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You searched for +publisher:"Temple University" +contributor:("Selzer, Michael E."). Showing records 1 – 3 of 3 total matches.

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Temple University

1. Srivastava, Isha Narain. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.

Degree: PhD, 2017, Temple University

Biomedical Neuroscience

Background and Purpose –The mammalian target of rapamycin (mTOR) pathway has been implicated in cellular responses to hypoxia and inflammation. Cerebral palsy (CP) is a neurodevelopmental disorder often linked to hypoxic and inflammatory injury to the brain, however, a role for mTOR modulation in CP has not been investigated. We hypothesized that mTOR inhibition would prevent neuronal death and diminish inflammation in a mouse model of CP. Methods – Post-natal day 6 mouse pups were subjected to hypoxia-ischemia and lipopolysaccharide-induced inflammation (HIL), a model of CP causing injury to several brain areas. Mice received rapamycin (5mg/kg) following HIL, and then daily for 3 subsequent days. The phospho-activation of the mTOR effector mTOR effector proteins S6, S6K and 4EBP as well as upstream negative regulators, TSC1 and Redd1, were assessed as an in vivo measure of the mTOR signaling cascade. Expression of hypoxia inducible factor 1 (HIF-1 alpha) was assayed as an indicator of hypoxia-mediated cellular injury. Neuronal cell death was defined with Fluoro-Jade C (FJC) and cleaved-caspase 3 (CC3), a marker of apoptosis. Autophagy was measured using Beclin-1 and LC3II expression. Lastly, neuroninflammation following HIL was evaluated by examining Iba-1 labeled microglia number and morphology, as well as P-STAT3 expression. Results – Neuronal death, HIF-1alpha expression, and numerous Iba-1 labeled microglia were evident at 24 and 48 hours following HIL. Basal mTOR signaling was unchanged by HIL. Coincident with persistent mTOR signaling, a decreased in Redd1 expression but not TSC1 was observed in HIL. Increased P-STAT3 expression was observed at 24 and 48 hours post-HIL. Rapamycin treatment following HIL significantly reduced neuronal death, decreased HIF-1 alpha and P-STAT3 expression, and microglial activation, coincident with enhanced expression of Beclin-1 and LC3II, markers of autophagy induction. Increase in neuronal death was observed with concomitant administration of rapamycin and chloroquine, an autophagy inhibitor. Administration of a S6K inhibitor, PF-4708671, following HIL also decreased FJC staining further supporting an mTOR-dependent effect of HIL. Conclusions – mTOR inhibition prevented neuronal cell death and diminished neuroinflammation in this model of CP. Persistent mTOR signaling following HIL suggests a failure of autophagy induction, which may contribute to neuronal death in CP. These results suggest that mTOR signaling may be a novel therapeutic target to reduce neuronal cell death in CP.

Temple University – Theses

Advisors/Committee Members: Crino, Peter;, Selzer, Michael E., Soprano, Dianne R., Ferguson, Tanya, Valencia, Ignacio;.

Subjects/Keywords: Neurosciences;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Srivastava, I. N. (2017). The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,346472

Chicago Manual of Style (16th Edition):

Srivastava, Isha Narain. “The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.” 2017. Doctoral Dissertation, Temple University. Accessed September 20, 2020. http://digital.library.temple.edu/u?/p245801coll10,346472.

MLA Handbook (7th Edition):

Srivastava, Isha Narain. “The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.” 2017. Web. 20 Sep 2020.

Vancouver:

Srivastava IN. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Sep 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,346472.

Council of Science Editors:

Srivastava IN. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,346472


Temple University

2. Srivastava, Isha Narain. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.

Degree: PhD, 2017, Temple University

Biomedical Neuroscience

Background and Purpose –The mammalian target of rapamycin (mTOR) pathway has been implicated in cellular responses to hypoxia and inflammation. Cerebral palsy (CP) is a neurodevelopmental disorder often linked to hypoxic and inflammatory injury to the brain, however, a role for mTOR modulation in CP has not been investigated. We hypothesized that mTOR inhibition would prevent neuronal death and diminish inflammation in a mouse model of CP. Methods – Post-natal day 6 mouse pups were subjected to hypoxia-ischemia and lipopolysaccharide-induced inflammation (HIL), a model of CP causing injury to several brain areas. Mice received rapamycin (5mg/kg) following HIL, and then daily for 3 subsequent days. The phospho-activation of the mTOR effector mTOR effector proteins S6, S6K and 4EBP as well as upstream negative regulators, TSC1 and Redd1, were assessed as an in vivo measure of the mTOR signaling cascade. Expression of hypoxia inducible factor 1 (HIF-1 alpha) was assayed as an indicator of hypoxia-mediated cellular injury. Neuronal cell death was defined with Fluoro-Jade C (FJC) and cleaved-caspase 3 (CC3), a marker of apoptosis. Autophagy was measured using Beclin-1 and LC3II expression. Lastly, neuroninflammation following HIL was evaluated by examining Iba-1 labeled microglia number and morphology, as well as P-STAT3 expression. Results – Neuronal death, HIF-1alpha expression, and numerous Iba-1 labeled microglia were evident at 24 and 48 hours following HIL. Basal mTOR signaling was unchanged by HIL. Coincident with persistent mTOR signaling, a decreased in Redd1 expression but not TSC1 was observed in HIL. Increased P-STAT3 expression was observed at 24 and 48 hours post-HIL. Rapamycin treatment following HIL significantly reduced neuronal death, decreased HIF-1 alpha and P-STAT3 expression, and microglial activation, coincident with enhanced expression of Beclin-1 and LC3II, markers of autophagy induction. Increase in neuronal death was observed with concomitant administration of rapamycin and chloroquine, an autophagy inhibitor. Administration of a S6K inhibitor, PF-4708671, following HIL also decreased FJC staining further supporting an mTOR-dependent effect of HIL. Conclusions – mTOR inhibition prevented neuronal cell death and diminished neuroinflammation in this model of CP. Persistent mTOR signaling following HIL suggests a failure of autophagy induction, which may contribute to neuronal death in CP. These results suggest that mTOR signaling may be a novel therapeutic target to reduce neuronal cell death in CP.

Temple University – Theses

Advisors/Committee Members: Crino, Peter;, Selzer, Michael E., Soprano, Dianne R., Ferguson, Tanya, Valencia, Ignacio;.

Subjects/Keywords: Neurosciences;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Srivastava, I. N. (2017). The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,446570

Chicago Manual of Style (16th Edition):

Srivastava, Isha Narain. “The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.” 2017. Doctoral Dissertation, Temple University. Accessed September 20, 2020. http://digital.library.temple.edu/u?/p245801coll10,446570.

MLA Handbook (7th Edition):

Srivastava, Isha Narain. “The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy.” 2017. Web. 20 Sep 2020.

Vancouver:

Srivastava IN. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Sep 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,446570.

Council of Science Editors:

Srivastava IN. The Role of Mammalian Target of Rapamycin (mTOR) in a Mouse Model of Cerebral Palsy. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,446570


Temple University

3. Merkel, Steven Franklin. Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates.

Degree: PhD, 2017, Temple University

Pathology

Recent clinical and preclinical reports have identified traumatic brain injury (TBI) as an important risk factor affecting the development of substance use disorders (SUDs). Notably, these studies show that factors like age at the time of injury and TBI severity may increase the risk of substance abuse behavior post-TBI. Furthermore, radiological assessments in clinical TBI populations have observed neuropathology in select brain regions that form key neurocircuits that mediate drug reward and drug-seeking behavior. Therefore, the effects of TBI on the function of these brain structures may influence the risk of substance abuse behavior following brain injury. In order to test the effect of experimental TBI on substance abuse behavior, we utilized two premiere preclinical models: 1) the controlled cortical impact (CCI) model of experimental TBI and 2) a biased, three-phase, cocaine conditioned place preference (CPP) assay. Furthermore, we characterized the effect of experimental TBI on

Temple University – Theses

Advisors/Committee Members: Ramirez, Servio, Persidsky, Yuri;, Rawls, Scott M., Selzer, Michael E., Langford, Dianne;.

Subjects/Keywords: Medicine; Pathology; Neurosciences;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Merkel, S. F. (2017). Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,450997

Chicago Manual of Style (16th Edition):

Merkel, Steven Franklin. “Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates.” 2017. Doctoral Dissertation, Temple University. Accessed September 20, 2020. http://digital.library.temple.edu/u?/p245801coll10,450997.

MLA Handbook (7th Edition):

Merkel, Steven Franklin. “Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates.” 2017. Web. 20 Sep 2020.

Vancouver:

Merkel SF. Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Sep 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,450997.

Council of Science Editors:

Merkel SF. Effects of Traumatic Brain Injury on Addiction-Like Behavior and Their Neuropathological Correlates. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,450997

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