225807"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225807/Salvatore_Gentile"><img alt="Research paper thumbnail of Salvatore Gentile" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Salvatore Gentile</div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We report the case of a patient who developed typical cluster headache attacks and was diagnosed ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We report the case of a patient who developed typical cluster headache attacks and was diagnosed as having multiple scle-rosis (MS) at the same time. The headache attacks resolved after i.v. treatment with methylpred-nisolone. MR imaging showed a pontine demyelinating lesion involving the trigeminal nerve root inlet area, on the same side as the pain. The association between cluster headache and MS has been rarely described before. This case suggests that in patients with clus-ter headache neuroimaging is often useful in order to exclude structur-al lesions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225807"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225807"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225807; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225807]").text(description); $(".js-view-count[data-work-id=93225807]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225807; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225807']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225807]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225807,"title":"Salvatore Gentile","translated_title":"","metadata":{"abstract":"We report the case of a patient who developed typical cluster headache attacks and was diagnosed as having multiple scle-rosis (MS) at the same time. 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The association between cluster headache and MS has been rarely described before. This case suggests that in patients with clus-ter headache neuroimaging is often useful in order to exclude structur-al lesions.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198051,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.775.6094\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225806"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225806/DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply"><img alt="Research paper thumbnail of DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply</div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Ó The Author(s) 2011. This article is published with open access at Springerlink.com</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225806"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225806"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225806; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225806]").text(description); $(".js-view-count[data-work-id=93225806]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225806; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225806']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225806]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225806,"title":"DOI 10.1007/s10194-011-0396-3 LETTER TO THE EDITOR Suggested randomized, controlled trial for frovatriptan: a reply","translated_title":"","metadata":{"abstract":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","publication_date":{"day":null,"month":null,"year":2013,"errors":{}}},"translated_abstract":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","internal_url":"https://www.academia.edu/93225806/DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply","translated_internal_url":"","created_at":"2022-12-19T01:20:45.709-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"DOI_10_1007_s10194_011_0396_3_LETTER_TO_THE_EDITOR_Suggested_randomized_controlled_trial_for_frovatriptan_a_reply","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Ó The Author(s) 2011. This article is published with open access at Springerlink.com","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[],"urls":[{"id":27198050,"url":"http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.288.3445\u0026rep=rep1\u0026type=pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225805"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225805/Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone"><img alt="Research paper thumbnail of Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone</div><div class="wp-workCard_item"><span>Panminerva medica</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225805"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225805"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225805; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225805]").text(description); $(".js-view-count[data-work-id=93225805]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225805; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225805']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225805]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225805,"title":"Detection of Exon 8 mutations in sqstm1/p62 gene by mutation-specific restriction enzyme digestion: a sensitive screening for Paget disease of bone","translated_title":"","metadata":{"publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Panminerva medica"},"translated_abstract":null,"internal_url":"https://www.academia.edu/93225805/Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone","translated_internal_url":"","created_at":"2022-12-19T01:20:45.595-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Detection_of_Exon_8_mutations_in_sqstm1_p62_gene_by_mutation_specific_restriction_enzyme_digestion_a_sensitive_screening_for_Paget_disease_of_bone","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":null,"owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":74780,"name":"Mutation","url":"https://www.academia.edu/Documents/in/Mutation"},{"id":901876,"name":"Sensitivity and Specificity","url":"https://www.academia.edu/Documents/in/Sensitivity_and_Specificity"},{"id":3647178,"name":"DNA Restriction Enzymes","url":"https://www.academia.edu/Documents/in/DNA_Restriction_Enzymes"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225803"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225803/_Neuroendocrinologic_aspects_of_epilepsy_"><img alt="Research paper thumbnail of [Neuroendocrinologic aspects of epilepsy]" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">[Neuroendocrinologic aspects of epilepsy]</div><div class="wp-workCard_item"><span>Minerva medica</span><span>, Jan 3, 1984</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although the literature recognises the involvement of neuropeptide structures in the genesis of e...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225803"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225803]").text(description); $(".js-view-count[data-work-id=93225803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225803,"title":"[Neuroendocrinologic aspects of epilepsy]","translated_title":"","metadata":{"abstract":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","publication_date":{"day":3,"month":1,"year":1984,"errors":{}},"publication_name":"Minerva medica"},"translated_abstract":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","internal_url":"https://www.academia.edu/93225803/_Neuroendocrinologic_aspects_of_epilepsy_","translated_internal_url":"","created_at":"2022-12-19T01:20:45.343-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"_Neuroendocrinologic_aspects_of_epilepsy_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Although the literature recognises the involvement of neuropeptide structures in the genesis of epilepsy, only tentative preliminary data are available at present. Experiments indicate that neuropeptides primarily involved in the genesis of epilepsy are leuencephalin, metencephalin and beta-endorphin. Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances. A qualitative and/or quantitative change to the GABA-neuropeptide balance may also be involved in convulsive disorders; decreased GABA fluid levels have been identified in both severely epileptic patients and infants with febrile convulsions. Neuropeptide modulation and GABAergic neurotransmission clearly therefore play a major role in the regulation of cortical bioelectrical activity. It is therefore likely that their interaction is involved in the genesis of epilepsy.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":161,"name":"Neuroscience","url":"https://www.academia.edu/Documents/in/Neuroscience"},{"id":7648,"name":"Epilepsy","url":"https://www.academia.edu/Documents/in/Epilepsy"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":57556,"name":"Hippocampus","url":"https://www.academia.edu/Documents/in/Hippocampus"},{"id":176503,"name":"Synaptic Transmission","url":"https://www.academia.edu/Documents/in/Synaptic_Transmission"},{"id":219680,"name":"Minerva Medica","url":"https://www.academia.edu/Documents/in/Minerva_Medica"},{"id":651604,"name":"Seizures","url":"https://www.academia.edu/Documents/in/Seizures"},{"id":1530411,"name":"Convulsion","url":"https://www.academia.edu/Documents/in/Convulsion"},{"id":1619808,"name":"Gamma-Aminobutyric Acid","url":"https://www.academia.edu/Documents/in/Gamma-Aminobutyric_Acid"},{"id":2558779,"name":"Gabaergic","url":"https://www.academia.edu/Documents/in/Gabaergic"},{"id":2583478,"name":"Neuropeptide","url":"https://www.academia.edu/Documents/in/Neuropeptide"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225802"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225802/Tumor_Necrosis_Factor_%CE%91_Gene_and_Cerebral_Aneurysms"><img alt="Research paper thumbnail of Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms</div><div class="wp-workCard_item"><span>Neurosurgery</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, im...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225802"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225802"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225802; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225802]").text(description); $(".js-view-count[data-work-id=93225802]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225802; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225802']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225802]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225802,"title":"Tumor Necrosis Factor-Α Gene and Cerebral Aneurysms","translated_title":"","metadata":{"abstract":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_date":{"day":null,"month":null,"year":2007,"errors":{}},"publication_name":"Neurosurgery"},"translated_abstract":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","internal_url":"https://www.academia.edu/93225802/Tumor_Necrosis_Factor_%CE%91_Gene_and_Cerebral_Aneurysms","translated_internal_url":"","created_at":"2022-12-19T01:20:45.199-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Tumor_Necrosis_Factor_Α_Gene_and_Cerebral_Aneurysms","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"The pathogenesis of intracranial aneurysms is still uncertain. In addition to atherosclerosis, immunological factors may play a role in the disease. Recent studies have suggested that tumor necrosis factor-alpha (TNF-alpha), one of the main proinflammatory cytokines, may play a key role in the formation and rupture of cerebral aneurysms. The purpose of this study is to evaluate the association of a functionally active polymorphism (-308 G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) in the TNF-alpha gene with the risk and the clinical features of aneurysmal subarachnoid hemorrhage. A total of 171 consecutive aneurysmal subarachnoid hemorrhage patients and 144 healthy controls were involved in the study. Computed tomographic scan findings were assessed by Fisher grade; clinical neurological assessment was performed using the Hunt and Hess grading system. Patients and controls were genotyped for the-308 biallelic (G\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;A) polymorphism of the TNF-alpha gene. The TNF-alpha G allele was significantly more frequent in patients than in controls (chi2 = 5.59; P = 0.0181) and homozygosity for the G allele, compared with remaining genotypes, was associated with a significantly increased risk of aneurysmal subarachnoid hemorrhage (odds ratio = 2.20; 95% confidence interval = 1.29\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;odds ratio\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;3.75). Allelic and genotypic frequencies of the examined polymorphism were not significantly different in disease subgroups. The different TNF-alpha genotypes do not seem to significantly modify the main clinical features of the disease. Our data suggests that the TNF-alpha gene or a linked locus significantly modulates the risk for aneurysmal subarachnoid hemorrhage. Additional studies in different populations are warranted to confirm our findings.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":650,"name":"Neurosurgery","url":"https://www.academia.edu/Documents/in/Neurosurgery"},{"id":3855,"name":"Polymorphism","url":"https://www.academia.edu/Documents/in/Polymorphism"},{"id":4670,"name":"Pathogenesis","url":"https://www.academia.edu/Documents/in/Pathogenesis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":73153,"name":"Genetic Testing","url":"https://www.academia.edu/Documents/in/Genetic_Testing"},{"id":174502,"name":"Incidence","url":"https://www.academia.edu/Documents/in/Incidence"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":437772,"name":"Odds ratio","url":"https://www.academia.edu/Documents/in/Odds_ratio"},{"id":622589,"name":"Risk Assessment","url":"https://www.academia.edu/Documents/in/Risk_Assessment-2"},{"id":1004200,"name":"Allele","url":"https://www.academia.edu/Documents/in/Allele"},{"id":1159938,"name":"Cerebral Aneurysm","url":"https://www.academia.edu/Documents/in/Cerebral_Aneurysm"},{"id":1239755,"name":"Neurosciences","url":"https://www.academia.edu/Documents/in/Neurosciences"},{"id":2482159,"name":"DNA mutational analysis","url":"https://www.academia.edu/Documents/in/DNA_mutational_analysis"},{"id":3208250,"name":"Intracranial aneurysm","url":"https://www.academia.edu/Documents/in/Intracranial_aneurysm"}],"urls":[{"id":27198049,"url":"https://journals.lww.com/00006123-200704000-00012"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225801"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225801/Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population"><img alt="Research paper thumbnail of Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population</div><div class="wp-workCard_item"><span>Journal of Neurology, Neurosurgery & Psychiatry</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Several lines of evidence indicate a role for inflammatory processes in the development of cerebr...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G&amp;gt;C and -572 G&amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G&amp;lt;C and the -572 G&amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225801"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225801"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225801; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225801]").text(description); $(".js-view-count[data-work-id=93225801]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225801; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225801']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225801]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225801,"title":"Interleukin 6 gene polymorphisms are not associated with aneurysmal subarachnoid haemorrhage in an Italian population","translated_title":"","metadata":{"abstract":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","publisher":"BMJ","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Journal of Neurology, Neurosurgery \u0026 Psychiatry"},"translated_abstract":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","internal_url":"https://www.academia.edu/93225801/Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population","translated_internal_url":"","created_at":"2022-12-19T01:20:45.096-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Interleukin_6_gene_polymorphisms_are_not_associated_with_aneurysmal_subarachnoid_haemorrhage_in_an_Italian_population","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"Several lines of evidence indicate a role for inflammatory processes in the development of cerebral aneurysms. Recently, polymorphisms in the promoter region of the interleukin 6 (IL6) gene were shown to be associated with intracranial aneurysmal disease. The purpose of this study was to verify the association of two functionally active polymorphisms (-174 G\u0026amp;gt;C and -572 G\u0026amp;gt;C) in the promoter region of the IL6 gene with the risk and clinical features of aneurysmal subarachnoid haemorrhage (SAH) in an Italian population. A total of 179 consecutive aneurysmal SAH patients and 156 healthy controls were involved in the study. Cases and controls were genotyped for the -174 G\u0026amp;lt;C and the -572 G\u0026amp;lt;C biallelic polymorphisms of the IL6 gene. The frequencies of different promoter haplotypes were compared between cases and controls. Allelic and genotypic frequencies of the examined polymorphism were not significantly different between cases and controls. Inferred haplotypes were not significantly different in both groups. Finally, the different IL6 genotypes did not seem to significantly modify the main clinical features of the disease. Our study did not confirm the association between functionally active polymorphisms in the IL6 gene and the risk of aneurysmal SAH in an Italian population. Additional studies in different populations are warranted to clarify the role of the IL6 gene in the pathogenesis of aneurysmal SAH.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":45213,"name":"Italy","url":"https://www.academia.edu/Documents/in/Italy"},{"id":67362,"name":"Italian","url":"https://www.academia.edu/Documents/in/Italian"},{"id":86952,"name":"Haplotypes","url":"https://www.academia.edu/Documents/in/Haplotypes"},{"id":99773,"name":"Disease","url":"https://www.academia.edu/Documents/in/Disease"},{"id":223022,"name":"Italiano","url":"https://www.academia.edu/Documents/in/Italiano"},{"id":289271,"name":"Aged","url":"https://www.academia.edu/Documents/in/Aged"},{"id":306990,"name":"Gene Polymorphism","url":"https://www.academia.edu/Documents/in/Gene_Polymorphism"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":1004200,"name":"Allele","url":"https://www.academia.edu/Documents/in/Allele"},{"id":1591688,"name":"Haplotype","url":"https://www.academia.edu/Documents/in/Haplotype"},{"id":1924712,"name":"Interleukin","url":"https://www.academia.edu/Documents/in/Interleukin"},{"id":3203621,"name":"Gene frequency","url":"https://www.academia.edu/Documents/in/Gene_frequency"},{"id":3208250,"name":"Intracranial aneurysm","url":"https://www.academia.edu/Documents/in/Intracranial_aneurysm"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225800"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" rel="nofollow" href="https://www.academia.edu/93225800/Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache"><img alt="Research paper thumbnail of Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title">Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache</div><div class="wp-workCard_item"><span>Headache: The Journal of Head and Face Pain</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P&amp;amp;amp;lt;0.01 and &amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225800"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225800"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225800; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225800]").text(description); $(".js-view-count[data-work-id=93225800]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225800; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225800']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=93225800]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225800,"title":"Decreased Sensitivity of 5-HT1D Receptors in Chronic Tension-Type Headache","translated_title":"","metadata":{"abstract":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Headache: The Journal of Head and Face Pain"},"translated_abstract":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","internal_url":"https://www.academia.edu/93225800/Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache","translated_internal_url":"","created_at":"2022-12-19T01:20:44.967-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Decreased_Sensitivity_of_5_HT1D_Receptors_in_Chronic_Tension_Type_Headache","translated_slug":"","page_count":null,"language":"en","content_type":"Work","summary":"To assess the sensitivity of 5-HT1D receptors in chronic tension-type headache using sumatriptan as a pharmacological probe. Previous studies have suggested involvement of serotonergic systems in chronic tension-type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5-HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo. We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension-type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo. Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P\u0026amp;amp;amp;lt;0.01 and \u0026amp;amp;amp;lt;0.05) altered in CTTH patients in comparison with controls. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in CTTH.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. Pinessi","url":"https://unito.academia.edu/LPinessi"},"attachments":[],"research_interests":[{"id":154,"name":"Endocrinology","url":"https://www.academia.edu/Documents/in/Endocrinology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":52562,"name":"Growth Hormone","url":"https://www.academia.edu/Documents/in/Growth_Hormone"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":64657,"name":"Prolactin","url":"https://www.academia.edu/Documents/in/Prolactin"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":72938,"name":"Placebo","url":"https://www.academia.edu/Documents/in/Placebo"},{"id":97269,"name":"Chronic Disease","url":"https://www.academia.edu/Documents/in/Chronic_Disease"},{"id":103107,"name":"Migraine","url":"https://www.academia.edu/Documents/in/Migraine"},{"id":103108,"name":"Headache","url":"https://www.academia.edu/Documents/in/Headache"},{"id":161176,"name":"The","url":"https://www.academia.edu/Documents/in/The"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":312279,"name":"Serotonin Receptors","url":"https://www.academia.edu/Documents/in/Serotonin_Receptors"},{"id":612548,"name":"Tension-Type Headache","url":"https://www.academia.edu/Documents/in/Tension-Type_Headache"},{"id":1961440,"name":"Agonist","url":"https://www.academia.edu/Documents/in/Agonist"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="93225799"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease"><img alt="Research paper thumbnail of Autonomic responses and pain perception in Alzheimer’s disease" class="work-thumbnail" src="https://attachments.academia-assets.com/96021233/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease">Autonomic responses and pain perception in Alzheimer’s disease</a></div><div class="wp-workCard_item"><span>European Journal of Pain</span><span>, 2000</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzh...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9da47f564d41fe3f358440b42dd88cc7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":96021233,"asset_id":93225799,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/96021233/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="93225799"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="93225799"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 93225799; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=93225799]").text(description); $(".js-view-count[data-work-id=93225799]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 93225799; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='93225799']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "9da47f564d41fe3f358440b42dd88cc7" } } $('.js-work-strip[data-work-id=93225799]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":93225799,"title":"Autonomic responses and pain perception in Alzheimer’s disease","translated_title":"","metadata":{"publisher":"Wiley","ai_title_tag":"Autonomic Responses and Pain in Alzheimer’s Disease","grobid_abstract":"We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.","publication_date":{"day":null,"month":null,"year":2000,"errors":{}},"publication_name":"European Journal of Pain","grobid_abstract_attachment_id":96021233},"translated_abstract":null,"internal_url":"https://www.academia.edu/93225799/Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease","translated_internal_url":"","created_at":"2022-12-19T01:20:44.758-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32055065,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":96021233,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/96021233/thumbnails/1.jpg","file_name":"eujp.2000.018520221219-1-wz36l9.pdf","download_url":"https://www.academia.edu/attachments/96021233/download_file","bulk_download_file_name":"Autonomic_responses_and_pain_perception.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/96021233/eujp.2000.018520221219-1-wz36l9-libre.pdf?1671447353=\u0026response-content-disposition=attachment%3B+filename%3DAutonomic_responses_and_pain_perception.pdf\u0026Expires=1743102266\u0026Signature=LV-ojb7w1hC6RJ32wX7MBhIstKNg2Z9RTkBCmVGdKCmZfq3zLQu3M3FmUFoFLoX0jiIYwrEpp3crpCVDrd-apQ4r-IYNImD6Lz~iWaDDy0O5t5Lgf31MWJ3NA4hEz8T194Hrn3pRYVrZ8SKuxATazejf~jogUsjpD5Gwdt9Iz~r5omLmZZtXJYBuL8PRVnSyiyetOWu-81GZ1C7JHQOhytqPDMTEC4J70B58jludJ0hoTzJIA9VCr4VwDTWgazVnkt3cOfSEgyFmLK6UAx8OZkZj6mfdL-IeaKP4XcLvvgCpz09WRk6fmoMr6dhDAgchb0QXobnLxAYS10FpXugdng__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Autonomic_responses_and_pain_perception_in_Alzheimer_s_disease","translated_slug":"","page_count":8,"language":"en","content_type":"Work","summary":"We analysed the effects of electrical noxious stimulation on the autonomic nervous system of Alzheimer's disease (AD) patients who were assessed by means of the Mini Mental State Examination test (MMSE). To do this, we used electrical stimuli at two different intensities: just above pain threshold and twice pain threshold. We recorded heart rate and systolic blood pressure by using conventional electrocardiography and finger photo-plethysmography. When a pain stimulus just above threshold was delivered, AD patients were found to have blunted autonomic responses compared to controls of the same age. Similarly, prestimulus expectation produced a less pronounced increase of the responses in AD patients compared to the controls. However, when the painful stimulus was increased to twice the pain threshold, the systolic blood pressure increase of AD patients did not differ from the controls, whereas heart rate increase was still slightly diminished. By contrast, pain perception was similar in the two groups when the stimulus was at pain threshold, whereas it was blunted in AD patients when the stimulus was twice the pain threshold. These findings show that in AD mild noxious stimulation produces blunted autonomic responses and normal pain perception, whereas strong noxious stimulation produces quasi-normal autonomic responses and blunted pain perception. These results indicate that AD patients have an increased threshold for both autonomic activation and pain tolerance.","owner":{"id":32055065,"first_name":"L.","middle_initials":null,"last_name":"Pinessi","page_name":"LPinessi","domain_name":"unito","created_at":"2015-06-10T02:16:45.282-07:00","display_name":"L. 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