Dissertations / Theses on the topic '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.
Full textPh.D.
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 cardiac function and reduce mortality. The purpose of this study is to investigate on how TTCCs (T-type calcium channels) affect cardiomyocyte proliferation. In mice after birth, the major TTCC expressed in the heart is Cav3.1/α1G, and therefore we used Cav3.1/α1G transgenic (TG), knockout (-/-) and wild type mice respectively to define the role of TTCC in cardiomyocyte proliferation. In neonatal mouse ventricular myocyte (NMVMs) right after birth, there is almost no TTCC after birth in α1G-/- NMVMs, whereas there are around 35% NMVMs in wild type (WT) show TTCC. On day 7 after birth, there are no T-type calcium currents in both α1G-/- NMVMs and WT NMVMs. Using BrdU, a DNA synthesis marker, we identified plenty of BrdU positive cardiomyocyte during the first seven days after birth. Cardiomyocyte is special due to its double nucleation property. Our cell cycle studies showed that there is significant difference in cell cycle distribution between α1G-/- and WT NMVMs on day seven after birth. Significantly more NMVMs are arrested in G1 phase in α1G-/-, compared to WT NMVMs. Even until 2 month old, there are still significantly more mono-nucleated cardiomyocyte in α1G-/- than in WT. In conclusion, all these evidence showed that blocking T-type calcium channel could partially prevent binucleation from happening and stop cardiomyocytes withdrawal from cell cycle. Mononucleated cardiomyocyte is still able to proliferate. Hence, mononucleated cardiomyocytes in adult still have potential to proliferation because these cardiomyoctes are arrested in their cell-cycle before their terminal differentiation, which could offer a novel approach for cardiac repair.
Temple University--Theses
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.
Full textPejović, 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.
Full textMcVicker, 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.
Full textMakarewich, 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.
Full textPh.D.
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+-dependent activation of calcineurin (Cn)-nuclear factor of activated T cells (NFAT) signaling. The puzzling feature of this hypertrophic signaling is that the cytosolic [Ca2+] that controls contractility appears to be separate from the [Ca2+] which activates Cn-NFAT signaling. The overarching theme of this dissertation is to explore the source and spatial constraints of pathological hypertrophic signaling Ca2+ and to investigate how it is possible that sensitive and finely tuned Ca2+-dependent signaling pathways are regulated in the background of massive Ca2+ fluctuations that oscillate between 100nM and upwards of 1-2μM during each cardiac contractile cycle. L-type Ca2+ channels (LTCCs) are a major source of Ca2+ entry in cardiac myocytes and are known to play an integral role in the initiation of myocyte excitation contraction-coupling (EC-coupling). We performed a number of experiments to show that a small population of LTCCs reside outside of EC-coupling domains within caveolin (Cav-3) signaling microdomains where they provide a local source of Ca2+ to activate Cn-NFAT signaling. We designed a Cav-targeted LTCC blocker that could eliminate Cn-NFAT activation but did not reduce myocyte contractility. The activity of Cav-targeted LTCCs could also be upregulated to enhance hypertrophic signaling without affecting contractility. Therefore, we believe that caveolae-localized LTCCs do not participate in EC-coupling, but instead act locally to control the coordinated activation of Cn-NFAT signaling that drives pathological remodeling. Transient Receptor Potential (TRP) channels are also thought to provide a source of Ca2+ for activation of hypertrophic signaling. The canonical family of TRP channels (TRPC) is expressed at low levels in normal adult cardiac tissue, but these channels are upregulated in disease conditions which implicates them as stress response molecules that could potentially provide a platform for hypertrophic Ca2+ signaling. We show evidence that TRPC channel abundance and function increases in cardiac stress conditions, such as myocardial infarction (MI), and that these channels are associated with hypertrophic responses, likely through a Ca2+ microdomain effect. While we found that TRPC channels housed in caveolae membrane microdomains provides a source of [Ca2+] for induction of cardiac hypertrophy, this effect also requires interplay with LTCCs. We also found that TRPC channels have negative effects on cardiac contractility, which we believe are due to local activation of Ca2+/calmodulin-dependent protein kinase (CaMKII) and subsequent modulation of ryanodine receptors (RyRs). Further, we found that inhibiting TRPC channels in a mouse model of MI led to increased basal myocyte contractility and reduced hypertrophy and cardiac structural and functional remodeling, as well as increased survival. Collectively, the data presented in this dissertation provides comprehensive evidence that Ca2+ regulation of Cn-NFAT signaling and resultant pathological hypertrophy can be coordinated by spatially localized and regulated Ca2+ channels. The compartmentalization of LTCCs and TRPC channels in caveolae membrane microdomains along with pathological hypertrophy signaling effectors makes for an attractive explanation for how Ca2+-dependent signaling pathways are regulated under conditions of continual Ca2+ transients that mediate cardiac contraction during each heart beat. Elucidation of additional Ca2+ signaling microdomains in adult cardiac myocytes will be important in more comprehensively resolving how myocytes differentiate between signaling versus contractile Ca2+.
Temple University--Theses
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.
Full textDeJong, 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.
Full textHoffman, 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.
Full textPh.D.
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 receptors. Basal cytosolic Ca2+ levels are maintained at around 100nM. The mitochondria begins clearing GPRC-depended cytosolic Ca2+elevation after a short time delay during which the cytosolic Ca2+ concentration exceeds 3M. Then, the mitochondria sacrifices a portion of its membrane potential to drive Ca2+ influx across the mitochondrial inner membrane into the matrix. The membrane potential of the mitochondria is created in part by the electron transport, which while transferring electrons, ejects protons from the matrix to the inner membrane space. The rapid mitochondrial Ca2+ uptake decreases mitochondrial membrane potential thus reducing or fully collapsing the mitochondria's ability to generate ATP. This uncoupling of the electron transport chain results in ROS production and decreased cell survival. Mitochondria provide the body with energy that allows a heart to beat, a brain to store memories, and fuels locomotive function. As a stand-alone energy generator, the mitochondria would be interesting, but not dynamic. The dynamic flow of information to the mitochondria through Ca2+ signaling with all the components of symbiotic precision is a true biological phenomenon. In the mitochondria, a complex Ca2+ buffering system of channels, pores, and exchangers directly affects the conversion of chemical potential to ATP. Recent, discoveries of the Ca2+ uniporter (MCU) and other system components have provided the tools to tackle levels of mitochondrion physiologic studies that were not possible only a couple of years ago. There remains a great need for advancement in the understanding of mitochondrial bioenergetics, and undoubtedly, the mitochondria will be viewed as a determinant factor for survival. The mitochondrial inner membrane through its curious construction of 3:1 protein to lipid ratio, carefully regulates the permeability of ions and metabolites. The transport of Ca2+ and other small ions across the inner membrane is an essential signaling pathway for mitochondrial maintenance of metabolic functions, but the mechanisms are still unclear due to a lack of mitochondrial systems biology. For example, the oligomeric MCU with two transmembrane domains is a core component of the major Ca2+ import pathway in mitochondria, and ablation of MCU lowers mitochondrial Ca2+ uptake, however portions such as the highly conserved linker between the two transmembrane was unstudied until recently. Other complex components such as MICU1 and MCUR1, which negatively and positively regulate MCU, are beginning to have their mechanism solved. MICU1 is associated with the mitochondrial inner membrane and has two EF hands, which indicated a possible role in Ca2+ sensing. This role as a Ca2+ sensor proved to be necessary for proper MICU1 inhibition of MCU, but not determinant of MICU1/MCU interaction. MICU1, MCUR1, and MCU are modified in numerous diseases in which a particular component is disproportionately expressed. This is in part due to the classical coupling of gene function to associated transcription factor meaning that because MICU1, MCUR1, and MCU have a Ca2+ flux function, their transcription is also probably controlled by Ca2+ and is altered in chronic inflammation or hypoxic systems such as Ca2+ overload during ischemia/reperfusion. In spite of the low affinity of uniporter, mitochondrial Ca2+ overload occurs due to the close proximity of mitochondria to the ER, however physical tethering of the mitochondria and ER is still not widely accepted. When Ca2+ is physiologically cleared from the cytosol to the mitochondria, it acts as a synchronizing signal to the numerous EF hands present on inner membrane transmembrane proteins and matrix-targeted proteins. . Synchronization of mitochondrial activities is critical for efficiency which has direct implication for both cell growth or damage through the byproduct of inefficiency, mROS (superoxide). Therefore, the EF hands and other Ca2+ response elements enhance the ratio of ATP to superoxide, thus supporting mitogenic function and healthy growth. The inefficient flow of energy leads to dysfunction such as the release of reactive oxygen species (ROS) from the mitochondria. ROS carries its own energy in the chemical form of a radical. This translates into thermodynamically favorable but harmful cellular damage. Sustained import of Ca2+ results in electron transport malfunction followed by loss of membrane potential as seen in ischemia. A common EF hand motif exists on many calcium sensitive proteins. This helix-loop-helix topology recognizes a specific range of calcium concentrations based on the primary and tertiary structure of the domain. Thus, not all EF hands are active at a given physiological Ca2+ concentrations. The Ca2+ is situated in the loop portion by 12 key interactions in a pentagonal bipyramidal geometry. The position of 12th residue supplies two of the interacting oxygen atoms for Ca2+ binding and are conserved as either Glutamate or Aspartate. EF-hand containing proteins do not necessarily transport Ca2+ alone, as many other solutes have also been reported. The EF hand motif can be found on many mitochondrial sensors including LETM-1, MICU1, and non- Ca2+ transporters (Nakayama, Moncrief et al. 1992), suggesting Ca2+ is often the synchronizing signaling molecule but not necessarily transported by the mitochondrial channel of interest. The discovery of the uniporter (MCU) is an exciting event in the field, as many relationships between different transport mechanisms affecting Ca2+ and membrane potential will be elucidated. One such relationship that should be explored is between the uniporter and inorganic phosphate exchange. This relationship may modulate cell death through a critical uptake dynamic between adenine, phosphate and Ca2+ through alternative pathways such as solute carriers. Mitochondrial carriers are crucial for transport across the inner membrane. There are two groups of Ca2+ binding solute carriers in the mitochondria, the aspartate/glutamate carriers (Palmieri, Pardo et al. 2001) and the ATP-magnesium carriers (SCaMC) (Satrustegui, Pardo et al. 2007). Carrier proteins transport molecules by changing shape and therefore can be saturated. Solute carrier activators have been previously reported to include Ca2+, adenosine 3'5'-cyclic monophosphate, protein kinases, and inositol polyphosphates (Dransfield and Aprille 1993). Other previous work has also reported transport of multiple different solutes (Fiermonte, De Leonardis et al. 2004). The higher eukaryote, vertebrate calcium systems, should functionally if not physically interact with conserved lower eukaryote systems such as solute carriers. All known mitochondrial carriers are members of the same family based on three tandem repeats and are predicted to function as oligomers. The human family of these inner mitochondrial membrane proteins is SLC25, and members of the SLC25 family have been identified as the cause of Stanley Syndrome and Amish Microcephaly suggesting the importance of SLC25. SLC25A23 has been proposed to be an ATP-Mg/Pi exchange carrier that allows for both uptake and release of ATP-Mg from mitochondria. As a putative ADP/Pi translocase, it is an interesting component as both ADP and Pi have been shown to play a role in cell survival and cell death. This SLC25A family member is likely to be the critical regulator of these two dynamic molecules. These carriers are stimulated by submicromolar Ca2+ to regulate adenine nucleotide levels in the cytosol and mitochondria. Previous literature has shown SLC25A25 knockout to have little effect on mouse metabolism. SLC25A24 has been shown to be involved in ADP/ATP ratios in the mitochondrial matrix resulting in cytosolic Ca2+ buffering enhancement (21). The functions of SLC25A23 largely remain unknown. It should be pointed out that SLC25A23, SLC25A24, and SLC25A25, Ca2+ induced changes, are not necessarily based on Ca2+ as a channel solute. The ATP/ADP maintained by SLC25 family members may contribute to Ca2+ uptake in the mitochondria and therefore may play a role in cell death through PTP opening. PTP opening is a point of convergence for many cell death pathways. The PTP, which behaves as a voltage-operated channel, can be triggered to open by high mitochondrial Ca2+, ROS, or low membrane potential. In previous studies, SLC25A24 knockdown resulted in increased PTP opening and decreased Ca2+ buffering. Solute carrier family 25 (mitochondrial carrier; phosphate carrier), which includes SLC25A23, SLC25A24, and SLC25A25, transport solutes across the inner membrane, are predicted to form six transmembrane domains sensitive to Ca2+ due to four Ca2+ binding EF hand motifs, and localize to the mitochondria (del Arco and Satrustegui 1998; Iijima, Yamamoto et al. 2001). Based on membrane topology predictions, SLC25 isoforms contain six transmembrane domains with several EF hand motifs. Although the solute carriers in the SCaMC family have been hypothesized to transport adenine, (Aprille 1988) they have never been fully characterized. Mitochondrial solute carriers are found only in eukaryotes (Carafoli and Lehninger 1971; Uribe, Rangel et al. 1992; Palmieri 2004), however Sal1 in yeast has high sequence homology (Kucejova, Li et al. 2008). SLC25A25 knockout was reported to have little effects on mouse metabolism. SLC25A24 has been shown to be involved in ADP/ATP ratios in the mitochondrial matrix resulting in cytosolic Ca2+ buffering enhancement (Traba, Del Arco et al. 2011). The functions of these solute carriers in mitochondrial Ca2+ uptake and mitochondrial ROS are largely unknown.
Temple University--Theses
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.
Full textObolensky, 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.
Full textPerera, Naomi Tessa. "ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/13519.
Full textSpasevska, Ivana. "The role of EGR-1 and calcium influx in the antitumor activity of anti-CD20 monoclonal antibodies." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1304/document.
Full textAnti-CD20 monoclonal antibodies (mAbs) are an essential component of the treatment of patients with non-Hodgkin's lymphoma and chronic lymphocytic leukemia (CLL). They mediate their antitumor effects by activating the immune system or by direct apoptotic signaling in target cells. In a previous preclinical study, we showed that treatment with anti-CD20 mAbs, rituximab and GA101, resulted in upregulated expression of early growth factor 1 (EGR-1) (Dalle et al. 2011). EGR-1 is a calcium (Ca2+) regulated transcription factor and CD20 is hypothesized to regulate transmembrane Ca2+ flux. Therefore, we aimed to assess the role of EGR-1 and Ca2+ flux in the cytotoxic activity of anti-CD20 mAbs. We have shown that EGR-1 expression is rapidly upregulated in CD20+ cells following rituximab and GA101 exposure. Decreasing EGR-1 expression by shRNA abolishes the direct cytotoxic effect of GA101 both in vitro and in vivo, indicating that EGR-1 is required for CD20-mediated cell death. Additionally, the overexpression of EGR-1 enhances the cytotoxic activity of GA101 both in vitro and in vivo. Furthermore, our results indicate that anti-CD20 mAbs induce calcium influx. Blocking the Ca2+ flux with calcium channel blockers (CCB) abolishes EGR-1 induction and impaires the GA101 efficacy in vivo and ex vivo in CLL blood samples. More importantly, our data indicate that patients receiving CCBs and anti-CD20 therapy have worst progression free survival and overall survival. In conclusion we have identified EGR-1 as a potential biomarker to predict response to anti-CD20 therapy. We demonstrated that co-treatement with CCBs negatively impacts the outcome of patients receiving anti-CD20 mAbs
Cifelli, Carlo. "Impairment of force development in K(ATP) channel deficient skeletal muscle involves calcium ion influx through L-type calcium ion channels." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27342.
Full textShailes, Sarah. "Regulation of calcium influx and reactive oxygen species production during infection of legumes by rhizobia." Thesis, University of East Anglia, 2014. https://ueaeprints.uea.ac.uk/48752/.
Full textKhawaja, Rabia Raheel. "Role of calcium influx through glutamate receptors in white matter brain injury and oligodendrocyte regeneration." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/583654.
Full textPh.D.
Calcium-influx through ionotropic glutamate receptors expressed on non-excitable cells, such as CNS glia, may regulate important cell events via intracellular signaling mechanisms. Oligodendrocytes and oligodendrocyte progenitors (OPCs), two glial populations supporting CNS myelination and myelin repair, express AMPA and NMDA receptors. Although calcium-influx through these receptors is thought to cause glutamate excitotoxicity to oligodendrocytes in CNS injuries, more recent studies suggest that AMPA or NMDA receptor-mediated synaptic transmission between neurons and OPCs plays a positive role in neuronal activity-dependent oligodendrocyte development and regeneration. Given the opposing roles of glutamate receptors in oligodendrocyte death and repair, the clinical relevance of these receptors in white matter injuries remain unclear. Another major challenge for exploring the role of these receptors in white matter injuries is that OPCs and neurons express a similar complement of AMPA and NMDA receptor subunits, which has complicated the interpretation of pharmacological manipulations and global genetic deletion approaches. To define the cell autonomous role of AMPA and NMDA receptor-mediated calcium signaling in oligodendroglia, I abolished the calcium influx through glutamate receptors using two different genetic approaches, and examined their impacts on oligodendrocyte development, injury-induced cell death, and regeneration. First, I employed a new mouse line which allows overexpression of GluA2, the calcium-impermeable AMPA receptor subunit, in a Cre activity-dependent manner. After crossing these mice with OPC- or oligodendrocyte-lineage-specific Cre mice, I applied hypoxic-ischemic injury to these multiple transgenic mice. Surprisingly, even though AMPA receptor-mediated calcium influx was blocked in OPCs, oligodendrogenesis or myelin integrity was not affected. However, GluA2 overexpression significantly promoted oligodendrocyte regeneration and OPC proliferation after injury, while the same manipulation in oligodendrocytes did not protect them from the initial cell loss. Moreover, GluA2 overexpression also stimulated transcriptional activities linked to myelinogenesis, even without injury. Second, I used conditional knockout mice for Grin1, the gene encoding an essential subunit of NMDA receptor complexes. As with GluA2 overexpressing mice, the removal of NMDA receptors from OPCs or all oligodendroglia did not significantly change normal oligodendrocyte development. However, the ablation of NMDA receptor in OPCs exacerbated oligodendrocyte loss by impairing new oligodendrogenesis in hypoxic-ischemic injury. These results suggest that neither AMPA receptors nor NMDA receptors mediate glutamate excitotoxicity in oligodendrocytes in neonatal hypoxic-ischemic injury. Instead, these receptors play distinct roles in post-injury oligodendrocyte development: AMPA receptor-mediated calcium suppresses oligodendrocyte regeneration, and NMDA receptor signaling supports oligodendrocyte regeneration after injury.
Temple University--Theses
Egunlusi, Ayodeji Olatunde. "Novel norbornane derivatives as potential neuroprotective agents." University of Western Cape, 2020. http://hdl.handle.net/11394/7339.
Full textNeurodegenerative disorders are characterised by progressive loss of the brain’s physiological functions as a result of gradual degeneration of neurons in the central nervous system. Even though they are classified as diseases of the elderly, occurrence earlier in life is possible, but that would suggest the influence of genetic and/or environmental factors. Due to the continuous rise in modernisation and industrialisation over the years, there has been an increase in incidence and prevalence of neurodegenerative disorders. With the advances in technology and life expectancy, the rates of the common forms (Alzheimer’s disease and Parkinson’s disease), are expected to increase exponentially by 2050. Unfortunately, there is still no clinically approved treatment or therapy to slow down or halt the degenerative process as most registered drugs only offer symptomatic relief. Confounding this issue is the lack of definite mechanism of neurodegeneration, which is still poorly defined and not completely understood. Nonetheless, the pathology of most neurodegenerative disorders is believed to be a combination of interrelated processes that eventually leads to neuronal cell death. Among the postulated processes, the impact of excitotoxicity mediated by NMDA receptor over-activation is prominent and it is implicated in virtually all neurodegenerative disorders. With this basic insight, it is believed that molecules capable of inhibiting NMDA receptors and associated calcium channels, without affecting the normal physiological functions of the brain, could potentially serve as good neuroprotective drugs. Competitive and uncompetitive blockers (MK-801 and ketamine) have been explored, but none were clinically accepted due to undesirable side effects such as hallucinations, sedation and depression. However, NGP1-01, a polycyclic cage molecule, has been shown to be neuroprotective through modulation of NMDA receptors and voltage gated calcium channels and attenuation of MPP+ -induced toxicity. A similar approach could be useful in the design and development of new neuroprotective drugs. The aim of this study was to synthesise a series of open and rearranged cage-like molecules and explore their neuroprotective potential in neuroblastoma SH-SY5Y cells. The proposed structures, with norbornane scaffolds that contained different moieties, were designed to structurally resemble NGP1-01 and MK-801. Once synthesised, the compounds were purified and characterised, and were evaluated for their biological activities. Compounds were first screened for cytotoxicity at different concentrations. Thereafter, they were evaluated for neuroprotective effects against MPP+ -induced excitotoxicity and for calcium flux modulatory effects on NMDA receptor and voltage gated calcium channels. The norbornane derivatives were synthesised and characterised, and all final products were afforded in sufficient yields. All compounds with the exception of two compounds displayed good cytotoxic profiles towards the SH-SY5Y neuroblastoma cells at 10 µM, 50 µM and 100 µM concentrations as they demonstrated percentage cell viabilities close to 100% (control treated cells). Only two compounds showed percentage cell viability of 51% and 59% at 100 µM. Utilising the same cell line, all compounds, tested at 10 µM, attenuated MPP+ -induced toxicity after 24 hours of exposure to a neurotoxin. This was evident in the 23% to 53% enhancement (significant with p < 0.05) in cell viability when compared to the MPP+ only treated cells. In comparison to known NMDA receptor and/or voltage gated calcium channel blockers (MK-801, NGP1-01 or nimodipine), the synthesised compounds demonstrated mono or dual inhibition of calcium channels as they effectively attenuated calcium influx by blocking NMDA receptors and/or voltage gated calcium channels expressed in neuroblastoma SHSY5Y cells. This group of compounds were found to be more potent NMDA receptor inhibitors, probably due to similarities with MK-801 and memantine, than voltage gated calcium channel inhibitors. All compounds demonstrated moderate to good calcium inhibitory effects at NMDA receptors in the range of 23% to 70% while a selected few displayed very little or no activity at the voltage gated calcium channels. In conclusion, 27 compounds with norbornane scaffolds were successfully synthesised and evaluated for cytotoxicity and neuroprotection. The abilities of the synthesised compounds to protect neurons from the neurotoxin MPP+ and reduce calcium flux into neuronal cells were successfully demonstrated. These characteristics are essential in neuroprotection as they may prove significant in halting or slowing down the disease progression. The compounds showing a good cytotoxicity profile, neuroprotective effects and ability to reduce calcium overload, could potentially act as neuroprotective agents with good safety profiles or contribute as lead structures to the development and design of structurally related molecules that could clinically benefit people with neurodegenerative disorders.
Bretherton, Nicola. "The effect of cis-5,8,11,14,17-eicosapentaenoic acid upon the contractile mechanisms linked to calcium influx and the mobilisation of intracellular calcium in aortic smooth muscle." Thesis, Aston University, 1998. http://publications.aston.ac.uk/10988/.
Full textRicker, Ellen M. "The inhibitory effects of opioids on voltage-gated calcium influx in neonatal rat carotid body type I cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1424262410.
Full textDe, Paula Daisy Maria Bentes [UNIFESP]. "Estudo do mecanismo molecular de transfecção mediada por ultrassom." Universidade Federal de São Paulo (UNIFESP), 2010. http://repositorio.unifesp.br/handle/11600/9564.
Full textO ultrassom (US) vem sendo amplamente utilizado para melhorar a eficiência de transfecção de vetores não-virais. No entanto, o mecanismo pelo qual o US promove a entrega de DNA nas células ainda é pouco entendido. Este fenômeno é normalmente atribuído a sonoporação. Porém, com base em experimentos anteriores realizados em nosso laboratório, suspeitamos que outro mecanismo esteja envolvido no processo de captação de DNA. Para estudar o mecanismo de entrega, um vetor plasmideal expressando EGFP (pEGFP-N3, 4,7 kb) foi utilizado para transfectar células NIH3T3 com um aparelho de US terapêutico sem a adição de microbolhas. Em condições de insonação de 2 W/cm2, duty cycle de 20% por 30s o US promoveu cerca de 40% de eficiência de transfecção, mas com 1 W/cm2 resultou em níveis muito baixos de transfecção. Fixados esses parâmetros, também foi avaliada a produção de espécies reativas de oxigênio (ROS), o aumento da concentração intracelular de cálcio ([Ca2+]i) e as alterações no potencial de membrana através de microscopia confocal. A produção de ROS foi aumentada durante a insonação, sendo interrompida logo que o US foi desligado. A [Ca2+]i também foi aumentada durante a exposição ao US, mas seus níveis não retornaram ao basal durante os 3 minutos de observação. Porém, 1 W/cm2 não foi suficiente para mobilizar o cálcio durante a insonação, e o influxo de cálcio teve início apenas 12 segundos após o término do US. Quando expostas ao US, as células também apresentaram mudanças no potencial de membrana atingindo um estado de hiperpolarização, retornando ao estado normal logo que o US foi desligado. A alteração desses três parâmetros pelo US sugere que a entrega de DNA plasmideal deva ocorrer por endocitose. Por fim, utilizando DNA plasmideal fluorescente, mostramos que esta molécula entra na célula via endocitose mediada por clatrina.
Ultrasound (US) has been widely used to improve the efficiency of non-viral vector transfection. However, the mechanism that enables the uptake of plasmid DNA in cells by US insonation is poorly understood, but it is typically attributed to sonoporation. Based on our previous results, we hypothesized that other mechanisms, such as endocytosis, are involved in this process. To explore the mechanism of plasmid DNA uptake, a plasmid vector expressing EGFP (pEGFP-N3: 4.7 kb) was used to transfect NIH3T3 cells using a therapeutic US without microbubbles and was monitored in real-time using a confocal microscope. We achieved about 40% transfection efficiency when we applied 2 W/cm2 with 20% of duty-cycle for 30 s, but 1 W/cm2 resulted in a very low level of transfection. In these experiments, the production of reactive oxygen species was augmented during the insonation but was stopped soon after turning off the US. Calcium influx was also augmented during the insonation, but its level did not return to basal levels following the 3-min observation period. However, 1 W/cm2 was not sufficient to mobilize calcium influx during the insonation, and calcium influx began 12 s after turning off the US. US insonation also changed the cell membrane potential to promote a hyperpolarization state, which returned to the normal state soon after turning off the US. The alteration of these parameters by US indicates the uptake of plasmid DNA by endocytosis. Finally, using a fluorescently labeled plasmid, we showed that this molecule enters into cells via clathrin-mediated endocytosis, not via caveolin-1.
TEDE
BV UNIFESP: Teses e dissertações
Mulligan, Sean Joseph. "Characterization of mitral cell presynaptic calcium influx and synaptic transmission in an in vitro, en bloc frog forebrain preparation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ37597.pdf.
Full textYang, Heng. "TRPM4, a non selective cation-permeable channel regulates Foxp3+ regulatory T cells suppressive function and survival trough modulating calcium influx." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114840.
Full textTRPM4, a Ca2+-activated non-selective cation ion channel is an important regulator of Ca2+ signaling and cell activation in conventional T cells, but its role in Foxp3+ Tregs function remains unknown. Using a model in which Trpm4 gene was selectively invalidated in Foxp3+ Tregs population (Foxp3(YFP)Cre+Trpm4flox/flox mice) we have shown in different in vivo models of acute and chronic inflammation that TRPM4 is an important regulator of Tregs functions and survival. In a model of primary carcinogenesis induced by methylcholantrene (3-MCA) or implanted fibrosarcoma (MCA205 model), in which Tregs role has been documented, lack of TRPM4 expression and function induced significantly decreased incidence and tumor growth. We found that within chronic inflammatory and hypoxic tumor microenvironment, TRPM4 protected Tregs from ATP-induced cell death and therefore promoted tumor initiation and progression. In contrast, TRPM4 deficiency in Tregs favored IFN-g-mediated spontaneous anti-tumor immune response. Thus, through inhibiting Ca2+ influx, TRPM4 acts as a negative modulator of Tregs suppressive functions and protects Tregs from activation-induced cell death
Zhang, Zehua [Verfasser], Matthias [Akademischer Betreuer] Engel, and Peter [Gutachter] Reeh. "The modulatory effects of STW 5 and Menthacarin on cellular calcium ion influx in vitro / Zehua Zhang ; Gutachter: Peter Reeh ; Betreuer: Matthias Engel." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2020. http://d-nb.info/1224101979/34.
Full textZanatta, Leila. "Mechanism of action of 1(alfa),25-dihydroxyvitamin D3 on cytochrome P-450 aromatase, calcium influx and gamma glutamyl transpeptidase in rat testis." Florianópolis, SC, 2011. http://repositorio.ufsc.br/xmlui/handle/123456789/95390.
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Daziano, Guillaume. "Rôle du propeptide de la sortiline et de ses dérivés dans les mécanismes de survie de la cellule bêta pancréatique." Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ6025.
Full textIn 2019, the International Diabetes Federation revealed that nearly 500 million people have diabetes worldwide. It is estimated that this incidence will reach 700 million people by 2045. In addition to the financial aspect of treatment, diabetes is a real public health issue. Indeed, the deleterious hyperglycemic environment associated with diabetes is could induce serious complications, leading to a functional alteration of many organs such as the heart, the brain or the kidney. Insulin resistance associated with the deterioration of insulin secretion and the loss of pancreatic beta cell mass are the main characteristics of type 2 diabetes. Thus, in order to improve the management of diabetic patients, the identification of a controlled therapeutic approach to protect beta cell mass and promote insulin secretion only in response to glucose and without side effects, appears ideal.The laboratory has identified the endogenous PE and its synthetic derivatives Spadin and Mini-Spadin as selective inhibitors of TREK-1 potassium channels. By this mechanism, the peptides showed also a strong antidepressant potential by modulating serotonin secretion, neuronal proliferation and survival. At the peripheral level, Spadin has been described in vitro and in vivo as a peptide with an incretin effect comparable to that of exendin-4, an antidiabetic commonly used in the clinic. Thus, following this study and by analogy to the protective effects observed on the neuron, we hypothesized that PE and its derivatives may have a beneficial role in the survival mechanisms in the pancreatic beta-cell.In this thesis, we demonstrate that endogenous PE and its derivatives protect beta cells from apoptosis induced by the chronic presence of the pro-inflammatory and diabetogenic interleukin IL-1β, as well as from an acute toxic shock induced by staurosporine. Furthermore, analysis of intracellular mechanisms reveals that these peptides cause an increase in intracellular calcium concentration, activate the ERK and Akt proliferative and survival pathways, and maintain CREB transcriptional factor activity in a deleterious environment via a calmodulin kinase-dependent pathway.Thus, this work shows that PE and its synthetic derivatives protect the pancreatic beta-cell and initiate virtuous cellular processes through an original PKA-independent signaling pathway, where membrane potential and calcium play a crucial role. This suggests the sortilin-derived peptides as a new class of pancreatic beta-cell protective molecules
Vachel, Laura. "Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP." Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT2303/document.
Full textTRP (Transient Receptor Potential) channels are keys actors of Ca2+ homeostasis. Several of these channels are involved in the Ca2+ influx of bronchial epithelial cells, including TRPC6 which is implicated in a functional coupling with the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) channel. CFTR mutation leads Cystic Fibrosis (CF) disease and causes abnormal Ca2+ homeostasis trought an increased of Ca2+ influx in CF bronchial epithelial cells. Our objective is to investigate the implication of TRP channels in abnormal Ca2+ influx of CF bronchial epithelial cells.We showed that CFTR down regulates TRPC6 activity whereas Ca2+ influx through TRPC6 potentiates G551D-CFTR, activated by VX-770. We propose a new therapeutic strategy that combines a CFTR potentiator and a specific activator of TRPC6. Then, we focused on the role of TRPV channels, particularly TRPV5 and TRPV6, in Ca2+ influx of bronchial epithelial cells. We observed that constitutive Ca2+ influx, related to TRPV5/TRPV6 activity, was twice higher in CF cells due to the increase of TRPV6 activity. The expression of PLC-δ1, an enzyme that negatively regulates TRPV6 activity, is dramatically decreased in CF cells. The correction of F508del-CFTR trafficking allows TRPV6 activity normalization but do not restore PLC-δ1 expression level in CF cells, suggesting a more complex control of TRPV6 in bronchial epithelial cells
Qu, Mengdi. "Molecular mechanism underlying CaMK1D-dependent function in AgRP neurons." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ029.
Full textDisruption of stress response mechanisms in organisms can lead to cellular dysfunction and diseases like metabolic syndrome. Energy balance is mainly regulated by the central nervous system (CNS), which integrates hormonal, neuronal, and dietary signals from various tissues. Dysfunction in this system is linked to obesity and metabolic syndrome, both precursors to type 2 diabetes (T2D). Our laboratory discovered that calcium/calmodulin-dependent protein kinase ID (CaMK1D), a gene associated with T2D, promotes ghrelin-mediated food intake in mice. However, CaMK1D signaling in NPY/AgRP neurons still remains questions. In this work, we proformed RNA sequencing using the GT1-7 hypothalamic cell line. To this end, we found that CalHM6 is a downstream target of CaMK1D signaling. CalHM6 mRNA levels were significantly upregulated in CaMK1D-/- cells and downregulated when CaMK1D was re-expressed. This was confirmed in vivo in the hypothalamus of CaMK1D-/- mice. CalHM6, likely a voltage-gated calcium channel, showed increased intracellular Ca2+ levels in response to ghrelin in CaMK1D-/- cells compared to CaMK1D+/+ cells using jGCamps method. Altogether, our work showed CalHM6 is a novel target of CaMK1D. High CaMK1D, leading to low CalHM6 expression, may enhance food intake and obesity by modulating calcium-dependent signaling in NPY/AgRP neuron
Sabourin, Jessica. "Influx cationique dépendant des canaux TRPCs dans les cellules musculaires squelettiques : régulation par le complexe dystrophine/alpha1-syntrophine et par la voie PLC : implication dans la dystrophie musculaire de Duchenne." Poitiers, 2009. http://theses.edel.univ-poitiers.fr/theses/2009/Sabourin-Jessica/2009-Sabourin-Jessica-These.pdf.
Full textThe dystrophin is a cytoskeleton protein normally expressed underneath the sarcolemma of skeletal muscle. The lack of this protein in Duchenne Muscular Dystrophy leads to muscle necrosis and to increased intracellular free calcium in the cytoplasm. Actually, the link between calcium mishandling and the absence of dystrophin is not well established and the aim of my study is to demonstrate it. Our works showed that cationic influx activated by calcium depletion of sarcoplasmic reticulum is strongly increased. We identified TRPC1 and TRPC4 channels supporting cationic influx in myotubes expressing mini-dystrophin. We also described for the first time a molecular link between dystrophin and TRPC1/TRPC4 channels, the alpha1-syntrophin. We suggested that normal regulation of syntrophin overexpression leads to reduction of abnormal cationic influx in dystrophin-deficient myotubes. Conversely, alpha1-syntrophin repression leads to increased cationic entry in myotubes expressing mini-dystrophin. The presence at normal level of this protein appears to be crucial for normal regulation of TRPC1/TRPC4 channels in skeletal muscle. On the other hand, we demonstrated an increased cationic influx supported by TRPC in dystrophin-deficient myotubes, which seems to be potentiated by PLC/PKC pathway
Rossato, Mateus Fortes. "Eriodictiol: um flavonóide antagonista do receptor trpv1 com atividade antioxidante." Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/11134.
Full textThe transient receptor potential vanilloid 1 (TRPV1) is a calcium permeable channel responsible for the transduction and modulation of acute and chronic pain signaling, being a potential target for treatment of different pain disorders. In spite of that, AMG517, a TRPV1 antagonist, presents several clinical limitations, such as the development of severe hypertermia. The aim of this study was to investigate the possible interaction of the flavonoid eriodictyol with the TRPV1 receptor and its putative antinociceptive and hyperthermic effect. Eriodictyol was able to displace the [3H]-resiniferatoxin binding (IC50 = 47 (21 - 119) nM) and to inhibit the calcium influx mediated by capsaicin (IC50 = 44 (16 125) nM), suggesting that eriodictyol acts as a TRPV1 antagonist. Moreover, eriodictyol induces antinociception in the intraplantar capsaicin test, with maximal effect of 49±10 and 64±4% of inhibition for oral (ED50 = 2 (1-5) mg/kg) and intrathecal (ED50 = 2 (1-3) nmol/site) routes, respectively. Concomitantly, eriodictyol did not induce any alteration on body temperature or locomotor activity. Orally administered eriodictyol (4.5 mg/kg) prevented the nociception induced by intrathecal injection of capsaicin (72±6% of inhibition), the non-protein thiol loss and the 3-nitrotyronise (3-NT) formation induced by capsaicin in spinal cord. Eriodictyol (4.5 mg/kg, p.o.) also reduced the thermal hyperalgesia (100% of inhibition) and mechanical allodynia (62±9% of inhibition) elicited by complete Freund s adjuvant (CFA) paw injection. In conclusion, Eriodictyol acts as an antagonist of TRPV1 receptor and an antioxidant, inducing antinociception without some side effects and limitations expected for TRPV1 antagonists, as hyperthermia.
O receptor de potencial transiente vanilóide 1 (TRPV1) é um canal iônico permeável a cátions ativado por uma série de estímulos nocivos, como calor, acidificação e agentes irritantes como a capsaicina. Este receptor é responsável pela detecção e transmissão da dor aguda e crônica. Devido a isso, substâncias que modulem a atividade deste receptor apresentam um potencial clínico para o tratamento da dor. Assim, este trabalho objetiva a possível interação do flavonóide eriodictiol com o receptor TRPV1. Inicialmente, observamos que o eriodictiol foi capaz de deslocar o radioligante [3H]-resiniferatoxina, em ensaio de união específica, do receptor TRPV1 com uma concentração inibitória 50% (IC50) de 46.9 (20.70 - 118.9) nM. Ao mesmo tempo, o eriodictiol também inibiu o influxo de cálcio estimulado por capsaicina com IC50 de 44,4 (15,6 125,1) nM, sugerindo que este aja como um antagonista do receptor. Além disso, também observamos que o eriodictiol induz antinocicepção no teste da capsaicina intraplantar com efeito máximo de 49,0±10.5 e 63,9±4.0 % de inibição máxima para o tratamento oral e intratecal, respectivamente, e com uma dose efetiva 50% (DE50) de 2,4 (1,0 5,5) mg/kg 2,2 (1,6 2,9) nmol/site, respectivamente. Além disso, não observamos alterações na atividade locomotora ou temperatura corporal dos animais. A administração oral de eriodictiol também foi capaz de prevenir a nocicepção induzida por capsaicina intratecal (71,7±5,7 % de inibição). Ao mesmo tempo, o eriodictiol também aboliu a hiperalgesia térmica e reduziu a alodínia mecânica (62,4±9,2 %) induzidas por adjuvante completo de Freund. Da mesma forma, o eriodictiol também preveniu totalmente a diminuição de tiois não protéicos e formação de 3-nitrotirosina (3-NT) espinhais induzidas por capsaicina, ao passo que apresentou atividade antioxidante direta no texto de neutralização do radical ABTS. Em conclusão, nossos resultados mostram que o eriodictiol age como um antagonista do receptor TRPV1, com atividade antioxidante, induzindo antinocicepção sem os efeitos colaterais e limitações esperados para antagonistas do receptor TRPV1.
Shoji, Emi. "Early pathogenesis of Duchenne muscular dystrophy modelled in patient-derived human induced pluripotent stem cells." Kyoto University, 2015. http://hdl.handle.net/2433/200495.
Full textSharma, Rajan. "Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds." University of the Western Cape, 2017. http://hdl.handle.net/11394/6228.
Full textAmong neurological disorders, many of the most devastating disorders are neurodegenerative. Modern research associates excitotoxicity to a variety of neuropathological conditions, suggesting that the neurodegenerative diseases with distinct etiologies may have excitotoxicity as a common pathway. Excitotoxicity occurs through over-stimulation of receptors for excitatory neurotransmitters like the N-methyl-D-aspartate (NMDA) receptors. Due to the relevance of NMDA receptors and excitotoxic processes, the antagonism or modulation of NMDA receptors is used as a therapeutic tool against neurodegenerative diseases. NMDA receptor activity can be modulated by S-nitrosylation and this modulation of NMDA receptor activity can be utilised in the development of neuroprotective drugs.
Djillani, Alaeddine. "Caractérisation des canaux calciques dans les polynucléaires neutrophiles : rôle dans la phagocytose et la production des radicaux libres oxygénés." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-01069097.
Full textAmpem, Prince Tuffour. "The Transient Receptor Potential Canonical 3 (TRPC3) Channel: Novel Role in Endothelial Cell Apoptosis and its Impact on Atherosclerosis." University of Toledo Health Science Campus / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=mco1493230041479167.
Full textLangford, Peter R. "c-Met Initiates Epithelial Scattering through Transient Calcium Influxes and NFAT-Dependent Gene Transcription." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/3186.
Full textBarbar, Élie. "Effets de la 4-aminopyridine sur le lymphocyte T Jurkat influx calcique, induction de l'apoptose et perméation d'ions." Thèse, Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/4245.
Full textWaiczies, Sonia. "Modulation of human antigen-specific T-cell response therapeutic implications for multiple sclerosis /." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969681844.
Full textGaldino, Jos? Nildo. "Influ?ncia do teor e granulometria da calcita e da temperatura de sinteriza??o no desenvolvimento de massas cer?micas para revestimento poroso(BIII)." Universidade Federal do Rio Grande do Norte, 2010. http://repositorio.ufrn.br:8080/jspui/handle/123456789/15903.
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This work aims at studying the influence of the concentration of calcite, its grain size and sintering temperature to obtain porous coating formulations that meet the design specifications. The experiments involved the physical-chemical and mineralogical caracterization of the raw materials, and mechanical tests on specimens dried and sintered, performing a planning mixture and factorial experiment, using the response surface methodology. The ceramic bodies studied were prepared by dry process, characterized, placed in conformity by uniaxial pressing and sintered at temperatures of 940 ? C, 1000?C, 1060?C, 1120?C and 1180?C using a fast-firing cycle. The crystalline phases formed during sintering at temperatures under study, revealed the presence of anorthite and wolastonite, and quartz-phase remaining. These phases were mainly responsible for the physical and mechanical properties of the sintered especimens. The results shown that as increases the participation of carbonate in the composition of ceramic bodies there is an increase of water absorption and a slight reduction in linear shrinkage for all sintering temperatures. As for the mechanical strength it was observed that it tended to decrease for sintering at temperatures between 940 ? C and 1060 ? C and to increase for sintering at temperatures above 1060 ? C occurring with greater intensity for compositions with higher content of calcite. The resistence decreased with increasing participation of quartz in all sintering temperatures. The decrease in grain size of calcite caused a slight increase in water absorption for formulation with the same concentration of carbonate, remaining virtually unchanged the results of linear shrinkage and mechanical strength. In conclusion, porous ceramic coating (BIII) can be obtained using high concentrations of calcite and keeping the properties required in technical standards and that the particle size of calcite can be used as tuning parameter for the properties of ceramic products.
Este trabalho objetiva estudar a influ?ncia da concentra??o de calcita, sua granulometria e temperatura de sinteriza??o na obten??o de formula??es para revestimento poroso que atendam as especifica??es da norma. Os experimentos envolveram a caracteriza??o f?sico qu?mica e mineral?gica das mat?rias-primas, e ensaios mec?nicos nos corpos de prova secos e sinterizados, precedendo-se de um planejamento de experimento de mistura e fatorial, com o uso da metodologia de superf?cie de resposta. As massas cer?micas estudadas foram preparadas pelo processo via seca, caracterizada, conformada por prensagem uniaxial e sinterizadas nas temperaturas de 940?C, 1000?C, 1060?C, 1120?C, e 1180?C utilizando um ciclo de sinteriza??o r?pido. As fases cristalina formadas durante a sinteriza??o nas temperaturas em estudo, revelaram a presen?a de anortita e wolastonita, al?m de quartzo com fase remanescente. Estas fases foram as principais respons?veis pelas propriedades f?sico-mec?nica dos corpos de provas sinterizados. Verificou-se que conforme se aumenta a participa??o do carbonato na composi??o das massas cer?micas ocorre um incremento de absor??o de ?gua e uma pequena redu??o da retra??o linear para todas as temperaturas de sinteriza??o. J? para a resist?ncia mec?nica houve uma tend?ncia de redu??o para sinteriza??o entre 940?C e 1060?C e aumento para sinteriza??o acima da temperatura de 1060?C ocorrendo com maior intensidade para formula??es com maior teor de calcita, e houve diminui??o da resist?ncia com o aumento da participa??o do quartzo em todas as temperaturas de sinteriza??o. A diminui??o da granulometria da calcita provocou um leve aumento na Absor??o de ?gua para formula??o com a mesma concentra??o desse carbonato mantendo praticamente inalterados os resultados de retra??o linear e resist?ncia mec?nica. Conclui-se que produtos cer?micos para revestimento poroso (BIII) podem ser obtidos utilizando altas concentra??es de calcita e mantendo-se as propriedades exigidas em normas t?cnicas e que a granulometria da calcita pode ser usada como par?metro de ajuste para as propriedades dos produtos cer?micos
Oliveira, Gislaine Alves de. "A ação espasmolítica do óleo essencial de Lippia microphylla Cham. e de seus constituintes majoritários envolve o bloqueio do influxo de cálcio em íleo de cobaia." Universidade Federal da Paraíba, 2014. http://tede.biblioteca.ufpb.br:8080/handle/tede/6824.
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The essential oil extracted from aerial parts of Lippia microphylla Cham. (Verbenaceae) (LM-OE) presents as major compounds thymol and carvacrol. The aim of this study was to investigate and to characterize oil LM-OE spasmolytic effect on guinea pig ileum, as well to verify if this effect is due its major compunds, thymol and carvacrol. Were performed measures of isometric and isotonic contractions and cytosolic calcium. LM-OE inhibited phasic contractions induced by 10-6 M of histamine or carbachol (CCh) (IC50 = 15.8 ± 2.3 e 24.4 ± 2.9 μg/mL, respectively). In a similar manner, thymol, carvacrol and thymol/carvacrol mixture antagonized histamine- (IC50 = 14.2 ± 1.6; 13.6 ± 1.3 e 13 ± 2.1 μg/mL, respectively) ou CCh- (IC50 = 21.3 ± 3.8; 16 ± 2.6 e 27.9 ± 4.8 μg/mL, respectively) induced phasic contractions. Compared with LM-OE, in neither case was difference. In the same way, LM-OE relaxed pre-contracted organ by 40 mM of KCl, 10-5 M of CCh or 10-6 M of histamine (EC50 = 7.6 ± 0.8; 7.2 ± 1.3 e 6.8 ± 0.6 μg/mL, respectively), being equipotent in the three situations. As CaV are common step on pathway of these three contractile agents, we hypothesized that somehow LM-OE would blocking Ca2+ influx by these channels. Once probably the major compounds are biological markers for this specie, we evaluated their effect upon tonic contraction induced by 40 mM of KCl. We found that thymol, carvacrol and thymol/carvacrol mixture relaxed the ileum in a significant and concentration-dependent manner (EC50 = 5.1 ± 1.1; 11.5 ± 1 e 5.1 ± 1.1 μg/mL, respectively), being carvacrol the least potent among the three, they did not showed statistic difference when compared with LM-OE. To confirm the hypothesis of CaV participation on LM-OE spasmolytic action, were performed cumulative concentration-response curves to CaCl2 in a nominal without Ca2+ depolarizing medium in absence (control) and LM-OE presence, witch one antagonize these contractions besides to relaxes the organ when it was pre-contracted by S-(-)-Bay K 8644 (EC50 = 8.5 ± 1.5 μg/mL), a selective CaV 1, agonist confirming that the CaV subtype involved is CaV 1. The fact of CsCl, a K+ channels nonselective blocker, has not changed the relaxing potency of LM-OE oil on ileum pre-contracted with 10-5 M CCh, discard the hypothesis of positive modulation of these channels, which would lead to an indirect blockade of CaV. In experiments with ileum circular layer, LM-OE antagonized phasic contractions induced by 10-6 M of CCh (IC50 = 30.1 ± 1.5 μg/mL), that suggests a negative modulation of the Ca2+ intracellular signaling by LM-OE oil to exert its spasmolytic effect. Viability of layer longitudinal smooth muscle cells was evaluated in the absence and presence of 81 μg/mL LM-OE oil, and no cell death was verify during 2 h of contact with cells LM-OE oil. In the presence of LM-OE oil, the intensity of fluorescence in intestinal guinea pig myocytes stimulated by histamine was reduced as a result of the reduction of calcium cytosolic concentration ([Ca2+]c). In conclusion, the LM-OE oil act by blocking calcium influx through CaV1, possibly by inhibiting intracellular Ca2+ signaling and reducing [Ca2+]c, to promote its spasmolytic effect in guinea pig ileum
O óleo essencial extraído das partes aéreas de Lippia microphylla Cham. (Verbenaceae) (LM-OE) apresenta como componentes majoritários o timol e o carvacrol. O objetivo deste trabalho foi investigar e caracterizar o efeito espasmolítico do óleo LM-OE em íleo de cobaia, bem como verificar se este efeito era devido aos seus constituintes majoritários. Foram realizadas medidas de contrações isotônicas e isométricas e do cálcio citosólico. O óleo LM-OE inibiu as contrações fásicas induzidas por 10-6 M de histamina ou de carbacol (CCh) (CI50 = 15,8 ± 2,3 e 24,4 ± 2,9 μg/mL, respectivamente). Da mesma forma, o timol, o carvacrol e a mistura timol/carvacrol antagonizaram as contrações fásicas induzidas por histamina (CI50 = 14,2 ± 1,6; 13,6 ± 1,3 e 13,0 ± 2,1 μg/mL, respectivamente) ou por CCh (CI50 = 21,3 ± 3,8; 16,0 ± 2,6 e 27,9 ± 4,8 μg/mL, respectivamente). Quando comparado com o óleo, não houve diferença em nenhum dos casos. Do mesmo modo, o óleo LM-OE relaxou, de maneira equipotente, o órgão pré-contraído com 40 mM de KCl, com 10-5 M de CCh ou com 10-6 M de histamina (CE50 = 7,6 ± 0,8; 7,2 ± 1,3 e 6,8 ± 0,6 μg/mL, respectivamente). Como o passo comum na via de sinalização destes agentes contráteis são os canais de cálcio dependentes de voltagem (CaV), hipotetizou-se que de alguma forma o óleo estaria impedindo o influxo de Ca2+ através destes canais. Visto que provavelmente os componentes majoritários são os marcadores biológicos para esta espécie, avaliou-se o efeito dos mesmos sobre a contração tônica induzida por 40 mM de KCl. Observou-se que o timol, o carvacrol e a mistura timol/carvacrol relaxaram o órgão de maneira significante e dependente de concentração (CE50 = 5,1 ± 1,1; 11,5 ± 1 e 5,1 ± 1,1 μg/mL, respectivamente), sendo o carvacrol o menos potente entre os três, os quais se mostraram equipotentes ao óleo LM-OE. Para confirmar a hipótese da participação dos CaV no mecanismo espasmolítico do óleo LM-OE, foram feitas curvas concentrações-resposta cumulativas ao CaCl2 em meio despolarizante nominalmente sem Ca2+ na ausência (controle) e na presença do óleo LM-OE, o qual antagonizou essas contrações, além de relaxar o órgão pré-contraído com S-(-)-Bay K 8644 (CE50 = 8,5 ± 1,5 μg/mL), agonista seletivo dos CaV1, confirmando assim que o subtipo de CaV envolvido é o CaV1. O fato do CsCl, um bloqueador não seletivo dos canais de K+, não ter alterado a potência relaxante do óleo LM-OE no íleo pré-contraído com 10-5 M de CCh, descarta a hipótese da modulação positiva desses canais, o que levaria a um bloqueio indireto dos CaV. Em experimentos utilizando a camada circular do íleo de cobaia, o óleo antagonizou as contrações fásicas induzidas por 10-6 M de CCh (CI50 = 30,1 ± 1,5 μg/mL), o que sugere uma possível inibição da sinalização intracelular de Ca2+ para exercer seu efeito espasmolítico. A viabilidade das células musculares lisas da camada longitudinal foi avaliada na ausência e na presença de 81 μg/mL do óleo LM-OE, não havendo morte celular no período 2 h de contato das células com o óleo LM-OE. Na presença do óleo LM-OE, a intensidade de fluorescência em miócitos intestinais de cobaia estimulados por histamina foi reduzida em consequência da redução da [Ca2+]c. Em conclusão, o óleo LM-OE age por impedir o influxo de cálcio através dos CaV1, por possivelmente inibir a sinalização intracelular de Ca2+ e redução da concentração citosólica desse íon, para promover seu efeito espasmolítico em íleo isolado de cobaia
Ferraz, Sandro Aparecido. "Estimativa do influxo de calcio por meio de canais tipo L em miocitos cardiacos isolados de ratos neonatos e adultos." [s.n.], 2003. http://repositorio.unicamp.br/jspui/handle/REPOSIP/260336.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia Eletrica e de Computação
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Doutorado
Leite, Jocelmo Cassio de Araujo. "Desenvolvimento embrionário de Ouriços-do-mar da espécie Echinometra lucunter (Linnaeus, 1758) envolve influxo de cálcio através dos canais de cálcio sensíveis à voltagem." Universidade Federal da Paraíba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/6871.
Full textCoordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Ca2+ is an intracellular messenger that controls a wide range of physiological functions through changes in its cytosolic concentration ([Ca2+]c). The increase in [Ca2+]c is derived of mobilization from intracellular stores or influx through channels, especially voltage-gated (Cav), present on cell surface. According to scientific literature, sea urchins embryogenesis is a process induced exclusively by the release of Ca2+ from the endoplasmic reticulum, and Ca2+ influx is not necessary for this process. However, there are studies in several species of the animal kingdom where Ca2+ influx is crucial for embryogenesis. Therefore, the aim of this study was to evaluate the involvement of Ca2+ influx at fertilization and embryonic development of Echinometra lucunter, a species of sea urchins with wide distribution on Brazilian coast. Thereby, eggs and embryos of E. lucunter were treated with various pharmacological tools and fertilization and embryonic development were monitored. Incubation of gametes in Ca2+ free medium inhibited fertilization and embryo treatment with Ca2+ chelators blocked embryonic development, suggesting that extracellular Ca2+ is essential for both processes. Cav blockers nifedipine, diltiazem and verapamil were also effective in blocking fertilization and embryo development, showing the importance of these channels to embryogenesis of E. lucunter. Inhibitory effect on embryo development is not associated with modulation of ABC superfamily proteins, since embryonic development was not affected, even under inhibition of these proteins. Verapamil inhibitory effect was reversed by prior addition of valinomycin which may be related to a probable increase of [Ca2+]c induced by K+ ionophore. ouabain, a Na+/K+-ATPase blocker that activates the reverse mode of Na+ /Ca2+, also reversed inhibition of development induced by verapamil. The reversal was not observed when compounds were added to embryos after verapamil, suggesting a temporal profile in inhibitory effect of these blockers. Inhibitory effects of verapamil and Ca2+ chelator EGTA were time-dependent, being absent 50 minutes after fertilization, suggesting that Ca2+ influx is seminal only in the first minutes of embryonic development. However, intracellular Ca2+ is essential for embryogenesis, since treatments with BAPTA-AM (chelator of intracellular Ca2+) and chlorpromazine or Trifluoperazine (Ca2+-calmodulin complex blockers) inhibited E. lucunter embryogenesis. Additionally, it was found that the rotundifolone, a plant-derived compound with vasorelaxing activity, attributed to the blockade of Cav, inhibited E. lucunter embryonic development showing an inhibitory profile similar to observed in vascular smooth muscle. Therefore, these results suggest that Ca2+ influx is essential for Echinometra lucunter embryogenesis and certify the embryonic development of this animal as appropriated pharmacological model for the investigation of natural and synthetic products that interferes in Ca2+ cellular dynamics.
O Ca2+ é um mensageiro intracelular que controla uma ampla variedade de funções fisiológicas por meio de alterações na sua concentração citosólica ([Ca2+]c). O aumento na [Ca2+]c é derivado da liberação a partir de estoques intracelulares ou do influxo através dos canais, principalmente os sensíveis à voltagem (Cav), presentes na superfície celular. De acordo com a literatura científica, a embriogênese de ouriços-do-mar é um processo regulado exclusivamente pela liberação de Ca2+ a partir do retículo endoplasmático, sendo o influxo dispensável para esse processo. Entretanto, há relatos em diversas espécies do reino animal onde o influxo de Ca2+ é crucial para a embriogênese. Portanto, o objetivo deste trabalho foi avaliar a participação do influxo de Ca2+ na fertilização e no desenvolvimento embrionário de Echinometra lucunter, uma espécie de ouriço-do-mar com ampla distribuição na costa Brasileira. Dessa forma, óvulos e embriões de E. lucunter foram tratados com diversas ferramentas farmacológicas e a fertilização e o desenvolvimento embrionário monitorados. A incubação dos gametas em meio isento de Ca2+ inibiu a fertilização e o tratamento dos embriões com quelantes de Ca2+ bloqueou o desenvolvimento embrionário, sugerindo que o Ca2+ extracelular é fundamental para ambos os processos. Os bloqueadores de Cav nifedipina, diltiazem e verapamil também foram eficazes no bloqueio da fertilização e do desenvolvimento embrionário, indicando a importância desses canais para a embriogênese de E. lucunter. O efeito inibitório sobre o desenvolvimento embrionário não está associado à modulação de proteínas da superfamília ABC, uma vez que o desenvolvimento embrionário ocorreu de forma normal, mesmo com a inibição dessas proteínas. O efeito inibitório do verapamil foi revertido pela adição prévia de valinomicina e tal fato pode estar relacionado a um provável aumento da [Ca2+]c induzido por este ionóforo de K+. A ouabaína, um bloqueador da Na+/K+-ATPase, capaz de ativar o modo reverso do trocador Na+/Ca2+, também reverteu a inibição do desenvolvimento induzida pelo verapamil. Essa reversão não foi observada quando os compostos foram adicionados aos embriões após o verapamil, sugerindo uma relação temporal no efeito inibitório desses bloqueadores. O efeito inibitório do verapamil e do quelante de Ca2+ EGTA foi dependente de tempo, sendo ausente 50 minutos após a fertilização, sugerindo que o influxo de Ca2+ é um fator determinante apenas nos primeiros minutos do desenvolvimento embrionário. Contudo, o Ca2+ intracelular é indispensável para a embriogênese, uma vez que os tratamentos com o BAPTA-AM, um quelante intracelular de Ca2+, e com trifluoperazina ou clorpromazina, bloqueadores do complexo Ca2+-calmodulina, inibiram a embriogênese de E. lucunter. Adicionalmente, foi verificado que a rotundifolona, um composto de origem vegetal com atividade vaso-relaxante atribuída ao bloqueio dos Cav, inibiu o desenvolvimento embrionário de E. lucunter, obtendo um perfil inibitório similar ao observado em musculatura lisa vascular. Portanto, esses resultados sugerem que o influxo de Ca2+ é essencial para a embriogênese de Echinometra lucunter e legitima o desenvolvimento embrionário desse animal como um excelente modelo farmacológico para a prospecção de produtos naturais e sintéticos bioativos que interferem na dinâmica celular do Ca2+.
Zanotto, Camila Ziliotto. "Papel da O-glicosilação com N-acetil-glucosamina (O-GlcNAc) no influxo e recaptação de cálcio pelo retículo sarcoplasmático em aorta de ratos: análise funcional." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-09092013-133940/.
Full textGlycosylation with O-linked -N-acetyl-glucosamine (O-GlcNAc) is a highly dynamic post-translational modification. The process of O-GlcNAc is controlled by two enzymes: the OGT enzyme catalyses the addition of N-acetyl-glucosamine to the hydroxyl group of serine and threonine residues of a target protein, while OGA catalyzes the cleavage of O-GlcNAc from post-translationally-modified proteins. Proteins with an important role in vascular function are targets of O-GlcNAc and increased levels of proteins modified by O-GlcNAc increase vascular reactivity to contractile stimuli. The regulation of intracellular calcium (Ca2+) concentration, including the activation of STIM1/Orai1, is key in the control of vascular tone. The stromal interaction molecules (STIM) act as sensors of intracellular Ca2+ stores whereas the Orai proteins represent subunits of the Ca2+ release-activated Ca2+ channels (CRAC). We hypothesized that increased levels of vascular O-GlcNAc proteins augment vascular contractile responses by altering mechanisms that regulate the intracellular Ca2+. Rat thoracic aortas were incubated with PugNAc (OGA selective inhibitor, ) for 24h. Using an experimental protocol that evaluates contractions induced by Ca2+ influx and release, we demonstrated that incubation with PugNAc increases contractile responses to phenylephrine (PE) as well as the contraction induced by Ca2+ influx, after depletion of intracellular Ca2+ stores. The CRAC channel blockers, 2-APB (100 ) and gadolinium (Gd3+, 100 ), significantly reduced the contractions induced by Ca2+ influx in aortas incubated with PugNAc. Furthermore, these aortas showed increased STIM1 protein expression, which could result in increased influx of Ca2+ and, in turn, increase vascular contraction. The contraction induced by the release of intracellular Ca2+ stores, stimulated by caffeine (20 mM) and serotonin (10 ), was increased in aortas incubated with PugNAc. The Ca2+-ATPase (SERCA) inhibitor thapsigargin produced similar effects in arteries incubated with PugNAc or vehicle, despite the increased SERCA protein expression in aortas incubated with PugNAc. Since PKC is activated by increases in intracellular Ca2+ and arteries incubated with PugNAc show activation of PKC, we determined whether the activity of proteins that are targets of PKC was increased in PugNAc-treated aortas. Incubation with PugNAc increased the expression of phosphorylated forms of CPI-17, MYPT-1 and MLC. Together, these results suggest that activation of STIM1/Orai1, increased release of intracellular Ca2+ and PKC activation may represent mechanisms that modulate vascular responses upon increased O-GlcNAc proteins.
Menasché, Philippe. "Étude expérimentale des solutions cardioplégiques : applications à la chirurgie cardiaque." Paris 11, 1987. http://www.theses.fr/1987PA112086.
Full textRosso, Angela. "Estudo do envolvimento iônico e de proteínas cinases no mecanismo de ação da 1-a,25(OH)2 vitamina D3, no influxo de cálcio em células de Sertoli e em testículos de ratos." reponame:Repositório Institucional da UFSC, 2012. http://repositorio.ufsc.br/xmlui/handle/123456789/94538.
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Tendo em mente que a 1,25D3, produto final do metabolismo da vitamina D3 é essencial para a integridade do sistema reprodutor masculino, e que, a homeostase do Ca+2 desempenha papel chave em muitos processos envolvidos na espermatogênese, avaliamos o efeito em nível membranar da 1,25D3 sobre o metabolismo do Ca+2 em testículo inteiro e célula de Sertoli de ratos imaturos. Foi demonstrado que em após 60 minutos de pré-incubação com o hormônio, não hove variação da captação basal de 45Ca+2 nos tempos de incubação de 30, 60, 150, 300 e 600 segundos. No tempo de incubação de 60 segundos, foi verificado que a 1,25D3 tem a capacidade de aumentar a captação de 45Ca+2 do meio extracelular em diferentes doses em ambos modelos experimentais, sendo este evento independente da ação genômica. Em testículos, observou-se que doses entre 10-15M e 10-9M foram eficazes em aumentar a captação de 45Ca+2, sendo o maior efeito evidenciado da dose de 10-10M (106%). Utilizando esta dose, foi demonstrado que os canais de CCDV do tipo L e T são as principais vias de entrada do íon nas células testiculares, e que há necessidade da manutenção das correntes de K+ e Cl- para que ocorra este evento. Em células de Sertoli também não foi verificada a variação da captação basal de 45Ca+2. Neste sistema, foi verificado que no tempo de 60 segundos de incubação, o hormônio foi capaz de elevar a captação de 45Ca+2 entre as doses de 10-12M e 10-8 M, onde a dose de 10-12 M aumentou em torno de140% a capatação do íon. Já a dose de 10-10 M elevou em 89% o influxo do íon. Desta forma, utilizando a dose de 10-10 M, verificamos que as células de Sertoli comportam- se assim como os testículos: há necessitadade da ativação dos CCDV-L e T para a entrada do Ca+2 assim como das correntes de K+ e Cl-. Também foi verificado que em células de Sertoli há necessidade da ativação das proteínas PKC e p38MAPK para a capatação de Ca+2 estimulada pela 1,25D3. Alé, disso, as proteínas PI3K e ERK1/2 também estão em parte envolvidas neste processo. Por fim, avaliamos que a integridade dos microtúbulos e a atividade dos canais ClC3 faz-se necessária para que ocorra a entrada do íon nas células de Sertoli, sendo esta elevação do íon necessária para que ocorra o processo de secreção celular já demosntrada anteriormente pela 1,25D3.
Silva, Neto Gilson da. "Estudo de Mat?rias-Primas do Rio Grande do Norte para Uso em Revestimento Poroso: Influ?ncia do teor de dolomita e temperatura de calcina??o nas propriedades f?sico-mec?nicas." Universidade Federal do Rio Grande do Norte, 2007. http://repositorio.ufrn.br:8080/jspui/handle/123456789/12875.
Full textThe state of Rio Grande do Norte presents a great potentiality for the production of ceramic tiles because of having natural raw material in quantity and quality making its economical exploration possible, beyond the great energetic differential of the state, the natural g?s. This works aims to study the influence of the dolomite and granulometry concentration and calcinations temperature in the obtaining of formulations for porous coverings which have to be coherent to the project,s specifications. The experiments have involved the physical-chemical and mineralogical characterizations of raw materials and mechanical tests in the dry and burnt proof bodies preceding a mixture experiment planning with the use of the response surface methodology, in order to get the best raw materials combinations to produce a ceramic mass with specific properties. The twelve ceramic masses studied in this work were prepared by the via dry process, characterized, shaped by uniaxial pressing and sinterized in the temperatures of 940?C, 1000?C, 1060?C, 1120?C and 1180?C, using a fast burning cycle. The crystalline phases formed during the sintering in the temperatures in study have revealed the presence of anorthite and diopside beyond quartz with a remaining phase. These phases were the main responsible ones by the physical- mechanical properties of the sinterized proof bodies. The proof bodies after the sintering stage have presented water absorption higher than 10% and a good dimensional stability in all studied temperatures. However, the flexural breaking strength results in the temperatures of 940?C, 1000?C and 1060?C, under the temperature zone of the vitrification of ceramic whiteware do not reach the flexural breaking strength specific for the porous wall tile (15 MPa), but in the temperature of 1120?C next to the vitrification temperature zone, some whiteware ceramic (formulations) has reached the specified value for the porous wall tile. The results of this work have showed that the studied raw materials have great importance for used in the production of porous wall tiles (BIII)
Rio Grande do Norte apresenta uma grande potencialidade para produ??o de revestimento cer?mico, haja vista, possuir mat?rias-primas naturais em quantidade e qualidade possibilitando sua explora??o econ?mica, al?m do grande diferencial energ?tico do Estado, que ? o g?s natural. Este trabalho objetiva estudar a influ?ncia da concentra??o de dolomita, sua granulometria e temperatura de sinteriza??o na obten??o de formula??es para revestimento poroso que atendam as especif?ca??es do projeto. Os experimentos envolveram a caracteriza??o f?sico qu?mico e mineral?gica das mat?rias-primas, e ensaios mec?nicos nos corpos de prova secos e queimados, precedendo-se de um planejamento de experimento de mistura, com o uso da metodologia de superf?cie de resposta, a fim de se obter as melhores combina?oes das mat?rias-primas para produzir massa cer?mica com propriedades especif?cas. As doze massas cer?micas estudadas foram preparadas pelo processo via seca, caracterizadas, conformadas por presagem uniaxial e sinterizadas nas temperaturas de 940?C, 1000?C, 1060?C, 1120?C, e 1180?C, utilizando um ciclo de queima r?pido. As fases cristalina formadas durante a sinteriza??o nas temperaturas em estudo, revelaram a presen?a de anortita e diopsita, al?m de quartzo com fase remanescente. Estas fases foram as principais respons?veis pelas propriedades f?sico-mec?nicas dos corpos de provas sinterizados. As fases cristalina formadas durante a sinteriza??o nas temperaturas em estudo, revelaram a presen?a de anortita e diopsita, al?m de quartzo com fase remanescente. Estas fases foram as principais respons?veis pelas propriedades f?sico-mec?nicas dos corpos de provas sinterizados. Os corpos de prova ap?s sinteriza??o apresentaram absor??o de ?gua superior a 10%, e uma boa estabilidade dimensional em todas as temperaturas estudadas, entretanto, os resultados da tens?o de ruptura ? flex?o nas temperaturas ( 940?C, 1000?C,e1060?C) abaixo da faixa de temperatura de gresifica?ao das massas cer?micas, n?o atigiram o valor de TRF especificado para revestimento poroso(15 MPa), por?m, na temperatura de 1120?C pr?xima da faixa da temperatura de gresifica??o, algumas massas cer?micas (formula??es) j? atingiram o valor especificado para revestimento poroso. Os resultados desse trabalho mostraram que, as mat?rias primas estudadas possuem grande potencial para serem utilizadas na fabrica??o de revestimento poroso (BIII)
Kuo-Jung, Lo, and 羅國榮. "Store depletion-induced calcium influx in." Thesis, 1998. http://ndltd.ncl.edu.tw/handle/35075435790662562236.
Full text國防醫學院
生物化學研究所
86
Using the fluorescent Ca2+ indicator fura-2, we found that, in cultured rat cerebellar astrocytes, a sustained increase of cytosolic Ca2+ concentration ([Ca2+]i) was induced by ATP or angiotensin II (AGII) following a transient increase of [Ca2+]i in the presence of extracellular Ca2+, while it was not seen in the absence of extracellular Ca2+, [Ca2+]i being declined to the basal level. Similarly, a slow and sustained [Ca2+]i increase, or a slow but not sustained [Ca2+]i increase was observed after intracellular Ca2+ pump was inhibited by thapsigargin (TG) in the presence or absence of extracellular Ca2+, respectively. These results suggest the existence of store-operated Ca2+ channel (SOC) in rat cerebellar astrocytes. This is further evidenced by the fact that 12 min after TG-induced stores depletion had occurred, [Ca2+]i remained in the sustained phase upon removal of TG, while it rapidly declined to the basal level after extracellular Ca2+ was removed. These results also indicate that activation of SOC was not dependent on its direct interaction with TG. Similar results were observed after Ca2+ stores were depleted by cyclopiazonic acid (CPA). This TG-induced, extracellular Ca2+-sensitive [Ca2+]i increase was highly dependent on the time period of TG exposure. Thus, Ca2+ influx could be detected as early as 2 min after TG exposure, while it was not fully activated until 12 min further suggesting that SOC was not activated until significant degree of Ca2+ stores were depleted. SOC could be detected earlier and TG-induced [Ca2+]i increase was greater in cells bathed in Na+ free buffer than those bathed in normal Na+ containing buffer indicating that SOC is a nonselective cation channel and Ca2+ influx was enhanced in the absence of Na+ since the competetion of Ca2+ with Na+ was no longer existing. However, using the fluorescent Na+ indicator, SBFI, [Na+]i increase was not detected after cells had been exposed to TG. Furthermore, the TG-activated cation channel was not permeable to Sr2+ or Ba2+, either. Using whole cell voltage clamp technique and step-pulse recordings from a holding potential of -70 mV to a test potential of -100 mV, a 60 - 100 pA inward current was activated by TG-induced Ca2+ stores depletion. The current-voltage curve of TG-activated current showed a linear relationship with the reversal poitential ranged from -5 to 0 mV in the presence of high internal Cs+ and external Na+. The amplitude of TG-activated current remained the same in Na+-free external solution, while it was larger at higher concentrations of external Ca2+. Taken together, our results suggest that SOC in rat cerebellar astrocytes is preferentially permeable to Ca2+. Similar SOC activity was seen in human embryonic kidney 293 cells (HEK293 cells) which is nonexcitable cells, while excitable cells, including rat cerebellar granule cells and procine aortic smooth muscle cells, did not display SOC. We next examined whether the activity of SOC was regulated by phosporylation by measuring the fura-2 fluorescence quench induced by Mn2+ influx via SOC. Addition of Mn2+ to the bathing buffer caused a slight but significant fluorescence quench and further fluorescence quench was induced 2 min after coadministration of Mn2+ and TG simultaneously. Pretreatment of cells with staurosporine, a Ser/Thr protein kinase inhibitor, enhanced the TG-induced fluorescence quench, while genistein, a tyrosine kinase inhibitor, had no effect on it indicating that dephosphorylation of Ser/Thr residues of proteins enhanced the SOC activity. This is further supported by the fact that promotion phosphorylation by phorbol 12-myristate 13-acetate or okadaic acid abolished TG-induced fluorescence quench. In conclusion, in rat cerebellar astrocytes, SOC is activated by depletion of Ca2+ store and its activity is regulated by phosporylation and dephosphorylation.
"Regulation of TRPC3-mediated Ca2+ influx and flow-induced Ca2+ influx." Thesis, 2006. http://library.cuhk.edu.hk/record=b6074196.
Full text"June 2006."
2+ in the title is superscript.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2006.
Includes bibliographical references (p. 131-150).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
E-Fong, Kao, and 高一峰. "Capacitative Calcium Influx in C6 Glioma Cells." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/01870397043096944408.
Full textYoo, Andrew. "Role of calcium influx in process extension of oligodendrocytes." Thesis, 1998. http://hdl.handle.net/2429/8375.
Full textShan, Ke, and 單可. "Mitochondrial ROS release triggered by calcium influx activates autophagy." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/uuc72e.
Full text國立臺灣大學
生化科學研究所
107
Autophagy, a self-digestive mechanism, is vital for cellular functions and health. During starvation, autophagosomes form mainly at the endoplasmic reticulum (ER)-mitochondria contact sites. However, how cells timely induce autophagy at these sites are unclear. We aimed to elucidate the roles of ER and mitochondrial calcium-reactive oxygen species (ROS) signaling in autophagosome formation at these sites. We used confocal live-cell imaging to monitor autophagy activity in the absence or presence of calcium and ROS inhibitors. We found that autophagy activity burst at 10-15 minutes of starvation. The autophagy burst was preceded by mitochondrial calcium influx, mitochondrial ROS production and release; the inhibition of these phenomena abolished autophagy burst. Previously, our lab saw Atg4, an LC3 de-conjugating enzyme, was inhibited in the same time frame. Additionally, autophagy induced by plasma membrane damage was also controlled by mitochondrial ROS release. Taken together, we propose that during short-term starvation, mitochondrial calcium influx induces ROS production and release. ROS then facilitate autophagy by local Atg4 inhibition. This calcium-ROS signaling pathway may represent a general autophagy regulatory mechanism in starvation, plasma membrane damage and other autophagy stimuli that involve calcium perturbations.
Hickey, Charlene. "Calcium influx and release controls neuroendocrine cell secretion and excitability." Thesis, 2009. http://hdl.handle.net/1974/5166.
Full textThesis (Master, Physiology) -- Queen's University, 2009-09-18 19:30:32.957
"Role of agonist- and flow-induced caclium influx in vascular tone control." 2004. http://library.cuhk.edu.hk/record=b6073718.
Full text"December 2004."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2004.
Includes bibliographical references (p. 179-204)
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.