Open Access. Powered by Scholars. Published by Universities.®

Life Sciences Commons

Open Access. Powered by Scholars. Published by Universities.®

Articles 1 - 4 of 4

Full-Text Articles in Life Sciences

Francisella Tularensis Catalase Restricts Immune Function By Impairing Trpm2 Channel Activity, Nicole Lynn Flaherty Jan 2015

Francisella Tularensis Catalase Restricts Immune Function By Impairing Trpm2 Channel Activity, Nicole Lynn Flaherty

Legacy Theses & Dissertations (2009 - 2024)

As an innate defense mechanism, macrophages produce reactive species that weaken pathogens and serve as secondary messengers to modify signaling responses involved in immune function. The gram-negative bacterium F. tularensis utilizes its antioxidant armature to limit the host immune response but the mechanism behind this suppression has not been defined. Here we establish that F. tularensis limits Ca2+ entry thereby limiting actin reorganization and IL-6 production in a redox-dependent fashion. Wild-type (LVS) or catalase deficient F. tularensis (∆katG) show distinct profiles in their H2O2 scavenging capacity, 1 pM/sec and 0.015 pM/sec, respectively. Murine alveolar macrophages infected with ∆katG display distinct …


The Postsynaptic Regulation Of Synaptic Strength In Drosophila, Daniel Michael Gertner Jan 2014

The Postsynaptic Regulation Of Synaptic Strength In Drosophila, Daniel Michael Gertner

Legacy Theses & Dissertations (2009 - 2024)

Postsynaptic Ca2+ plays an important role in synaptic homeostasis and synaptic plasticity. Postsynaptic Ca2+ signals have been shown to regulate synaptic transmission at the Drosophila larval neuromuscular junction (NMJ), however, these signals have not been well characterized. This will explore how these signals regulate synaptic strength and what channels are involved. In previous lab experiments Ca2+ transients were observed during evoked and spontaneous release (Desai and Lnenicka, 2011). It was further demonstrated that a reduction in synaptic strength occurs following synaptic stimulation. It was hypothesized that the increase in postsynaptic Ca2+ following synaptic stimulation activates the gCS and causes a …


Mechanisms Of Age-Related Inflammation And Cancer : The Synergistic Effect Of Oxidants And Calcium, Donald A. Mccarthy Jan 2014

Mechanisms Of Age-Related Inflammation And Cancer : The Synergistic Effect Of Oxidants And Calcium, Donald A. Mccarthy

Legacy Theses & Dissertations (2009 - 2024)

The accumulation of senescent cells during the process of aging has been implicated as causal in numerous age-related pathologies. Senescent cells adopt a secretory phenotype consisting of many factors including matrix remodeling enzymes, growth factors, cytokines, and chemokines. Their secretory nature is the primary reason that they are associated with disease, but it remains unclear why they become so inflammatory. Using primary human fibroblasts cultured to senescence, we mechanistically determined why senescent cells are such potent inducers of inflammation. Our findings indicate that the early production of the cytokine Interleukin 1-α (IL-1α) is central to this transition. We found that …


Calcium Regulation And Transmitter Release At Drosophila Larval Neuromuscular Junction, Tao He Jan 2011

Calcium Regulation And Transmitter Release At Drosophila Larval Neuromuscular Junction, Tao He

Legacy Theses & Dissertations (2009 - 2024)

Calcium ions act as the most versatile 2nd messenger and are involved in an incredibly broad spectrum of biological processes. Proper cellular Ca2+ homeostasis is paramount in maintaining normal cell growth, functions, survival and programmed death. Hence, understanding Ca2+ regulation has been a goal of and a hot topic in cutting-edge biological research for decades. Recently, the advent of a new generation of Ca2+ indicators has made a major contribution to advances in understanding Ca2+ regulation (Grynkiewicz et al., 1985). Likewise, the application of Drosophila melanogaster as an animal model has provided tantalizing clues and fueled the progress of research …