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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
101

Radiation induced DNA damage response in carriers of the breast cancer gene mutation BRCA1

Lamont, Jayne Margaret January 2000 (has links)
No description available.
102

An investigation of iron metabolism in cells of the mononuclear phagocyte system

Davies, Euryl Howell January 1989 (has links)
No description available.
103

The interaction of pH with the calcium paradox of the heart

Chatamra, Krai-Rith January 1994 (has links)
No description available.
104

Regulation of the stress proteins calreticulin and Grp75 in response to amino acid deprivation of Chinese hamster overy cells

Heal, Richard January 1997 (has links)
No description available.
105

A comparison of selected cell formation algorithms : a simulation-based scheduling approach

Eltohmi, Omer Ahmed January 1996 (has links)
No description available.
106

Retroviral mediated expression of B-galactosidase in mouse cells

Clarke, A. R. January 1988 (has links)
No description available.
107

Genomic Approaches to Identifying Transcriptional Targets of AP-1, CREB and JNK Signaling in the Nervous System of Drosophila melanogaster

Etter, Paul Dezso January 2005 (has links)
Although a few regulators of memory and addiction have been identified, the biochemical pathways that mediate the development of addiction and memory remain poorly understood. In addition, important questions remain as to how these two phenomena can persist for so long, sometimes for the entire life of an individual.Signaling molecules and transcription factors are activated in response to stimuli that induce long-term neuronal plastic changes. The transcription factor CREB (cAMP-responsive element binding protein) is clearly involved in triggering processes of addiction and memory, but its sustained activation following a course of chronic drug exposure (or learning) returns to baseline within days [1]. Even the enduring increased levels of deltaFosB (a Fos family transcription factor that couples with other proteins in the AP-1 family to form transcriptional activator/repressor complexes) observed in regions of the mammalian brain following chronic drug exposure, persists for only weeks or months. Thus, although CREB and deltaFosB probably initiate the very stable behavioral changes seen with addiction and memory, their alterations cannot mediate those behavioral changes per se [1]. Long-term up- or down-regulation of molecules downstream of these transcription factors, or others, must be responsible for the enduring modifications in synaptic connectivity and structure believed to be required for the maintenance of these durable behavioral states [2].Many believe that more rapid progress will be made toward understanding the molecular basis of addiction if research efforts proceed hand-in-hand with, rather than in isolation from, the overlapping neurobiological study of learning and memory [1, 2]. The importance and utility of using simple model systems such as Drosophila and Aplysia to identify and characterize genes involved in long-term synaptic plasticity, and hence memory formation, is well documented [3-5]. Identification and functional analyses of neuronal genes transcriptionally regulated by AP-1 and CREB in Drosophila would elaborate on molecular mechanisms of long-term plasticity and hence help us understand, and perhaps manipulate, processes that underlie addiction and memory.
108

Extracellular Regulation of Nitric Oxide Signaling via Soluble Guanylate Cyclase

Ramanathan, Saumya January 2012 (has links)
Nitric Oxide (NO) regulates cardiovascular homeostasis by binding to soluble guanylate cyclase (sGC), leading to cGMP production, reduced cytosolic calcium concentration ([Ca²⁺]ᵢ) and vasorelaxation. Thrombospondin-1 (TSP-1), a secreted matricellular protein, was recently discovered to inhibit NO signaling and sGC activity. Inhibition of sGC requires binding to cell-surface receptor CD47. Here, I show that a TSP-1 C-terminal fragment (E3CaG1) readily inhibits sGC in Jurkat T cells, and that inhibition requires an increase in [Ca²⁺]ᵢ. Using digital imaging microscopy on live cells, I further show that E3CaG1 binding results in a substantial increase in [Ca²⁺]ᵢ, up to 300 nM. Addition of angiotensin II, a potent vasoconstrictor known to increase [Ca²⁺]ᵢ, also strongly inhibits sGC activity. sGC isolated from calcium-treated cells or from cell-free lysates supplemented with Ca²⁺ remains inhibited, while addition of kinase inhibitors staurosporine, genistein, PP1 or PP2 reverse inhibition, indicating inhibition likely involves a tyrosine kinase, more specifically, a src family kinase. Rat sGC is also inhibited by lysates supplemented with Ca²⁺, suggesting that the site of modification is at an evolutionarily conserved residue. Inhibition is through an increase in K(m) for GTP, which rises to 834 μM for the NO-stimulated protein, a 13-fold increase over the uninhibited protein. Compounds YC-1 and BAY 41-2272, allosteric stimulators of sGC that are of interest for treating hypertension, overcome E3CaG1-mediated inhibition of NO-ligated sGC. Taken together, these data suggest that sGC not only lowers [Ca²⁺]ᵢ in response to NO, inducing vasodilation, but is also inhibited by high [Ca²⁺]ᵢ, providing a fine balance between signals for vasodilation and vasoconstriction.
109

Cytokines and their inhibition within the central nervous system in chronic relasping experimental allergic encephalomyelitis

Hall, Deborah Jean January 1990 (has links)
No description available.
110

The role of the tyrosine phosphatase CD45 in B and C T cell development

Mee, Patrick Joseph January 1999 (has links)
No description available.

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