Дисертації з теми "Molecular Physiology and Pharmacology"
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Bahnasi, Yahya Mohamed. "Molecular physiology and pharmacolgy of TRPC5 ion channels." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496554.
Повний текст джерелаElnakish, Mohammad T. "Mechanisms and Functional Consequences of Cardiac Remodeling: Role of Myocardial Rac1 and Vascular Profilin1 Genes." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1363694358.
Повний текст джерелаBonilla, Ingrid Marie. "Acquired Electrophysiological Remodeling and Cardiac Arrhythmias." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396024058.
Повний текст джерелаSzabo, Elod Zala. "Molecular and cellular properties of the human brain Na+H+ exchanger isoform 5." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38420.
Повний текст джерелаPharmacological analyses demonstrated that H+ i-activated 22Na+ influx mediated by NHE5 was inhibited by several classes of drugs at half-maximal concentrations that were intermediate to those determined for the high-affinity NHE1 and the low-affinity NHE3 isoforms. Kinetic analyses showed that the extracellular Na+-dependence of NHE5 activity followed a simple hyperbolic relationship and, unlike other NHE isoforms, the intracellular H+-dependence also exhibited first-order kinetics. Extracellular monovalent cations, such as H+ and Li+, but not K+, acted as effective competitive inhibitors of 22Na+ influx by NHE5.
To find novel interacting proteins that are involved in NHE5 regulation, a yeast two-hybrid screen of human brain cDNA library was conducted using NHE5 as bait. A clone encoding the AMP-activated protein kinase (AMPK) alpha2 subunit was further analyzed. AMPK is a serine/threonine kinase that is activated by elevated ratios of [AMP]/[ATP], regulating various biological processes in response to hypoxia or exercise. AMPK alpha2 binds NHE5 in vitro and in vivo, and directly phosphorylates it in vitro. Activation of endogenous AMPK by AICAR, a membrane permeable AMP analogue, as well as heterologous expression of the full-length and constitutive active forms of alpha2 subunit increased the transporter activity measured by 22Na+ influx.
The regulatory protein arrestin3 was also found to interact with NHE5 in the yeast two-hybrid screen. Arrestins were previously shown to associate with and regulate transmembrane proteins of the G protein-coupled receptor family. We demonstrate that NHE5 binds arrestin3 both in vitro and in vivo; and the binding is phosphorylation-dependent. When co-expressed in CHO cells, arrestin3 and NHE5 co-localize, and arrestin3 expression seems to attenuate the basal activity of the transporter. The data presented in this thesis reveals new aspects of both NHE regulation, and AMPK and arrestin function.
Zicha, Stephen. "Molecular basis for ion current heterogeneity in normal and diseased hearts." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85660.
Повний текст джерелаHere, we describe the variable dependence on repolarizing K+ currents in different species as being the result of the lack of Ito subunits in guinea pig heart with a greater expression of IK subunits, while rabbits express all hypothesized Ito subunits, but express IK subunits at low levels. Humans are found to lie in between these two species in terms of the expression of these voltage-gated K+ channel subunits. The specialized function of certain regions of the heart, such as the ventricles and the SAN, have been attributed to the heterologous expression of Ito and the pacemaker current (I f) respectively. Here were demonstrate that both Kv4.3 and KchIP2 gradients underlie an observed Ito transmural gradient and contribute to the dispersion of repolarization, while a greater expression of HCN2 and HCN4 subunits in the SAN compared to the right atrium account for the larger I f current in this region. Cardiovascular diseases such as congestive heart failure (CHF) have been associated with ion channel remodelling. Here, we report the finding of changes in Nav1.5, Kv4.3, HCN2 and HCN4 expression which may underlie some of the electrophysiological changes associated with this disease. Furthermore, we characterise a genetic polymorphism which is associated with another disease, atrial fibrillation.
The heterologous expression of voltage-gated ion channel subunits may account for many of the species-, region- and disease-specific differences which have been observed in the heart. Such heterogeneity contributes to the proper functioning of the heart under normal conditions, but may also contribute to the pathogenesis of cardiovascular disease.
Richman, Jeremy Golding 1970. "Characterization of α₂-adrenergic receptor localization and functional responses". Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282583.
Повний текст джерелаSinha, Sayantani. "Role of TRPA1 and TRPV1 in Propofol Induced Vasodilation." Thesis, Kent State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618926.
Повний текст джерелаAims: Propofol, clinically named as Diprivan is an intravenous anesthetic known to cause hypotension in patients presenting for surgery. We have investigated the vasodilatory signaling cascade by which propofol causes hypotension using both in vivo and in vitro experimental approaches.
Methods and Results: Using high-fidelity microtip transducer catheter, mean arterial blood pressure (MAP) was measured in control, transient receptor potential ankyrin subtype 1 knock-out (TRPA1-/-), transient receptor potential vanilloid 1 knock-out (TRPV1-/-) and TRPA1-TRPV1 double-knockout mice (TRPAV-/-) in the presence and absence of L-NAME (an endothelial nitric oxide synthase inhibitor) and penitrem A [a big-conductance calcium gated (BKCa) channel inhibitor]. To further support our in-vivo data, murine coronary microvessels were isolated and cannulated for vasoreactivity studies. Furthermore, NO production from endothelial cells isolated from mouse aorta was also measured and immunocytochemical (ICC) studies were performed to show the intracellular localization of TRPA1 and TRPV1. Our in-vivo data shows that the characteristic propofol-induced depressor response is dependent on TRPA1-NO-BKCa pathway. Interestingly, vasoreactivity studies in isolated murine left anterior ascending (LAD) arteries demonstrate that TRPA1 and TRPV1 communicate with each other and propofol-induced vasodilation is dependent on both TRPA1 and TRPV1. Moreover our data also suggest that NO production and BK channel activation are the downstream mediators in this pathway. Finally, we demonstrate that NO production is attenuated in primary endothelial cells isolated from TRPAV-/- mice. ICC data also shows the co-localization of these channels in mouse aortic endothelial cells.
Conclusions: This is the first study which has shown that propofol-induced vasodilation involves TRPA1 in-vivo and also there is an implication of cross-talk between TRPA1 and TRPV1 in the coronary bed. Furthermore by understanding the mechanisms by which this anesthetic causes hypotension and coronary dilation will help to mitigate the potential harmful side-effects of anesthesia in patients with little cardiovascular reserve. This will in turn ensure a better and faster post-operative recovery in patients, especially benefiting those suffering from diabetes and other cardiovascular disorders.
Harris, Tanoya L. "Ouabain Regulates Caveolin-1 Vesicle Trafficking by a Src-Dependent Mechanism." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1333732028.
Повний текст джерелаBarr, Larry A. "The Role of Calcium in the Regulation of Pathological Hypertrophy." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/254617.
Повний текст джерелаPh.D.
Pathological hypertrophy leads to cardiac dysfunction and heart failure. It is not clearly defined how this process occurs in the cardiomyocyte, or how the pathology can be effectively treated. There are numerous processes that lead to pathological hypertrophy. We developed two models to study pathological hypertrophy and the role that Ca2+ plays. In one model, we administered clinical doses of the leukemia therapeutic drug imatinib to neonatal ventricular cardiomyocytes. This drug has recently been found to be cardiotoxic, and we set out to understand if Ca2+ is involved. In the second model, we developed mice with overexpression of the Ca2+ entrance channel, the L-type calcium channel (LTCC), which leads to pathological hypertrophy over time. We instituted a chronic exercise regimen on these mice to learn if physiological hypertrophy can ameliorate detrimental aspects of pathological hypertrophy. After cardiomyocytes were treated with imatinib, they expressed enhanced Ca2+ activity. Levels of atrial natriuretic peptide (ANP) were up, signifying pathological hypertrophy. We determined that Ca2+ was activating Calcineurin, leading to translocation of nuclear factor of activated T-cells (NFAT) into the nucleus, resulting in hypertrophy. This activity was blocked by Ca2+ and Calcineurin inhibitors. We concluded that imatinib causes Ca2+ induced pathological hypertrophy. When mice with LTCC overexpression were exercised, they exhibited enhanced cardiac function. They also had thicker septal walls and increased chamber diameter, hallmarks of physiological hypertrophy. Heart weight to body weight ratio was significantly higher after exercise. When isolated hearts were administered ischemia/reperfusion injury, the exercised hearts showed a significant improvement in recovery compared to sedentary LTCC overexpressed hearts. Calcium activity was enhanced at the cardiomyocyte level in both mouse lines of exercised mice. In conclusion, hearts with a pathological hypertrophic phenotype can enhance function and achieve cardioprotection through chronic exercise.
Temple University--Theses
Blatherwick, Eleanor Q. "Imaging mass spectrometry approaches for the detection and localisation of drug compounds and small molecules in tissue." Thesis, University of Warwick, 2013. http://wrap.warwick.ac.uk/57257/.
Повний текст джерелаShin, Jong M. "Role of C121A in mGluR2 homodimeric expression and function." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5576.
Повний текст джерелаVohra, Hiba Z. "Molecular Targets of Psychedelics and Their Role in Behavioral Models of Hallucinogenic Action." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6012.
Повний текст джерелаPandey, Varunkumar Girijaprasad. "The Effect of Glucocorticoids on Regulation of the Human Angiotensinogen Gene and Blood Pressure." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1378647891.
Повний текст джерелаMuchhala, Karan Hitesh. "An investigation on the role of β-arrestin 2, protein kinase C and sex on the mechanism of morphine tolerance in the mouse ileum". VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6074.
Повний текст джерелаNarayanaswami, Vidya. "DIET-INDUCED OBESITY: DOPAMINERGIC AND BEHAVIORAL MECHANISMS AS OUTCOMES AND PREDICTORS." UKnowledge, 2013. http://uknowledge.uky.edu/pharmacy_etds/12.
Повний текст джерелаRavilla, Nagendra Babu. "K-Cl Cotransport: Role of KCC3 in cellular Potassium (K) homeostasis in KCC3- transfected HEK-293 cells." Wright State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=wright1377519708.
Повний текст джерелаSINHA, SAYANTANI. "Role of TRPA1 and TRPV1 in Propofol Induced Vasodilation." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1384901930.
Повний текст джерелаAbdul, Majid Aman Shah Bin. "The influence of selected sulphur containing compounds on retinal cell death : neuroprotective effects of hydrogen sulphide in a glaucoma model." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:bfb5ec82-9141-4784-94a8-0df3ce9d9471.
Повний текст джерелаHirsch, Alexander M. "Embryonic Stem Cell-Derived Exosomes Increase the Antiproliferative Activity of Doxorubicin in Breast Cancer." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5981.
Повний текст джерелаAhmad, Faizzan Syed. "A novel human stem cell platform for probing adrenoceptor signaling in iPSC derived cardiomyocytes including those with an adult atrial phenotype." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:17972018-6750-4e5c-8cc9-42e9c381f531.
Повний текст джерелаPark, Sung H. "High Affinity Block of ICl,swell by Thiol-Reactive Small Molecules." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4433.
Повний текст джерелаYan, Dejun. "THE EFFECT OF CURCUMIN ON LEWIS LUNG CARCINOMA." Bowling Green State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1308588440.
Повний текст джерелаVallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/913.
Повний текст джерелаVallaster, Markus Parzival. "Intergenerational Effects of Nicotine in an Animal Model of Paternal Nicotine Exposure." eScholarship@UMMS, 2008. http://escholarship.umassmed.edu/gsbs_diss/913.
Повний текст джерелаRagas, Moner A. "Refining a Post-Stroke Pharmacological and Physical Treatment to Reduce Infarct Volume or Improve Functional Recovery, Using Gene Expression Changes in the Peri-Infarct Region to Examine Potential Mechanisms in Male and Female Rats." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1470395029.
Повний текст джерелаAppleby, Hollie Leanne. "Orai channel physiology and pharmacology." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/15950/.
Повний текст джерелаPrachanronarong, Kristina L. "Understanding Drug Resistance and Antibody Neutralization Escape in Antivirals: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/840.
Повний текст джерелаNovozhilova, Ekaterina B. "Physiology and pharmacology of flatworm muscle." [Ames, Iowa : Iowa State University], 2008.
Знайти повний текст джерелаSpratt, James Christopher Samuel. "Endothelin : cardiovascular pharmacology, physiology & pathophysiology." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23202.
Повний текст джерелаStechschulte, Lance A. "The Co-chaperones FKBP51 and PP5 Control Nuclear Receptor Phosphorylation and Adipogenesis." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1370871316.
Повний текст джерелаOrdway, Gregory A. "Molecular Pharmacology of Antidepressants." Digital Commons @ East Tennessee State University, 2006. https://dc.etsu.edu/etsu-works/8657.
Повний текст джерелаMaharjan, Chandra Kumar. "Interaction of Na+/K+ ATPase with Bcl-2 Proteins: Isolated Enzyme vs Epithelial Cell Extracts." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1464692938.
Повний текст джерелаCumming, Paul Kenneth. "Pharmacology of cerebral histamine." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30687.
Повний текст джерелаMedicine, Faculty of
Graduate
Bolton, John Francis. "Urinary tract smooth muscle physiology and pharmacology." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432685.
Повний текст джерелаPearson, Hugh Anthony. "Physiology and pharmacology of insect calcium channels." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308295.
Повний текст джерелаFarquhar, Michelle Jane. "Molecular pharmacology of chimeric peptides." Thesis, University of Wolverhampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247780.
Повний текст джерелаBarkan, Kerry. "An investigation into glucagon receptor pharmacology." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/98781/.
Повний текст джерелаBaker, Jillian G. "Molecular pharmacology of β-adrenoceptor ligands." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401579.
Повний текст джерелаSlusarczyk, Adrian L. (Adrian Lukas). "Molecular imaging with engineered physiology." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104229.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references (pages 125-133).
Using molecular imaging in vivo, biomolecular and cellular phenomena can be investigated within their relevant physiological context, addressing a central challenge for 21st century biomedicine and basic research. To advance neuroscience in particular, molecular-level measurements across the brain inside the intact organism are required. However, existing imaging strategies and available probes have been limited by serious constraints. Magnetic resonance imaging (MRI) provides deeper tissue penetration depth than optical imaging and better spatial resolution and greater versatility in sensor design than radioactive probes. The most important drawback for MRI probes has been the need for high concentrations in the micromolar to millimolar range, leading to analyte sequestration, complications for noninvasive brain delivery, and toxicity. Efforts to address the sensitivity problem, such as nuclear hyperpolarization, introduce their own technical constraints and so far lack generality. Here, we introduce a conceptually novel molecular imaging technique based on artificially induced physiological perturbations, enabling molecular MRI with nanomolar sensitivity. In this imaging strategy, we take advantage of blood as an abundant endogenous source of contrast compatible with multiple imaging modalities including MRI and optical imaging to decouple the concentration requirement for molecular sensing from the concentration requirement for imaging contrast. Highly potent vasoactive peptides are engineered to respond to specific biomolecular phenomena of interest at nanomolar concentrations by inducing dilation of the microvasculature, increased local bloodflow, and consequently, large changes in T₂*-weighted MRI contrast. This principle is exploited to design activatable probes for protease activity based on the calcitonin gene-related peptide (CGRP) and validate them for brain imaging in live rats; to use CGRP as a genetic reporter for cell tracking; and to create fusions of a vasoactive peptide from flies to previously characterized antibodies capable of crossing the blood-brain barrier (BBB), suggesting the possibility of minimally invasive brain delivery of such probes. We demonstrate the feasibility of highly sensitive molecular MRI with vasoactive probes at concentrations compatible with in situ expression of probes and delivery across the BBB, and show that vasoactive peptides are a versatile platform for MRI probe design which promises unprecedented in vivo molecular insights for biomedicine and neuroscience.
by Adrian L. Slusarczyk.
Ph. D.
Thornton, S. "The physiology and pharmacology of oxytocin during human pregnancy." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234659.
Повний текст джерелаSam, Cynthia Laura Sandra. "Atrial myocyte physiology and pharmacology in health and disease." Thesis, Kingston University, 2013. http://eprints.kingston.ac.uk/27782/.
Повний текст джерелаFerro, Charles Joseph. "Endothelin in man : studies in pharmacology, physiology and pathophysiology." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/21238.
Повний текст джерелаLiu, Tongyu. "Ethanol Effect on Three Distinct Types of Ependymal Cells and the Intracellular Calcium Oscillation Property." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1396351727.
Повний текст джерелаMcGonigle, Ian Vincent. "Molecular pharmacology of an insect GABA receptor." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/226857.
Повний текст джерелаWhittaker, Steven Robert. "The molecular pharmacology of purine CDK inhibitors." Thesis, Institute of Cancer Research (University Of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404908.
Повний текст джерелаKasorn, Anongnard. "The molecular pharmacology of lysophosphatidic acid receptors." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441003.
Повний текст джерелаLee, Ka Cheong. "Molecular pharmacology of DNA topoisomerase II drugs." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3780.
Повний текст джерелаLin, Kuan-Hung. "Viral Proteases as Drug Targets and the Mechanisms of Drug Resistance: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/841.
Повний текст джерелаLin, Kuan-Hung. "Viral Proteases as Drug Targets and the Mechanisms of Drug Resistance: A Dissertation." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/841.
Повний текст джерелаKnight, Anthony. "A systems pharmacology approach to the adenosine A1 receptor." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/75201/.
Повний текст джерела