Academic literature on the topic 'Molecular Physiology and Pharmacology'
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Journal articles on the topic "Molecular Physiology and Pharmacology"
Kiehn, Johann, Antonio E. Lacerda, Barbara Wible, and Arthur M. Brown. "Molecular Physiology and Pharmacology of HERG." Circulation 94, no. 10 (November 15, 1996): 2572–79. http://dx.doi.org/10.1161/01.cir.94.10.2572.
Full textUEDA, Hiroshi, and Makoto INOUE. "Molecular pharmacology and physiology of nociceptin." Folia Pharmacologica Japonica 114, no. 6 (1999): 347–56. http://dx.doi.org/10.1254/fpj.114.347.
Full textBleakman, D. "Kainate receptor pharmacology and physiology." Cellular and Molecular Life Sciences (CMLS) 56, no. 7-8 (November 1, 1999): 558–66. http://dx.doi.org/10.1007/s000180050453.
Full textMasaki, Tomoh, Masashi Yanagisawa, and Katsutoshi Goto. "Physiology and pharmacology of endothelins." Medicinal Research Reviews 12, no. 4 (July 1992): 391–421. http://dx.doi.org/10.1002/med.2610120405.
Full textFisher, James W. "Erythropoietin: Physiology and Pharmacology Update." Experimental Biology and Medicine 228, no. 1 (January 2003): 1–14. http://dx.doi.org/10.1177/153537020322800101.
Full textNakanishi, Shigetada. "Molecular physiology of glutamate receptors." Japanese Journal of Pharmacology 67 (1995): 7. http://dx.doi.org/10.1016/s0021-5198(19)35554-4.
Full textBrooks, G. T. "Comprehensive insect physiology, biochemistry and pharmacology." Insect Biochemistry 15, no. 5 (January 1985): i—xiv. http://dx.doi.org/10.1016/0020-1790(85)90131-3.
Full textCiarimboli, Giuliano. "Physiology, Biochemistry, and Pharmacology of Transporters for Organic Cations." International Journal of Molecular Sciences 22, no. 2 (January 13, 2021): 732. http://dx.doi.org/10.3390/ijms22020732.
Full textAnderson, Warwick P. "Molecular biology in the service of physiology, pharmacology and endocrinology." Clinical and Experimental Pharmacology and Physiology 22, no. 12 (December 1995): 934. http://dx.doi.org/10.1111/j.1440-1681.1995.tb02329.x.
Full textde Almeida, Luiz G. N., Hayley Thode, Yekta Eslambolchi, Sameeksha Chopra, Daniel Young, Sean Gill, Laurent Devel, and Antoine Dufour. "Matrix Metalloproteinases: From Molecular Mechanisms to Physiology, Pathophysiology, and Pharmacology." Pharmacological Reviews 74, no. 3 (June 23, 2022): 712–68. http://dx.doi.org/10.1124/pharmrev.121.000349.
Full textDissertations / Theses on the topic "Molecular Physiology and Pharmacology"
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.
Full textElnakish, 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.
Full textBonilla, Ingrid Marie. "Acquired Electrophysiological Remodeling and Cardiac Arrhythmias." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396024058.
Full textSzabo, 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.
Full textPharmacological 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.
Full textHere, 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.
Full textSinha, Sayantani. "Role of TRPA1 and TRPV1 in Propofol Induced Vasodilation." Thesis, Kent State University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3618926.
Full textAims: 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.
Full textBarr, 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.
Full textPh.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/.
Full textBooks on the topic "Molecular Physiology and Pharmacology"
1953-, Webb David J., ed. Molecular biology and pharmacology of the endothelins. New York: Springer, 1995.
Find full textKenakin, Terrence P. Molecular pharmacology: A short course. Cambridge, Mass: Blackwell Science, 1997.
Find full textMorad, Martin, Setsuro Ebashi, Wolfgang Trautwein, and Yoshihisa Kurachi, eds. Molecular Physiology and Pharmacology of Cardiac Ion Channels and Transporters. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-3990-8.
Full textBurch, Ronald M. Molecular biology and pharmacology of bradykinin receptors. Austin: R.G. Landes, 1993.
Find full textGlossmann, H. Methods in Pharmacology: Molecular and Cellular Biology of Pharmacological Targets. Boston, MA: Springer US, 1993.
Find full textVitamin D: Physiology, molecular biology, and clinical applications. 2nd ed. [New York]: Humana Press, 2010.
Find full text1929-, Inoki Reizo, Kudō Teruo 1929-, and Olgart Leif 1938-, eds. Dynamic aspects of dental pulp: Molecular biology, pharmacology and pathophysiology. London: Chapman and Hall, 1990.
Find full textSternberg, Esther M., and Lewis L. Judd. Glucocorticoids and mood: Clinical manifestations, risk factors and molecular mechanisms. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2009.
Find full textP, Czech Michael, ed. Molecular basis of insulin action. New York: Plenum Press, 1985.
Find full textNestler, Eric J. Molecular Neuropharmacology. New York: McGraw-Hill, 2008.
Find full textBook chapters on the topic "Molecular Physiology and Pharmacology"
Benn, Caroline. "Physiology and Treatment of Hyperuricemia and Gout." In Encyclopedia of Molecular Pharmacology, 1234–43. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_10042.
Full textBenn, Caroline. "Physiology and Treatment of Hyperuricemia and Gout." In Encyclopedia of Molecular Pharmacology, 1–10. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_10042-1.
Full textCui, Meng, Lucas Cantwell, Andrew Zorn, and Diomedes E. Logothetis. "Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications." In Pharmacology of Potassium Channels, 277–356. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/164_2021_501.
Full textBorn, W., and J. A. Fischer. "Calcitonin Gene Products: Molecular Biology, Chemistry, and Actions." In Physiology and Pharmacology of Bone, 569–616. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77991-6_16.
Full textMartin, T. J. "Parathyroid Hormone-Related Protein: Molecular Biology, Chemistry, and Actions." In Physiology and Pharmacology of Bone, 617–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77991-6_17.
Full textFrench, Deborah. "The Molecular Pathology of Glanzmann’s Thrombasthenia." In Handbook of Platelet Physiology and Pharmacology, 394–423. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5049-5_18.
Full textJohnston, Graham A. R. "Molecular Biology, Pharmacology, and Physiology of GABAC Receptors." In The GABA Receptors, 297–323. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2597-1_11.
Full textLehmann-Horn, F., and R. Rüdel. "Molecular pathophysiology of voltage-gated ion channels." In Reviews of Physiology, Biochemistry and Pharmacology, 195–268. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/3-540-61343-9_9.
Full textBenos, Dale J., Sonia Cunningham, R. Randall Baker, K. Beth Beason, Youngsuk Oh, and Peter R. Smith. "Molecular characteristics of amiloride-sensitive sodium channels." In Reviews of Physiology, Biochemistry and Pharmacology, 31–113. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/bfb0036122.
Full textPette, Dirk, and Robert S. Staron. "Cellular and molecular diversities of mammalian skeletal muscle fibers." In Reviews of Physiology, Biochemistry and Pharmacology, 1–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/3540528806_3.
Full textConference papers on the topic "Molecular Physiology and Pharmacology"
Lu, Yi-Ru, and Yu-Hsin Chiu. "Physiology and pharmacology of ATP-releasing pannexin 1 channels." In THE 4TH INTERNATIONAL CONFERENCE ON LIFE SCIENCE AND TECHNOLOGY (ICoLiST). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0112732.
Full textJerde, Travis J., and Stephen Y. Nakada. "The Role of Pharmacology in Ureteral Physiology and Expulsive Therapy." In RENAL STONE DISEASE: 1st Annual International Urolithiasis Research Symposium. AIP, 2007. http://dx.doi.org/10.1063/1.2723585.
Full textOrdu, Y., J. Augustin, E. V. Hodenberg, V. Bode, and J. Harenberg. "COMPARATIVE CLINICAL PHARMACOLOGY OF LOW MOLECULAR WEIGHT HEPARINS IN MAN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643228.
Full textBielby-Clarke, Keren. "0161 Enhancing Anatomy, Physiology And Pharmacology Teaching In A New Undergraduate Pharmacy Curriculum Using Simulation Technology." In Association for Simulated Practice in Healthcare Annual Conference 11–13 November 2014 Abstracts. The Association for Simulated Practice in Healthcare, 2014. http://dx.doi.org/10.1136/bmjstel-2014-000002.184.
Full text"Anti-tumor Molecular Mechanism of Steroidal Drugs Based on Network Pharmacology." In 2018 3rd International Conference on Life Sciences, Medicine, and Health. Francis Academic Press, 2018. http://dx.doi.org/10.25236/iclsmh.18.020.
Full textOuyang, Xinyao. "Molecular mechanism of catalpol in the treatment of diabetes mellitus based on network pharmacology and molecular docking." In 3RD INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2020). AIP Publishing, 2021. http://dx.doi.org/10.1063/5.0048403.
Full textBarth, Connor W., Lei G. Wang, Antonio Montaño, Alexander L. Antaris, Jonathan M. Sorger, and Summer L. Gibbs. "Pharmacology of near infrared nerve-specific fluorophores for fluorescence-guided nerve sparing surgical procedures." In Molecular-Guided Surgery: Molecules, Devices, and Applications VII, edited by Summer L. Gibbs, Brian W. Pogue, and Sylvain Gioux. SPIE, 2021. http://dx.doi.org/10.1117/12.2583265.
Full textPiermarini, Peter M. "The molecular physiology of inward rectifier potassium (Kir) channels in mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93039.
Full textTekutskaya, E., I. Raybova, and Lyubov Ramazanovna Gusaruk. "THE DEGREE OF OXIDATIVE DAMAGE TO DNA IN VITRO AS A MOLECULAR PREDICTOR OF DISORDERS CAUSED BY EPIGENETIC AND EXOGENOUS FACTORS." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.49.
Full textKawachi, N., N. Suzui, S. Ishii, S. Ito, N. S. Ishioka, K. Kikuchi, T. Tsukamoto, T. Kusakawa, and F. Fujimaki. "Molecular imaging for plant physiology: Imaging of carbon translocation to sink organs." In 2009 IEEE Nuclear Science Symposium and Medical Imaging Conference (NSS/MIC 2009). IEEE, 2009. http://dx.doi.org/10.1109/nssmic.2009.5402366.
Full textReports on the topic "Molecular Physiology and Pharmacology"
Tabita, F. R. Summer Workshop: Molecular Basis, Physiology and Diversity of Microbial Adaptation. Office of Scientific and Technical Information (OSTI), May 2002. http://dx.doi.org/10.2172/836588.
Full textHeven Sze. Regulating Intracellular Calcium in Plants: From Molecular Genetics to Physiology. Office of Scientific and Technical Information (OSTI), June 2008. http://dx.doi.org/10.2172/932554.
Full textUnsworth, Nancy. The Physiology and Molecular Biology of Iron Nutrition for Cyanobacteria. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6413.
Full textZeikus, J. G. Molecular Physiology of Succinic Acid Based Fermentation In Anaerobes: Control of Chemical Yield by CO2 Fixation and Electron Donors. Office of Scientific and Technical Information (OSTI), May 2003. http://dx.doi.org/10.2172/1183577.
Full textHulata, Gideon, Thomas D. Kocher, Micha Ron, and Eyal Seroussi. Molecular Mechanisms of Sex Determination in Cultured Tilapias. United States Department of Agriculture, October 2010. http://dx.doi.org/10.32747/2010.7697106.bard.
Full textLaBonte, Don, Etan Pressman, Nurit Firon, and Arthur Villordon. Molecular and Anatomical Characterization of Sweetpotato Storage Root Formation. United States Department of Agriculture, December 2011. http://dx.doi.org/10.32747/2011.7592648.bard.
Full textBloch, Guy, Gene E. Robinson, and Mark Band. Functional genomics of reproduction and division of labor in a key non-Apis pollinator. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699867.bard.
Full textFait, Aaron, Grant Cramer, and Avichai Perl. Towards improved grape nutrition and defense: The regulation of stilbene metabolism under drought. United States Department of Agriculture, May 2014. http://dx.doi.org/10.32747/2014.7594398.bard.
Full textSavaldi-Goldstein, Sigal, and Siobhan M. Brady. Mechanisms underlying root system architecture adaptation to low phosphate environment. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600024.bard.
Full textLers, Amnon, Majid R. Foolad, and Haya Friedman. genetic basis for postharvest chilling tolerance in tomato fruit. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7600014.bard.
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