Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for +publisher:"Temple University" +contributor:("Sullivan, Kathleen E.;"). Showing records 1 – 2 of 2 total matches.

Search Limiters

Last 2 Years | English Only

No search limiters apply to these results.

▼ Search Limiters


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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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 26, 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. 26 Oct 2020.

Vancouver:

Bagashev A. MOLECULAR MECHANISM OF HIV-1 TAT INDUCED NEURONAL DYSFUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 26]. 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. Gallo, Paul Matthew. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.

Degree: PhD, 2017, Temple University

Microbiology and Immunology

Systemic lupus erythematosus (SLE) is complex autoimmune disease in which autoantibodies form against double stranded DNA (dsDNA) and nuclear antigens. Autoantigen immune complexes form, deposit in the vasculature, and cause multisystem organ damage. Both genetic and environmental factors contribute to the development of SLE. This thesis will explore three major themes found in the study of SLE: 1) Bacterial infection as an environmental trigger, 2) cytokine dysregulation in immune cells, and 3) the treatment of end organ damage in the form of lupus nephritis. Viral infections have long been associated with the development of systemic autoimmune disease, but the mechanisms by which chronic bacterial infections may promote autoimmunity remain unclear. In chapter three we show that a component of bacterial biofilms, the amyloid-like protein “curli”, irreversibly forms fibers with bacterial or eukaryotic DNA during biofilm formation. This interaction accelerates amyloid polymerization and creates potent immunogenic complexes that activate immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in SLE. When given systemically, curli/DNA composites trigger immune activation and production of autoantibodies in lupus-prone and wild type mice. We also found that infection with curli-producing bacteria triggered higher autoantibody titers in lupus-prone mice compared to curli-deficient bacteria. These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity. Cytokine dysregulation is also common in SLE patients. Serum cytokines are often elevated during active disease, including type I IFNs and IL-10. In chapter four we demonstrate that Il10 is a type I IFN response gene and has increased basal expression in dendritic cells (DCs) derived from pre-disease lupus-prone Sle1,2,3 mice. We show that Sle1,2,3-derived DCs overproduce IL-10 in response to TLR ligands and that this is the result of autocrine signaling though the type I IFN receptor (IFNAR). These results suggest that dysregulation of cytokine signaling in the myeloid compartment may contribute to IL-10 dysregulation in SLE. Renal disease remains a major cause of morbidity and mortality in SLE. A number of mouse models of chronic kidney disease have implicated the EGFR-family receptors in the progression of renal fibrosis and dysfunction. In chapter five we show that renal expression of ErbB2 is increased in murine lupus. We therefore asked if EGFR-family inhibition could prevent murine lupus nephritis. To test this possibility we used lapatinib, an EGFR-ErbB2 dual kinase inhibitor, in an IFN-accelerated model of murine lupus. We found that lapatinib administration lowered autoantibody levels but worsened renal disease. Lapatinib failure to treat murine lupus nephritis despite lowered autoantibody levels suggests EGFR-family signaling is…

Advisors/Committee Members: Gallucci, Stefania;, Cohen, Philip L., Ganea, Doina, Monestier, Marc, Tukel, Cagla, Sullivan, Kathleen E.;.

Subjects/Keywords: Biomechanics; Accounting;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Gallo, P. M. (2017). The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,452916

Chicago Manual of Style (16th Edition):

Gallo, Paul Matthew. “The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.” 2017. Doctoral Dissertation, Temple University. Accessed October 26, 2020. http://digital.library.temple.edu/u?/p245801coll10,452916.

MLA Handbook (7th Edition):

Gallo, Paul Matthew. “The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.” 2017. Web. 26 Oct 2020.

Vancouver:

Gallo PM. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Oct 26]. Available from: http://digital.library.temple.edu/u?/p245801coll10,452916.

Council of Science Editors:

Gallo PM. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,452916

.