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You searched for +publisher:"Temple University" +contributor:("Persidsky, Yuri;"). Showing records 1 – 3 of 3 total matches.

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Temple University

1. Bagashev, Asen. MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION.

Degree: PhD, 2014, Temple University

Cell Biology

In the early years of the AIDS epidemic, being infected with the virus that causes the disease was considered a virtual death sentence. But with the development of highly active antiretroviral therapy (HAART), many infected with HIV-1 are living much longer. In fact, it is estimated that by 2015, about half of all HIV-positive individuals will be older than 50. Yet those over 50 also progress to AIDS faster than adults in their 20s or 30s. And those in the younger age bracket, even those responding well to antiretroviral therapy, still exhibit illnesses and clinical conditions commonly associated with older people, such as HIV-associated neurocognitive disorders (HAND), certain cancers, liver and bones diseases. For the most part, the reasons for this have remained a mystery. However, one may ask, how in the absence of circulating detected virus, viral proteins could cause this kind of damage. The answer is that eradication of latent viruses still unsuccessful and studies showed the persistence of HIV-1 in brain cells as well as the presence of viral proteins in CSF. This notion was supported by the compelling neuropathological data suggesting that the loss of Synaptic Plasticity occurs with the ongoing presence of virus and despite HAART. Clinically, these neuropathological data manifest by a gradual loss of working memory and learning disability, which promote alteration of synaptic plasticity that may manifest by symptoms similar to the ones observed in aged brain or what is called PREMATURE BRAIN AGING. Anatomically, working memory and learning ability functions are assured by neurons of the hippocampus, a brain area known-to-be affected by HIV-1 proteins. Mechanistically, several laboratories, including ours, demonstrated that viral proteins perform their functions through deregulation of several molecular pathways that can cause mitochondrial damage (such as depletion of mitochondrial calcium and release of ROS), inhibition of axonal transport leading to prevent neuronal communications or loss of long-term potentiation (LTP). Interestingly, CREB and BDNF proteins have been shown to play an important role in this phenomenon directly or through its downstream target genes. In here, we examined the impact of HIV-1 Tat on CREB-BDNF pathway and whether Tat is using this pathway to cause neuronal deregulation.

Temple University – Theses

Advisors/Committee Members: Sawaya, Bassel E., Kirby, Lynn;, Abood, Mary Ellen, Persidsky, Yuri, Sullivan, Kathleen E.;.

Subjects/Keywords: Neurosciences; Molecular biology; Virology

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

APA (6th Edition):

Bagashev, A. (2014). MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,255791

Chicago Manual of Style (16th Edition):

Bagashev, Asen. “MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION.” 2014. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,255791.

MLA Handbook (7th Edition):

Bagashev, Asen. “MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION.” 2014. Web. 30 Oct 2020.

Vancouver:

Bagashev A. MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,255791.

Council of Science Editors:

Bagashev A. MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,255791


Temple University

2. Zhang, Lixiao. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.

Degree: PhD, 2017, Temple University

Pharmacology

Background: Epidemiology, clinical trials and meta-analysis studies have established that Hyperhomocysteinemia (HHcy) is an independent risk factor for stroke. However, the exact molecular mechanism underlying the HHcy-induced risk of stroke is unclear. Our study aims to investigate the role of HHcy in stroke. Methods and results: We established a mice mode of focal ischemic stroke, termed transient Middle Cerebral Artery Occlusion (tMCAO) and conducted surgery on a mice model of HHcy (plasma homocysteine level ~150μM), in which a Zn2+ inducible human cystathionine β-synthase (CBS) transgene was introduced to circumvent the neonatal lethality of the CBS gene deficiency (Tg-hCBS Cbs-/- mice). Fourteen-week-old male mice were used in the experiment. A student’s t-test was used for the evaluation of the statistical significance between the two groups. For the comparison across multiple groups, one-way ANOVA was used. We found that HHcy 1) increased the infarction volume from 42.3 ± 4.9 mm

Temple University – Theses

Advisors/Committee Members: Wang, Hong;, Yang, Xiao-Feng, Ashby, Barrie, Persidsky, Yuri, Eguchi, Satoru, Yu, Jun, Zhow, Bin;.

Subjects/Keywords: Health sciences; Pharmacology; Biology;

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

APA (6th Edition):

Zhang, L. (2017). HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,450002

Chicago Manual of Style (16th Edition):

Zhang, Lixiao. “HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.” 2017. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,450002.

MLA Handbook (7th Edition):

Zhang, Lixiao. “HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.” 2017. Web. 30 Oct 2020.

Vancouver:

Zhang L. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,450002.

Council of Science Editors:

Zhang L. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,450002


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;

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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 October 30, 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. 30 Oct 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 Oct 30]. 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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