Relevant bibliographies by topics / Calcium channels – Animal models

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Calcium channels – Animal models'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Calcium channels – Animal models"

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Kamp, Marcel A., Maxine Dibué, Toni Schneider, Hans-Jakob Steiger, and Daniel Hänggi. "Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia." Stroke Research and Treatment 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/382146.

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Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion channel expression and function is initiated, with acute and long-term effects differing from each other. Initial hypoperfusion after exposure of cerebral vessels to oxyhemoglobin correlates with a suppression of voltage-gated potassium channel activity, whereas delayed cerebral vasospasm involves chan
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Kazama, Itsuro. "Roles of Lymphocyte Kv1.3-Channels in the Pathogenesis of Renal Diseases and Novel Therapeutic Implications of Targeting the Channels." Mediators of Inflammation 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/436572.

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Delayed rectifier K+-channels (Kv1.3) are predominantly expressed in T lymphocytes. Based on patch-clamp studies, the channels play crucial roles in facilitating the calcium influx necessary to trigger lymphocyte activation and proliferation. Using selective channel inhibitors in experimental animal models,in vivostudies then revealed the clinically relevant relationship between the channel expression and the pathogenesis of autoimmune diseases. In renal diseases, in which “chronic inflammation” or “the overstimulation of cellular immunity” is responsible for the pathogenesis, the overexpressi
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Uchitel, Osvaldo D., Carlota González Inchauspe, and Mariano N. Di Guilmi. "Calcium channels and synaptic transmission in familial hemiplegic migraine type 1 animal models." Biophysical Reviews 6, no. 1 (December 3, 2013): 15–26. http://dx.doi.org/10.1007/s12551-013-0126-y.

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Bakowski, Daniel, Fraser Murray, and Anant B. Parekh. "Store-Operated Ca2+ Channels: Mechanism, Function, Pharmacology, and Therapeutic Targets." Annual Review of Pharmacology and Toxicology 61, no. 1 (January 6, 2021): 629–54. http://dx.doi.org/10.1146/annurev-pharmtox-031620-105135.

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Calcium (Ca2+) release–activated Ca2+ (CRAC) channels are a major route for Ca2+ entry in eukaryotic cells. These channels are store operated, opening when the endoplasmic reticulum (ER) is depleted of Ca2+, and are composed of the ER Ca2+ sensor protein STIM and the pore-forming plasma membrane subunit Orai. Recent years have heralded major strides in our understanding of the structure, gating, and function of the channels. Loss-of-function and gain-of-function mutants combined with RNAi knockdown strategies have revealed important roles for the channel in numerous human diseases, making the
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Tano, Jean-Yves, and Maik Gollasch. "Hypoxia and ischemia-reperfusion: a BiK contribution?" American Journal of Physiology-Heart and Circulatory Physiology 307, no. 6 (September 15, 2014): H811—H817. http://dx.doi.org/10.1152/ajpheart.00319.2014.

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Over the last decades, cardiovascular disease has become the primary cause of death in the Western world, and this trend is expanding throughout the world. In particular, atherosclerosis and the subsequent vessel obliterations are the primary cause of ischemic disease (stroke and coronary heart disease). Excess calcium influx into the cells is one of the major pathophysiological mechanisms important for ischemic injury in the brain and heart in humans. The large-conductance calcium-activated K+ channels (BK) are thus interesting candidates to protect against excess calcium influx and the event
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Falcón, Débora, Isabel Galeano-Otero, Marta Martín-Bórnez, María Fernández-Velasco, Isabel Gallardo-Castillo, Juan A. Rosado, Antonio Ordóñez, and Tarik Smani. "TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease." Cells 9, no. 1 (January 10, 2020): 173. http://dx.doi.org/10.3390/cells9010173.

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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal mode
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Prestori, Francesca, Francesco Moccia, and Egidio D’Angelo. "Disrupted Calcium Signaling in Animal Models of Human Spinocerebellar Ataxia (SCA)." International Journal of Molecular Sciences 21, no. 1 (December 27, 2019): 216. http://dx.doi.org/10.3390/ijms21010216.

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Spinocerebellar ataxias (SCAs) constitute a heterogeneous group of more than 40 autosomal-dominant genetic and neurodegenerative diseases characterized by loss of balance and motor coordination due to dysfunction of the cerebellum and its efferent connections. Despite a well-described clinical and pathological phenotype, the molecular and cellular events that underlie neurodegeneration are still poorly undaerstood. Emerging research suggests that mutations in SCA genes cause disruptions in multiple cellular pathways but the characteristic SCA pathogenesis does not begin until calcium signaling
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Crotti, Lia, Katja E. Odening, and Michael C. Sanguinetti. "Heritable arrhythmias associated with abnormal function of cardiac potassium channels." Cardiovascular Research 116, no. 9 (May 19, 2020): 1542–56. http://dx.doi.org/10.1093/cvr/cvaa068.

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Abstract Cardiomyocytes express a surprisingly large number of potassium channel types. The primary physiological functions of the currents conducted by these channels are to maintain the resting membrane potential and mediate action potential repolarization under basal conditions and in response to changes in the concentrations of intracellular sodium, calcium, and ATP/ADP. Here, we review the diversity and functional roles of cardiac potassium channels under normal conditions and how heritable mutations in the genes encoding these channels can lead to distinct arrhythmias. We briefly review
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Schoepf, Clemens L., Maximilian Zeidler, Lisa Spiecker, Georg Kern, Judith Lechner, Kai K. Kummer, and Michaela Kress. "Selected Ionotropic Receptors and Voltage-Gated Ion Channels: More Functional Competence for Human Induced Pluripotent Stem Cell (iPSC)-Derived Nociceptors." Brain Sciences 10, no. 6 (June 3, 2020): 344. http://dx.doi.org/10.3390/brainsci10060344.

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Preclinical research using different rodent model systems has largely contributed to the scientific progress in the pain field, however, it suffers from interspecies differences, limited access to human models, and ethical concerns. Human induced pluripotent stem cells (iPSCs) offer major advantages over animal models, i.e., they retain the genome of the donor (patient), and thus allow donor-specific and cell-type specific research. Consequently, human iPSC-derived nociceptors (iDNs) offer intriguingly new possibilities for patient-specific, animal-free research. In the present study, we chara
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Othman and Hamurtekin. "A New Pain Killer from the Nature: N-Type Calcium Channels Blockers." Proceedings 40, no. 1 (February 8, 2020): 47. http://dx.doi.org/10.3390/proceedings2019040047.

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N-type calcium channels (Neuronal-type Calcium channel, Cav2.2) is a member of high voltage activated calcium channels. There are two native small peptides for N-type calcium channels (NTCC) directly which are derived from cone snail, ω-conotoxin-GVIA isolated from Conus geographus and ω-conotoxin-MVIIA (SNX-111, Ziconotide, PrialtTM), from Conus magus which both directly block the α1-ion conducting pore. NTCCs, have been shown to play a key role in nociceptive transmission due to their strategic location, presynaptically in afferent C & Aᵹ fiber terminals and postsynaptically in descendin
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Dissertations / Theses on the topic "Calcium channels – Animal models"

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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain d
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Diffley, Leonie. "Calcium regulation and ion channel remodelling in an animal model of heart failure." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493676.

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CHF is a complex disease that results in the remodelling of the heart at every level, from the gross anatomy down to the levels of the ion channel resulting in aberrant signalling and contractile dysfunction. The QT interval of the cardiac ECG is frequently increased in heart failure, suggesting ion channel remodelling which has proarrhythmic consequences. One of the aims of this study was to determine the changes that occur from the in vivo level, down to the level of the ion channel that may contribute to arrhythmogenesis.
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DeRemigio, Hilary. "Markov chain models of instantaneously coupled intracellular calcium channels." W&M ScholarWorks, 2008. https://scholarworks.wm.edu/etd/1539623334.

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Localized calcium elevations known as calcium puffs or sparks are cellular signals arising from cooperative activity of clusters of inositol 1,4,5-trisphosphate receptors (IP3Rs) or ryanodine receptors (RyRs) located at calcium release sites on the endoplasmic or sarcoplasmic reticulum membrane. When Markov chain models of these intracellular calcium-regulated calcium channels are coupled via a mathematical representation of the calcium microdomain, simulated calcium release sites may exhibit the phenomenon of "stochastic calcium excitability" where the IP3Rs or RyRs open and close in a concer
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Calcraft, Peter James. "Two-pore channels and NAADP-dependent calcium signalling." Thesis, St Andrews, 2010. http://hdl.handle.net/10023/888.

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Muller, Yunhua Li 1963. "Developmentally regulated expression of the calcium-dependent potassium channel and calcium channels during maturation of the rat cerebellum." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282231.

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Potassium channels govern the duration and frequency of excitable membrane events, and thus may regulate voltage-dependent signals that are important in neuronal development. This study assesses the developmental expression of two classes of K⁺ channels in vivo and in vitro in the rat cerebellum. In vivo, the level of mslo-related transcript for the Ca²⁺-dependent K⁺ channel (KCa) was shown by Northern analysis to be upregulated during development, whereas transcripts for delayed rectifier (KD) channels remained fairly constant. The same pattern of in vivo development was demonstrated with fun
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Matias, Madeleine Gundayao. "Animal calcium release-activated calcium (CRAC) channels are homologous and derived from the ubiquitous Cation Diffusion Facilitators." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453033.

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Thesis (M.S.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed June 25, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 48-51).
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Giannattasio, Bartolomeo. "Characterization of ATP receptors and voltage-dependent calcium ion channels in cardiovascular cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=case1060781044.

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Giblin, Kathryn Anne. "Is epilepsy a preventable disorder? New evidence from animal models." Yale University, 2010. http://ymtdl.med.yale.edu/theses/available/etd-03052010-144943/.

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Epilepsy accounts for 0.5% of the global burden of disease, and primary prevention of epilepsy represents one of the three 2007 NINDS Epilepsy Research Benchmarks. Efforts to understand and intervene in the process of epileptogenesis have yielded fruitful preventative strategies in animal models. This article reviews the current understanding of epileptogenesis, introduces the concept of a "critical period" for epileptogenesis, and examines strategies for epilepsy prevention in animal models of both acquired and genetic epilepsies. As proof of principle, we investigated whether early preventat
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Rakers, Cordula Marijke [Verfasser]. "The role of glial calcium changes in animal models of stroke / Cordula Marijke Rakers." Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/1121105599/34.

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Kaurstad, Guri. "Cardiomyocyte function and calcium handling in animal models of inborn and aquired maximal oxygen uptake." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for sirkulasjon og bildediagnostikk, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-16549.

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Hjertemuskelcellefunksjon og kalsiumhåndtering i dyremodeller med medfødt og ervervet maksimalt oksygenopptak Hjerte-karsykdommer er i dag årsaken til flest dødsfall i Europa. Selv om det er kjent at et høyt maksimalt oksygenopptak kan virke beskyttende mot hjerte-karsykdom både hos friske og de med økt risiko, vil studier av de underliggende mekanismene bidra med verdifull informasjon til utvikling av fremtidige retningslinjer for behandling og forebygging av hjertekarsykdom. Maksimalt oksygenopptak er hos de fleste av oss avhengig av hjertets slagvolum som igjen bestemmes av hjertemuskelcel
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Books on the topic "Calcium channels – Animal models"

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Rodger, Claire. The anticonvulsant profiles of two calcium channel antagonists in animal models of epilepsy. Manchester: University of Manchester, 1993.

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The effect of calcium antagonists on the normoxic and the ischaemic myocardium: Studies in rat and guinea-pig cardiac preparations. Amsterdam: [s.n.], 1989.

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S, Sideman, Beyar Rafael, Landesberg Amir, and New York Academy of Sciences, eds. Interactive and integrative cardiology. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Felling, Ryan J. Targets for Neuroprotection in Ischemic Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0111.

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Cerebral ischemia or hypoxia-ischemia initiate a cascade of biochemical events including impaired reuptake of glutamate into perisynaptic glia causing glutamate flooding, calcium fluxing through NMDA glutamate channels, activation of neuronal nitric oxide synthetase, and impaired mitochondrial ATP production. In animal models it is possible to block these steps and protect the brain but the temporal window of protection after the insult lasts only a few hours. Recombinant TPA is clinically protective if given within 3 hours of stroke, but other agents have not been shown to protect brain tissu
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Asher, Ornoy, ed. Animal models of human related calcium metabolic disorders. Boca Raton, Fla: CRC Press, 1995.

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(Editor), Stephan Frings, and Jonathan Bradley (Editor), eds. Transduction Channels in Sensory Cells. Wiley-VCH, 2004.

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Bradley, Jonathan, and Stephan Frings. Transduction Channels in Sensory Cells. Wiley & Sons, Incorporated, John, 2006.

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Bradley, Jonathan, and Stephan Frings. Transduction Channels in Sensory Cells. Wiley-VCH Verlag GmbH, 2005.

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Stephan, Frings, and Bradley Jonathan 1961-, eds. Transduction channels in sensory cells. Weinheim: Wiley-VCH, 2004.

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(Editor), H. Leon Bradlow, Jack Fishman (Editor), and Michael P. Osborne (Editor), eds. Cancer Prevention: Novel Nutrient and Pharmaceutical Developments (Annals of the New York Academy of Sciences, V. 889). New York Academy of Sciences, 1999.

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Book chapters on the topic "Calcium channels – Animal models"

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Oh-Hora, Masatsugu, and Xiuyuan Lu. "Function of Orai/Stim Proteins Studied in Transgenic Animal Models." In Calcium Entry Channels in Non-Excitable Cells, 107–26. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-6.

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Scheuer, Todd. "Bacterial Sodium Channels: Models for Eukaryotic Sodium and Calcium Channels." In Voltage Gated Sodium Channels, 269–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_13.

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Kostyuk, Platon, and Sergei Mironov. "Theoretical Models for Calcium Channels in Nerve Cells." In Water and Ions in Biological Systems, 17–26. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4899-0424-9_4.

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Smith-Swintosky, V. L., and M. P. Mattson. "Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration." In Cell and Animal Models in Aging and Dementia Research, 29–45. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9350-1_3.

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FOX, LYLE, ATSUSHI UEDA, BRETT BERKE, I.-FENG PENG, and CHUN-FANG WU. "Movement Disorders in Drosophila Mutants of Potassium Channels and Biogenic Amine Pathways." In Animal Models of Movement Disorders, 487–504. Elsevier, 2005. http://dx.doi.org/10.1016/b978-012088382-0/50045-1.

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Khan, Saeed R. "Animal Models of Calcium Oxalate Kidney Stone Formation." In Animal Models for the Study of Human Disease, 483–98. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-415894-8.00021-x.

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Groff, Jeffrey R., Hilary DeRemigio, and Gregory D. Smith. "Markov Chain Models of Ion Channels and Calcium Release Sites." In Stochastic Methods in Neuroscience, 29–64. Oxford University Press, 2009. http://dx.doi.org/10.1093/acprof:oso/9780199235070.003.0002.

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Cohen, Bertram I., and Erwin H. Mosbach. "Effects of Bile Acids and Sterols in Animal Models of Colorectal Cancer." In Calcium, Vitamin D, and Prevention of Colon Cancer, 209–27. CRC Press, 2018. http://dx.doi.org/10.1201/9781351070386-12.

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Baimbridge, K. G., I. Mody, J. A. Shacklock, and J. J. Miller. "CALBINDIN D28k AND ANIMAL MODELS OF EPILEPSY11Supported by a Canadian MRC Program Grant to K.G.B, and J.J.M." In Calcium-Binding Proteins in Health and Disease, 615–17. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-12-521040-9.50115-7.

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Fajmut, Aleš. "Molecular Mechanisms and Targets of Cyclic Guanosine Monophosphate (cGMP) in Vascular Smooth Muscles." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97708.

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Molecular mechanisms and targets of cyclic guanosine monophosphate (cGMP) accounting for vascular smooth muscles (VSM) contractility are reviewed. Mathematical models of five published mechanisms are presented, and four novel mechanisms are proposed. cGMP, which is primarily produced by the nitric oxide (NO) dependent soluble guanylate cyclase (sGC), activates cGMP-dependent protein kinase (PKG). The NO/cGMP/PKG signaling pathway targets are the mechanisms that regulate cytosolic calcium ([Ca2+]i) signaling and those implicated in the Ca2+-desensitization of the contractile apparatus. In addition to previous mathematical models of cGMP-mediated molecular mechanisms targeting [Ca2+]i regulation, such as large-conductance Ca2+-activated K+ channels (BKCa), Ca2+-dependent Cl− channels (ClCa), Na+/Ca2+ exchanger (NCX), Na+/K+/Cl− cotransport (NKCC), and Na+/K+-ATPase (NKA), other four novel mechanisms are proposed here based on the existing but perhaps overlooked experimental results. These are the effects of cGMP on the sarco−/endo- plasmic reticulum Ca2+-ATPase (SERCA), the plasma membrane Ca2+-ATPase (PMCA), the inositol 1,4,5-trisphosphate (IP3) receptor channels type 1 (IP3R1), and on the myosin light chain phosphatase (MLCP), which is implicated in the Ca2+-desensitization. Different modeling approaches are presented and discussed, and novel model descriptions are proposed.
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Conference papers on the topic "Calcium channels – Animal models"

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DEREMIGIO, HILARY, PETER KEMPER, M. DREW LAMAR, and GREGORY D. SMITH. "MARKOV CHAIN MODELS OF COUPLED INTRACELLULAR CALCIUM CHANNELS: KRONECKER STRUCTURED REPRESENTATIONS AND BENCHMARK STATIONARY DISTRIBUTION CALCULATIONS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0035.

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Zhou, Yilu, Lauren Resutek, Liyun Wang, and X. Lucas Lu. "Effects of Bisphosphonate on Long-Term Culture of Cartilage Allografts." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14635.

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Zoledronic acid (ZA), an FDA approved bisphosphonate (BP) medicine, is widely used for the treatment of osteoclast-related bone loss diseases [1]. Our previous study has found that systemic administration of ZA could dramatically suppress the development of post-traumatic osteoarthritis (PTOA) in the DMM (destabilization of the medial meniscus) mouse model, a model recapitulating the altered joint loading associated with PTOA [2]. This finding is consistent with a few similar studies using different animal models [3]. However, little is known about the cellular and biochemical mechanisms of BP
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Marshall, Lauren, Andra Frost, Tim Fee, and Joel Berry. "Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.

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Drug development platforms such as two-dimensional (2D) in vitro cell culture systems and in vivo animal studies do not accurately predict human in vivo effectiveness of candidate therapeutics [1]. Cell culture systems have limited similarities to primary human cells and tissues as only one cell type is employed and animal studies have a generally limited ability to recapitulate human drug response as different species have differences in metabolism, physiology, and behavior. Mike Leavitt, a former U.S. Secretary of Health and Human Services, has stated that “currently, nine out of ten experim
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Emerson, David R., and Robert W. Barber. "Designing Efficient Microvascular Networks Using Conventional Microfabrication Techniques." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18312.

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The ability to fabricate networks of micro-channels that obey the biological properties of bifurcating structures found in nature suggests that it is possible to construct artificial vasculatures or bronchial structures. These devices could aid in the desirable objective of eliminating many forms of animal testing. In addition, the ability to precisely control hydraulic conductance could allow designers to create specific concentration gradients that would allow biologists to correlate the behavior of cells. In 1926, Murray found that there was an optimum branching ratio between the diameters
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