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class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://univ-lille1.academia.edu/MSalzet"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://univ-lille1.academia.edu/MSalzet">Michel Salzet</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Université des Sciences et Technologies de Lille (Lille-1)</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://pitt.academia.edu/VladimirTyurin"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://pitt.academia.edu/VladimirTyurin">Vladimir Tyurin</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of Pittsburgh</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://independent.academia.edu/ValentinaKapralova"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://independent.academia.edu/ValentinaKapralova">Valentina Kapralova</a></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://independent.academia.edu/ValerianKagan"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://independent.academia.edu/ValerianKagan">Valerian Kagan</a></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://independent.academia.edu/NicholasWinograd"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://independent.academia.edu/NicholasWinograd">Nicholas Winograd</a></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://independent.academia.edu/WalterShaw"><img class="profile-avatar u-positionAbsolute" alt="Walter Shaw" border="0" onerror="if (this.src != 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Pittsburgh</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://independent.academia.edu/MarisolLeon46"><img class="profile-avatar u-positionAbsolute" alt="Marisol Leon" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/271539014/121747673/111082897/s200_marisol.leon.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://independent.academia.edu/MarisolLeon46">Marisol Leon</a></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://utad.academia.edu/FranciscoPeixoto"><img class="profile-avatar u-positionAbsolute" border="0" alt="" src="//a.academia-assets.com/images/s200_no_pic.png" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://utad.academia.edu/FranciscoPeixoto">Francisco Peixoto</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">Universidade de Trás-os-Montes e Alto Douro (UTAD)</p></div></div><div class="suggested-user-card"><div class="suggested-user-card__avatar social-profile-avatar-container"><a href="https://medbiotech.academia.edu/EvaSzabo"><img class="profile-avatar u-positionAbsolute" alt="Eva Szabo" border="0" onerror="if (this.src != '//a.academia-assets.com/images/s200_no_pic.png') this.src = '//a.academia-assets.com/images/s200_no_pic.png';" width="200" height="200" src="https://0.academia-photos.com/243098507/97726582/86815601/s200_eva.szabo.jpg" /></a></div><div class="suggested-user-card__user-info"><a class="suggested-user-card__user-info__header ds2-5-body-sm-bold ds2-5-body-link" href="https://medbiotech.academia.edu/EvaSzabo">Eva Szabo</a><p class="suggested-user-card__user-info__subheader ds2-5-body-xs">University of Pécs</p></div></div></ul></div><div class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="33280586" href="https://www.academia.edu/Documents/in/Human_Sciences"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/AndrewAmoscato","location":"/AndrewAmoscato","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/AndrewAmoscato","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Human Sciences"]}" data-trace="false" data-dom-id="Pill-react-component-ec5540c3-a516-40bd-9440-01b0bca4aded"></div> <div id="Pill-react-component-ec5540c3-a516-40bd-9440-01b0bca4aded"></div> </a></div></div></div></div><div class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Andrew Amoscato</h3></div><div class="js-work-strip profile--work_container" data-work-id="114169406"><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/114169406/Mapping_of_phospholipids_by_MALDI_imaging_MALDI_MSI_realities_and_expectations"><img alt="Research paper thumbnail of Mapping of phospholipids by MALDI imaging (MALDI-MSI): realities and expectations" class="work-thumbnail" src="https://attachments.academia-assets.com/110937648/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/114169406/Mapping_of_phospholipids_by_MALDI_imaging_MALDI_MSI_realities_and_expectations">Mapping of phospholipids by MALDI imaging (MALDI-MSI): realities and expectations</a></div><div class="wp-workCard_item"><span>Chemistry and Physics of Lipids</span><span>, Jul 1, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has emerged as ...</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">Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has emerged as a novel powerful MS methodology that has the ability to generate both molecular and spatial information within a tissue section. Application of this technology as a new type of biochemical lipid microscopy may lead to new discoveries of the lipid metabolism and biomarkers associated with area-specific alterations or damage under stress/disease conditions such as traumatic brain injury or acute lung injury, among others. However there are limitations in the range of what it can detect as compared with liquid chromatography-MS (LC-MS) of a lipid extract from a tissue section. The goal of the current work was to critically consider remarkable new opportunities along with the limitations and approaches for further improvements of MALDI-MSI. Based on our experimental data and assessments, improvements of the spectral and spatial resolution, sensitivity and specificity towards low abundance species of lipids are proposed. This is followed by a review of the current literature, including methodologies that other laboratories have used to overcome these challenges.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2ef751b699e2ae5928ce3edbf1667809" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937648,"asset_id":114169406,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937648/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169406"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169406"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169406; 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$(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="114169404"><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/114169404/Imaging_mass_spectrometry_reveals_loss_of_polyunsaturated_cardiolipins_in_the_cortical_contusion_hippocampus_and_thalamus_after_traumatic_brain_injury"><img alt="Research paper thumbnail of Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury" class="work-thumbnail" src="https://attachments.academia-assets.com/110937649/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/114169404/Imaging_mass_spectrometry_reveals_loss_of_polyunsaturated_cardiolipins_in_the_cortical_contusion_hippocampus_and_thalamus_after_traumatic_brain_injury">Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury</a></div><div class="wp-workCard_item"><span>Journal of Neurochemistry</span><span>, Sep 26, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traumatic brain injury (TBI) leads to changes in ion fluxes, alterations in mitochondrial functio...</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">Traumatic brain injury (TBI) leads to changes in ion fluxes, alterations in mitochondrial function and increased generation of reactive oxygen species, resulting in secondary tissue damage. Mitochondria play important signaling roles in coordination of multiple metabolic platforms in addition to their well-known role in bioenergetics. Mitochondrial signaling strongly depends on cardiolipin (CL), a mitochondria-specific structurally unusual anionic phospholipid containing four fatty acyl chains. While our previous reports indicated that CL is selectively oxidized and presents itself as a target for the redox therapy following TBI, the topography of changes of CL in the injured brain remained to be defined. Here we present a MALDI imaging study which reports regio-specific changes in CL, in a controlled cortical impact (CCI) model of TBI in rats. MALDI imaging revealed that TBI caused early decreases in CL in the contusional cortex, ipsilateral hippocampus and thalamus with the most highly unsaturated CL species being most susceptible to loss. Phosphatidylinositol was the only other lipid species that exhibited a significant decrease, albeit to a lesser extent than CL. Signals for other lipids remained unchanged. This is the first study evaluating the spatial distribution of CL loss after acute brain injury. We propose that the CL loss may constitute an upstream mechanism for CL-driven signaling in different brain regions as an early response mechanism and may also underlie the bioenergetic changes that occur in hippocampal, cortical and thalamic mitochondria after TBI.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ee90a79b2fd469eb04f60fa2d9a7dade" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937649,"asset_id":114169404,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937649/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169404"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169404"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169404; 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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="114169402"><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/114169402/Mass_spectrometry_based_oxidative_lipidomics_and_lipid_imaging_applications_in_traumatic_brain_injury"><img alt="Research paper thumbnail of Mass-spectrometry based oxidative lipidomics and lipid imaging: applications in traumatic brain injury" class="work-thumbnail" src="https://attachments.academia-assets.com/110937646/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/114169402/Mass_spectrometry_based_oxidative_lipidomics_and_lipid_imaging_applications_in_traumatic_brain_injury">Mass-spectrometry based oxidative lipidomics and lipid imaging: applications in traumatic brain injury</a></div><div class="wp-workCard_item"><span>Journal of Neurochemistry</span><span>, Nov 19, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lipids, particularly phospholipids, are fundamental to central nervous system (CNS) tissue archit...</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">Lipids, particularly phospholipids, are fundamental to central nervous system (CNS) tissue architecture and function. Endogenous polyunsaturated fatty acid chains of phospholipids possess cis-double bonds each separated by one methylene group. These phospholipids are very susceptible to free-radical attack and oxidative modifications. A combination of analytical methods including different versions of chromatography and mass spectrometry allows obtaining detailed information on the content and distribution of lipids and their oxidation products thus constituting the newly emerging field of oxidative lipidomics. It is becoming evident that specific oxidative modifications of lipids are critical to a number of cellular functions, disease states and responses to oxidative stresses. Oxidative lipidomics is beginning to provide new mechanistic insights into traumatic brain injury (TBI) which may have significant translational potential for development of therapies in acute CNS insults. In particular, selective oxidation of a mitochondria-specific phospholipid, cardiolipin, has been associated with the initiation and progression of apoptosis in injured neurons thus indicating new drug discovery targets. Further, imaging mass-spectrometry represents an exciting new opportunity for correlating maps of lipid profiles and their oxidation products with structure and neuropathology. This review is focused on these most recent advancements in the field of lipidomics and oxidative lipidomics based on the applications of mass-spectrometry and imaging mass-spectrometry as they relate to studies of phospholipids in TBI.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="05904bfd93819434bc6812f76b4c611f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937646,"asset_id":114169402,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937646/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169402"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169402"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169402; 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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="114169389"><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/114169389/Redox_phospho_lipidomics_of_signaling_in_inflammation_and_programmed_cell_death"><img alt="Research paper thumbnail of Redox (phospho)lipidomics of signaling in inflammation and programmed cell death" class="work-thumbnail" src="https://attachments.academia-assets.com/110937662/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/114169389/Redox_phospho_lipidomics_of_signaling_in_inflammation_and_programmed_cell_death">Redox (phospho)lipidomics of signaling in inflammation and programmed cell death</a></div><div class="wp-workCard_item"><span>Journal of Leukocyte Biology</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In addition to the known prominent role of polyunsaturated (phospho)lipids as structural blocks 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">In addition to the known prominent role of polyunsaturated (phospho)lipids as structural blocks of biomembranes, there is an emerging understanding of another important function of these molecules as a highly diversified signaling language utilized for intra- and extracellular communications. Technological developments in high-resolution mass spectrometry facilitated the development of a new branch of metabolomics, redox lipidomics. Analysis of lipid peroxidation reactions has already identified specific enzymatic mechanisms responsible for the biosynthesis of several unique signals in response to inflammation and regulated cell death programs. Obtaining comprehensive information about millions of signals encoded by oxidized phospholipids, represented by thousands of interactive reactions and pleiotropic (patho)physiological effects, is a daunting task. However, there is still reasonable hope that significant discoveries, of at least some of the important contributors to the overall...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="27bef88dadbce06f44f5d0ef81830b02" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937662,"asset_id":114169389,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937662/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169389"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169389"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169389; 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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="108120979"><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/108120979/Identification_of_Human_Aldehyde_Dehydrogenase_1_Family_Member_A1_as_a_Novel_CD8_T_Cell_Defined_Tumor_Antigen_in_Squamous_Cell_Carcinoma_of_the_Head_and_Neck"><img alt="Research paper thumbnail of Identification of Human Aldehyde Dehydrogenase 1 Family Member A1 as a Novel CD8+ T-Cell–Defined Tumor Antigen in Squamous Cell Carcinoma of the Head and Neck" class="work-thumbnail" src="https://attachments.academia-assets.com/106589650/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/108120979/Identification_of_Human_Aldehyde_Dehydrogenase_1_Family_Member_A1_as_a_Novel_CD8_T_Cell_Defined_Tumor_Antigen_in_Squamous_Cell_Carcinoma_of_the_Head_and_Neck">Identification of Human Aldehyde Dehydrogenase 1 Family Member A1 as a Novel CD8+ T-Cell–Defined Tumor Antigen in Squamous Cell Carcinoma of the Head and Neck</a></div><div class="wp-workCard_item"><span>Cancer Research</span><span>, 2007</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Few epitopes are available for vaccination therapy of patients with squamous cell carcinoma of th...</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">Few epitopes are available for vaccination therapy of patients with squamous cell carcinoma of the head and neck (SCCHN). Using a tumor-specific CTL, aldehyde dehydrogenase 1 family member A1 (ALDH1A1) was identified as a novel tumor antigen in SCCHN. Mass spectral analysis of peptides in tumor-derived lysates was used to determine that the CTL line recognized the HLA-A*0201 (HLA-A2) binding ALDH1A188-96 peptide. Expression of ALDH1A1 in established SCCHN cell lines, normal mucosa, and primary keratinocytes was studied by quantitative reverse transcription-PCR and immunostaining. Protein expression was further defined by immunoblot analysis, whereas ALDH1A1 activity was measured using ALDEFLUOR. ALDH1A188-96 peptide was identified as an HLA-A2–restricted, naturally presented, CD8+ T-cell–defined tumor peptide. ALDH1A188-96 peptide-specific CD8+ T cells recognized only HLA-A2+ SCCHN cell lines, which overexpressed ALDH1A1, as well as targets transfected with ALDH1A1 cDNA. 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Using a tumor-specific CTL, aldehyde dehydrogenase 1 family member A1 (ALDH1A1) was identified as a novel tumor antigen in SCCHN. Mass spectral analysis of peptides in tumor-derived lysates was used to determine that the CTL line recognized the HLA-A*0201 (HLA-A2) binding ALDH1A188-96 peptide. Expression of ALDH1A1 in established SCCHN cell lines, normal mucosa, and primary keratinocytes was studied by quantitative reverse transcription-PCR and immunostaining. Protein expression was further defined by immunoblot analysis, whereas ALDH1A1 activity was measured using ALDEFLUOR. ALDH1A188-96 peptide was identified as an HLA-A2–restricted, naturally presented, CD8+ T-cell–defined tumor peptide. ALDH1A188-96 peptide-specific CD8+ T cells recognized only HLA-A2+ SCCHN cell lines, which overexpressed ALDH1A1, as well as targets transfected with ALDH1A1 cDNA. 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=100452677]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452677,"title":"1475: Detection of Brain Cardiolipins in Plasma After Cardiac Arrest","internal_url":"https://www.academia.edu/100452677/1475_Detection_of_Brain_Cardiolipins_in_Plasma_After_Cardiac_Arrest","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[]}, 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="100452676"><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/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis"><img alt="Research paper thumbnail of Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/101273116/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/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis">Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Apoptosis has been identified recently as a component of many cardiac pathologies. However, the p...</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">Apoptosis has been identified recently as a component of many cardiac pathologies. However, the potential triggers of programmed cell death in the heart and the involvement of specific metabolic pathway(s) are less well characterized. Detachment of cytochrome c from the mitochondrial inner membrane is a necessary first step for cytochrome c release into the cytosol and initiation of apoptosis. The saturated long chain fatty acid, palmitate, induces apoptosis in rat neonatal cardiomyocytes and diminishes content of the mitochondrial anionic phospholipid, cardiolipin. These changes are accompanied by 1) acyl chain saturation of phosphatidic acid and phosphatidylglycerol, 2) large increases in the levels of these two phospholipids, and 3) a decline in cardiolipin synthesis. Although cardiolipin synthase activity is unchanged, saturated phosphatidylglycerol is a poor substrate for this enzyme. Under these conditions, decreased cardiolipin synthesis and release of cytochrome c are directly and significantly correlated. The results suggest that phosphatidylglycerol saturation and subsequent decreases in cardiolipin affect the association of cytochrome c with the inner mitochondrial membrane, directly influencing the pathway to cytochrome c release and subsequent apoptosis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fb2e6eb7d076d3d025560b11ebd40885" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273116,"asset_id":100452676,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273116/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452676"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452676"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452676; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452676]").text(description); $(".js-view-count[data-work-id=100452676]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452676; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452676']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "fb2e6eb7d076d3d025560b11ebd40885" } } $('.js-work-strip[data-work-id=100452676]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452676,"title":"Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis","internal_url":"https://www.academia.edu/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[{"id":101273116,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/101273116/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/101273116/download_file","bulk_download_file_name":"Decreased_Cardiolipin_Synthesis_Correspo.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/101273116/pdf-libre.pdf?1681933809=\u0026response-content-disposition=attachment%3B+filename%3DDecreased_Cardiolipin_Synthesis_Correspo.pdf\u0026Expires=1740158365\u0026Signature=CHbZSlfNMLu1ApCeUSU-VOwghW4oImEI2eeX9~TyMqpJLsQaZyssOjiMkUkwG1fn74-gDGBrdHH3fg98X4qZNDEb~n5nTQLSPeV6K6413TATQF-lLng~JuCuEsd9uo8-N~qREuxwaCvofSWax7M5woqAJAL6T0r-QwhOg4xKwaU4F1A6VKYEp7p7fkHaMlchAIA9l8v4ZM9LkSwT5YUmIRUDqBJt52JgIKCpC1j4c8-zwWN27RIR4S4PttN87sd3jYhTvGb0Gi~Lf8Z8ZnIwzFwFB0Ew3-vYtLroNsuUXv-MsiCzk52onq1p1QkXESh3MmIpYGHG4AaWtGdEz8f8Cw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="100452675"><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/100452675/Aberrant_cardiolipin_metabolism_is_associated_with_cognitive_deficiency_and_hippocampal_alteration_in_tafazzin_knockdown_mice"><img alt="Research paper thumbnail of Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice" class="work-thumbnail" src="https://attachments.academia-assets.com/101273115/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/100452675/Aberrant_cardiolipin_metabolism_is_associated_with_cognitive_deficiency_and_hippocampal_alteration_in_tafazzin_knockdown_mice">Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta. Molecular basis of disease</span><span>, 2018</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cardiolipin (CL) is a key mitochondrial phospholipid essential for mitochondrial energy productio...</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">Cardiolipin (CL) is a key mitochondrial phospholipid essential for mitochondrial energy production. CL is remodeled from monolysocardiolipin (MLCL) by the enzyme tafazzin (TAZ). Loss-of-function mutations in the gene which encodes TAZ results in a rare X-linked disorder called Barth Syndrome (BTHS). The mutated TAZ is unable to maintain the physiological CL:MLCL ratio, thus reducing CL levels and affecting mitochondrial function. BTHS is best known as a cardiac disease, but has been acknowledged as a multi-syndrome disorder, including cognitive deficits. Since reduced CL levels has also been reported in numerous neurodegenerative disorders, we examined how TAZ-deficiency impacts cognitive abilities, brain mitochondrial respiration and the function of hippocampal neurons and glia in TAZ knockdown (TAZ kd) mice. We have identified for the first time the profile of changes that occur in brain phospholipid content and composition of TAZ kd mice. The brain of TAZ kd mice exhibited reduce...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fb13594ca713362b043b410137c9a70f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273115,"asset_id":100452675,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273115/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452675"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452675"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452675; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452675]").text(description); $(".js-view-count[data-work-id=100452675]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452675; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452675']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="100452674"><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/100452674/Gas_Cluster_Ion_Beam_Time_of_Flight_Secondary_Ion_Mass_Spectrometry_High_Resolution_Imaging_of_Cardiolipin_Speciation_in_the_Brain_Identification_of_Molecular_Losses_after_Traumatic_Injury"><img alt="Research paper thumbnail of Gas Cluster Ion Beam Time-of-Flight Secondary Ion Mass Spectrometry High-Resolution Imaging of Cardiolipin Speciation in the Brain: Identification of Molecular Losses after Traumatic Injury" class="work-thumbnail" src="https://attachments.academia-assets.com/101273123/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/100452674/Gas_Cluster_Ion_Beam_Time_of_Flight_Secondary_Ion_Mass_Spectrometry_High_Resolution_Imaging_of_Cardiolipin_Speciation_in_the_Brain_Identification_of_Molecular_Losses_after_Traumatic_Injury">Gas Cluster Ion Beam Time-of-Flight Secondary Ion Mass Spectrometry High-Resolution Imaging of Cardiolipin Speciation in the Brain: Identification of Molecular Losses after Traumatic Injury</a></div><div class="wp-workCard_item"><span>Analytical chemistry</span><span>, Jan 18, 2017</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Gas cluster ion beam-secondary ion mass spectrometry (GCIB-SIMS) has shown the full potential of ...</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">Gas cluster ion beam-secondary ion mass spectrometry (GCIB-SIMS) has shown the full potential of mapping intact lipids in biological systems with better than 10 μm lateral resolution. This study investigated further the capability of GCIB-SIMS in imaging high-mass signals from intact cardiolipin (CL) and gangliosides in normal brain and the effect of a controlled cortical impact model (CCI) of traumatic brain injury (TBI) on their distribution. A combination of enzymatic and chemical treatments was employed to suppress the signals from the most abundant phospholipids (phosphatidylcholine (PC) and phosphatidylethanolamine (PE)) and enhance the signals from the low-abundance CLs and gangliosides to allow their GCIB-SIMS detection at 8 and 16 μm spatial resolution. Brain CLs have not been observed previously using other contemporary imaging mass spectrometry techniques at better than 50 μm spatial resolution. High-resolution images of naive and injured brain tissue facilitated the comp...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ba6f50f99055df40c596c36f587d4db5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273123,"asset_id":100452674,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273123/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452674"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452674"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452674; 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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="100452673"><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/100452673/Global_assessment_of_oxidized_free_fatty_acids_in_brain_reveals_an_enzymatic_predominance_to_oxidative_signaling_after_trauma"><img alt="Research paper thumbnail of Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma" class="work-thumbnail" src="https://attachments.academia-assets.com/101273112/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/100452673/Global_assessment_of_oxidized_free_fatty_acids_in_brain_reveals_an_enzymatic_predominance_to_oxidative_signaling_after_trauma">Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta</span><span>, Jan 24, 2017</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traumatic brain injury (TBI) is a major health problem associated with significant morbidity and ...</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">Traumatic brain injury (TBI) is a major health problem associated with significant morbidity and mortality. The pathophysiology of TBI is complex involving signaling through multiple cascades, including lipid peroxidation. Oxidized free fatty acids, a prominent product of lipid peroxidation, are potent cellular mediators involved in induction and resolution of inflammation and modulation of vasomotor tone. While previous studies have assessed lipid peroxidation after TBI, to our knowledge no studies have used a systematic approach to quantify the global oxidative changes in free fatty acids. In this study, we identified and quantified 244 free fatty acid oxidation products using a newly developed global liquid chromatography tandem-mass spectrometry (LC-MS/MS) method. This methodology was used to follow the time course of these lipid species in the contusional cortex of our pediatric rat model of TBI. We show that oxidation peaked at 1h after controlled cortical impact and was progr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f0bf21ed1f14e50977b63bc6531335b4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273112,"asset_id":100452673,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273112/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452673"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452673"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452673; 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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="100452672"><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/100452672/Known_unknowns_of_cardiolipin_signaling_The_best_is_yet_to_come"><img alt="Research paper thumbnail of Known unknowns of cardiolipin signaling: The best is yet to come" class="work-thumbnail" src="https://attachments.academia-assets.com/101273121/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/100452672/Known_unknowns_of_cardiolipin_signaling_The_best_is_yet_to_come">Known unknowns of cardiolipin signaling: The best is yet to come</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta</span><span>, Jan 4, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Since its discovery 75years ago, a wealth of knowledge has accumulated on the role of cardiolipin...</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">Since its discovery 75years ago, a wealth of knowledge has accumulated on the role of cardiolipin, the hallmark phospholipid of mitochondria, in bioenergetics and particularly on the structural organization of the inner mitochondrial membrane. A surge of interest in this anionic doubly-charged tetra-acylated lipid found in both prokaryotes and mitochondria has emerged based on its newly discovered signaling functions. Cardiolipin displays organ, tissue, cellular and transmembrane distribution asymmetries. A collapse of the membrane asymmetry represents a pro-mitophageal mechanism whereby externalized cardiolipin acts as an &quot;eat-me&quot; signal. Oxidation of cardiolipin&#39;s polyunsaturated acyl chains - catalyzed by cardiolipin complexes with cytochrome c. - is a pro-apoptotic signal. The messaging functions of myriads of cardiolipin species and their oxidation products are now being recognized as important intracellular and extracellular signals for innate and adaptive immune...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c27a8c96c8f041d7e9d54afed9c36b0c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273121,"asset_id":100452672,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273121/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452672"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452672"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452672; 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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="100452671"><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/100452671/Biosynthesis_of_oxidized_lipid_mediators_via_lipoprotein_associated_phospholipase_A2hydrolysis_of_extracellular_cardiolipin_induces_endothelial_toxicity"><img alt="Research paper thumbnail of Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2hydrolysis of extracellular cardiolipin induces endothelial toxicity" class="work-thumbnail" src="https://attachments.academia-assets.com/101273088/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/100452671/Biosynthesis_of_oxidized_lipid_mediators_via_lipoprotein_associated_phospholipase_A2hydrolysis_of_extracellular_cardiolipin_induces_endothelial_toxicity">Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2hydrolysis of extracellular cardiolipin induces endothelial toxicity</a></div><div class="wp-workCard_item"><span>American Journal of Physiology-Lung Cellular and Molecular Physiology</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We (66) have previously described an NSAID-insensitive intramitochondrial biosynthetic pathway in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We (66) have previously described an NSAID-insensitive intramitochondrial biosynthetic pathway involving oxidation of the polyunsaturated mitochondrial phospholipid, cardiolipin (CL), followed by hydrolysis [by calcium-independent mitochondrial calcium-independent phospholipase A2-γ (iPLA2γ)] of oxidized CL (CLox), leading to the formation of lysoCL and oxygenated octadecadienoic metabolites. We now describe a model system utilizing oxidative lipidomics/mass spectrometry and bioassays on cultured bovine pulmonary artery endothelial cells (BPAECs) to assess the impact of CLox that we show, in vivo, can be released to the extracellular space and may be hydrolyzed by lipoprotein-associated PLA2(Lp-PLA2). Chemically oxidized liposomes containing bovine heart CL produced multiple oxygenated species. Addition of Lp-PLA2hydrolyzed CLox and produced (oxygenated) monolysoCL and dilysoCL and oxidized octadecadienoic metabolites including 9- and 13-hydroxyoctadecadienoic (HODE) acids. CLox cau...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e356a891ce253080be76532e0665701f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273088,"asset_id":100452671,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273088/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452671"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452671"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452671; 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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="100452670"><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/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection"><img alt="Research paper thumbnail of Development of small molecule mitochondria-targeted antioxidants for radioprotection" 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/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection">Development of small molecule mitochondria-targeted antioxidants for radioprotection</a></div><div class="wp-workCard_item"><span>Cancer Research</span><span>, Apr 15, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">4410 We have previously demonstrated that overexpression of MnSOD protects cells from irradiation...</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">4410 We have previously demonstrated that overexpression of MnSOD protects cells from irradiation damage by reduction of superoxide and inhibition of subsequent production of peroxynitrite resulting in stabilization of the mitochondria. To develop new compounds for radioprotection we have attached a gramicidin (GS)-peptide isotere linker that facilitates transportation of proteins into the mitochondria to the antioxidant 4-amino-Tempo (4-AT) and the nitric oxide synthase (NOS) inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) to concentrate the inhibitions in the mitochondria. Initial experiments were performed with two GS-Tempo derivatives (XJB-5-125 or XJB-5-131) or two AMT derivatives (XJB-5-127 or XJB-5-133). To demonstrate concentration of the compounds into the mitochondria, 32D cl 3 cells were incubated in the presence of 100 μM of XJB-5-125, XJB-5-127, XJB-5-131, XJB-5-133, tempol or AMT for 1 hour at which time the mitochondria were isolated and analyzed by mass spectrometry. There was no detectable uptake of 4-AT or AMT into the mitochondria but there was significant uptake of XJB-5-125, 127, 131 or 133 in the mitochondria. Localization of 4-AT to the mitochondria using the mitochondrial leader sequence resulted in increased radiation resistance. Irradiation survival curves were performed on 32D cl 3 cells incubated in 100 μM XJB-5-125, 10 μM XJB-5-131 or 100 μM 4-AT for 1 hour and irradiated to doses ranging from 0 to 800 cGy. The cells were plated in methylcellulose and colonies of greater than 50 cells were counted 7 days later. Cells incubated in XJB-5-125 or XJB-5-131 had increased radiation resistance as shown by an increased shoulder on the survival curve (n=18.24) compared to 32D cl 3 cells only or cells incubated in 4-AT (n=7.47 or 5.82, respectively). The mitochondrial localized AMT (XJB-5-127 or XJB-5-133) also exhibited increased radiation resistance. Irradiation survival curves were performed by incubating 32D cl 3 cells for 1 hour in 10 or 100 μM AMT, XJB-5-127 or XJB-5-133 and irradiating the cells at doses ranging from 0 to 800 cGy. Radiation survival curves at 10 μM revealed no significant change in the D0 between AMT and the mitochondrial linked XJB-5-125 or XJB-5-133. At 100 μM there was a significant increase in the D0 of 1.925 Gy for AMT compared to 1.281 for control 32D cl 3. The two AMT conjugates with the mitochondria linker had a higher D0 of 2.771 or 3.317 Gy compared to the AMT of 1.925 and the 32D cl 3 at 1.281. Using probes specific for peroxynitrite, 32D cl 3 cells incubated in 10 μM or 100 μM of XJB-5-127 or XJB-5-133 produced no peroxynitrite following irradiation while control cells or cells incubated in AMT produced peroxynitrite. The mitochondrial localization was necessary in preventing production of peroxynitrite. These results demonstrate the importance of localization of antioxidants or NOS inhibitors to the mitochondria in protecting cells from irradiation.</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="100452670"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452670"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452670; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452670]").text(description); $(".js-view-count[data-work-id=100452670]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452670; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452670']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=100452670]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452670,"title":"Development of small molecule mitochondria-targeted antioxidants for radioprotection","internal_url":"https://www.academia.edu/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[]}, 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="100452669"><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/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced"><img alt="Research paper thumbnail of Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced" class="work-thumbnail" src="https://attachments.academia-assets.com/101273104/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/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced">Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Induction of apoptosis in dendritic cells (DC) is one of the escape mechanisms of tumor cells fro...</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">Induction of apoptosis in dendritic cells (DC) is one of the escape mechanisms of tumor cells from the immune surveillance system. This study aimed to clarify the underlying mechanisms of tumor-induced DC apoptosis. The supernatants (SN) of murine tumor cell lines B16 (melanoma), MCA207, and MCA102 (fibrosarcoma) increased C16 and C24 ceramide as determined by electrospray mass spectrometry and induced apoptosis in bone marrow-derived DC. N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous ceramide, enhanced DC apoptosis and ceramide levels in the presence of tumor SN. Pretreatment with L-cycloserine, an inhibitor of de novo ceramide synthesis, or phorbol ester, 12-O-tetradecanoylphorbol-13-acetate reduced endogenous ceramide levels and protected DC from tumor-induced apoptosis. However, other DC survival factors, including LPS and TNF-␣, failed to do so. The protective activity of 12-O-tetradecanoylphorbol-13-acetate is abrogated by pretreatment with phosphoinositide 3-kinase (PI3K) inhibitor, LY294002. Therefore, down-regulation of PI3K is the major facet of tumor-induced DC apoptosis. Tumor SN, N-oleoylethanolamine, or PDMP suppressed Akt, NF-B, and bcl-x L in DC, suggesting that the accumulation of ceramide impedes PI3K-mediated survival signals. Taken together, ceramide mediates tumor-induced DC apoptosis by down-regulation of the PI3K pathway.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bba872c683a391f744edaea35c6b01dc" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273104,"asset_id":100452669,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273104/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452669"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452669"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452669; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452669]").text(description); $(".js-view-count[data-work-id=100452669]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452669; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452669']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bba872c683a391f744edaea35c6b01dc" } } $('.js-work-strip[data-work-id=100452669]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452669,"title":"Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced","internal_url":"https://www.academia.edu/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[{"id":101273104,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/101273104/thumbnails/1.jpg","file_name":"3773.pdf","download_url":"https://www.academia.edu/attachments/101273104/download_file","bulk_download_file_name":"Dendritic_Cell_Apoptosis_Ceramide_Mediat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/101273104/3773-libre.pdf?1681933817=\u0026response-content-disposition=attachment%3B+filename%3DDendritic_Cell_Apoptosis_Ceramide_Mediat.pdf\u0026Expires=1740158365\u0026Signature=HQJi~1e8KDOlaqPFfgiZQugzHFTjXT-UF-bBxfibzdq5xCXBFxA9WMCgwY2wPakx6dBujLz~SJ8GuX79SdLEowy8bPGscTTfSok--hdf36v8AYuTO72a-ITJvTXYE6b4UQ4iGxfNM9mVxeQc9a6YSatZ5yILE9A~BPISdNWRLsZL8nhVC020DN8dHak1XFcQqUK~DnwodTbrUHthzPs4gEzRwVUeJmmcf0sdhRM3BpB5LwtJC5G0e--kL~Q6Fo-dyJ75FZAxUjNEYXtsHwJWZ0AYDKdgpwpdy7EpPH~ipn2NBWUPIeyxcnFViQKbUu063Y-4U17hjHGjUnLAg~ikhQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="100452668"><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/100452668/Defects_of_Lipid_Synthesis_Are_Linked_to_the_Age_Dependent_Demyelination_Caused_by_Lamin_B1_Overexpression"><img alt="Research paper thumbnail of Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression" class="work-thumbnail" src="https://attachments.academia-assets.com/101273117/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/100452668/Defects_of_Lipid_Synthesis_Are_Linked_to_the_Age_Dependent_Demyelination_Caused_by_Lamin_B1_Overexpression">Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression</a></div><div class="wp-workCard_item"><span>The Journal of neuroscience : the official journal of the Society for Neuroscience</span><span>, Jan 26, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lamin B1 is a component of the nuclear lamina and plays a critical role in maintaining nuclear ar...</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">Lamin B1 is a component of the nuclear lamina and plays a critical role in maintaining nuclear architecture, regulating gene expression and modulating chromatin positioning. We have previously shown that LMNB1 gene duplications cause autosomal dominant leukodystrophy (ADLD), a fatal adult onset demyelinating disease. The mechanisms by which increased LMNB1 levels cause ADLD are unclear. To address this, we used a transgenic mouse model where Lamin B1 overexpression is targeted to oligodendrocytes. These mice showed severe vacuolar degeneration of the spinal cord white matter together with marked astrogliosis, microglial infiltration, and secondary axonal damage. Oligodendrocytes in the transgenic mice revealed alterations in histone modifications favoring a transcriptionally repressed state. Chromatin changes were accompanied by reduced expression of genes involved in lipid synthesis pathways, many of which are known to play important roles in myelin regulation and are preferentiall...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a49cb75c491c1c1f481fc1a94e208305" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273117,"asset_id":100452668,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273117/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452668"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452668"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452668; 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} }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="100452666"><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/100452666/Oxidative_Lipidomics_of_Apoptosis_Quantitative_Assessment_of_Phospholipid_Hydroperoxides_in_Cells_and_Tissues"><img alt="Research paper thumbnail of Oxidative Lipidomics of Apoptosis: Quantitative Assessment of Phospholipid Hydroperoxides in Cells and Tissues" class="work-thumbnail" src="https://attachments.academia-assets.com/101273131/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/100452666/Oxidative_Lipidomics_of_Apoptosis_Quantitative_Assessment_of_Phospholipid_Hydroperoxides_in_Cells_and_Tissues">Oxidative Lipidomics of Apoptosis: Quantitative Assessment of Phospholipid Hydroperoxides in Cells and Tissues</a></div><div class="wp-workCard_item"><span>Methods in Molecular Biology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxidized phospholipids play essential roles in execution of mitochondrial stage of apoptosis and ...</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">Oxidized phospholipids play essential roles in execution of mitochondrial stage of apoptosis and clearance of apoptotic cells. The identification and quantification of oxidized phospholipids generated during apoptosis can be successfully achieved by oxidative lipidomics. With this approach, diverse molecular species of phospholipids and their hydroperoxides are identified and characterized by soft-ionization mass-spectrometry techniques such as electrospray ionization (ESI). Quantitative assessment of lipid hydroperoxides is performed by fluorescence HPLC-based protocol. The protocol is based on separation of phospholipids using two-dimensional-highperformance thin-layer chromatography (2-D-HPTLC). Phospholipids are hydrolyzed using phospholipase A 2. The fatty acid hydroperoxides (FA-OOH) released is quantified by a fluorometric assay using Amplex red reagent and microperoxidase-11 (MP-11). Detection limit of this protocol is 1-2 pmol of lipid hydroperoxides. Lipid arrays vs. oxidized lipid arrays can be performed by comparing the abundance of phospholipids with the abundance of oxidized phospholipids. Using oxidative lipidomics approach we show that the pattern of phospholipid oxidation during apoptosis is nonrandom and does not follow their abundance in several types of cells undergoing apoptosis and a variety of disease states. This has important implications for evaluation of apoptosis in vivo. The anionic phospholipids, cardiolipin (CL) and phosphatidylserine (PS), are the preferred peroxidation substrates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="83f54d27ec2d2350d7bad6420f96c636" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273131,"asset_id":100452666,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273131/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452666"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452666"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452666; 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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="100452664"><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/100452664/Low_glucose_enhanced_TRAIL_cytotoxicity_is_mediated_through_the_ceramide_Akt_FLIP_pathway"><img alt="Research paper thumbnail of Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide–Akt–FLIP pathway" class="work-thumbnail" src="https://attachments.academia-assets.com/101273087/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/100452664/Low_glucose_enhanced_TRAIL_cytotoxicity_is_mediated_through_the_ceramide_Akt_FLIP_pathway">Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide–Akt–FLIP pathway</a></div><div class="wp-workCard_item"><span>Oncogene</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To examine whether the tumor microenvironment alters cytokine-induced cytotoxicity, human prostat...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To examine whether the tumor microenvironment alters cytokine-induced cytotoxicity, human prostate adenocarcinoma DU-145 cells were exposed to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and/or glucose deprivation, a common characteristic of the tumor microenvironment. TRAIL alone reduced cell survival in a dose-dependent manner. Glucose deprivation alone induced no cytotoxicity within 4 h. However, the combination of TRAIL (50 ng/ml) and glucose deprivation for 4 h increased cell death and PARP cleavage by promoting activation of caspase-8 and caspase-3, relative to that of TRAIL alone. Similar results were observed in human colorectal carcinoma CX-1 cells. Data from immunoblotting analysis reveal that glucose deprivation-enhanced TRAIL cytotoxicity is inversely related to the intracellular level of FLICE inhibitory protein (FLIP) but not that of death receptor 5 (DR5). Results from mass spectrometry show that glucose deprivation elevates ceramide. The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP. Taken together, the present studies suggest that glucose deprivation enhances TRAIL-induced cytotoxicity through the ceramide ± Akt ± FLIP pathway.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b329eea76e5f6289532d4c4288807256" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273087,"asset_id":100452664,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273087/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452664"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452664"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452664; 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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="3269875" id="papers"><div class="js-work-strip profile--work_container" data-work-id="114169406"><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/114169406/Mapping_of_phospholipids_by_MALDI_imaging_MALDI_MSI_realities_and_expectations"><img alt="Research paper thumbnail of Mapping of phospholipids by MALDI imaging (MALDI-MSI): realities and expectations" class="work-thumbnail" src="https://attachments.academia-assets.com/110937648/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/114169406/Mapping_of_phospholipids_by_MALDI_imaging_MALDI_MSI_realities_and_expectations">Mapping of phospholipids by MALDI imaging (MALDI-MSI): realities and expectations</a></div><div class="wp-workCard_item"><span>Chemistry and Physics of Lipids</span><span>, Jul 1, 2012</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has emerged as ...</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">Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has emerged as a novel powerful MS methodology that has the ability to generate both molecular and spatial information within a tissue section. Application of this technology as a new type of biochemical lipid microscopy may lead to new discoveries of the lipid metabolism and biomarkers associated with area-specific alterations or damage under stress/disease conditions such as traumatic brain injury or acute lung injury, among others. However there are limitations in the range of what it can detect as compared with liquid chromatography-MS (LC-MS) of a lipid extract from a tissue section. The goal of the current work was to critically consider remarkable new opportunities along with the limitations and approaches for further improvements of MALDI-MSI. Based on our experimental data and assessments, improvements of the spectral and spatial resolution, sensitivity and specificity towards low abundance species of lipids are proposed. This is followed by a review of the current literature, including methodologies that other laboratories have used to overcome these challenges.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2ef751b699e2ae5928ce3edbf1667809" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937648,"asset_id":114169406,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937648/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169406"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169406"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169406; 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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="114169404"><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/114169404/Imaging_mass_spectrometry_reveals_loss_of_polyunsaturated_cardiolipins_in_the_cortical_contusion_hippocampus_and_thalamus_after_traumatic_brain_injury"><img alt="Research paper thumbnail of Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury" class="work-thumbnail" src="https://attachments.academia-assets.com/110937649/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/114169404/Imaging_mass_spectrometry_reveals_loss_of_polyunsaturated_cardiolipins_in_the_cortical_contusion_hippocampus_and_thalamus_after_traumatic_brain_injury">Imaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injury</a></div><div class="wp-workCard_item"><span>Journal of Neurochemistry</span><span>, Sep 26, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traumatic brain injury (TBI) leads to changes in ion fluxes, alterations in mitochondrial functio...</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">Traumatic brain injury (TBI) leads to changes in ion fluxes, alterations in mitochondrial function and increased generation of reactive oxygen species, resulting in secondary tissue damage. Mitochondria play important signaling roles in coordination of multiple metabolic platforms in addition to their well-known role in bioenergetics. Mitochondrial signaling strongly depends on cardiolipin (CL), a mitochondria-specific structurally unusual anionic phospholipid containing four fatty acyl chains. While our previous reports indicated that CL is selectively oxidized and presents itself as a target for the redox therapy following TBI, the topography of changes of CL in the injured brain remained to be defined. Here we present a MALDI imaging study which reports regio-specific changes in CL, in a controlled cortical impact (CCI) model of TBI in rats. MALDI imaging revealed that TBI caused early decreases in CL in the contusional cortex, ipsilateral hippocampus and thalamus with the most highly unsaturated CL species being most susceptible to loss. Phosphatidylinositol was the only other lipid species that exhibited a significant decrease, albeit to a lesser extent than CL. Signals for other lipids remained unchanged. This is the first study evaluating the spatial distribution of CL loss after acute brain injury. We propose that the CL loss may constitute an upstream mechanism for CL-driven signaling in different brain regions as an early response mechanism and may also underlie the bioenergetic changes that occur in hippocampal, cortical and thalamic mitochondria after TBI.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ee90a79b2fd469eb04f60fa2d9a7dade" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937649,"asset_id":114169404,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937649/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169404"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169404"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169404; 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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="114169402"><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/114169402/Mass_spectrometry_based_oxidative_lipidomics_and_lipid_imaging_applications_in_traumatic_brain_injury"><img alt="Research paper thumbnail of Mass-spectrometry based oxidative lipidomics and lipid imaging: applications in traumatic brain injury" class="work-thumbnail" src="https://attachments.academia-assets.com/110937646/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/114169402/Mass_spectrometry_based_oxidative_lipidomics_and_lipid_imaging_applications_in_traumatic_brain_injury">Mass-spectrometry based oxidative lipidomics and lipid imaging: applications in traumatic brain injury</a></div><div class="wp-workCard_item"><span>Journal of Neurochemistry</span><span>, Nov 19, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lipids, particularly phospholipids, are fundamental to central nervous system (CNS) tissue archit...</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">Lipids, particularly phospholipids, are fundamental to central nervous system (CNS) tissue architecture and function. Endogenous polyunsaturated fatty acid chains of phospholipids possess cis-double bonds each separated by one methylene group. These phospholipids are very susceptible to free-radical attack and oxidative modifications. A combination of analytical methods including different versions of chromatography and mass spectrometry allows obtaining detailed information on the content and distribution of lipids and their oxidation products thus constituting the newly emerging field of oxidative lipidomics. It is becoming evident that specific oxidative modifications of lipids are critical to a number of cellular functions, disease states and responses to oxidative stresses. Oxidative lipidomics is beginning to provide new mechanistic insights into traumatic brain injury (TBI) which may have significant translational potential for development of therapies in acute CNS insults. In particular, selective oxidation of a mitochondria-specific phospholipid, cardiolipin, has been associated with the initiation and progression of apoptosis in injured neurons thus indicating new drug discovery targets. Further, imaging mass-spectrometry represents an exciting new opportunity for correlating maps of lipid profiles and their oxidation products with structure and neuropathology. This review is focused on these most recent advancements in the field of lipidomics and oxidative lipidomics based on the applications of mass-spectrometry and imaging mass-spectrometry as they relate to studies of phospholipids in TBI.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="05904bfd93819434bc6812f76b4c611f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937646,"asset_id":114169402,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937646/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169402"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169402"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169402; 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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="114169389"><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/114169389/Redox_phospho_lipidomics_of_signaling_in_inflammation_and_programmed_cell_death"><img alt="Research paper thumbnail of Redox (phospho)lipidomics of signaling in inflammation and programmed cell death" class="work-thumbnail" src="https://attachments.academia-assets.com/110937662/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/114169389/Redox_phospho_lipidomics_of_signaling_in_inflammation_and_programmed_cell_death">Redox (phospho)lipidomics of signaling in inflammation and programmed cell death</a></div><div class="wp-workCard_item"><span>Journal of Leukocyte Biology</span><span>, 2019</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In addition to the known prominent role of polyunsaturated (phospho)lipids as structural blocks 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">In addition to the known prominent role of polyunsaturated (phospho)lipids as structural blocks of biomembranes, there is an emerging understanding of another important function of these molecules as a highly diversified signaling language utilized for intra- and extracellular communications. Technological developments in high-resolution mass spectrometry facilitated the development of a new branch of metabolomics, redox lipidomics. Analysis of lipid peroxidation reactions has already identified specific enzymatic mechanisms responsible for the biosynthesis of several unique signals in response to inflammation and regulated cell death programs. Obtaining comprehensive information about millions of signals encoded by oxidized phospholipids, represented by thousands of interactive reactions and pleiotropic (patho)physiological effects, is a daunting task. However, there is still reasonable hope that significant discoveries, of at least some of the important contributors to the overall...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="27bef88dadbce06f44f5d0ef81830b02" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":110937662,"asset_id":114169389,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/110937662/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="114169389"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="114169389"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 114169389; 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Using a tumor-specific CTL, aldehyde dehydrogenase 1 family member A1 (ALDH1A1) was identified as a novel tumor antigen in SCCHN. Mass spectral analysis of peptides in tumor-derived lysates was used to determine that the CTL line recognized the HLA-A*0201 (HLA-A2) binding ALDH1A188-96 peptide. Expression of ALDH1A1 in established SCCHN cell lines, normal mucosa, and primary keratinocytes was studied by quantitative reverse transcription-PCR and immunostaining. Protein expression was further defined by immunoblot analysis, whereas ALDH1A1 activity was measured using ALDEFLUOR. ALDH1A188-96 peptide was identified as an HLA-A2–restricted, naturally presented, CD8+ T-cell–defined tumor peptide. ALDH1A188-96 peptide-specific CD8+ T cells recognized only HLA-A2+ SCCHN cell lines, which overexpressed ALDH1A1, as well as targets transfected with ALDH1A1 cDNA. 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Using a tumor-specific CTL, aldehyde dehydrogenase 1 family member A1 (ALDH1A1) was identified as a novel tumor antigen in SCCHN. Mass spectral analysis of peptides in tumor-derived lysates was used to determine that the CTL line recognized the HLA-A*0201 (HLA-A2) binding ALDH1A188-96 peptide. Expression of ALDH1A1 in established SCCHN cell lines, normal mucosa, and primary keratinocytes was studied by quantitative reverse transcription-PCR and immunostaining. Protein expression was further defined by immunoblot analysis, whereas ALDH1A1 activity was measured using ALDEFLUOR. ALDH1A188-96 peptide was identified as an HLA-A2–restricted, naturally presented, CD8+ T-cell–defined tumor peptide. ALDH1A188-96 peptide-specific CD8+ T cells recognized only HLA-A2+ SCCHN cell lines, which overexpressed ALDH1A1, as well as targets transfected with ALDH1A1 cDNA. 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dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=100452677]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452677,"title":"1475: Detection of Brain Cardiolipins in Plasma After Cardiac Arrest","internal_url":"https://www.academia.edu/100452677/1475_Detection_of_Brain_Cardiolipins_in_Plasma_After_Cardiac_Arrest","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[]}, 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="100452676"><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/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis"><img alt="Research paper thumbnail of Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis" class="work-thumbnail" src="https://attachments.academia-assets.com/101273116/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/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis">Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis</a></div><div class="wp-workCard_item"><span>Journal of Biological Chemistry</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Apoptosis has been identified recently as a component of many cardiac pathologies. However, the p...</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">Apoptosis has been identified recently as a component of many cardiac pathologies. However, the potential triggers of programmed cell death in the heart and the involvement of specific metabolic pathway(s) are less well characterized. Detachment of cytochrome c from the mitochondrial inner membrane is a necessary first step for cytochrome c release into the cytosol and initiation of apoptosis. The saturated long chain fatty acid, palmitate, induces apoptosis in rat neonatal cardiomyocytes and diminishes content of the mitochondrial anionic phospholipid, cardiolipin. These changes are accompanied by 1) acyl chain saturation of phosphatidic acid and phosphatidylglycerol, 2) large increases in the levels of these two phospholipids, and 3) a decline in cardiolipin synthesis. Although cardiolipin synthase activity is unchanged, saturated phosphatidylglycerol is a poor substrate for this enzyme. Under these conditions, decreased cardiolipin synthesis and release of cytochrome c are directly and significantly correlated. The results suggest that phosphatidylglycerol saturation and subsequent decreases in cardiolipin affect the association of cytochrome c with the inner mitochondrial membrane, directly influencing the pathway to cytochrome c release and subsequent apoptosis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fb2e6eb7d076d3d025560b11ebd40885" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273116,"asset_id":100452676,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273116/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452676"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452676"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452676; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452676]").text(description); $(".js-view-count[data-work-id=100452676]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452676; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452676']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "fb2e6eb7d076d3d025560b11ebd40885" } } $('.js-work-strip[data-work-id=100452676]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452676,"title":"Decreased Cardiolipin Synthesis Corresponds with Cytochromec Release in Palmitate-induced Cardiomyocyte Apoptosis","internal_url":"https://www.academia.edu/100452676/Decreased_Cardiolipin_Synthesis_Corresponds_with_Cytochromec_Release_in_Palmitate_induced_Cardiomyocyte_Apoptosis","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[{"id":101273116,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/101273116/thumbnails/1.jpg","file_name":"pdf.pdf","download_url":"https://www.academia.edu/attachments/101273116/download_file","bulk_download_file_name":"Decreased_Cardiolipin_Synthesis_Correspo.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/101273116/pdf-libre.pdf?1681933809=\u0026response-content-disposition=attachment%3B+filename%3DDecreased_Cardiolipin_Synthesis_Correspo.pdf\u0026Expires=1740158365\u0026Signature=CHbZSlfNMLu1ApCeUSU-VOwghW4oImEI2eeX9~TyMqpJLsQaZyssOjiMkUkwG1fn74-gDGBrdHH3fg98X4qZNDEb~n5nTQLSPeV6K6413TATQF-lLng~JuCuEsd9uo8-N~qREuxwaCvofSWax7M5woqAJAL6T0r-QwhOg4xKwaU4F1A6VKYEp7p7fkHaMlchAIA9l8v4ZM9LkSwT5YUmIRUDqBJt52JgIKCpC1j4c8-zwWN27RIR4S4PttN87sd3jYhTvGb0Gi~Lf8Z8ZnIwzFwFB0Ew3-vYtLroNsuUXv-MsiCzk52onq1p1QkXESh3MmIpYGHG4AaWtGdEz8f8Cw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="100452675"><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/100452675/Aberrant_cardiolipin_metabolism_is_associated_with_cognitive_deficiency_and_hippocampal_alteration_in_tafazzin_knockdown_mice"><img alt="Research paper thumbnail of Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice" class="work-thumbnail" src="https://attachments.academia-assets.com/101273115/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/100452675/Aberrant_cardiolipin_metabolism_is_associated_with_cognitive_deficiency_and_hippocampal_alteration_in_tafazzin_knockdown_mice">Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta. Molecular basis of disease</span><span>, 2018</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Cardiolipin (CL) is a key mitochondrial phospholipid essential for mitochondrial energy productio...</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">Cardiolipin (CL) is a key mitochondrial phospholipid essential for mitochondrial energy production. CL is remodeled from monolysocardiolipin (MLCL) by the enzyme tafazzin (TAZ). Loss-of-function mutations in the gene which encodes TAZ results in a rare X-linked disorder called Barth Syndrome (BTHS). The mutated TAZ is unable to maintain the physiological CL:MLCL ratio, thus reducing CL levels and affecting mitochondrial function. BTHS is best known as a cardiac disease, but has been acknowledged as a multi-syndrome disorder, including cognitive deficits. Since reduced CL levels has also been reported in numerous neurodegenerative disorders, we examined how TAZ-deficiency impacts cognitive abilities, brain mitochondrial respiration and the function of hippocampal neurons and glia in TAZ knockdown (TAZ kd) mice. We have identified for the first time the profile of changes that occur in brain phospholipid content and composition of TAZ kd mice. The brain of TAZ kd mice exhibited reduce...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="fb13594ca713362b043b410137c9a70f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273115,"asset_id":100452675,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273115/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452675"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452675"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452675; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452675]").text(description); $(".js-view-count[data-work-id=100452675]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452675; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452675']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(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="100452674"><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/100452674/Gas_Cluster_Ion_Beam_Time_of_Flight_Secondary_Ion_Mass_Spectrometry_High_Resolution_Imaging_of_Cardiolipin_Speciation_in_the_Brain_Identification_of_Molecular_Losses_after_Traumatic_Injury"><img alt="Research paper thumbnail of Gas Cluster Ion Beam Time-of-Flight Secondary Ion Mass Spectrometry High-Resolution Imaging of Cardiolipin Speciation in the Brain: Identification of Molecular Losses after Traumatic Injury" class="work-thumbnail" src="https://attachments.academia-assets.com/101273123/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/100452674/Gas_Cluster_Ion_Beam_Time_of_Flight_Secondary_Ion_Mass_Spectrometry_High_Resolution_Imaging_of_Cardiolipin_Speciation_in_the_Brain_Identification_of_Molecular_Losses_after_Traumatic_Injury">Gas Cluster Ion Beam Time-of-Flight Secondary Ion Mass Spectrometry High-Resolution Imaging of Cardiolipin Speciation in the Brain: Identification of Molecular Losses after Traumatic Injury</a></div><div class="wp-workCard_item"><span>Analytical chemistry</span><span>, Jan 18, 2017</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Gas cluster ion beam-secondary ion mass spectrometry (GCIB-SIMS) has shown the full potential of ...</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">Gas cluster ion beam-secondary ion mass spectrometry (GCIB-SIMS) has shown the full potential of mapping intact lipids in biological systems with better than 10 μm lateral resolution. This study investigated further the capability of GCIB-SIMS in imaging high-mass signals from intact cardiolipin (CL) and gangliosides in normal brain and the effect of a controlled cortical impact model (CCI) of traumatic brain injury (TBI) on their distribution. A combination of enzymatic and chemical treatments was employed to suppress the signals from the most abundant phospholipids (phosphatidylcholine (PC) and phosphatidylethanolamine (PE)) and enhance the signals from the low-abundance CLs and gangliosides to allow their GCIB-SIMS detection at 8 and 16 μm spatial resolution. Brain CLs have not been observed previously using other contemporary imaging mass spectrometry techniques at better than 50 μm spatial resolution. High-resolution images of naive and injured brain tissue facilitated the comp...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ba6f50f99055df40c596c36f587d4db5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273123,"asset_id":100452674,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273123/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452674"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452674"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452674; 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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="100452673"><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/100452673/Global_assessment_of_oxidized_free_fatty_acids_in_brain_reveals_an_enzymatic_predominance_to_oxidative_signaling_after_trauma"><img alt="Research paper thumbnail of Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma" class="work-thumbnail" src="https://attachments.academia-assets.com/101273112/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/100452673/Global_assessment_of_oxidized_free_fatty_acids_in_brain_reveals_an_enzymatic_predominance_to_oxidative_signaling_after_trauma">Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta</span><span>, Jan 24, 2017</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Traumatic brain injury (TBI) is a major health problem associated with significant morbidity and ...</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">Traumatic brain injury (TBI) is a major health problem associated with significant morbidity and mortality. The pathophysiology of TBI is complex involving signaling through multiple cascades, including lipid peroxidation. Oxidized free fatty acids, a prominent product of lipid peroxidation, are potent cellular mediators involved in induction and resolution of inflammation and modulation of vasomotor tone. While previous studies have assessed lipid peroxidation after TBI, to our knowledge no studies have used a systematic approach to quantify the global oxidative changes in free fatty acids. In this study, we identified and quantified 244 free fatty acid oxidation products using a newly developed global liquid chromatography tandem-mass spectrometry (LC-MS/MS) method. This methodology was used to follow the time course of these lipid species in the contusional cortex of our pediatric rat model of TBI. We show that oxidation peaked at 1h after controlled cortical impact and was progr...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f0bf21ed1f14e50977b63bc6531335b4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273112,"asset_id":100452673,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273112/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452673"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452673"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452673; 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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="100452672"><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/100452672/Known_unknowns_of_cardiolipin_signaling_The_best_is_yet_to_come"><img alt="Research paper thumbnail of Known unknowns of cardiolipin signaling: The best is yet to come" class="work-thumbnail" src="https://attachments.academia-assets.com/101273121/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/100452672/Known_unknowns_of_cardiolipin_signaling_The_best_is_yet_to_come">Known unknowns of cardiolipin signaling: The best is yet to come</a></div><div class="wp-workCard_item"><span>Biochimica et biophysica acta</span><span>, Jan 4, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Since its discovery 75years ago, a wealth of knowledge has accumulated on the role of cardiolipin...</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">Since its discovery 75years ago, a wealth of knowledge has accumulated on the role of cardiolipin, the hallmark phospholipid of mitochondria, in bioenergetics and particularly on the structural organization of the inner mitochondrial membrane. A surge of interest in this anionic doubly-charged tetra-acylated lipid found in both prokaryotes and mitochondria has emerged based on its newly discovered signaling functions. Cardiolipin displays organ, tissue, cellular and transmembrane distribution asymmetries. A collapse of the membrane asymmetry represents a pro-mitophageal mechanism whereby externalized cardiolipin acts as an &quot;eat-me&quot; signal. Oxidation of cardiolipin&#39;s polyunsaturated acyl chains - catalyzed by cardiolipin complexes with cytochrome c. - is a pro-apoptotic signal. The messaging functions of myriads of cardiolipin species and their oxidation products are now being recognized as important intracellular and extracellular signals for innate and adaptive immune...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c27a8c96c8f041d7e9d54afed9c36b0c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273121,"asset_id":100452672,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273121/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452672"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452672"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452672; 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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="100452671"><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/100452671/Biosynthesis_of_oxidized_lipid_mediators_via_lipoprotein_associated_phospholipase_A2hydrolysis_of_extracellular_cardiolipin_induces_endothelial_toxicity"><img alt="Research paper thumbnail of Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2hydrolysis of extracellular cardiolipin induces endothelial toxicity" class="work-thumbnail" src="https://attachments.academia-assets.com/101273088/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/100452671/Biosynthesis_of_oxidized_lipid_mediators_via_lipoprotein_associated_phospholipase_A2hydrolysis_of_extracellular_cardiolipin_induces_endothelial_toxicity">Biosynthesis of oxidized lipid mediators via lipoprotein-associated phospholipase A2hydrolysis of extracellular cardiolipin induces endothelial toxicity</a></div><div class="wp-workCard_item"><span>American Journal of Physiology-Lung Cellular and Molecular Physiology</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">We (66) have previously described an NSAID-insensitive intramitochondrial biosynthetic pathway in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">We (66) have previously described an NSAID-insensitive intramitochondrial biosynthetic pathway involving oxidation of the polyunsaturated mitochondrial phospholipid, cardiolipin (CL), followed by hydrolysis [by calcium-independent mitochondrial calcium-independent phospholipase A2-γ (iPLA2γ)] of oxidized CL (CLox), leading to the formation of lysoCL and oxygenated octadecadienoic metabolites. We now describe a model system utilizing oxidative lipidomics/mass spectrometry and bioassays on cultured bovine pulmonary artery endothelial cells (BPAECs) to assess the impact of CLox that we show, in vivo, can be released to the extracellular space and may be hydrolyzed by lipoprotein-associated PLA2(Lp-PLA2). Chemically oxidized liposomes containing bovine heart CL produced multiple oxygenated species. Addition of Lp-PLA2hydrolyzed CLox and produced (oxygenated) monolysoCL and dilysoCL and oxidized octadecadienoic metabolites including 9- and 13-hydroxyoctadecadienoic (HODE) acids. CLox cau...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e356a891ce253080be76532e0665701f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273088,"asset_id":100452671,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273088/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452671"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452671"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452671; 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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="100452670"><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/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection"><img alt="Research paper thumbnail of Development of small molecule mitochondria-targeted antioxidants for radioprotection" 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/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection">Development of small molecule mitochondria-targeted antioxidants for radioprotection</a></div><div class="wp-workCard_item"><span>Cancer Research</span><span>, Apr 15, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">4410 We have previously demonstrated that overexpression of MnSOD protects cells from irradiation...</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">4410 We have previously demonstrated that overexpression of MnSOD protects cells from irradiation damage by reduction of superoxide and inhibition of subsequent production of peroxynitrite resulting in stabilization of the mitochondria. To develop new compounds for radioprotection we have attached a gramicidin (GS)-peptide isotere linker that facilitates transportation of proteins into the mitochondria to the antioxidant 4-amino-Tempo (4-AT) and the nitric oxide synthase (NOS) inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) to concentrate the inhibitions in the mitochondria. Initial experiments were performed with two GS-Tempo derivatives (XJB-5-125 or XJB-5-131) or two AMT derivatives (XJB-5-127 or XJB-5-133). To demonstrate concentration of the compounds into the mitochondria, 32D cl 3 cells were incubated in the presence of 100 μM of XJB-5-125, XJB-5-127, XJB-5-131, XJB-5-133, tempol or AMT for 1 hour at which time the mitochondria were isolated and analyzed by mass spectrometry. There was no detectable uptake of 4-AT or AMT into the mitochondria but there was significant uptake of XJB-5-125, 127, 131 or 133 in the mitochondria. Localization of 4-AT to the mitochondria using the mitochondrial leader sequence resulted in increased radiation resistance. Irradiation survival curves were performed on 32D cl 3 cells incubated in 100 μM XJB-5-125, 10 μM XJB-5-131 or 100 μM 4-AT for 1 hour and irradiated to doses ranging from 0 to 800 cGy. The cells were plated in methylcellulose and colonies of greater than 50 cells were counted 7 days later. Cells incubated in XJB-5-125 or XJB-5-131 had increased radiation resistance as shown by an increased shoulder on the survival curve (n=18.24) compared to 32D cl 3 cells only or cells incubated in 4-AT (n=7.47 or 5.82, respectively). The mitochondrial localized AMT (XJB-5-127 or XJB-5-133) also exhibited increased radiation resistance. Irradiation survival curves were performed by incubating 32D cl 3 cells for 1 hour in 10 or 100 μM AMT, XJB-5-127 or XJB-5-133 and irradiating the cells at doses ranging from 0 to 800 cGy. Radiation survival curves at 10 μM revealed no significant change in the D0 between AMT and the mitochondrial linked XJB-5-125 or XJB-5-133. At 100 μM there was a significant increase in the D0 of 1.925 Gy for AMT compared to 1.281 for control 32D cl 3. The two AMT conjugates with the mitochondria linker had a higher D0 of 2.771 or 3.317 Gy compared to the AMT of 1.925 and the 32D cl 3 at 1.281. Using probes specific for peroxynitrite, 32D cl 3 cells incubated in 10 μM or 100 μM of XJB-5-127 or XJB-5-133 produced no peroxynitrite following irradiation while control cells or cells incubated in AMT produced peroxynitrite. The mitochondrial localization was necessary in preventing production of peroxynitrite. These results demonstrate the importance of localization of antioxidants or NOS inhibitors to the mitochondria in protecting cells from irradiation.</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="100452670"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452670"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452670; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452670]").text(description); $(".js-view-count[data-work-id=100452670]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452670; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452670']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=100452670]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452670,"title":"Development of small molecule mitochondria-targeted antioxidants for radioprotection","internal_url":"https://www.academia.edu/100452670/Development_of_small_molecule_mitochondria_targeted_antioxidants_for_radioprotection","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[]}, 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="100452669"><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/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced"><img alt="Research paper thumbnail of Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced" class="work-thumbnail" src="https://attachments.academia-assets.com/101273104/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/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced">Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Induction of apoptosis in dendritic cells (DC) is one of the escape mechanisms of tumor cells fro...</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">Induction of apoptosis in dendritic cells (DC) is one of the escape mechanisms of tumor cells from the immune surveillance system. This study aimed to clarify the underlying mechanisms of tumor-induced DC apoptosis. The supernatants (SN) of murine tumor cell lines B16 (melanoma), MCA207, and MCA102 (fibrosarcoma) increased C16 and C24 ceramide as determined by electrospray mass spectrometry and induced apoptosis in bone marrow-derived DC. N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous ceramide, enhanced DC apoptosis and ceramide levels in the presence of tumor SN. Pretreatment with L-cycloserine, an inhibitor of de novo ceramide synthesis, or phorbol ester, 12-O-tetradecanoylphorbol-13-acetate reduced endogenous ceramide levels and protected DC from tumor-induced apoptosis. However, other DC survival factors, including LPS and TNF-␣, failed to do so. The protective activity of 12-O-tetradecanoylphorbol-13-acetate is abrogated by pretreatment with phosphoinositide 3-kinase (PI3K) inhibitor, LY294002. Therefore, down-regulation of PI3K is the major facet of tumor-induced DC apoptosis. Tumor SN, N-oleoylethanolamine, or PDMP suppressed Akt, NF-B, and bcl-x L in DC, suggesting that the accumulation of ceramide impedes PI3K-mediated survival signals. Taken together, ceramide mediates tumor-induced DC apoptosis by down-regulation of the PI3K pathway.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bba872c683a391f744edaea35c6b01dc" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273104,"asset_id":100452669,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273104/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452669"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452669"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452669; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=100452669]").text(description); $(".js-view-count[data-work-id=100452669]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 100452669; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='100452669']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-a9bf3a2bc8c89fa2a77156577594264ee8a0f214d74241bc0fcd3f69f8d107ac.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bba872c683a391f744edaea35c6b01dc" } } $('.js-work-strip[data-work-id=100452669]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":100452669,"title":"Dendritic Cell Apoptosis Ceramide Mediates Tumor-Induced","internal_url":"https://www.academia.edu/100452669/Dendritic_Cell_Apoptosis_Ceramide_Mediates_Tumor_Induced","owner_id":33280586,"coauthors_can_edit":true,"owner":{"id":33280586,"first_name":"Andrew","middle_initials":null,"last_name":"Amoscato","page_name":"AndrewAmoscato","domain_name":"independent","created_at":"2015-07-23T05:53:06.934-07:00","display_name":"Andrew Amoscato","url":"https://independent.academia.edu/AndrewAmoscato"},"attachments":[{"id":101273104,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/101273104/thumbnails/1.jpg","file_name":"3773.pdf","download_url":"https://www.academia.edu/attachments/101273104/download_file","bulk_download_file_name":"Dendritic_Cell_Apoptosis_Ceramide_Mediat.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/101273104/3773-libre.pdf?1681933817=\u0026response-content-disposition=attachment%3B+filename%3DDendritic_Cell_Apoptosis_Ceramide_Mediat.pdf\u0026Expires=1740158365\u0026Signature=HQJi~1e8KDOlaqPFfgiZQugzHFTjXT-UF-bBxfibzdq5xCXBFxA9WMCgwY2wPakx6dBujLz~SJ8GuX79SdLEowy8bPGscTTfSok--hdf36v8AYuTO72a-ITJvTXYE6b4UQ4iGxfNM9mVxeQc9a6YSatZ5yILE9A~BPISdNWRLsZL8nhVC020DN8dHak1XFcQqUK~DnwodTbrUHthzPs4gEzRwVUeJmmcf0sdhRM3BpB5LwtJC5G0e--kL~Q6Fo-dyJ75FZAxUjNEYXtsHwJWZ0AYDKdgpwpdy7EpPH~ipn2NBWUPIeyxcnFViQKbUu063Y-4U17hjHGjUnLAg~ikhQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}]}, 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="100452668"><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/100452668/Defects_of_Lipid_Synthesis_Are_Linked_to_the_Age_Dependent_Demyelination_Caused_by_Lamin_B1_Overexpression"><img alt="Research paper thumbnail of Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression" class="work-thumbnail" src="https://attachments.academia-assets.com/101273117/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/100452668/Defects_of_Lipid_Synthesis_Are_Linked_to_the_Age_Dependent_Demyelination_Caused_by_Lamin_B1_Overexpression">Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression</a></div><div class="wp-workCard_item"><span>The Journal of neuroscience : the official journal of the Society for Neuroscience</span><span>, Jan 26, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Lamin B1 is a component of the nuclear lamina and plays a critical role in maintaining nuclear ar...</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">Lamin B1 is a component of the nuclear lamina and plays a critical role in maintaining nuclear architecture, regulating gene expression and modulating chromatin positioning. We have previously shown that LMNB1 gene duplications cause autosomal dominant leukodystrophy (ADLD), a fatal adult onset demyelinating disease. The mechanisms by which increased LMNB1 levels cause ADLD are unclear. To address this, we used a transgenic mouse model where Lamin B1 overexpression is targeted to oligodendrocytes. These mice showed severe vacuolar degeneration of the spinal cord white matter together with marked astrogliosis, microglial infiltration, and secondary axonal damage. Oligodendrocytes in the transgenic mice revealed alterations in histone modifications favoring a transcriptionally repressed state. Chromatin changes were accompanied by reduced expression of genes involved in lipid synthesis pathways, many of which are known to play important roles in myelin regulation and are preferentiall...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a49cb75c491c1c1f481fc1a94e208305" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273117,"asset_id":100452668,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273117/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452668"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452668"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452668; 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} }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="100452666"><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/100452666/Oxidative_Lipidomics_of_Apoptosis_Quantitative_Assessment_of_Phospholipid_Hydroperoxides_in_Cells_and_Tissues"><img alt="Research paper thumbnail of Oxidative Lipidomics of Apoptosis: Quantitative Assessment of Phospholipid Hydroperoxides in Cells and Tissues" class="work-thumbnail" src="https://attachments.academia-assets.com/101273131/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/100452666/Oxidative_Lipidomics_of_Apoptosis_Quantitative_Assessment_of_Phospholipid_Hydroperoxides_in_Cells_and_Tissues">Oxidative Lipidomics of Apoptosis: Quantitative Assessment of Phospholipid Hydroperoxides in Cells and Tissues</a></div><div class="wp-workCard_item"><span>Methods in Molecular Biology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Oxidized phospholipids play essential roles in execution of mitochondrial stage of apoptosis and ...</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">Oxidized phospholipids play essential roles in execution of mitochondrial stage of apoptosis and clearance of apoptotic cells. The identification and quantification of oxidized phospholipids generated during apoptosis can be successfully achieved by oxidative lipidomics. With this approach, diverse molecular species of phospholipids and their hydroperoxides are identified and characterized by soft-ionization mass-spectrometry techniques such as electrospray ionization (ESI). Quantitative assessment of lipid hydroperoxides is performed by fluorescence HPLC-based protocol. The protocol is based on separation of phospholipids using two-dimensional-highperformance thin-layer chromatography (2-D-HPTLC). Phospholipids are hydrolyzed using phospholipase A 2. The fatty acid hydroperoxides (FA-OOH) released is quantified by a fluorometric assay using Amplex red reagent and microperoxidase-11 (MP-11). Detection limit of this protocol is 1-2 pmol of lipid hydroperoxides. Lipid arrays vs. oxidized lipid arrays can be performed by comparing the abundance of phospholipids with the abundance of oxidized phospholipids. Using oxidative lipidomics approach we show that the pattern of phospholipid oxidation during apoptosis is nonrandom and does not follow their abundance in several types of cells undergoing apoptosis and a variety of disease states. This has important implications for evaluation of apoptosis in vivo. The anionic phospholipids, cardiolipin (CL) and phosphatidylserine (PS), are the preferred peroxidation substrates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="83f54d27ec2d2350d7bad6420f96c636" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273131,"asset_id":100452666,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273131/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452666"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452666"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452666; 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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="100452664"><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/100452664/Low_glucose_enhanced_TRAIL_cytotoxicity_is_mediated_through_the_ceramide_Akt_FLIP_pathway"><img alt="Research paper thumbnail of Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide–Akt–FLIP pathway" class="work-thumbnail" src="https://attachments.academia-assets.com/101273087/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/100452664/Low_glucose_enhanced_TRAIL_cytotoxicity_is_mediated_through_the_ceramide_Akt_FLIP_pathway">Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide–Akt–FLIP pathway</a></div><div class="wp-workCard_item"><span>Oncogene</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To examine whether the tumor microenvironment alters cytokine-induced cytotoxicity, human prostat...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To examine whether the tumor microenvironment alters cytokine-induced cytotoxicity, human prostate adenocarcinoma DU-145 cells were exposed to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and/or glucose deprivation, a common characteristic of the tumor microenvironment. TRAIL alone reduced cell survival in a dose-dependent manner. Glucose deprivation alone induced no cytotoxicity within 4 h. However, the combination of TRAIL (50 ng/ml) and glucose deprivation for 4 h increased cell death and PARP cleavage by promoting activation of caspase-8 and caspase-3, relative to that of TRAIL alone. Similar results were observed in human colorectal carcinoma CX-1 cells. Data from immunoblotting analysis reveal that glucose deprivation-enhanced TRAIL cytotoxicity is inversely related to the intracellular level of FLICE inhibitory protein (FLIP) but not that of death receptor 5 (DR5). Results from mass spectrometry show that glucose deprivation elevates ceramide. The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP. Taken together, the present studies suggest that glucose deprivation enhances TRAIL-induced cytotoxicity through the ceramide ± Akt ± FLIP pathway.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b329eea76e5f6289532d4c4288807256" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":101273087,"asset_id":100452664,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/101273087/download_file?s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="100452664"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="100452664"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 100452664; 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