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class="profile--tab_heading_container">Papers by Mohammad Ebrahimkhani</h3></div><div class="js-work-strip profile--work_container" data-work-id="102073320"><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/102073320/Genetically_engineering_self_organization_of_human_pluripotent_stem_cells_into_a_liver_bud_like_tissue_using_Gata6"><img alt="Research paper thumbnail of Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6" class="work-thumbnail" src="https://attachments.academia-assets.com/102435689/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/102073320/Genetically_engineering_self_organization_of_human_pluripotent_stem_cells_into_a_liver_bud_like_tissue_using_Gata6">Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6</a></div><div class="wp-workCard_item"><span>Nature communications</span><span>, Jan 6, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative me...</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">Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative medicine. While most of the methods using these cells have focused on deriving homogenous populations of specialized cells, there has been modest success in producing hiPSC-derived organotypic tissues or organoids. Here we present a novel approach for generating and then co-differentiating hiPSC-derived progenitors. With a genetically engineered pulse of GATA-binding protein 6 (GATA6) expression, we initiate rapid emergence of all three germ layers as a complex function of GATA6 expression levels and tissue context. Within 2 weeks we obtain a complex tissue that recapitulates early developmental processes and exhibits a liver bud-like phenotype, including haematopoietic and stromal cells as well as a neuronal niche. Collectively, our approach demonstrates derivation of complex tissues from hiPSCs using a single autologous hiPSCs as source and generates a range of stromal cells that co-deve...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3ecd9e8fc66ab30439fd0363cd26cfb3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435689,"asset_id":102073320,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435689/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073320"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073320"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073320; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073320]").text(description); $(".js-view-count[data-work-id=102073320]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073320; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073320']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073320, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "3ecd9e8fc66ab30439fd0363cd26cfb3" } } $('.js-work-strip[data-work-id=102073320]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073320,"title":"Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6","translated_title":"","metadata":{"abstract":"Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative medicine. 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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" rel="nofollow" href="https://www.academia.edu/102073317/342810_Lung_Liver_Interactions_A_Multi_Scale_In_Vitro_Systems_Analysis">342810 Lung-Liver Interactions: A Multi-Scale In Vitro Systems Analysis</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Individual cells integrate many external cues — including those that arise from various extracell...</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">Individual cells integrate many external cues — including those that arise from various extracellular matrix components, mechanical stimulation and soluble signals from adjacent and even distant cells — to generate a basal phenotype and respond to perturbations in their environment [1]. Yet, to capture the complexity of human physiology in vitro demands the evaluation of interacting cell types coexisting in a hierarchical 3-dimensional structure influenced by gradients in nutrients, mechanics, and cell composition. Ultimately, to computationally model integrated responses of multiple cells types (including immune cells) requires the need to assess systems under both homeostatic and pathologic conditions. In this study, we propose to integrate communication between lung-liver tissue modules. 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Res.</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9af0ec3e3e659e8f4d4f66b3d529c5d9" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435686,"asset_id":102073315,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435686/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073315"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073315"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073315; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073315]").text(description); $(".js-view-count[data-work-id=102073315]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073315; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073315']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073315, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "9af0ec3e3e659e8f4d4f66b3d529c5d9" } } $('.js-work-strip[data-work-id=102073315]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073315,"title":"A reversible model for periportal fibrosis and a refined alternative to bile duct ligation","translated_title":"","metadata":{"publisher":"Oxford University Press (OUP)","grobid_abstract":"MC. 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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="102073314"><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/102073314/Effect_of_morphine_on_ischemia_reperfusion_injury_Experimental_study_in_testicular_torsion_rat_model"><img alt="Research paper thumbnail of Effect of morphine on ischemia-reperfusion injury: Experimental study in testicular torsion rat model" class="work-thumbnail" src="https://attachments.academia-assets.com/102435687/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/102073314/Effect_of_morphine_on_ischemia_reperfusion_injury_Experimental_study_in_testicular_torsion_rat_model">Effect of morphine on ischemia-reperfusion injury: Experimental study in testicular torsion rat model</a></div><div class="wp-workCard_item"><span>Urology</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="629ce1d54a66f6204a541da940f8cfe5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435687,"asset_id":102073314,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435687/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073314"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073314"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073314; 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "629ce1d54a66f6204a541da940f8cfe5" } } $('.js-work-strip[data-work-id=102073314]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073314,"title":"Effect of morphine on ischemia-reperfusion injury: Experimental study in testicular torsion rat model","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Objectives. To investigate the effects of morphine on reperfusion injury due to testicular torsion-detorsion (T/D). Methods. We divided 36 adult male Sprague-Dawley rats into six groups. Testicular ischemia was achieved by twisting the right testis 720°counterclockwise for 1 hour, and reperfusion was allowed for 4 hours after detorsion. The baseline group was for basal normal values. The sham-operated group served as the control group. The T/D group underwent 1 hour of testicular torsion and 4 hours of detorsion. The morphine group received pretreatment with intravenous morphine sulfate (10 mg/kg) just before detorsion. The naltrexone group received an intravenous injection of naltrexone HCl (20 mg/kg) 15 minutes before detorsion. The naltrexone/morphine group received intravenous administration of naltrexone HCl (20 mg/kg) 15 minutes before detorsion and morphine sulfate (10 mg/kg) just before detorsion. Results. The ipsilateral malondialdehyde levels in the T/D group were significantly greater than in the control and baseline groups. Moreover, the ipsilateral testicular malondialdehyde values in the morphine group were significantly lower than in the T/D and naltrexone/morphine groups. Also, significant decreases occurred in catalase and superoxide dismutase activities in the T/D group compared with the control and baseline groups. These values were significantly greater in the morphine group than in the T/D and naltrexone/morphine groups. The ipsilateral testes of all groups that underwent testicular torsion showed similar histopathologic changes. Conclusions. Morphine increased the ipsilateral intratesticular antioxidant markers during the reperfusion phase after unilateral testicular torsion, which was eventually reflected in lower testicular malondialdehyde levels. 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class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/102073312/All_human_microphysical_model_of_metastasis_therapy"><img alt="Research paper thumbnail of All-human microphysical model of metastasis therapy" class="work-thumbnail" src="https://attachments.academia-assets.com/102435656/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/102073312/All_human_microphysical_model_of_metastasis_therapy">All-human microphysical model of metastasis therapy</a></div><div class="wp-workCard_item"><span>Stem Cell Research &amp; Therapy</span><span>, 2013</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9a720bfa0aeb168ae5855381ee282f54" 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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/102073310/CRISPR_transcriptional_repression_devices_and_layered_circuits_in_mammalian_cells"><img alt="Research paper thumbnail of CRISPR transcriptional repression devices and layered circuits in mammalian cells" class="work-thumbnail" src="https://attachments.academia-assets.com/102435685/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/102073310/CRISPR_transcriptional_repression_devices_and_layered_circuits_in_mammalian_cells">CRISPR transcriptional repression devices and layered circuits in mammalian cells</a></div><div class="wp-workCard_item"><span>Nature Methods</span><span>, 2014</span></div><div class="wp-workCard_item 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in mammalian cells","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"A key obstacle to creating sophisticated genetic circuits has been the lack of scalable device libraries. Here we present a modular transcriptional repression architecture based on clustered regularly interspaced palindromic repeats (CRISPR) system and examine approaches for regulated expression of guide RNAs in human cells. Subsequently we demonstrate that CRISPR regulatory devices can be layered to create functional cascaded circuits, which provide a valuable toolbox for engineering purposes. Engineered biological circuits provide insights into the underlying biology of living cells and offer potential solutions to a range of medical and industrial challenges 1, 2. A prerequisite for efficient engineering of such sophisticated circuits is the availability of a library of regulatory devices that can be connected in various contexts to create new and Correspondence should be addressed to R.W.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Nature 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href="https://www.academia.edu/102073309/Stimulating_healthy_tissue_regeneration_by_targeting_the_5_HT2B_receptor_in_chronic_liver_disease"><img alt="Research paper thumbnail of Stimulating healthy tissue regeneration by targeting the 5-HT2B receptor in chronic liver disease" class="work-thumbnail" src="https://attachments.academia-assets.com/102435702/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/102073309/Stimulating_healthy_tissue_regeneration_by_targeting_the_5_HT2B_receptor_in_chronic_liver_disease">Stimulating healthy tissue regeneration by targeting the 5-HT2B receptor in chronic liver disease</a></div><div class="wp-workCard_item"><span>Nature Medicine</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span 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class="js-work-strip profile--work_container" data-work-id="102073308"><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/102073308/Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells"><img alt="Research paper thumbnail of Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073308/Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells">Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells</a></div><div class="wp-workCard_item"><span>Molecular and Cellular Biochemistry</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The level of activity of the telomerase has been shown to correlate with the degree of invasivene...</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 level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. In addition, cellular redox state is believed to regulate the secretion of matrix metalloproteinase-2 (MMP-2). To determine the effect of anti-sense telomerase treatment of prostate cancer cells on MMP-2 activity, and the reactive oxygen and nitrogen species (two effectors of cellular redox state). Anti-sense oligonucleotide against RNA component of human telomerase (hTR) was introduced into the cells using Fugene-6 transfection reagent. The activity of telomerase was assessed using Telomere Repeat Amplification Protocol (TRAP assay). Activity of matrix metalloproteinase-2 (MMP-2) was determined by zymography. Levels of intracellular reactive oxygen species (ROS) and nitric oxide metabolites were measured by dichlorofluorescein diacetate (DCFH-DA) staining and Griess reagent, respectively. The level of apoptosis was determined using TUNEL assay. TRAP assay showed more than 90% inhibition of telomerase activity after 72 h of transfection. Pro-MMP-2 activity was decreased down to 50% of the control levels. Intracellular reactive oxygen species were also significantly decreased. Neither apoptosis rate nor the level of nitric oxide metabolites was significantly different between anti-sense treated and control cells. Concomitant reduction of the pro-MMP-2 secretion and ROS in PC-3 cells following hTR inhibition suggests that over-activity of telomerase in cancer cells might increase the level of matrix metalloproteinase-2 and thus, be directly involved in the invasion process through enhancement of intracellular oxidative stress.</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="102073308"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073308"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073308; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073308]").text(description); $(".js-view-count[data-work-id=102073308]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073308; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073308']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073308, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073308]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073308,"title":"Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells","translated_title":"","metadata":{"abstract":"The level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. In addition, cellular redox state is believed to regulate the secretion of matrix metalloproteinase-2 (MMP-2). To determine the effect of anti-sense telomerase treatment of prostate cancer cells on MMP-2 activity, and the reactive oxygen and nitrogen species (two effectors of cellular redox state). Anti-sense oligonucleotide against RNA component of human telomerase (hTR) was introduced into the cells using Fugene-6 transfection reagent. The activity of telomerase was assessed using Telomere Repeat Amplification Protocol (TRAP assay). Activity of matrix metalloproteinase-2 (MMP-2) was determined by zymography. Levels of intracellular reactive oxygen species (ROS) and nitric oxide metabolites were measured by dichlorofluorescein diacetate (DCFH-DA) staining and Griess reagent, respectively. The level of apoptosis was determined using TUNEL assay. TRAP assay showed more than 90% inhibition of telomerase activity after 72 h of transfection. Pro-MMP-2 activity was decreased down to 50% of the control levels. Intracellular reactive oxygen species were also significantly decreased. Neither apoptosis rate nor the level of nitric oxide metabolites was significantly different between anti-sense treated and control cells. Concomitant reduction of the pro-MMP-2 secretion and ROS in PC-3 cells following hTR inhibition suggests that over-activity of telomerase in cancer cells might increase the level of matrix metalloproteinase-2 and thus, be directly involved in the invasion process through enhancement of intracellular oxidative stress.","publisher":"Springer Nature","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Molecular and Cellular Biochemistry"},"translated_abstract":"The level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. In addition, cellular redox state is believed to regulate the secretion of matrix metalloproteinase-2 (MMP-2). To determine the effect of anti-sense telomerase treatment of prostate cancer cells on MMP-2 activity, and the reactive oxygen and nitrogen species (two effectors of cellular redox state). Anti-sense oligonucleotide against RNA component of human telomerase (hTR) was introduced into the cells using Fugene-6 transfection reagent. The activity of telomerase was assessed using Telomere Repeat Amplification Protocol (TRAP assay). Activity of matrix metalloproteinase-2 (MMP-2) was determined by zymography. Levels of intracellular reactive oxygen species (ROS) and nitric oxide metabolites were measured by dichlorofluorescein diacetate (DCFH-DA) staining and Griess reagent, respectively. The level of apoptosis was determined using TUNEL assay. TRAP assay showed more than 90% inhibition of telomerase activity after 72 h of transfection. Pro-MMP-2 activity was decreased down to 50% of the control levels. Intracellular reactive oxygen species were also significantly decreased. Neither apoptosis rate nor the level of nitric oxide metabolites was significantly different between anti-sense treated and control cells. Concomitant reduction of the pro-MMP-2 secretion and ROS in PC-3 cells following hTR inhibition suggests that over-activity of telomerase in cancer cells might increase the level of matrix metalloproteinase-2 and thus, be directly involved in the invasion process through enhancement of intracellular oxidative stress.","internal_url":"https://www.academia.edu/102073308/Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells","translated_internal_url":"","created_at":"2023-05-20T06:51:45.211-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":14292,"name":"Oxidative Stress","url":"https://www.academia.edu/Documents/in/Oxidative_Stress"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":39865,"name":"Telomerase","url":"https://www.academia.edu/Documents/in/Telomerase"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":1186610,"name":"DNA binding proteins","url":"https://www.academia.edu/Documents/in/DNA_binding_proteins"},{"id":1256747,"name":"Oxidation-Reduction","url":"https://www.academia.edu/Documents/in/Oxidation-Reduction"},{"id":1296969,"name":"Molecular and Cellular Biochemistry","url":"https://www.academia.edu/Documents/in/Molecular_and_Cellular_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1920779,"name":"Matrix Metalloproteinase","url":"https://www.academia.edu/Documents/in/Matrix_Metalloproteinase"},{"id":3143442,"name":"Prostate carcinoma","url":"https://www.academia.edu/Documents/in/Prostate_carcinoma"},{"id":3205111,"name":"Prostatic neoplasms","url":"https://www.academia.edu/Documents/in/Prostatic_neoplasms"},{"id":3978516,"name":"Telomerase Reverse Transcriptase","url":"https://www.academia.edu/Documents/in/Telomerase_Reverse_Transcriptase"},{"id":4045320,"name":"Matrix metalloproteinase inhibitors","url":"https://www.academia.edu/Documents/in/Matrix_metalloproteinase_inhibitors"}],"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="102073307"><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/102073307/Homocysteine_alterations_in_experimental_cholestasis_and_its_subsequent_cirrhosis"><img alt="Research paper thumbnail of Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis" class="work-thumbnail" src="https://attachments.academia-assets.com/102435703/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/102073307/Homocysteine_alterations_in_experimental_cholestasis_and_its_subsequent_cirrhosis">Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="840fb7ee728130fb860b841d40d7aeae" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435703,"asset_id":102073307,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435703/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073307"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073307"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073307; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073307]").text(description); $(".js-view-count[data-work-id=102073307]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073307; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073307']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073307, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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); 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Impaired liver function can alter Hcy metabolism. The aim of the present study was to determine plasma Hcy alterations in acute obstructive cholestasis and the subsequent biliary cirrhosis. Cholestasis was induced by bile duct ligation and sham-operated and unoperated rats were used as controls. The animals were studied on the days 7th, 14th, 21st and 28th after the operation. Plasma Hcy, cysteine, methionine, nitric oxide (NO) and liver S-adenosyl-methionine (SAM), S-adenosyl-homocysteine (SAH), SAM to SAH ratio and glutathione were measured. Chronic L-NAME treatment was also included in the study. Plasma Hcy concentrations were transiently elevated by the day 14th after bile duct ligation (P b 0.01) and subsequently returned to control levels. Similar relative fluctuations in plasma Hcy were observed in BDL rats after intraperitoneal methionine overload. Plasma methionine, cysteine and nitrite and nitrate were significantly increased after bile duct ligation. SAM to SAH ratio was diminished by the 1st week of cholestasis and remained significantly decreased throughout the study. These events were accompanied by a decrease in GSH to GSSG ratio in the liver. Chronic L-NAME treatment improved SAM to SAH ratio and prevented the elevation of plasma Hcy and methionine (P b 0.05) while couldn't influence the other parameters. In conclusion, this study demonstrates alterations in plasma Hcy and liver SAM and SAH contents in precirrhotic","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Life 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Sciences","url":"https://www.academia.edu/Documents/in/Life_Sciences"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":118450,"name":"Glutathione","url":"https://www.academia.edu/Documents/in/Glutathione"},{"id":165519,"name":"Liver Function","url":"https://www.academia.edu/Documents/in/Liver_Function"},{"id":195983,"name":"Homocysteine","url":"https://www.academia.edu/Documents/in/Homocysteine"},{"id":413194,"name":"Analysis of 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="102073306"><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/102073306/Obstructive_cholestasis_alters_intestinal_transit_in_mice_role_of_opioid_system"><img alt="Research paper thumbnail of Obstructive cholestasis alters intestinal transit in mice: role of opioid system" class="work-thumbnail" src="https://attachments.academia-assets.com/102435699/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/102073306/Obstructive_cholestasis_alters_intestinal_transit_in_mice_role_of_opioid_system">Obstructive cholestasis alters intestinal transit in mice: role of opioid system</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a7c46ceb029b7d87e82d5770582ccab5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435699,"asset_id":102073306,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435699/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073306"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073306"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073306; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073306]").text(description); $(".js-view-count[data-work-id=102073306]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073306; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073306']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + 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WowProfile.WorkStripView({ el: this, workJSON: {"id":102073306,"title":"Obstructive cholestasis alters intestinal transit in mice: role of opioid system","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Acute cholestasis is associated with increased activity of the endogenous opioid system. It is also known that opioid receptor agonists like morphine decrease the intestinal transit. The purpose of the present study was to investigate the effect of cholestasis on the small intestine transit and the possible involvement of opioid system in this phenomenon in mice. Cholestasis was induced by bile duct-ligation and intestinal transit was measured with charcoal meal and calculation of percent of transit through small intestine. The effect of chronic administration of naltrexone and acute pretreatment with morphine on intestinal transit was evaluated in bile duct-ligated (BDL) as well as unoperated (CTL) and sham-operated (SHAM) animals. The plasma alkaline phosphatase and alanine aminotransferase activities were also measured. A significant decrease in small intestine transit (%transit) was observed in BDL mice compared to SHAM animals, which was prominent even after 24 h of cholestasis. Chronic pretreatment with an opioid receptor antagonist, naltrexone, (10 mg/kg, i.p for 2, 4 or 6 days) completely restored the cholestasis-induced decrease in %transit to that of control animals. Although the acute administration of morphine (2 mg/kg, s.c.) 20 min before charcoal feeding caused a significant decrease in the intestinal transit of CTL and SHAM animals, it did not decrease the %transit of BDL animals on the day 5 after operation. Our findings show that acute cholestasis is associated with a prominent decrease in small intestine transit in mice and opioid receptors maybe involved in this phenomenon.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Life 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/></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/102073305/The_c_Rel_subunit_of_nuclear_factor_%CE%BAB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation">The c-Rel subunit of nuclear factor-κB regulates murine liver inflammation, wound-healing, and hepatocyte proliferation</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in l...</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 this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.</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="102073305"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073305"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073305; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073305]").text(description); $(".js-view-count[data-work-id=102073305]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073305; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073305']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073305, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073305]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073305,"title":"The c-Rel subunit of nuclear factor-κB regulates murine liver inflammation, wound-healing, and hepatocyte proliferation","translated_title":"","metadata":{"abstract":"In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Hepatology"},"translated_abstract":"In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.","internal_url":"https://www.academia.edu/102073305/The_c_Rel_subunit_of_nuclear_factor_%CE%BAB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation","translated_internal_url":"","created_at":"2023-05-20T06:51:44.540-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"The_c_Rel_subunit_of_nuclear_factor_κB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":8991,"name":"Wound Healing","url":"https://www.academia.edu/Documents/in/Wound_Healing"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37773,"name":"Hepatology","url":"https://www.academia.edu/Documents/in/Hepatology"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":144048,"name":"Hepatitis","url":"https://www.academia.edu/Documents/in/Hepatitis"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":404319,"name":"Liver regeneration","url":"https://www.academia.edu/Documents/in/Liver_regeneration"},{"id":432593,"name":"Hepatocytes","url":"https://www.academia.edu/Documents/in/Hepatocytes"},{"id":664203,"name":"Hepatocyte","url":"https://www.academia.edu/Documents/in/Hepatocyte"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":2922788,"name":"Liver injury","url":"https://www.academia.edu/Documents/in/Liver_injury"},{"id":3789880,"name":"Medical biochemistry and metabolomics","url":"https://www.academia.edu/Documents/in/Medical_biochemistry_and_metabolomics"}],"urls":[{"id":31597727,"url":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fhep.23385"}]}, 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="102073303"><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/102073303/Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver"><img alt="Research paper thumbnail of Wound healing and local neuroendocrine regulation in the injured liver" class="work-thumbnail" src="https://attachments.academia-assets.com/102435681/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/102073303/Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver">Wound healing and local neuroendocrine regulation in the injured liver</a></div><div class="wp-workCard_item"><span>Expert Reviews in Molecular Medicine</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hepatic wound-healing response is a complex process involving many different cell types and f...</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 hepatic wound-healing response is a complex process involving many different cell types and factors. It leads to the formation of excessive matrix and a fibrotic scar, which ultimately disrupts proper functioning of the liver and establishes cirrhosis. Activated hepatic myofibroblasts, which are derived from cells such as hepatic stellate cells (HSCs), play a key role in this process. Upon chronic liver injury, there is an upregulation in the local neuroendocrine system and it has recently been demonstrated that activated HSCs express specific receptors and respond to different components of this system. Neuroendocrine factors and their receptors participate in a complex network that modulates liver inflammation and wound healing, and controls the development and progression of liver fibrosis. The first part of this review provides an overview of the molecular mechanisms governing hepatic wound healing. In the second section, we explore important components of the hepatic neuroe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9bbe3019d6cf15fc0d67d322dc955eb9" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435681,"asset_id":102073303,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435681/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073303"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073303"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073303; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073303]").text(description); $(".js-view-count[data-work-id=102073303]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073303; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073303']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073303, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "9bbe3019d6cf15fc0d67d322dc955eb9" } } $('.js-work-strip[data-work-id=102073303]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073303,"title":"Wound healing and local neuroendocrine regulation in the injured liver","translated_title":"","metadata":{"abstract":"The hepatic wound-healing response is a complex process involving many different cell types and factors. 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In the second section, we explore important components of the hepatic neuroe...","publisher":"Cambridge University Press (CUP)","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Expert Reviews in Molecular Medicine"},"translated_abstract":"The hepatic wound-healing response is a complex process involving many different cell types and factors. It leads to the formation of excessive matrix and a fibrotic scar, which ultimately disrupts proper functioning of the liver and establishes cirrhosis. Activated hepatic myofibroblasts, which are derived from cells such as hepatic stellate cells (HSCs), play a key role in this process. Upon chronic liver injury, there is an upregulation in the local neuroendocrine system and it has recently been demonstrated that activated HSCs express specific receptors and respond to different components of this system. Neuroendocrine factors and their receptors participate in a complex network that modulates liver inflammation and wound healing, and controls the development and progression of liver fibrosis. The first part of this review provides an overview of the molecular mechanisms governing hepatic wound healing. 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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="102073302"><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/102073302/Matrix_metalloproteinase_2_secretion_in_WEHI_164_fibrosarcoma_cells_is_nitric_oxide_related_and_modified_by_morphine"><img alt="Research paper thumbnail of Matrix metalloproteinase 2 secretion in WEHI 164 fibrosarcoma cells is nitric oxide-related and modified by morphine" class="work-thumbnail" src="https://attachments.academia-assets.com/102435694/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/102073302/Matrix_metalloproteinase_2_secretion_in_WEHI_164_fibrosarcoma_cells_is_nitric_oxide_related_and_modified_by_morphine">Matrix metalloproteinase 2 secretion in WEHI 164 fibrosarcoma cells is nitric oxide-related and modified by morphine</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3d8d2d9298739f9beca00567722eadbe" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435694,"asset_id":102073302,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435694/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073302"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073302"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073302; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073302]").text(description); $(".js-view-count[data-work-id=102073302]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073302; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073302']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073302, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "3d8d2d9298739f9beca00567722eadbe" } } $('.js-work-strip[data-work-id=102073302]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073302,"title":"Matrix metalloproteinase 2 secretion in WEHI 164 fibrosarcoma cells is nitric oxide-related and modified by morphine","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Matrix metalloproteinases (MMP) are ubiquitous enzymes involved in extracellular matrix remodeling, and as a consequence in a number of physiological and pathological states, including development, wound healing and cancer. A crucial feature of cancer progression and metastasis is the disruption of extracellular matrix, and spreading of proliferating cancer cells. Modulation of MMP is a main target of cancer research. Using the mouse fibrosarcoma cell line WEHI 164, producing high amounts of MMP-2, we investigated whether we could modulate its production. We report that MMP-2 is under the control of nitric oxide (NO)/nitric oxide synthase (NOS) system. In addition, we show that NOS activity is controlled by opioids in a non-opioid receptor-related manner. Finally, we provide evidence that morphine, when administrated at low, non-toxic concentrations (b 10 − 9 M) attenuates MMP-2 activity. We conclude that, as morphine is able to decrease metalloproteinase activity via the NO/ NOS system, it may have a place in the treatment of several sarcomas including fibrosarcoma.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"European Journal of 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Metalloproteinase","url":"https://www.academia.edu/Documents/in/Matrix_Metalloproteinase"},{"id":4045320,"name":"Matrix metalloproteinase inhibitors","url":"https://www.academia.edu/Documents/in/Matrix_metalloproteinase_inhibitors"}],"urls":[{"id":31597726,"url":"https://api.elsevier.com/content/article/PII:S0014299905012458?httpAccept=text/xml"}]}, 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="102073301"><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/102073301/Potentiation_of_anandamide_effects_in_mesenteric_beds_isolated_from_bile_duct_ligated_rats_role_of_nitric_oxide"><img alt="Research paper thumbnail of Potentiation of anandamide effects in mesenteric beds isolated from bile duct-ligated rats: role of nitric oxide" class="work-thumbnail" src="https://attachments.academia-assets.com/102435722/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/102073301/Potentiation_of_anandamide_effects_in_mesenteric_beds_isolated_from_bile_duct_ligated_rats_role_of_nitric_oxide">Potentiation of anandamide effects in mesenteric beds isolated from bile duct-ligated rats: role of nitric oxide</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f23e08014898ac685d381dbc4249c5f3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "f23e08014898ac685d381dbc4249c5f3" } } $('.js-work-strip[data-work-id=102073301]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073301,"title":"Potentiation of anandamide effects in mesenteric beds isolated from bile duct-ligated rats: role of nitric oxide","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Changes in vascular responsiveness are proposed as the basis for some of the cardiovascular complications in cholestasis. Cholestasis is also associated with accumulation of endogenous opioid peptides and evidence of nitric oxide (NO) overproduction. On the other hand, it is well known that anandamide, an endogenous cannabinoid ligand, causes hypotension and a decrease in systemic vascular resistance. In the present study, the possible role of the cannabinoid system in cholestasis-induced mesenteric vascular bed responsiveness was investigated. Mesenteric arteries of bile duct-ligated and sham-operated rats receiving daily administrations of saline were used for evaluating phenylephrine or anandamide dose-response, acute effects of N G-nitro-L-arginine methyl ester (L-NAME, 100 AM), a non-selective inhibitor of NO synthase (NOS), or naltrexone, an opioid receptors antagonist (1 AM). The other groups of bile duct-ligated and sham-operated rats received daily intraperitoneal administration of L-NAME (20 mg/kg/day), aminoguanidine, a selective inducible NOS (iNOS) inhibitor (150 mg/kg/day) or naltrexone (10 mg/kg/day). After 7 days, the superior mesenteric artery was cannulated and the mesenteric vascular bed was perfused according to the McGregor method. Anandamide-induced relaxation was significantly potentiated in mesenteric vascular beds of bile duct-ligated rats. Chronic treatment of bile duct-ligated animals with L-NAME and aminoguanidine blocked this hyperresponsiveness while the hyperresponsiveness was potentiated at large doses of anandamide on chronic treatment of these animals with naltrexone. Although acute L-NAME treatment of mesenteric beds completely blocked the anandamide-induced vasorelaxation in sham-operated rats, this vasorelaxation still was present in bile duct-ligated animals. Anandamide-induced vasorelaxation remained unaffected after acute naltrexone treatment of mesenteric beds in both bile duct-ligated and sham-operated rats. Our results indicate that (1) there is enhanced anandamideinduced vasorelaxation in cholestatic rats, probably due to a defect in cannabinoid or vanilloid receptors and (2) NO overproduction may be involved in cholestasis-induced vascular hyperresponsiveness.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"European Journal of 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data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway"><img alt="Research paper thumbnail of Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway">Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric o...</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 endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.</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="102073300"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073300"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073300; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073300]").text(description); $(".js-view-count[data-work-id=102073300]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073300; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073300']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073300, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073300]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073300,"title":"Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway","translated_title":"","metadata":{"abstract":"The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.","publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"European Journal of Pharmacology"},"translated_abstract":"The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.","internal_url":"https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway","translated_internal_url":"","created_at":"2023-05-20T06:51:43.313-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":154,"name":"Endocrinology","url":"https://www.academia.edu/Documents/in/Endocrinology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":12981,"name":"Enzyme Inhibitors","url":"https://www.academia.edu/Documents/in/Enzyme_Inhibitors"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":159958,"name":"Acetylcholine","url":"https://www.academia.edu/Documents/in/Acetylcholine"},{"id":178753,"name":"Penis","url":"https://www.academia.edu/Documents/in/Penis"},{"id":279027,"name":"European","url":"https://www.academia.edu/Documents/in/European"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":555120,"name":"Arginine","url":"https://www.academia.edu/Documents/in/Arginine"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1272871,"name":"Muscle Relaxation","url":"https://www.academia.edu/Documents/in/Muscle_Relaxation"},{"id":1358142,"name":"Methyl Ester","url":"https://www.academia.edu/Documents/in/Methyl_Ester"},{"id":1509324,"name":"Arachidonic Acid","url":"https://www.academia.edu/Documents/in/Arachidonic_Acid"},{"id":1866509,"name":"Indomethacin","url":"https://www.academia.edu/Documents/in/Indomethacin"},{"id":2611583,"name":"cholestasis","url":"https://www.academia.edu/Documents/in/cholestasis"},{"id":3881526,"name":"In Vitro Techniques","url":"https://www.academia.edu/Documents/in/In_Vitro_Techniques"}],"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="102073299"><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/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors"><img alt="Research paper thumbnail of The synergistic anticonvulsant effect of agmatine and morphine: Possible role of alpha 2-adrenoceptors" class="work-thumbnail" src="https://attachments.academia-assets.com/102435682/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/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors">The synergistic anticonvulsant effect of agmatine and morphine: Possible role of alpha 2-adrenoceptors</a></div><div class="wp-workCard_item"><span>Epilepsy Research</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="db856e7698aa9c29424e2a0d01747d2c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435682,"asset_id":102073299,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435682/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073299"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073299"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073299; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073299]").text(description); $(".js-view-count[data-work-id=102073299]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073299; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073299']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073299, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "db856e7698aa9c29424e2a0d01747d2c" } } $('.js-work-strip[data-work-id=102073299]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073299,"title":"The synergistic anticonvulsant effect of agmatine and morphine: Possible role of alpha 2-adrenoceptors","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Recent demonstrations of the anticonvulsant properties of agmatine suggest it may be considered as a potential adjunct for protection against seizure. We investigated the possibility of an additive anticonvulsant effect between low doses of agmatine and morphine. The thresholds for the clonic seizures induced by the intravenous administration of gamma-aminobutyric acid (GABA)-antagonist, pentylenetetrazole (PTZ) were assessed in mice. Morphine at lower doses (1-3 mg/kg) increased and at higher doses (30, 60 mg/kg) decreased the seizure threhsold. Pretreatment with a per se non-effective dose of agmatine (1 mg/kg) potentiated the anticonvulsant effect of morphine. The combination of subeffective doses of agmatine and morphine led to potent anticonvulsant effects. The proconvulsant effect of morphine was attenuated by agmatine. Yohimbine with a dose (1 mg/kg) incapable of affecting seizure threshold reversed the effect of agmatine on both anticonvulsant and proconvulsant effects of morphine. These results suggest that agmatine potentiates the anticonvulsant effect of morphine and alpha 2-adrenoceptors may be involved in this effect.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Epilepsy Research","grobid_abstract_attachment_id":102435682},"translated_abstract":null,"internal_url":"https://www.academia.edu/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors","translated_internal_url":"","created_at":"2023-05-20T06:51:43.160-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":102435682,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/102435682/thumbnails/1.jpg","file_name":"j.eplepsyres.2005.04.00320230520-1-9imgcf.pdf","download_url":"https://www.academia.edu/attachments/102435682/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"The_synergistic_anticonvulsant_effect_of.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/102435682/j.eplepsyres.2005.04.00320230520-1-9imgcf-libre.pdf?1684594568=\u0026response-content-disposition=attachment%3B+filename%3DThe_synergistic_anticonvulsant_effect_of.pdf\u0026Expires=1732425863\u0026Signature=LVZ-8vpZ8gq3t44SOIveBhlCA-n1E5e2pkK1LJkHUD6NX4I2kHZ03xOsc7uY8abfAji8MjLfiLZgxJEJ6~njagmKWpa6~rD6Bh9mJdrgueICRMm77dDqoFAkkz1MBhnB60kIS3gjgNsuSAiKJVjCkgU75oybjK0eGsT6M8MQFFtr4JQIioj6vkDtR4lPJXocNsIaKMANZ7FYpPIvbBNh58FPOv95P6cwNfkF2CjHrsSZ350Mpy8YjRFNTonyExE8Y5Y7ZBpSvW3J8Gm5D3jY8BjOpvwRP8Yv0bE9Bdp9u7h7uUxbtUhLGS74R-QrEhQPdFGcBGxhU3nEHZtZqobCDw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors","translated_slug":"","page_count":8,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad 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Dose","url":"https://www.academia.edu/Documents/in/Low_Dose"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":218374,"name":"Morphine","url":"https://www.academia.edu/Documents/in/Morphine"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":413194,"name":"Analysis of Variance","url":"https://www.academia.edu/Documents/in/Analysis_of_Variance"},{"id":651604,"name":"Seizures","url":"https://www.academia.edu/Documents/in/Seizures"},{"id":1225893,"name":"Effective Dose","url":"https://www.academia.edu/Documents/in/Effective_Dose"},{"id":1957847,"name":"Pentylenetetrazole","url":"https://www.academia.edu/Documents/in/Pentylenetetrazole"},{"id":1957848,"name":"Seizure threshold","url":"https://www.academia.edu/Documents/in/Seizure_threshold"},{"id":2661220,"name":"Agmatine","url":"https://www.academia.edu/Documents/in/Agmatine"},{"id":3509231,"name":"Yohimbine","url":"https://www.academia.edu/Documents/in/Yohimbine"},{"id":3545627,"name":"Drug synergism","url":"https://www.academia.edu/Documents/in/Drug_synergism"}],"urls":[{"id":31597725,"url":"https://api.elsevier.com/content/article/PII:S0920121105000768?httpAccept=text/xml"}]}, 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="102073298"><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/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis"><img alt="Research paper thumbnail of Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis">Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis</a></div><div class="wp-workCard_item"><span>Digestive Diseases and Sciences</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic ...</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">Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.</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="102073298"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073298"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073298; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073298]").text(description); $(".js-view-count[data-work-id=102073298]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073298; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073298']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073298, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073298]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073298,"title":"Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis","translated_title":"","metadata":{"abstract":"Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P \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;lt; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P \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;lt; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P \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;lt; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.","publisher":"Springer Science and Business Media LLC","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Digestive Diseases and Sciences"},"translated_abstract":"Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P \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;lt; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P \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;lt; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P \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;lt; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.","internal_url":"https://www.academia.edu/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis","translated_internal_url":"","created_at":"2023-05-20T06:51:42.988-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":93659,"name":"Digestive and Liver Diseases","url":"https://www.academia.edu/Documents/in/Digestive_and_Liver_Diseases"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":122402,"name":"Nitrates","url":"https://www.academia.edu/Documents/in/Nitrates"},{"id":204388,"name":"Vasoconstriction","url":"https://www.academia.edu/Documents/in/Vasoconstriction"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":244849,"name":"Hepatic Encephalopathy","url":"https://www.academia.edu/Documents/in/Hepatic_Encephalopathy"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":767931,"name":"Naltrexone","url":"https://www.academia.edu/Documents/in/Naltrexone"},{"id":956370,"name":"Opioid Receptor","url":"https://www.academia.edu/Documents/in/Opioid_Receptor"},{"id":1000359,"name":"Phenylephrine","url":"https://www.academia.edu/Documents/in/Phenylephrine"},{"id":1255525,"name":"Chronic Liver Disease","url":"https://www.academia.edu/Documents/in/Chronic_Liver_Disease"},{"id":1654024,"name":"Nitrites","url":"https://www.academia.edu/Documents/in/Nitrites"},{"id":2581997,"name":"splanchnic circulation","url":"https://www.academia.edu/Documents/in/splanchnic_circulation"},{"id":3430960,"name":"Mesentery","url":"https://www.academia.edu/Documents/in/Mesentery"},{"id":3589281,"name":"Ligation","url":"https://www.academia.edu/Documents/in/Ligation"},{"id":3635108,"name":"Superior mesenteric artery","url":"https://www.academia.edu/Documents/in/Superior_mesenteric_artery"}],"urls":[{"id":31597724,"url":"http://link.springer.com/content/pdf/10.1007/s10620-008-0261-7.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="102073297"><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/102073297/Lithium_inhibits_the_modulatory_effects_of_morphine_on_susceptibility_to_pentylenetetrazole_induced_clonic_seizure_in_mice_involvement_of_a_nitric_oxide_pathway"><img alt="Research paper thumbnail of Lithium inhibits the modulatory effects of morphine on susceptibility to pentylenetetrazole-induced clonic seizure in mice: involvement of a nitric oxide pathway" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073297/Lithium_inhibits_the_modulatory_effects_of_morphine_on_susceptibility_to_pentylenetetrazole_induced_clonic_seizure_in_mice_involvement_of_a_nitric_oxide_pathway">Lithium inhibits the modulatory effects of morphine on susceptibility to pentylenetetrazole-induced clonic seizure in mice: involvement of a nitric oxide pathway</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lithium has been reported to inhibit opioid-induced properties. The present study examined the ef...</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">Lithium has been reported to inhibit opioid-induced properties. The present study examined the effect of acute and chronic administration of lithium chloride (LiCl) on morphine&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s biphasic modulation of susceptibility to pentylenetetrazole (PTZ)-induced clonic seizure in mice. We also examined the possible involvement of nitric oxide (NO) pathway in lithium effect. Both acute (0.1 and 1 mg/kg) and chronic (same doses, 21 consecutive days) administration of LiCl completely inhibited the anticonvulsant and proconvulsant effects of morphine (at doses 1 and 30 mg/kg, respectively). A very low and per se noneffective dose of LiCl (0.05 mg/kg) significantly inhibited both phases of morphine effect when administered concomitant with a noneffective low dose of naloxone (0.1 mg/kg). The NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) at a per se noneffective dose of 0.3 mg/kg potentiated the inhibitory effects of low doses of LiCl (0.01 and 0.05 mg/kg) on both phases of morphine effect. l-arginine, a NO synthase substrate, at a per se noneffective dose of 30 mg/kg reversed the inhibitory effects of lithium (1 mg/kg). Lithium is capable of antagonizing both modulatory effects of morphine on seizure susceptibility even at relatively low doses. 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The present study examined the effect of acute and chronic administration of lithium chloride (LiCl) on morphine\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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s biphasic modulation of susceptibility to pentylenetetrazole (PTZ)-induced clonic seizure in mice. We also examined the possible involvement of nitric oxide (NO) pathway in lithium effect. Both acute (0.1 and 1 mg/kg) and chronic (same doses, 21 consecutive days) administration of LiCl completely inhibited the anticonvulsant and proconvulsant effects of morphine (at doses 1 and 30 mg/kg, respectively). 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="17875812" id="papers"><div class="js-work-strip profile--work_container" data-work-id="102073320"><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/102073320/Genetically_engineering_self_organization_of_human_pluripotent_stem_cells_into_a_liver_bud_like_tissue_using_Gata6"><img alt="Research paper thumbnail of Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6" class="work-thumbnail" src="https://attachments.academia-assets.com/102435689/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/102073320/Genetically_engineering_self_organization_of_human_pluripotent_stem_cells_into_a_liver_bud_like_tissue_using_Gata6">Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6</a></div><div class="wp-workCard_item"><span>Nature communications</span><span>, Jan 6, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative me...</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">Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative medicine. While most of the methods using these cells have focused on deriving homogenous populations of specialized cells, there has been modest success in producing hiPSC-derived organotypic tissues or organoids. Here we present a novel approach for generating and then co-differentiating hiPSC-derived progenitors. With a genetically engineered pulse of GATA-binding protein 6 (GATA6) expression, we initiate rapid emergence of all three germ layers as a complex function of GATA6 expression levels and tissue context. Within 2 weeks we obtain a complex tissue that recapitulates early developmental processes and exhibits a liver bud-like phenotype, including haematopoietic and stromal cells as well as a neuronal niche. Collectively, our approach demonstrates derivation of complex tissues from hiPSCs using a single autologous hiPSCs as source and generates a range of stromal cells that co-deve...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="3ecd9e8fc66ab30439fd0363cd26cfb3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435689,"asset_id":102073320,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435689/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073320"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073320"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073320; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073320]").text(description); $(".js-view-count[data-work-id=102073320]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073320; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073320']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073320, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "3ecd9e8fc66ab30439fd0363cd26cfb3" } } $('.js-work-strip[data-work-id=102073320]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073320,"title":"Genetically engineering self-organization of human pluripotent stem cells into a liver bud-like tissue using Gata6","translated_title":"","metadata":{"abstract":"Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative medicine. While most of the methods using these cells have focused on deriving homogenous populations of specialized cells, there has been modest success in producing hiPSC-derived organotypic tissues or organoids. Here we present a novel approach for generating and then co-differentiating hiPSC-derived progenitors. With a genetically engineered pulse of GATA-binding protein 6 (GATA6) expression, we initiate rapid emergence of all three germ layers as a complex function of GATA6 expression levels and tissue context. Within 2 weeks we obtain a complex tissue that recapitulates early developmental processes and exhibits a liver bud-like phenotype, including haematopoietic and stromal cells as well as a neuronal niche. Collectively, our approach demonstrates derivation of complex tissues from hiPSCs using a single autologous hiPSCs as source and generates a range of stromal cells that co-deve...","publication_date":{"day":6,"month":1,"year":2016,"errors":{}},"publication_name":"Nature communications"},"translated_abstract":"Human induced pluripotent stem cells (hiPSCs) have potential for personalized and regenerative medicine. While most of the methods using these cells have focused on deriving homogenous populations of specialized cells, there has been modest success in producing hiPSC-derived organotypic tissues or organoids. Here we present a novel approach for generating and then co-differentiating hiPSC-derived progenitors. With a genetically engineered pulse of GATA-binding protein 6 (GATA6) expression, we initiate rapid emergence of all three germ layers as a complex function of GATA6 expression levels and tissue context. 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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" rel="nofollow" href="https://www.academia.edu/102073317/342810_Lung_Liver_Interactions_A_Multi_Scale_In_Vitro_Systems_Analysis">342810 Lung-Liver Interactions: A Multi-Scale In Vitro Systems Analysis</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Individual cells integrate many external cues — including those that arise from various extracell...</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">Individual cells integrate many external cues — including those that arise from various extracellular matrix components, mechanical stimulation and soluble signals from adjacent and even distant cells — to generate a basal phenotype and respond to perturbations in their environment [1]. Yet, to capture the complexity of human physiology in vitro demands the evaluation of interacting cell types coexisting in a hierarchical 3-dimensional structure influenced by gradients in nutrients, mechanics, and cell composition. Ultimately, to computationally model integrated responses of multiple cells types (including immune cells) requires the need to assess systems under both homeostatic and pathologic conditions. In this study, we propose to integrate communication between lung-liver tissue modules. 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To investigate the effects of morphine on reperfusion injury due to testicular torsion-detorsion (T/D). Methods. We divided 36 adult male Sprague-Dawley rats into six groups. Testicular ischemia was achieved by twisting the right testis 720°counterclockwise for 1 hour, and reperfusion was allowed for 4 hours after detorsion. The baseline group was for basal normal values. The sham-operated group served as the control group. The T/D group underwent 1 hour of testicular torsion and 4 hours of detorsion. The morphine group received pretreatment with intravenous morphine sulfate (10 mg/kg) just before detorsion. The naltrexone group received an intravenous injection of naltrexone HCl (20 mg/kg) 15 minutes before detorsion. The naltrexone/morphine group received intravenous administration of naltrexone HCl (20 mg/kg) 15 minutes before detorsion and morphine sulfate (10 mg/kg) just before detorsion. Results. The ipsilateral malondialdehyde levels in the T/D group were significantly greater than in the control and baseline groups. Moreover, the ipsilateral testicular malondialdehyde values in the morphine group were significantly lower than in the T/D and naltrexone/morphine groups. Also, significant decreases occurred in catalase and superoxide dismutase activities in the T/D group compared with the control and baseline groups. These values were significantly greater in the morphine group than in the T/D and naltrexone/morphine groups. The ipsilateral testes of all groups that underwent testicular torsion showed similar histopathologic changes. Conclusions. Morphine increased the ipsilateral intratesticular antioxidant markers during the reperfusion phase after unilateral testicular torsion, which was eventually reflected in lower testicular malondialdehyde levels. Furthermore, this effect was mediated through the opioid 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Reperfusion Injury","url":"https://www.academia.edu/Documents/in/Ischemia_Reperfusion_Injury"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":129739,"name":"Anesthesia","url":"https://www.academia.edu/Documents/in/Anesthesia"},{"id":203521,"name":"tESTIS","url":"https://www.academia.edu/Documents/in/tESTIS"},{"id":215075,"name":"Experimental Study","url":"https://www.academia.edu/Documents/in/Experimental_Study"},{"id":218374,"name":"Morphine","url":"https://www.academia.edu/Documents/in/Morphine"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":732354,"name":"Rat 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class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/102073312/All_human_microphysical_model_of_metastasis_therapy"><img alt="Research paper thumbnail of All-human microphysical model of metastasis therapy" class="work-thumbnail" src="https://attachments.academia-assets.com/102435656/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/102073312/All_human_microphysical_model_of_metastasis_therapy">All-human microphysical model of metastasis therapy</a></div><div class="wp-workCard_item"><span>Stem Cell Research &amp; Therapy</span><span>, 2013</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9a720bfa0aeb168ae5855381ee282f54" 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102073312, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "9a720bfa0aeb168ae5855381ee282f54" } } $('.js-work-strip[data-work-id=102073312]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073312,"title":"All-human microphysical model of metastasis therapy","translated_title":"","metadata":{"publisher":"Springer Science and Business Media 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Metastasis is a multistep process whereby cells from the primary tumor invade or migrate through surrounding tissues and barrier matrices, disseminate via the vasculature (hematologic or lymphatic), arrest and extravasate at the metastatic niche, and ultimately survive and outgrow in this ectopic environment. Ectopic-site survival and subsequent proliferative outgrowth is the rate-limiting step in clinically evident disease [1,2]. Distant metastases are generally more resistant to treatments than the primary tumor [3], underscoring the need to develop more rational therapeutic approaches based on the molecular pathophysiology in the metastatic microenvironment [4]. Clinically undetectable metastases have serious implications for cancer patients; approximately one-third of women suff ered a metastatic relapse within 5 years post lumpectomy [5,6]. Th is late emergence implies that tumor cells disseminate early and survive undetected in ectopic sites [5,6]. Numerous three-dimensional models of tumor cells capture a subset of tumor behaviors [7-11]. A signifi cant gap exists in investigating how metastatic nodules interact with the host tissue due to the inherent small-scale dimensions of most microfl uidic devices, poor disease recapitulation by cell lines, and lack of a primary cell environment. 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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/102073310/CRISPR_transcriptional_repression_devices_and_layered_circuits_in_mammalian_cells"><img alt="Research paper thumbnail of CRISPR transcriptional repression devices and layered circuits in mammalian cells" class="work-thumbnail" src="https://attachments.academia-assets.com/102435685/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/102073310/CRISPR_transcriptional_repression_devices_and_layered_circuits_in_mammalian_cells">CRISPR transcriptional repression devices and layered circuits in mammalian cells</a></div><div class="wp-workCard_item"><span>Nature Methods</span><span>, 2014</span></div><div class="wp-workCard_item 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{"id":102073310,"title":"CRISPR transcriptional repression devices and layered circuits in mammalian cells","translated_title":"","metadata":{"publisher":"Springer Science and Business Media LLC","grobid_abstract":"A key obstacle to creating sophisticated genetic circuits has been the lack of scalable device libraries. Here we present a modular transcriptional repression architecture based on clustered regularly interspaced palindromic repeats (CRISPR) system and examine approaches for regulated expression of guide RNAs in human cells. Subsequently we demonstrate that CRISPR regulatory devices can be layered to create functional cascaded circuits, which provide a valuable toolbox for engineering purposes. Engineered biological circuits provide insights into the underlying biology of living cells and offer potential solutions to a range of medical and industrial challenges 1, 2. A prerequisite for efficient engineering of such sophisticated circuits is the availability of a library of regulatory devices that can be connected in various contexts to create new and Correspondence should be addressed to R.W.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Nature 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class="js-work-strip profile--work_container" data-work-id="102073308"><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/102073308/Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells"><img alt="Research paper thumbnail of Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073308/Concomitant_reduction_of_matrix_metalloproteinase_2_secretion_and_intracellular_reactive_oxygen_species_following_anti_sense_inhibition_of_telomerase_activity_in_PC_3_prostate_carcinoma_cells">Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells</a></div><div class="wp-workCard_item"><span>Molecular and Cellular Biochemistry</span><span>, 2005</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The level of activity of the telomerase has been shown to correlate with the degree of invasivene...</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 level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. In addition, cellular redox state is believed to regulate the secretion of matrix metalloproteinase-2 (MMP-2). To determine the effect of anti-sense telomerase treatment of prostate cancer cells on MMP-2 activity, and the reactive oxygen and nitrogen species (two effectors of cellular redox state). Anti-sense oligonucleotide against RNA component of human telomerase (hTR) was introduced into the cells using Fugene-6 transfection reagent. The activity of telomerase was assessed using Telomere Repeat Amplification Protocol (TRAP assay). Activity of matrix metalloproteinase-2 (MMP-2) was determined by zymography. Levels of intracellular reactive oxygen species (ROS) and nitric oxide metabolites were measured by dichlorofluorescein diacetate (DCFH-DA) staining and Griess reagent, respectively. The level of apoptosis was determined using TUNEL assay. TRAP assay showed more than 90% inhibition of telomerase activity after 72 h of transfection. Pro-MMP-2 activity was decreased down to 50% of the control levels. Intracellular reactive oxygen species were also significantly decreased. Neither apoptosis rate nor the level of nitric oxide metabolites was significantly different between anti-sense treated and control cells. Concomitant reduction of the pro-MMP-2 secretion and ROS in PC-3 cells following hTR inhibition suggests that over-activity of telomerase in cancer cells might increase the level of matrix metalloproteinase-2 and thus, be directly involved in the invasion process through enhancement of intracellular oxidative stress.</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="102073308"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073308"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073308; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073308]").text(description); $(".js-view-count[data-work-id=102073308]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073308; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073308']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073308, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073308]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073308,"title":"Concomitant reduction of matrix metalloproteinase-2 secretion and intracellular reactive oxygen species following anti-sense inhibition of telomerase activity in PC-3 prostate carcinoma cells","translated_title":"","metadata":{"abstract":"The level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. 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Pro-MMP-2 activity was decreased down to 50% of the control levels. Intracellular reactive oxygen species were also significantly decreased. Neither apoptosis rate nor the level of nitric oxide metabolites was significantly different between anti-sense treated and control cells. Concomitant reduction of the pro-MMP-2 secretion and ROS in PC-3 cells following hTR inhibition suggests that over-activity of telomerase in cancer cells might increase the level of matrix metalloproteinase-2 and thus, be directly involved in the invasion process through enhancement of intracellular oxidative stress.","publisher":"Springer Nature","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Molecular and Cellular Biochemistry"},"translated_abstract":"The level of activity of the telomerase has been shown to correlate with the degree of invasiveness in several tumor types. 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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="102073307"><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/102073307/Homocysteine_alterations_in_experimental_cholestasis_and_its_subsequent_cirrhosis"><img alt="Research paper thumbnail of Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis" class="work-thumbnail" src="https://attachments.academia-assets.com/102435703/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/102073307/Homocysteine_alterations_in_experimental_cholestasis_and_its_subsequent_cirrhosis">Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="840fb7ee728130fb860b841d40d7aeae" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435703,"asset_id":102073307,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435703/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073307"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073307"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073307; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073307]").text(description); $(".js-view-count[data-work-id=102073307]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073307; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073307']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073307, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "840fb7ee728130fb860b841d40d7aeae" } } $('.js-work-strip[data-work-id=102073307]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073307,"title":"Homocysteine alterations in experimental cholestasis and its subsequent cirrhosis","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Homocysteine (Hcy), an intermediate in methionine metabolism, has been proposed to be involved in hepatic fibrogenesis. Impaired liver function can alter Hcy metabolism. The aim of the present study was to determine plasma Hcy alterations in acute obstructive cholestasis and the subsequent biliary cirrhosis. Cholestasis was induced by bile duct ligation and sham-operated and unoperated rats were used as controls. The animals were studied on the days 7th, 14th, 21st and 28th after the operation. Plasma Hcy, cysteine, methionine, nitric oxide (NO) and liver S-adenosyl-methionine (SAM), S-adenosyl-homocysteine (SAH), SAM to SAH ratio and glutathione were measured. Chronic L-NAME treatment was also included in the study. Plasma Hcy concentrations were transiently elevated by the day 14th after bile duct ligation (P b 0.01) and subsequently returned to control levels. Similar relative fluctuations in plasma Hcy were observed in BDL rats after intraperitoneal methionine overload. Plasma methionine, cysteine and nitrite and nitrate were significantly increased after bile duct ligation. SAM to SAH ratio was diminished by the 1st week of cholestasis and remained significantly decreased throughout the study. These events were accompanied by a decrease in GSH to GSSG ratio in the liver. Chronic L-NAME treatment improved SAM to SAH ratio and prevented the elevation of plasma Hcy and methionine (P b 0.05) while couldn't influence the other parameters. In conclusion, this study demonstrates alterations in plasma Hcy and liver SAM and SAH contents in precirrhotic","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Life 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"profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="102073306"><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/102073306/Obstructive_cholestasis_alters_intestinal_transit_in_mice_role_of_opioid_system"><img alt="Research paper thumbnail of Obstructive cholestasis alters intestinal transit in mice: role of opioid system" class="work-thumbnail" src="https://attachments.academia-assets.com/102435699/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/102073306/Obstructive_cholestasis_alters_intestinal_transit_in_mice_role_of_opioid_system">Obstructive cholestasis alters intestinal transit in mice: role of opioid system</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a7c46ceb029b7d87e82d5770582ccab5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435699,"asset_id":102073306,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435699/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073306"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073306"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073306; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073306]").text(description); $(".js-view-count[data-work-id=102073306]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073306; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073306']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073306, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "a7c46ceb029b7d87e82d5770582ccab5" } } $('.js-work-strip[data-work-id=102073306]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073306,"title":"Obstructive cholestasis alters intestinal transit in mice: role of opioid system","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Acute cholestasis is associated with increased activity of the endogenous opioid system. It is also known that opioid receptor agonists like morphine decrease the intestinal transit. The purpose of the present study was to investigate the effect of cholestasis on the small intestine transit and the possible involvement of opioid system in this phenomenon in mice. Cholestasis was induced by bile duct-ligation and intestinal transit was measured with charcoal meal and calculation of percent of transit through small intestine. The effect of chronic administration of naltrexone and acute pretreatment with morphine on intestinal transit was evaluated in bile duct-ligated (BDL) as well as unoperated (CTL) and sham-operated (SHAM) animals. The plasma alkaline phosphatase and alanine aminotransferase activities were also measured. A significant decrease in small intestine transit (%transit) was observed in BDL mice compared to SHAM animals, which was prominent even after 24 h of cholestasis. Chronic pretreatment with an opioid receptor antagonist, naltrexone, (10 mg/kg, i.p for 2, 4 or 6 days) completely restored the cholestasis-induced decrease in %transit to that of control animals. Although the acute administration of morphine (2 mg/kg, s.c.) 20 min before charcoal feeding caused a significant decrease in the intestinal transit of CTL and SHAM animals, it did not decrease the %transit of BDL animals on the day 5 after operation. Our findings show that acute cholestasis is associated with a prominent decrease in small intestine transit in mice and opioid receptors maybe involved in this phenomenon.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Life 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Sciences","url":"https://www.academia.edu/Documents/in/Life_Sciences"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":204435,"name":"Alkaline phosphatase","url":"https://www.academia.edu/Documents/in/Alkaline_phosphatase"},{"id":218374,"name":"Morphine","url":"https://www.academia.edu/Documents/in/Morphine"},{"id":425213,"name":"Alanine Aminotransferase","url":"https://www.academia.edu/Documents/in/Alanine_Aminotransferase"},{"id":572282,"name":"Combination drug therapy","url":"https://www.academia.edu/Documents/in/Combination_drug_therapy"},{"id":711582,"name":"Opioid","url":"https://www.academia.edu/Documents/in/Opioid"},{"id":767931,"name":"Naltrexone","url":"https://www.academia.edu/Documents/in/Naltrexone"},{"id":956370,"name":"Opioid Receptor","url":"https://www.academia.edu/Documents/in/Opioid_Receptor"},{"id":1129054,"name":"Gastrointestinal Transit Time","url":"https://www.academia.edu/Documents/in/Gastrointestinal_Transit_Time"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2112739,"name":"Alanine Transaminase","url":"https://www.academia.edu/Documents/in/Alanine_Transaminase"},{"id":2611583,"name":"cholestasis","url":"https://www.academia.edu/Documents/in/cholestasis"},{"id":3789884,"name":"Pharmacology and pharmaceutical sciences","url":"https://www.academia.edu/Documents/in/Pharmacology_and_pharmaceutical_sciences"}],"urls":[{"id":31597728,"url":"https://api.elsevier.com/content/article/PII:S0024320504008318?httpAccept=text/xml"}]}, 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="102073305"><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/102073305/The_c_Rel_subunit_of_nuclear_factor_%CE%BAB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation"><img alt="Research paper thumbnail of The c-Rel subunit of nuclear factor-κB regulates murine liver inflammation, wound-healing, and hepatocyte proliferation" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073305/The_c_Rel_subunit_of_nuclear_factor_%CE%BAB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation">The c-Rel subunit of nuclear factor-κB regulates murine liver inflammation, wound-healing, and hepatocyte proliferation</a></div><div class="wp-workCard_item"><span>Hepatology</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in l...</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 this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.</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="102073305"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073305"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073305; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073305]").text(description); $(".js-view-count[data-work-id=102073305]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073305; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073305']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073305, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073305]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073305,"title":"The c-Rel subunit of nuclear factor-κB regulates murine liver inflammation, wound-healing, and hepatocyte proliferation","translated_title":"","metadata":{"abstract":"In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.","publisher":"Ovid Technologies (Wolters Kluwer Health)","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Hepatology"},"translated_abstract":"In this study, we determined the role of the nuclear factor-kappaB (NF-kappaB) subunit c-Rel in liver injury and regeneration. In response to toxic injury of the liver, c-Rel null (c-rel(-/-)) mice displayed a defect in the neutrophilic inflammatory response, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Expressed, and Secreted; also known as CCL5). The subsequent fibrogenic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced injury was also impaired and this was associated with deficiencies in the expression of fibrogenic genes, collagen I and alpha-smooth muscle actin, by hepatic stellate cells. We additionally report that c-Rel is required for the normal proliferative regeneration of hepatocytes in response to toxic injury and partial hepatectomy. Absence of c-Rel was associated with blunted and delayed induction of forkhead box M1 (FoxM1) and its downstream targets cyclin B1 and Cdc25C. Furthermore, isolated c-rel(-/-) hepatocytes expressed reduced levels of FoxM1 and a reduced rate of basal and epidermal growth factor-induced DNA synthesis. Chromatin immunoprecipitation revealed that c-Rel binding to the FoxM1 promoter is induced in the regenerating liver. c-Rel has multiple functions in the control of liver homeostasis and regeneration and is a transcriptional regulator of FoxM1 and compensatory hepatocyte proliferation.","internal_url":"https://www.academia.edu/102073305/The_c_Rel_subunit_of_nuclear_factor_%CE%BAB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation","translated_internal_url":"","created_at":"2023-05-20T06:51:44.540-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"The_c_Rel_subunit_of_nuclear_factor_κB_regulates_murine_liver_inflammation_wound_healing_and_hepatocyte_proliferation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":8991,"name":"Wound Healing","url":"https://www.academia.edu/Documents/in/Wound_Healing"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":37773,"name":"Hepatology","url":"https://www.academia.edu/Documents/in/Hepatology"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":123418,"name":"NF-kappa B","url":"https://www.academia.edu/Documents/in/NF-kappa_B"},{"id":144048,"name":"Hepatitis","url":"https://www.academia.edu/Documents/in/Hepatitis"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":404319,"name":"Liver regeneration","url":"https://www.academia.edu/Documents/in/Liver_regeneration"},{"id":432593,"name":"Hepatocytes","url":"https://www.academia.edu/Documents/in/Hepatocytes"},{"id":664203,"name":"Hepatocyte","url":"https://www.academia.edu/Documents/in/Hepatocyte"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":2922788,"name":"Liver injury","url":"https://www.academia.edu/Documents/in/Liver_injury"},{"id":3789880,"name":"Medical biochemistry and metabolomics","url":"https://www.academia.edu/Documents/in/Medical_biochemistry_and_metabolomics"}],"urls":[{"id":31597727,"url":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fhep.23385"}]}, 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="102073303"><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/102073303/Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver"><img alt="Research paper thumbnail of Wound healing and local neuroendocrine regulation in the injured liver" class="work-thumbnail" src="https://attachments.academia-assets.com/102435681/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/102073303/Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver">Wound healing and local neuroendocrine regulation in the injured liver</a></div><div class="wp-workCard_item"><span>Expert Reviews in Molecular Medicine</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hepatic wound-healing response is a complex process involving many different cell types and f...</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 hepatic wound-healing response is a complex process involving many different cell types and factors. It leads to the formation of excessive matrix and a fibrotic scar, which ultimately disrupts proper functioning of the liver and establishes cirrhosis. Activated hepatic myofibroblasts, which are derived from cells such as hepatic stellate cells (HSCs), play a key role in this process. Upon chronic liver injury, there is an upregulation in the local neuroendocrine system and it has recently been demonstrated that activated HSCs express specific receptors and respond to different components of this system. Neuroendocrine factors and their receptors participate in a complex network that modulates liver inflammation and wound healing, and controls the development and progression of liver fibrosis. The first part of this review provides an overview of the molecular mechanisms governing hepatic wound healing. In the second section, we explore important components of the hepatic neuroe...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="9bbe3019d6cf15fc0d67d322dc955eb9" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435681,"asset_id":102073303,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435681/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073303"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073303"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073303; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073303]").text(description); $(".js-view-count[data-work-id=102073303]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073303; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073303']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073303, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "9bbe3019d6cf15fc0d67d322dc955eb9" } } $('.js-work-strip[data-work-id=102073303]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073303,"title":"Wound healing and local neuroendocrine regulation in the injured liver","translated_title":"","metadata":{"abstract":"The hepatic wound-healing response is a complex process involving many different cell types and factors. It leads to the formation of excessive matrix and a fibrotic scar, which ultimately disrupts proper functioning of the liver and establishes cirrhosis. Activated hepatic myofibroblasts, which are derived from cells such as hepatic stellate cells (HSCs), play a key role in this process. Upon chronic liver injury, there is an upregulation in the local neuroendocrine system and it has recently been demonstrated that activated HSCs express specific receptors and respond to different components of this system. Neuroendocrine factors and their receptors participate in a complex network that modulates liver inflammation and wound healing, and controls the development and progression of liver fibrosis. The first part of this review provides an overview of the molecular mechanisms governing hepatic wound healing. In the second section, we explore important components of the hepatic neuroe...","publisher":"Cambridge University Press (CUP)","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Expert Reviews in Molecular Medicine"},"translated_abstract":"The hepatic wound-healing response is a complex process involving many different cell types and factors. It leads to the formation of excessive matrix and a fibrotic scar, which ultimately disrupts proper functioning of the liver and establishes cirrhosis. Activated hepatic myofibroblasts, which are derived from cells such as hepatic stellate cells (HSCs), play a key role in this process. Upon chronic liver injury, there is an upregulation in the local neuroendocrine system and it has recently been demonstrated that activated HSCs express specific receptors and respond to different components of this system. Neuroendocrine factors and their receptors participate in a complex network that modulates liver inflammation and wound healing, and controls the development and progression of liver fibrosis. The first part of this review provides an overview of the molecular mechanisms governing hepatic wound healing. In the second section, we explore important components of the hepatic neuroe...","internal_url":"https://www.academia.edu/102073303/Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver","translated_internal_url":"","created_at":"2023-05-20T06:51:43.943-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":102435681,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/102435681/thumbnails/1.jpg","file_name":"b6a20ea73c3ed19d7006f0ecb88077368997.pdf","download_url":"https://www.academia.edu/attachments/102435681/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Wound_healing_and_local_neuroendocrine_r.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/102435681/b6a20ea73c3ed19d7006f0ecb88077368997-libre.pdf?1684594581=\u0026response-content-disposition=attachment%3B+filename%3DWound_healing_and_local_neuroendocrine_r.pdf\u0026Expires=1732401362\u0026Signature=Ex4CFccMZfZErv5FYwSobgXk~A0CiUg6EuRoj6YIAaofUEtz61sQXzLUWEZRMRblO~BaAiOrjy8XqmScE1a47PDW74OF3E7YZPmQ4XKNpQ3YrUoSRDI9ZtcphcigyIH-yiKSqpAolVvESfu4oICJ0~xnDCMWHjnXhcx9M8J9mZ~B3VUXaEoTDvyxSTNIS1OZzj40pxmJ7Ab--MU~8wIpakSuVL~QXwWg52SVkcoXJr9syRKF3m6fR3v70S-ejuV6EytUxHLdHg6t2pOZvSUj3bLgEV9c5WGmWupHjNQ5b5OzIfZ92m9Wlf6QENdarNeiYEcYu8OwriBNFAs7XoFtXA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Wound_healing_and_local_neuroendocrine_regulation_in_the_injured_liver","translated_slug":"","page_count":19,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[{"id":102435681,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/102435681/thumbnails/1.jpg","file_name":"b6a20ea73c3ed19d7006f0ecb88077368997.pdf","download_url":"https://www.academia.edu/attachments/102435681/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Wound_healing_and_local_neuroendocrine_r.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/102435681/b6a20ea73c3ed19d7006f0ecb88077368997-libre.pdf?1684594581=\u0026response-content-disposition=attachment%3B+filename%3DWound_healing_and_local_neuroendocrine_r.pdf\u0026Expires=1732401362\u0026Signature=Ex4CFccMZfZErv5FYwSobgXk~A0CiUg6EuRoj6YIAaofUEtz61sQXzLUWEZRMRblO~BaAiOrjy8XqmScE1a47PDW74OF3E7YZPmQ4XKNpQ3YrUoSRDI9ZtcphcigyIH-yiKSqpAolVvESfu4oICJ0~xnDCMWHjnXhcx9M8J9mZ~B3VUXaEoTDvyxSTNIS1OZzj40pxmJ7Ab--MU~8wIpakSuVL~QXwWg52SVkcoXJr9syRKF3m6fR3v70S-ejuV6EytUxHLdHg6t2pOZvSUj3bLgEV9c5WGmWupHjNQ5b5OzIfZ92m9Wlf6QENdarNeiYEcYu8OwriBNFAs7XoFtXA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":8991,"name":"Wound Healing","url":"https://www.academia.edu/Documents/in/Wound_Healing"},{"id":9334,"name":"Inflammation","url":"https://www.academia.edu/Documents/in/Inflammation"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":60436,"name":"Cell Differentiation","url":"https://www.academia.edu/Documents/in/Cell_Differentiation"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":174804,"name":"Fibrosis","url":"https://www.academia.edu/Documents/in/Fibrosis"},{"id":469018,"name":"Neoplasms","url":"https://www.academia.edu/Documents/in/Neoplasms"},{"id":600778,"name":"Cirrhosis","url":"https://www.academia.edu/Documents/in/Cirrhosis"},{"id":777306,"name":"Hepatic Fibrosis","url":"https://www.academia.edu/Documents/in/Hepatic_Fibrosis"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1920778,"name":"Myofibroblast","url":"https://www.academia.edu/Documents/in/Myofibroblast"},{"id":3257003,"name":"Expert reviews","url":"https://www.academia.edu/Documents/in/Expert_reviews"}],"urls":[]}, dispatcherData: dispatcherData }); 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "3d8d2d9298739f9beca00567722eadbe" } } $('.js-work-strip[data-work-id=102073302]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073302,"title":"Matrix metalloproteinase 2 secretion in WEHI 164 fibrosarcoma cells is nitric oxide-related and modified by morphine","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Matrix metalloproteinases (MMP) are ubiquitous enzymes involved in extracellular matrix remodeling, and as a consequence in a number of physiological and pathological states, including development, wound healing and cancer. A crucial feature of cancer progression and metastasis is the disruption of extracellular matrix, and spreading of proliferating cancer cells. Modulation of MMP is a main target of cancer research. Using the mouse fibrosarcoma cell line WEHI 164, producing high amounts of MMP-2, we investigated whether we could modulate its production. We report that MMP-2 is under the control of nitric oxide (NO)/nitric oxide synthase (NOS) system. In addition, we show that NOS activity is controlled by opioids in a non-opioid receptor-related manner. Finally, we provide evidence that morphine, when administrated at low, non-toxic concentrations (b 10 − 9 M) attenuates MMP-2 activity. 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rats: role of nitric oxide" class="work-thumbnail" src="https://attachments.academia-assets.com/102435722/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/102073301/Potentiation_of_anandamide_effects_in_mesenteric_beds_isolated_from_bile_duct_ligated_rats_role_of_nitric_oxide">Potentiation of anandamide effects in mesenteric beds isolated from bile duct-ligated rats: role of nitric oxide</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f23e08014898ac685d381dbc4249c5f3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073301]").text(description); $(".js-view-count[data-work-id=102073301]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073301; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073301']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073301, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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: "f23e08014898ac685d381dbc4249c5f3" } } $('.js-work-strip[data-work-id=102073301]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073301,"title":"Potentiation of anandamide effects in mesenteric beds isolated from bile duct-ligated rats: role of nitric oxide","translated_title":"","metadata":{"publisher":"Elsevier BV","grobid_abstract":"Changes in vascular responsiveness are proposed as the basis for some of the cardiovascular complications in cholestasis. Cholestasis is also associated with accumulation of endogenous opioid peptides and evidence of nitric oxide (NO) overproduction. On the other hand, it is well known that anandamide, an endogenous cannabinoid ligand, causes hypotension and a decrease in systemic vascular resistance. In the present study, the possible role of the cannabinoid system in cholestasis-induced mesenteric vascular bed responsiveness was investigated. Mesenteric arteries of bile duct-ligated and sham-operated rats receiving daily administrations of saline were used for evaluating phenylephrine or anandamide dose-response, acute effects of N G-nitro-L-arginine methyl ester (L-NAME, 100 AM), a non-selective inhibitor of NO synthase (NOS), or naltrexone, an opioid receptors antagonist (1 AM). The other groups of bile duct-ligated and sham-operated rats received daily intraperitoneal administration of L-NAME (20 mg/kg/day), aminoguanidine, a selective inducible NOS (iNOS) inhibitor (150 mg/kg/day) or naltrexone (10 mg/kg/day). After 7 days, the superior mesenteric artery was cannulated and the mesenteric vascular bed was perfused according to the McGregor method. Anandamide-induced relaxation was significantly potentiated in mesenteric vascular beds of bile duct-ligated rats. Chronic treatment of bile duct-ligated animals with L-NAME and aminoguanidine blocked this hyperresponsiveness while the hyperresponsiveness was potentiated at large doses of anandamide on chronic treatment of these animals with naltrexone. Although acute L-NAME treatment of mesenteric beds completely blocked the anandamide-induced vasorelaxation in sham-operated rats, this vasorelaxation still was present in bile duct-ligated animals. Anandamide-induced vasorelaxation remained unaffected after acute naltrexone treatment of mesenteric beds in both bile duct-ligated and sham-operated rats. Our results indicate that (1) there is enhanced anandamideinduced vasorelaxation in cholestatic rats, probably due to a defect in cannabinoid or vanilloid receptors and (2) NO overproduction may be involved in cholestasis-induced vascular hyperresponsiveness.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"European Journal of 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data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway"><img alt="Research paper thumbnail of Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway">Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric o...</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 endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.</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="102073300"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073300"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073300; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073300]").text(description); $(".js-view-count[data-work-id=102073300]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073300; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073300']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073300, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073300]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073300,"title":"Time-dependent reduction of acetylcholine-induced relaxation in corpus cavernosum of cholestatic rats: role of nitric oxide and cyclooxygenase pathway","translated_title":"","metadata":{"abstract":"The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.","publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"European Journal of Pharmacology"},"translated_abstract":"The endothelium-dependent relaxation of corpus cavernosum smooth muscle and the roles of nitric oxide (NO) and arachidonic acid products of cyclooxygenase were investigated in non-operated, SHAM-operated, and bile duct-ligated rats. We further investigated the time-dependent alterations of corpus cavernosum relaxation in 2-, 7-, and 14-day bile duct-ligated animals. Acetylcholine produced concentration-dependent relaxation in phenylephrine-precontracted strips of corpus cavernosum. A significant reduction in the acetylcholine-induced relaxation was observed 2 days after bile duct ligation, and a greater reduction was observed on subsequent days. Incubation with 20 microM indomethacin reduced the acetylcholine-induced relaxation of the corpus cavernosum of unoperated rats while it had no effect in the corpus cavernosum of bile duct-ligated rats. Chronic treatment with Nomega-Nitro-L-Arginine Methyl Ester (L-NAME, 3 mg/kg/day, intraperitoneally) reduced the relaxation responses in the unoperated group while it had no effect in the bile duct-ligated group. These results show that acetylcholine-induced corporal relaxation is impaired in cholestatic rats, and this may be related to deficient nitric oxide production by the endothelium. The involvement of prostaglandins in this impairment seems unlikely.","internal_url":"https://www.academia.edu/102073300/Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway","translated_internal_url":"","created_at":"2023-05-20T06:51:43.313-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Time_dependent_reduction_of_acetylcholine_induced_relaxation_in_corpus_cavernosum_of_cholestatic_rats_role_of_nitric_oxide_and_cyclooxygenase_pathway","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":154,"name":"Endocrinology","url":"https://www.academia.edu/Documents/in/Endocrinology"},{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":12981,"name":"Enzyme Inhibitors","url":"https://www.academia.edu/Documents/in/Enzyme_Inhibitors"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":159958,"name":"Acetylcholine","url":"https://www.academia.edu/Documents/in/Acetylcholine"},{"id":178753,"name":"Penis","url":"https://www.academia.edu/Documents/in/Penis"},{"id":279027,"name":"European","url":"https://www.academia.edu/Documents/in/European"},{"id":382388,"name":"Nitric Oxide Synthase","url":"https://www.academia.edu/Documents/in/Nitric_Oxide_Synthase"},{"id":555120,"name":"Arginine","url":"https://www.academia.edu/Documents/in/Arginine"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1272871,"name":"Muscle Relaxation","url":"https://www.academia.edu/Documents/in/Muscle_Relaxation"},{"id":1358142,"name":"Methyl Ester","url":"https://www.academia.edu/Documents/in/Methyl_Ester"},{"id":1509324,"name":"Arachidonic Acid","url":"https://www.academia.edu/Documents/in/Arachidonic_Acid"},{"id":1866509,"name":"Indomethacin","url":"https://www.academia.edu/Documents/in/Indomethacin"},{"id":2611583,"name":"cholestasis","url":"https://www.academia.edu/Documents/in/cholestasis"},{"id":3881526,"name":"In Vitro Techniques","url":"https://www.academia.edu/Documents/in/In_Vitro_Techniques"}],"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="102073299"><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/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors"><img alt="Research paper thumbnail of The synergistic anticonvulsant effect of agmatine and morphine: Possible role of alpha 2-adrenoceptors" class="work-thumbnail" src="https://attachments.academia-assets.com/102435682/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/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors">The synergistic anticonvulsant effect of agmatine and morphine: Possible role of alpha 2-adrenoceptors</a></div><div class="wp-workCard_item"><span>Epilepsy Research</span><span>, 2005</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="db856e7698aa9c29424e2a0d01747d2c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":102435682,"asset_id":102073299,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/102435682/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&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="102073299"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073299"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073299; 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We investigated the possibility of an additive anticonvulsant effect between low doses of agmatine and morphine. The thresholds for the clonic seizures induced by the intravenous administration of gamma-aminobutyric acid (GABA)-antagonist, pentylenetetrazole (PTZ) were assessed in mice. Morphine at lower doses (1-3 mg/kg) increased and at higher doses (30, 60 mg/kg) decreased the seizure threhsold. Pretreatment with a per se non-effective dose of agmatine (1 mg/kg) potentiated the anticonvulsant effect of morphine. The combination of subeffective doses of agmatine and morphine led to potent anticonvulsant effects. The proconvulsant effect of morphine was attenuated by agmatine. Yohimbine with a dose (1 mg/kg) incapable of affecting seizure threshold reversed the effect of agmatine on both anticonvulsant and proconvulsant effects of morphine. These results suggest that agmatine potentiates the anticonvulsant effect of morphine and alpha 2-adrenoceptors may be involved in this effect.","publication_date":{"day":null,"month":null,"year":2005,"errors":{}},"publication_name":"Epilepsy Research","grobid_abstract_attachment_id":102435682},"translated_abstract":null,"internal_url":"https://www.academia.edu/102073299/The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors","translated_internal_url":"","created_at":"2023-05-20T06:51:43.160-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":102435682,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/102435682/thumbnails/1.jpg","file_name":"j.eplepsyres.2005.04.00320230520-1-9imgcf.pdf","download_url":"https://www.academia.edu/attachments/102435682/download_file?st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&st=MTczMjQyMjI2Myw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"The_synergistic_anticonvulsant_effect_of.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/102435682/j.eplepsyres.2005.04.00320230520-1-9imgcf-libre.pdf?1684594568=\u0026response-content-disposition=attachment%3B+filename%3DThe_synergistic_anticonvulsant_effect_of.pdf\u0026Expires=1732425863\u0026Signature=LVZ-8vpZ8gq3t44SOIveBhlCA-n1E5e2pkK1LJkHUD6NX4I2kHZ03xOsc7uY8abfAji8MjLfiLZgxJEJ6~njagmKWpa6~rD6Bh9mJdrgueICRMm77dDqoFAkkz1MBhnB60kIS3gjgNsuSAiKJVjCkgU75oybjK0eGsT6M8MQFFtr4JQIioj6vkDtR4lPJXocNsIaKMANZ7FYpPIvbBNh58FPOv95P6cwNfkF2CjHrsSZ350Mpy8YjRFNTonyExE8Y5Y7ZBpSvW3J8Gm5D3jY8BjOpvwRP8Yv0bE9Bdp9u7h7uUxbtUhLGS74R-QrEhQPdFGcBGxhU3nEHZtZqobCDw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"The_synergistic_anticonvulsant_effect_of_agmatine_and_morphine_Possible_role_of_alpha_2_adrenoceptors","translated_slug":"","page_count":8,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad 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Dose","url":"https://www.academia.edu/Documents/in/Low_Dose"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":218374,"name":"Morphine","url":"https://www.academia.edu/Documents/in/Morphine"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":413194,"name":"Analysis of Variance","url":"https://www.academia.edu/Documents/in/Analysis_of_Variance"},{"id":651604,"name":"Seizures","url":"https://www.academia.edu/Documents/in/Seizures"},{"id":1225893,"name":"Effective Dose","url":"https://www.academia.edu/Documents/in/Effective_Dose"},{"id":1957847,"name":"Pentylenetetrazole","url":"https://www.academia.edu/Documents/in/Pentylenetetrazole"},{"id":1957848,"name":"Seizure threshold","url":"https://www.academia.edu/Documents/in/Seizure_threshold"},{"id":2661220,"name":"Agmatine","url":"https://www.academia.edu/Documents/in/Agmatine"},{"id":3509231,"name":"Yohimbine","url":"https://www.academia.edu/Documents/in/Yohimbine"},{"id":3545627,"name":"Drug synergism","url":"https://www.academia.edu/Documents/in/Drug_synergism"}],"urls":[{"id":31597725,"url":"https://api.elsevier.com/content/article/PII:S0920121105000768?httpAccept=text/xml"}]}, 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="102073298"><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/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis"><img alt="Research paper thumbnail of Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" rel="nofollow" href="https://www.academia.edu/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis">Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis</a></div><div class="wp-workCard_item"><span>Digestive Diseases and Sciences</span><span>, 2008</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic ...</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">Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;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; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.</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="102073298"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073298"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073298; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073298]").text(description); $(".js-view-count[data-work-id=102073298]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073298; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073298']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073298, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073298]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073298,"title":"Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis","translated_title":"","metadata":{"abstract":"Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P \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;lt; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P \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;lt; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P \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;lt; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.","publisher":"Springer Science and Business Media LLC","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Digestive Diseases and Sciences"},"translated_abstract":"Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P \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;lt; 0.01). Chronic opioid receptor blockade significantly increased this parameter (P \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;lt; 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P \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;lt; 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.","internal_url":"https://www.academia.edu/102073298/Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis","translated_internal_url":"","created_at":"2023-05-20T06:51:42.988-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":270485136,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Opioid_Receptor_Blockade_Improves_Mesenteric_Responsiveness_in_Biliary_Cirrhosis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":270485136,"first_name":"Mohammad","middle_initials":null,"last_name":"Ebrahimkhani","page_name":"MohammadEbrahimkhani","domain_name":"independent","created_at":"2023-05-20T06:48:45.436-07:00","display_name":"Mohammad Ebrahimkhani","url":"https://independent.academia.edu/MohammadEbrahimkhani"},"attachments":[],"research_interests":[{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":65390,"name":"Internal Medicine","url":"https://www.academia.edu/Documents/in/Internal_Medicine"},{"id":93659,"name":"Digestive and Liver Diseases","url":"https://www.academia.edu/Documents/in/Digestive_and_Liver_Diseases"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":122402,"name":"Nitrates","url":"https://www.academia.edu/Documents/in/Nitrates"},{"id":204388,"name":"Vasoconstriction","url":"https://www.academia.edu/Documents/in/Vasoconstriction"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":244849,"name":"Hepatic Encephalopathy","url":"https://www.academia.edu/Documents/in/Hepatic_Encephalopathy"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":767931,"name":"Naltrexone","url":"https://www.academia.edu/Documents/in/Naltrexone"},{"id":956370,"name":"Opioid Receptor","url":"https://www.academia.edu/Documents/in/Opioid_Receptor"},{"id":1000359,"name":"Phenylephrine","url":"https://www.academia.edu/Documents/in/Phenylephrine"},{"id":1255525,"name":"Chronic Liver Disease","url":"https://www.academia.edu/Documents/in/Chronic_Liver_Disease"},{"id":1654024,"name":"Nitrites","url":"https://www.academia.edu/Documents/in/Nitrites"},{"id":2581997,"name":"splanchnic circulation","url":"https://www.academia.edu/Documents/in/splanchnic_circulation"},{"id":3430960,"name":"Mesentery","url":"https://www.academia.edu/Documents/in/Mesentery"},{"id":3589281,"name":"Ligation","url":"https://www.academia.edu/Documents/in/Ligation"},{"id":3635108,"name":"Superior mesenteric artery","url":"https://www.academia.edu/Documents/in/Superior_mesenteric_artery"}],"urls":[{"id":31597724,"url":"http://link.springer.com/content/pdf/10.1007/s10620-008-0261-7.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="102073297"><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/102073297/Lithium_inhibits_the_modulatory_effects_of_morphine_on_susceptibility_to_pentylenetetrazole_induced_clonic_seizure_in_mice_involvement_of_a_nitric_oxide_pathway"><img alt="Research paper thumbnail of Lithium inhibits the modulatory effects of morphine on susceptibility to pentylenetetrazole-induced clonic seizure in mice: involvement of a nitric oxide pathway" 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"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/102073297/Lithium_inhibits_the_modulatory_effects_of_morphine_on_susceptibility_to_pentylenetetrazole_induced_clonic_seizure_in_mice_involvement_of_a_nitric_oxide_pathway">Lithium inhibits the modulatory effects of morphine on susceptibility to pentylenetetrazole-induced clonic seizure in mice: involvement of a nitric oxide pathway</a></div><div class="wp-workCard_item"><span>Brain Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lithium has been reported to inhibit opioid-induced properties. The present study examined the ef...</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">Lithium has been reported to inhibit opioid-induced properties. The present study examined the effect of acute and chronic administration of lithium chloride (LiCl) on morphine&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s biphasic modulation of susceptibility to pentylenetetrazole (PTZ)-induced clonic seizure in mice. We also examined the possible involvement of nitric oxide (NO) pathway in lithium effect. Both acute (0.1 and 1 mg/kg) and chronic (same doses, 21 consecutive days) administration of LiCl completely inhibited the anticonvulsant and proconvulsant effects of morphine (at doses 1 and 30 mg/kg, respectively). A very low and per se noneffective dose of LiCl (0.05 mg/kg) significantly inhibited both phases of morphine effect when administered concomitant with a noneffective low dose of naloxone (0.1 mg/kg). The NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) at a per se noneffective dose of 0.3 mg/kg potentiated the inhibitory effects of low doses of LiCl (0.01 and 0.05 mg/kg) on both phases of morphine effect. l-arginine, a NO synthase substrate, at a per se noneffective dose of 30 mg/kg reversed the inhibitory effects of lithium (1 mg/kg). Lithium is capable of antagonizing both modulatory effects of morphine on seizure susceptibility even at relatively low doses. These inhibitory effects of lithium may also involve NO synthesis.</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="102073297"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="102073297"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 102073297; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=102073297]").text(description); $(".js-view-count[data-work-id=102073297]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 102073297; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='102073297']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 102073297, container: "", }); });</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-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.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" } } $('.js-work-strip[data-work-id=102073297]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":102073297,"title":"Lithium inhibits the modulatory effects of morphine on susceptibility to pentylenetetrazole-induced clonic seizure in mice: involvement of a nitric oxide pathway","translated_title":"","metadata":{"abstract":"Lithium has been reported to inhibit opioid-induced properties. The present study examined the effect of acute and chronic administration of lithium chloride (LiCl) on morphine\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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s biphasic modulation of susceptibility to pentylenetetrazole (PTZ)-induced clonic seizure in mice. We also examined the possible involvement of nitric oxide (NO) pathway in lithium effect. Both acute (0.1 and 1 mg/kg) and chronic (same doses, 21 consecutive days) administration of LiCl completely inhibited the anticonvulsant and proconvulsant effects of morphine (at doses 1 and 30 mg/kg, respectively). A very low and per se noneffective dose of LiCl (0.05 mg/kg) significantly inhibited both phases of morphine effect when administered concomitant with a noneffective low dose of naloxone (0.1 mg/kg). The NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) at a per se noneffective dose of 0.3 mg/kg potentiated the inhibitory effects of low doses of LiCl (0.01 and 0.05 mg/kg) on both phases of morphine effect. l-arginine, a NO synthase substrate, at a per se noneffective dose of 30 mg/kg reversed the inhibitory effects of lithium (1 mg/kg). Lithium is capable of antagonizing both modulatory effects of morphine on seizure susceptibility even at relatively low doses. These inhibitory effects of lithium may also involve NO synthesis.","publisher":"Elsevier BV","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Brain Research"},"translated_abstract":"Lithium has been reported to inhibit opioid-induced properties. The present study examined the effect of acute and chronic administration of lithium chloride (LiCl) on morphine\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;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s biphasic modulation of susceptibility to pentylenetetrazole (PTZ)-induced clonic seizure in mice. We also examined the possible involvement of nitric oxide (NO) pathway in lithium effect. Both acute (0.1 and 1 mg/kg) and chronic (same doses, 21 consecutive days) administration of LiCl completely inhibited the anticonvulsant and proconvulsant effects of morphine (at doses 1 and 30 mg/kg, respectively). A very low and per se noneffective dose of LiCl (0.05 mg/kg) significantly inhibited both phases of morphine effect when administered concomitant with a noneffective low dose of naloxone (0.1 mg/kg). The NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) at a per se noneffective dose of 0.3 mg/kg potentiated the inhibitory effects of low doses of LiCl (0.01 and 0.05 mg/kg) on both phases of morphine effect. l-arginine, a NO synthase substrate, at a per se noneffective dose of 30 mg/kg reversed the inhibitory effects of lithium (1 mg/kg). Lithium is capable of antagonizing both modulatory effects of morphine on seizure susceptibility even at relatively low doses. 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