Gotowe bibliografie tematyczne / Influx de calcium

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Influx de calcium”

Autor: Grafiati
Data publikacji: 2 listopada 2024
Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Influx de calcium"

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King, Leslie B., and Bruce D. Freedman. "B-lymphocyte calcium inFlux." Immunological Reviews 231, no. 1 (2009): 265–77. http://dx.doi.org/10.1111/j.1600-065x.2009.00822.x.

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Neher, Erwin. "Controls on calcium influx." Nature 355, no. 6358 (1992): 298–99. http://dx.doi.org/10.1038/355298a0.

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McCarthy, Nicola. "Calcium influx is moving." Nature Reviews Cancer 9, no. 4 (2009): 230–31. http://dx.doi.org/10.1038/nrc2629.

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GIBBONS, SIMON J., JAMES R. BRORSON, DAVID BLEAKMAN, PAUL S. CHARD, and RICHARD J. MILLER. "Calcium Influx and Neurodegeneration." Annals of the New York Academy of Sciences 679, no. 1 Markers of Ne (1993): 22–33. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18286.x.

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Vostal, J. G., and J. C. Fratantoni. "Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition." Biochemical Journal 295, no. 2 (1993): 525–29. http://dx.doi.org/10.1042/bj2950525.

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Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calci
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Ramagopal, M. V., and S. J. Mustafa. "Effect of adenosine and its analogues on calcium influx in coronary artery." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (1988): H1492—H1498. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1492.

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In the present study, we have investigated the changes in calcium influx during the relaxing responses to adenosine and its analogues. Calcium-45 influx was measured in bovine coronary artery rings in the presence of prostaglandin F2 alpha (10(-5) M) and KCl (50 and 100 mM). Prostaglandin F2 alpha and KCl caused increases in calcium influx. Prostaglandin F2 alpha produced a further contraction when added to rings maximally contracted with KCl (100 mM or higher), suggesting two different mechanisms for prostaglandin F2 alpha- and KCl-induced contractions. Similarly, a greater calcium influx was
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Davis, Michael J., and Neeraj R. Sharma. "Calcium-Release-Activated Calcium Influx in Endothelium." Journal of Vascular Research 34, no. 3 (1997): 186–95. http://dx.doi.org/10.1159/000159222.

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Capiod, Thierry. "Cell proliferation, calcium influx and calcium channels." Biochimie 93, no. 12 (2011): 2075–79. http://dx.doi.org/10.1016/j.biochi.2011.07.015.

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Chen, Huanmian, and Nevin A. Lambert. "Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus." Journal of Neurophysiology 78, no. 6 (1997): 3484–88. http://dx.doi.org/10.1152/jn.1997.78.6.3484.

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Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in den
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Wang, Z., M. Estacion, and L. J. Mordan. "Ca2+ influx via T-type channels modulates PDGF-induced replication of mouse fibroblasts." American Journal of Physiology-Cell Physiology 265, no. 5 (1993): C1239—C1246. http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1239.

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The role of low-threshold voltage-gated calcium channels (VGCC) in modulating extracellular calcium influx and proliferation was investigated in platelet-derived growth factor (PDGF)-stimulated C3H/10T1/2 mouse fibroblasts. Previous studies demonstrated that cell cycle progression after PDGF stimulation was dependent on extracellular calcium influx producing a sustained increase in the intracellular calcium concentration. In this study, PDGF-induced calcium influx, the sustained intracellular calcium increase, and progression to S phase were inhibited by nordihydroguariaretic acid (NDGA), an i
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Rozprawy doktorskie na temat "Influx de calcium"

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Wang, Fang. "DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?" Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214814.

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Physiology<br>Ph.D.<br>Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004; Levy, et al., 2002). Heart failure, by definition, is progressive deteriorating function of the heart due to progressive cardiac myocytes loss. Though after decades of endeavor of searching the pathophysiology and treatments for heart failure, it remains highly lethal. Therefore, it is vital to find novel therapies to help treat such chronic disease. Replace the lost cardiomyocyte with new ones could restore
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Yang, Meng. "Calcium influx, celluar signaling and the biology of candida albicans." Thesis, University of Aberdeen, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499748.

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<i>FIG1 </i>is a gene that encodes a transmembrane protein involved in calcium influx a process that is important for stress responses in pathogens fungi such as <i>Candida albicans.</i> A <i>Cafig1 </i>null mutant took up less calcium ions in mating than control strains confirming its role in Ca<sup>2+</sup> uptake.  Furthermore, <i>C. albicans </i>strains with deletions of <i>FIG1 </i>in other calcium channel mutant backgrounds displayed distinctive phenotypes under vegetative growth conditions, which suggested that Fig1 may be a regulator of other calcium influx systems. Using GFP and <i>La
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Pejović, Vojislav. "Glutamate induced potentiation of calcium influx in primary hippocampal culture neurons." [S.l.] : [s.n.], 2001. http://ArchiMeD.uni-mainz.de/pub/2001/0027/diss.pdf.

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McVicker, Clare Geldard. "Calcium influx mechanisms during mediator-induced responses in human airway smooth muscle." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404814.

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Makarewich, Catherine Anne. "MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/266828.

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Molecular and Cellular Physiology<br>Ph.D.<br>Pathological cardiac stressors, including persistent hypertension or damage from ischemic heart disease, induce a chronic demand for enhanced contractile performance of the heart. The cytosolic calcium (Ca2+) transient that regulates myocyte contraction must be persistently increased in disease states in order to maintain cardiac output to sustain the metabolic requirements of the body. Associated with this enhanced intracellular Ca2+ ([Ca2+]i) state is pathological cardiac myocyte hypertrophy, which results in large part from the activation of Ca2
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Kortekaas, Phaedra. "Development and function of calcium influx in pyramidal neurons of the hippocampal CA1 region." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/55584.

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DeJong, Danica. "Calcium Alleviates Symptoms in Hyperkalemic Periodic Paralysis by Reducing the Abnormal Sodium Influx." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23487.

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Hyperkalemic periodic paralysis, HyperKPP, is an inherited progressive disorder of the muscles caused by mutations in the voltage gated sodium channel (NaV1.4). The objectives of this thesis were to develop a technique for measurement symptoms in vivo using electromyography (EMG) and to determine the mechanism by which Ca2+ alleviates HyperKPP symptoms, since this is unknown. Increasing extracellular [Ca2+] ([Ca2+]e) from 1.3 to 4 mM did not result in any increases in45Ca2+ influx suggesting no increase in intracellular [Ca2+] ([Ca2+]i) acting on an intracellular signaling pathway or on an ion
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Hoffman, Nicholas. "Mitochondrial Calcium Influx is Determined by Multiple Protein Components Including SLC25A23 and MICU1." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/287159.

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Biochemistry<br>Ph.D.<br>Ca2+ control mechanisms employed by the cell at the plasma membrane include receptor operated, voltage-sensitive, and store operated channels for Ca2+ import. Upon entry into the cytosol, Ca2+ is sequestered by Ca2+ binding proteins, the endoplasmic reticulum (ER), or by mitochondria. The largest Ca2+ store in the cell is the ER where Ca2+ levels approach millimolar levels. The ER regulates cytosolic Ca2+ homeostasis by using Ca2+ binding proteins, the SERCA pump, second messenger Ca2+ release upon IP3 receptor activation, and Ca2+-induced Ca2+ release by ryanodine rec
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Torihashi, Shigeko, Toyoshi Fujimoto, Claudia Trost, Shinsuke Nakayama, and 茂子 鳥橋. "Calcium oscillation linked to pacemaking of interstitial cells of Cajal;Requirement of calcium influx and localisation of TRP4 in caveolae." The American Society for Biochemistry and Molecular Biology, 2002. http://hdl.handle.net/2237/7447.

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Obolensky, Anna. "Pharmacological modulation of calcium influx in freshly isolated rat lymphocytes and lymphoma cell lines." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249555.

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Książki na temat "Influx de calcium"

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Perrella, Joel. Effect of estrogen on glutamate-induced neuronal cell death and calcium influx. 2005.

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Heine, Christopher L. Malignant Hyperthermia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0025.

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In this chapter we discuss the pathophysiology of malignant hyperthermia, identify those who are known to be susceptible to MH, delineate how best to prepare the operating for those patients, and provide step by step treatment recommendations for patients that develop MH. Malignant hyperthermia (MH) is a pharmacogenetic disease. When susceptible individuals are exposed to a triggering agent, a hypermetabolic response develops. Succinylcholine and halogenated, inhaled anesthetics are triggers of MH. The MH reaction is initiated by a rapid influx of calcium ions into the myoplasm that triggers u
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Fomberstein, Kenneth, Marissa Rubin, Dipan Patel, John-Paul Sara, and Abhishek Gupta. Perioperative Opioid Analgesics of Use in Pain Management for Spine Surgery. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0004.

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This chapter compares the basic properties of several opioid analgesics and explores their applications in perioperative pain control in spine surgery. Parenteral opioids have long been the cornerstone of treatment for postoperative pain; they work by inhibiting voltage-gated calcium channels and increasing potassium influx, which results in reduced neuronal excitability, thereby inhibiting the ascending transmission of painful stimuli and activating the descending inhibitory pathways. This chapter reviews concepts including opioid conversion and rotation, opioid tolerance, and opioid cross-to
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Slimp, Jefferson C. Neurophysiology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0003.

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Any discussion of the pathomechanisms and treatments of MS benefits from an understanding of the physiology of the neuronal membrane and the action potential. Neurons and glia, are important for signal propagation, synaptic function, and neural development. The neuronal cell membrane, maintains different ionic environments inside and outside the cell, separating charge across the membrane and facilitating electrical excitability. Ion channels allow flow of sodium, potassium, and calcium ions across the membrane at selected times. At rest, potassium ion efflux across the membrane establishes th
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Części książek na temat "Influx de calcium"

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Belrose, Jillian C., Fabiana A. Caetano, Kai Yang, Brian M. W. Lockhart, Michael F. Jackson, and John F. MacDonald. "Mechanisms of Calcium Influx Following Stroke." In Metal Ion in Stroke. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9663-3_2.

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Petersen, O. H. "Control of Calcium Influx and Internal Calcium Release in Electrically Non-Excitable Cells." In Calcium Transport and Intracellular Calcium Homeostasis. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83977-1_2.

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Ghazal, Nasab, and Jennifer Q. Kwong. "Analyzing Mitochondrial Calcium Influx in Isolated Mitochondria." In Methods in Molecular Biology. Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-4164-4_12.

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Taschenberger, Holger, Kun-Han Lin, and Shuwen Chang. "Presynaptic Ca2+ Influx and Its Modulation at Auditory Calyceal Terminals." In Modulation of Presynaptic Calcium Channels. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6334-0_9.

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Colucci, Wilson S., and Giovanni Sperti. "Phorbol Esters Stimulate Calcium Influx via Voltage-Dependent Channels in A7r5 Vascular Smooth-Muscle Cells." In Cell Calcium Metabolism. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_9.

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Borowiec, Anne-Sophie, Gabriel Bidaux, and Thierry Capiod. "Are Calcium Channels More Important Than Calcium Influx for Cell Proliferation?" In Trends in Stem Cell Proliferation and Cancer Research. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_4.

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Yagodin, Sergey, Lynne A. Holtzclaw, and James T. Russell. "Subcellular calcium oscillators and calcium influx support agonist-induced calcium waves in cultured astrocytes." In Signal Transduction Mechanisms. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2015-3_15.

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Hanson, John B., Magaly Rincon, and Sharon A. Rogers. "Controls on Calcium Influx in Corn Root Cells." In Molecular and Cellular Aspects of Calcium in Plant Development. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2177-4_31.

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MacKenzie, E. T., and J. McCulloch. "Glutamate Antagonism as a Pharmacological Approach to Prevent Calcium Influx in Focal Cerebral Ischemia." In Cerebral Ischemia and Calcium. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-85863-5_22.

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Bers, Donald M. "Calcium influx and sarcoplasmic reticulum calcium release in cardiac excitation-contraction coupling." In Developments in Cardiovascular Medicine. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3311-8_5.

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Streszczenia konferencji na temat "Influx de calcium"

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Kulakova, M. V., M. D. Pakhomova, V. A. Bidiuk, and M. O. Agaphonov. "HYPERSENSITIVITY TO SODIUM DODECYL SULFATE IN OGATAEA YEASTS WITH INACTIVATED VACUOLAR CALCIUM ATPASE IS EXERTED BY CALCIUM INFLUX INTO THE CYTOSOL FROM ENVIRONMENT." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-251.

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Here we show that SDS provokes Cch1-independent Ca2+ influx into cytosol from the environment. The SDS hypersensitivity in mutants with inactivated Pmc1 results from inability to cope with the cytosolic calcium concentration increase, while Cch1 inactivation partially rescues this trait. This implies the presence of an additional Cch1 Ca2+ function beyond cellular Ca2+ transport.
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Jetta, Deekshitha, Deepika Verma, Mohammad M. Maneshi, and Susan Z. Hua. "Shear Stress Induced Calcium Dependent Nuclear Deformation in Epithelial Cells." In ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-87650.

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External mechanical forces can reach the cell nucleus causing changes in nuclear morphology, size and motility. A common explanation is that these forces are transmitted by surrounding cytoskeleton network through its linkage to nuclear envelope; shear stress causes reorganization of cytoskeleton, thus, the changes in nuclear shape. In this study, we measured nuclear shape and intracellular Ca2+ under fluid shear stress in MDCK cells using a parallel plate microfluidic chip. We show that fluid shear stress (1.1 dyn/cm2, 3 hrs) causes significant changes in nuclear shape in cells, from a flat d
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Lange, Ingo, and Dana-Lynn T. Koomoa. "Abstract 3781: MYCN-induced TRPM7 mediates calcium influx and promotes neuroblastoma cell migration." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3781.

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Mecklenburg, Anne, Anton Albrecht, Franziska Gniech, Cynthia Olotu, Sven Hammerschmidt, and Rainer Kiefmann. "In Pulmonary Endothelial Cells Calcium Signaling By S. Pneumoniae Is Regulated By Calcium Influx From The Extracellular Space But Also By Calcium Release From Intracellular Stores." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3281.

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Sadras, Francisco, Teneale A. Stewart, Melanie Robitaille, et al. "Abstract P6-06-15: Remodelling of calcium influx pathways in breast cancer associated fibroblasts." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p6-06-15.

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Xu, Ningyong, Donna L. Cioffi, Xiaogang Wang, Eugene A. Cioffi, Mikhail Alexeyev, and Troy Steves. "Orai1 Is A Critical Determinant Of Sodium Influx Through Store Operated Calcium Entry Channels." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5510.

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Fuzimoto, T., K. Fuzimura, and A. Kuramoto. "MEASUREMENT OF PLATELET IONIZED CALCIUM IN PATIENTS WITH MYELOPROLIFERATIVE DISORDERS BY AEQUORIN METHOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644573.

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In myeloproliferative disorders(MPD), bleeding tendency and thrombosis are encountered occasionally in the presence of high platelet counts. It has been reported that there are some abnormalities of membrane glycoprotein or arachidonate metabolism in platelets of MPD. We measured the intracellular change of calcium levels[Cai2+] after stimulation in platelets of the patients with MPD by Aequorin method. Eleven cases of chronic myelogenous leukemia(CML), 7 cases of polycythemia vera(PV), 4 cases of essential thrombocythemiaCET^ and 12 normal adults were studied, and as stimulators 0.5 U/ml thro
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Erickson, Geoffrey R., and Farshid Guilak. "Osmotic Stress Initiates Intracellular Calcium Waves in Chondrocytes Through Extracellular Influx and the Inositol Phosphate Pathway." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0580.

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Abstract The biophysical environment of the chondrocytes plays an important role in the health, turnover, and homeostasis of articular cartilage. Under normal physiologic loading, chondrocytes are exposed to a complex and diverse array of biophysical signals, including mechanical and osmotic stresses, fluid flow, and fluid pressures [4]. Due to the charged and hydrated nature of the extracellular matrix, mechanical compression causes exudation of interstitial fluid in cartilage, which alters the osmotic environment of the chondrocytes. Confocal microscopy studies have shown that chondrocytes l
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Monteith, Greg, Francisco Sadras, Teneale Stewart, et al. "Abstract 99: Remodeling of calcium influx pathways in models of cancer associated fibroblasts in breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-99.

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Monteith, Greg, Francisco Sadras, Teneale Stewart, et al. "Abstract 99: Remodeling of calcium influx pathways in models of cancer associated fibroblasts in breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-99.

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Raporty organizacyjne na temat "Influx de calcium"

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Yalovsky, Shaul, and Julian Schroeder. The function of protein farnesylation in early events of ABA signal transduction in stomatal guard cells of Arabidopsis. United States Department of Agriculture, 2002. http://dx.doi.org/10.32747/2002.7695873.bard.

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Loss of function mutations in the farnesyltransferase β subunit gene ERA1 (enhanced response to abscisic acid), cause abscisic acid hypersensitivity in seedlings and in guard cells. This results in slowed water loss of plants in response to drought. Farnesyltransferase (PFT) catalyses the attachment of the 15-carbon isoprenoid farnesyl to conserved cysteine residues located in a conserved C-terminal domain designated CaaX box. PFT is a heterodimeric protein comprised of an a and b sununits. The a subunit is shared between PFT and geranylgeranyltransferase-I (PGGTI) which catalyses the attachem
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