{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/79442"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/79442","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"The Effects of Immune Factor, TNFα, on Human Fetal Neural Development and Schizophrenia in a Cerebral Organoid Model","abstract":"M.S.","abstract_html":"M.S.","abstract_has_math":false,"creators":["Powell, Hanna"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Stachowiak, Ewa","Neuroscience"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-04-04T20:33:13Z","date_published":"2019-04-04T20:33:13Z","updated_at":"2026-07-27T19:05:19Z","subjects":["neurosciences","immunology","genetics"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/79442","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Stachowiak, Ewa","Neuroscience"]},{"key":"dc:creator","label":"Author","values":["Powell, Hanna"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-04-04T20:33:13Z","2019","2019-01-24 12:51:17"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["neurosciences","immunology","genetics"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/79442"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["M.S.","Schizophrenia (SZ) is a psychiatric disease, which affects approximately one percent of the global population. Schizophrenia is a neurodevelopmental disorder, which affects in utero brain development within the first trimester well before its clinical manifestation during adolescence. The symptoms that characterize SZ and lead to its diagnosis are typically divided into positive symptoms (dilutions, paranoia, etc.) and negative symptoms (decreases in cognitive functioning, social skills, executive functioning, etc.)(Millan, Fone, Steckler, & Horan, 2014) Over 300 genes were found to be altered in SZ affecting diverse developmental pathways which when dysregulated may increase the likelihood of disease manifestation. Recent studies indicate that the affected signaling pathways converge on and dysregulate the pan-ontogenetic INFS pathway (E. K. Stachowiak et al., 2017) However, genetics isn’t the only factor causing SZ, a number of environmental factors exist, which in combination with genetics has been proposed to influence the expression of the disease (Schmitt, Hasan, Gruber, & Falkai, 2011) ... This study focuses on the effect of immune factor, TNFα, on neurodevelopment during early pregnancy using the in vitro model of cerebral organoids (“mini brains”) to discover if there is a significant difference between neurodevelopment that occurs with and without maternal immune activation. In order to recapitulate this the organoids were treated with 50pg TNFα at two weeks of growth, the treatment lasted nine days and then the organoids were allowed two weeks to recover and then harvested at 37 days. The following four experimental groups were used: nontreated control (C), control treated with TNFα (C+TNFα), schizophrenia (SZ) and schizophrenia treated with TNFα (SZ+TNFα). The two untreated groups received only nutritional supplements during the nine-day treatment period."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The Effects of Immune Factor, TNFα, on Human Fetal Neural Development and Schizophrenia in a Cerebral Organoid Model"]}]}],"canonical_facts":{"dc:contributor":["Stachowiak, Ewa","Neuroscience"],"dc:creator":["Powell, Hanna"],"dc:date":["2019-04-04T20:33:13Z","2019","2019-01-24 12:51:17"],"dc:description":["M.S.","Schizophrenia (SZ) is a psychiatric disease, which affects approximately one percent of the global population. Schizophrenia is a neurodevelopmental disorder, which affects in utero brain development within the first trimester well before its clinical manifestation during adolescence. The symptoms that characterize SZ and lead to its diagnosis are typically divided into positive symptoms (dilutions, paranoia, etc.) and negative symptoms (decreases in cognitive functioning, social skills, executive functioning, etc.)(Millan, Fone, Steckler, & Horan, 2014) Over 300 genes were found to be altered in SZ affecting diverse developmental pathways which when dysregulated may increase the likelihood of disease manifestation. Recent studies indicate that the affected signaling pathways converge on and dysregulate the pan-ontogenetic INFS pathway (E. K. Stachowiak et al., 2017) However, genetics isn’t the only factor causing SZ, a number of environmental factors exist, which in combination with genetics has been proposed to influence the expression of the disease (Schmitt, Hasan, Gruber, & Falkai, 2011) ... This study focuses on the effect of immune factor, TNFα, on neurodevelopment during early pregnancy using the in vitro model of cerebral organoids (“mini brains”) to discover if there is a significant difference between neurodevelopment that occurs with and without maternal immune activation. In order to recapitulate this the organoids were treated with 50pg TNFα at two weeks of growth, the treatment lasted nine days and then the organoids were allowed two weeks to recover and then harvested at 37 days. The following four experimental groups were used: nontreated control (C), control treated with TNFα (C+TNFα), schizophrenia (SZ) and schizophrenia treated with TNFα (SZ+TNFα). The two untreated groups received only nutritional supplements during the nine-day treatment period."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/79442"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["neurosciences","immunology","genetics"],"dc:title":["The Effects of Immune Factor, TNFα, on Human Fetal Neural Development and Schizophrenia in a Cerebral Organoid Model"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T19:05:19Z"}