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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
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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.
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Showing 71 to 76 of 76 (0.022 seconds)Spelling suggestions: "subject:"iir"" "subject:"rair""
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Genetic and functional characterisation of killer cell immunoglobulin like receptors (KIR) of rhesus macaques (Macaca mulatta) / Genetische und funktionelle Charakterisierung der killer cell immunoglobulin like Rezeptoren (KIR) des Rhesusaffen (Macaca mulatta)Kruse, Philip Hermann 06 April 2010 (has links)
No description available.
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Modulation of gene expression by chronic stress in astroglia in hippocampus and prefrontal cortex of the rat / Modulation der Genexpression durch chronischen Stress in Astroglia im Hippocampus und im präfrontalen Kortex bei RattenAraya-Callís, Carolina 20 April 2012 (has links)
No description available.
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Characterisation of killer immunoglobulin-like receptors in rhesus macaques (Macaca mulatta) / Charakterisierung von killer immunoglobulin-like receptors von Rhesus Affen (Macaca mulatta)Hermes, Meike 13 July 2012 (has links)
No description available.
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Hydrogen Sulfide Regulation of Kir ChannelsHa, Junghoon 01 January 2017 (has links)
Inwardly rectifying potassium (Kir) channels establish and regulate the resting membrane potential of excitable cells in the heart, brain and other peripheral tissues. Phosphatidylinositol- 4,5-bisphosphate (PIP2) is a key direct activator of ion channels, including Kir channels. Gasotransmitters, such as carbon monoxide (CO), have been reported to regulate the activity of Kir channels by altering channel-PIP2 interactions. We tested, in a model system, the effects and mechanism of action of another important gasotransmitter, hydrogen sulfide (H2S) thought to play a key role in cellular responses under ischemic conditions. Direct administration of sodium hydrogen sulfide (NaHS), as an exogenous H2S source, and expression of cystathionine γ-lyase (CSE), a key enzyme that produces endogenous H2S in specific brain tissues, resulted in comparable current inhibition of several Kir2 and Kir3 channels. A “tag switch” assay provided biochemical evidence for sulfhydration of Kir3.2 channels. The extent of H2S regulation depended on the strength of channel-PIP2 interactions: H2S regulation was attenuated when strengthening channel-PIP2 interactions and was increased when channel-PIP2 interactions were weakened by depleting PIP2 levels via different manipulations. These H2S effects took place through specific cytoplasmic cysteine residues in Kir3.2 channels, where atomic resolution structures with PIP2 gives us insight as to how they may alter channel-PIP2 interactions. Mutation of these residues abolished H2S inhibition, and reintroduction of specific cysteine residues into the background of the mutant lacking cytoplasmic cysteine residues, rescued H2S inhibition. Molecular dynamics simulation experiments provided mechanistic insights as to how sulfhydration of specific cysteine residues could lead to changes in channel-PIP2 interactions and channel gating.
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KIR Channels in CO2 Central Chemoreception: Analysis with a Functional Genomics ApproachRojas, Asheebo 06 August 2007 (has links)
The process of respiration is a pattern of spontaneity and automatic motor control that originate in the brainstem. The mechanism by which the brainstem detects CO2 is termed central CO2 chemoreception (CCR). Since the early 1960’s there have been tremendous efforts placed on identification of central CO2 chemoreceptors (molecules that detect CO2). Even with these efforts, what a central CO2 chemoreceptor looks like remain unknown. To test the hypothesis that inward rectifier K+ (Kir) channels are CO2 sensing molecules in CCR, a series of experiments were carried out. 1) The first question asked was whether the Kir4.1-Kir5.1 channel is expressed in brainstem chemosensitive nuclei. Immunocytochemistry was performed on transverse medullary and pontine sections using antibodies raised against Kir4.1 and Kir5.1. Positive immunoassays for both Kir4.1 and Kir5.1 subunits were found in CO2 chemosensitive neurons. In the LC the Kir4.1 and Kir5.1 were co-expressed with the neurokinin-1 receptor that is the natural receptor for substance P. 2) The second question asked was whether the Kir4.1-Kir5.1 channel is subject to modulation by neurotransmitters critical for respiratory control. My studies demonstrated that indeed the Kir4.1-Kir5.1 channel is subject to modulation by substance P, serotonin and thyrotropin releasing hormone. 3) I performed studies to demonstrate the intracellular signaling system underlying the Kir4.1-Kir5.1 channel modulation by these neurotransmitters. The modulation by all three neurotransmitters was dependent upon the activation of protein kinase C (PKC). The Kir4.1-Kir5.1 but not the Kir4.1 channel was modulated by PKC. Both the Kir4.1 and Kir5.1 subunits can be phosphorylated by PKC in vitro. However, systematic mutational analysis failed to reveal the phosphorylation site. 4) The fourth question asked was whether Kir channels share a common pH gating mechanism that can be identified. Experiments were performed to understand the gating of the Kir6.2+SUR1 channel as specific sites for ligand binding and gating have been demonstrated. I identified a functional gate that was shared by multiple ligands that is Phe168 in the Kir6.2. Other Kir channels appear to share a similar gating mechanism. Taken together, these studies demonstrate the modulation of Kir channels in central CO2 chemoreception.
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Altered Skeletal Muscle Excitation-Contraction Coupling in the R6/2 Transgenic Mouse Model for Huntington's DiseaseMiranda, Daniel R. January 2021 (has links)
No description available.
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