Dissertations / Theses on the topic 'Influx'
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Davenport, R. "Mechanisms of toxic sodium influx in wheat." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598300.
Full textChuula, Luyando. "Mass influx refugee situations: law and practice." Master's thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/24995.
Full textLawson, Roderick A. "Neutrophils in bacterial pneumonia : influx and clearance." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/28407.
Full textAlgharaibeh, Mamoun. "Effect of influx of Eolian materials on soil formation." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/289093.
Full textPosel, Deborah. "Influx control and the construction of Apartheid, 1948-1961." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327979.
Full textJames, Nicholas Paul. "The role of auxin influx carrier in plant development." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275958.
Full textElton, Jessica. "Contending with privileged influx lessons from Boston's Mission Hill /." Diss., Connect to the thesis, 2004. http://thesis.haverford.edu/54/01/2004EltonJ.pdf.
Full textYang, 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 textBradley, J. E. "The Ca²⺠influx pathways of isolated urethra cells." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431451.
Full textAdelman, Sammy. "Influx control and the crisis in South Africa : 1979-1986." Thesis, University of Warwick, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328631.
Full textVibeke, Eggli Ann. "Mass refugee influx and the limits of public international law /." The Hague : M. Nijhoff publ, 2002. http://catalogue.bnf.fr/ark:/12148/cb39269232j.
Full textVelmurugan, Naveen. "Distributed dynamics of influx during MPD operations : modelling and estimation." Thesis, Université Paris sciences et lettres, 2020. http://www.theses.fr/2020UPSLM018.
Full textWhile drilling an oil well, unwanted influx of fluids from the reservoir may occur. This manuscript studies the dynamics of the resulting fluid flow in the wellbore and the reservoir, during managed pressure drilling (MPD) operations. We study the phenomena using first-principle approach that leads to a modified two phase flow model called the drift-flux model (DFM). The model takes the form of a hyperbolic system of transport equations, whereas the reservoir pressure dynamics is given by a parabolic diffusion equation. We propose appropriate numerical schemes for both. Then, we propose different observer designs to estimate the influx from the reservoir into the wellbore. The observers for the coupled wellbore-reservoir system take different forms, as we combine the distributed and the reduced order models for each system. We propose to use the choke pressure as a measurement that is typically available on a MPD operational site, i.e. topside sensing. However, availability of the bottom hole pressure modifies the observer design, in ways we detail. We show convergence of the observers to the true values of reservoir pore pressure and influx, in each case
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.
Full textKwan, Wai San. "SLCO influx transporters and variability in the disposition of Antiretroviral drugs." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526797.
Full text龔振輝 and Chun-fai Frederick Kung. "Influx of Western media to Asia and response of Asian governments." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31267191.
Full textTsai, Ke-Li. "Mechanisms of acid influx in the carotid body type I cell." Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:683bdddf-e8a0-4abb-8d68-35b9188057e0.
Full textKung, Chun-fai Frederick. "Influx of Western media to Asia and response of Asian governments /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1796314X.
Full textWang, 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
Shen, Ying. "Regulation of Ca2+ influx by cell shape in Swiss 3T3 cells." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548807.
Full textPineda, Christopher Julius. "Finding a Home: Latino Residential Influx into Progress Village, 1990-2010." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/6014.
Full textPaiva, Almino Afonso de Oliveira. "Avalia??o de uma fra??o polissacaridica da alga Lobophora variegata (Lamouroux) em modelo de artrite induzida em ratos por Zymosan." Universidade Federal do Rio Grande do Norte, 2010. http://repositorio.ufrn.br:8080/jspui/handle/123456789/18532.
Full textFucans seaweed Lobophora variegata estructures are known for their chemical and biological properties. In this study, we analyzed, the action of fucans L. variegata and the fractions purified with acetone in Zymosan-induced arthritis. After differential fractionation with acetone, six fractions were obtained and named F0.3, F0.5, F0.8, F1, F1.5 and F2. The results showed that the fraction F1 showed high yield (51.9%) and was chosen for studies of antioxidant activity and induced arthritis. Nuclear magnetic resonance (NMR) of 13C showed signals at 103.3 and 15.78 ppm that are assigned to links ?13 galactose and of the C6 methyl fucose, respectively. The infrared (IR) showed absorbance at 1238 and 850 cm-1 which are attributed to sulfate. The fraction F1 showed antioxidant activities in vitro. For analysis of inflammatory parameters chosen the polysaccharide was administered in different doses (25, 50 and 75 mg / kg ip, per body weight) and diclofenac sodium (5 mg / kg ip) and L-NAME (25 mg / kg ip) in groups of animals (n = 6). After 6 h, were analyzed for cellular influx and levels of nitrite. In experiment five days, were made analysis of swelling and serum TNF-?. Histopathological analysis were performed for confirmation of results. The fraction F1 (25, 50 and 75 mg / kg ip) reduced the cellular influx (52.1 to 96.7%) and nitric oxide levels (27.2 - 39%) compared to control group. The reduction of edema (63.4 - 100%) and serum TNF-? (p <0.001) were observed when the polysaccharide F1 administered at a dose (50 mg / kg) These results suggest that these heterofucanas of Lobophora variegata have besides the activity antioxidant and potential anti-inflammatory activity in arthritis induced by zymosan
Fucanas da alga Lobophora variegata s?o conhecidas por suas estruturas qu?micas e propriedades biol?gicas. Nesse estudo, analisou-se a a??o de fucanas de L. variegata e suas fra??es purificadas com acetona na artrite induzida por Zymosan. Ap?s fracionamento diferencial com acetona, 6 fra??es foram obtidas e nomeados F0.3, F0.5, F0.8, F1, F1.5 e F2. Os resultados mostraram que a fra??o F1 apresentou alto rendimento (51,9%) e foi escolhida para estudos da atividade antioxidante e artrite induzida. A resson?ncia magn?tica nuclear (RMN) de 13C mostrou sinais a 103,3 e 15,78 ppm que s?o atribu?dos ?s liga??es ?1 3 da galactose e metil do C6 da fucose, respectivamente. O infravermelho (IV) mostrou absorb?ncia a 1238 e 850 cm-1 que s?o atribu?das ao sulfato. A fra??o F1 apresentou atividades antioxidantes in vitro. Para an?lise de par?metros inflamat?rios a fra??o polissacar?dica escolhida foi administrada em diferentes doses (25, 50 e 75 mg/kg i.p, por peso corporal), assim como diclofenaco de s?dio (5 mg/kg i.p.) e L-NAME (25 mg/kg i.p.) em grupos de animais (n=6). Depois de 6 h, foram realizadas an?lises de influxo celular e n?veis de nitrito. Em experimento de cinco dias, foram efetuadas analises de edema e TNF-? s?rico. An?lises histopatol?gicas foram realizadas para confirma??o de resultados. A fra??o F1 (25, 50 e 75 mg/kg i.p.) reduziu o influxo celular (52,1 ? 96,7%) e os n?veis ?xido n?trico (27,2 ? 39%) em rela??o ao grupo controle. A redu??o do edema (63,4 - 100%) e TNF-? s?rico (p < 0,001) foram observadas quando administrado o polissacar?deo F1 na dosagem (50 mg/kg) Esses resultados sugerem que essas heterofucanas de Lobophora variegata possuem al?m da atividade antioxidante, potencial atividade anti-inflamat?ria na artrite induzida por zymosan
Tomoda, Takako School of Sociology UNSW. "The loanword (Gairaigo) influx into the Japanese language: contemporary perceptions and responses." Awarded by:University of New South Wales. School of Sociology, 2005. http://handle.unsw.edu.au/1959.4/22997.
Full textBurwell, Isaac Ronald. "The responses of diatoms to the influx of tephras into lacustrine environments." Thesis, University of Canterbury. Geology, 2003. http://hdl.handle.net/10092/6775.
Full textMartucci, Tony. "Characterisation of a family of putative auxin influx carrier genes in strawberry." Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272805.
Full textYemm, Anthony Alan. "Molecular characterisation of the putative auxin influx carrier, AUX1 from Arabidopsis thaliana." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250523.
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 textQuément, Fanny. "« Mutable as sound » : mutations des influx sonores dans l’œuvre de Seamus Heaney." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCA113.
Full textThis thesis questions the presence and metamorphoses of sound in the works of Seamus Heaney, ultimately bringing the experience of the printed text and that of audio recordings into comparison. Based on a study of the author’s essays, poems and commercialised recordings, it retraces the trajectory of sound influxes from the perception of soundwaves in the environment to the emission of the voice, via their recreation in writing. The phrase “sound influx” is meant to revive the aquatic metaphor in the catachretic compound “soundwave.” It also invites to detect undercurrents by ear and study them from the perspective of the listener, taking into account their reception and absoption as much as their broadcasting.In order to show that each poem is a sound event of its own kind, it analyses the process through which the sonic environment is turned into a poetic soundscape which then becomes part of other environments when orally performed. Borrowing concepts from Sound Studies, it highlights the dynamic but elusive nature of sound, identifies and questions the conductive properties of a writing that also makes room for silence, and reflects, along with Heaney, on listening as a notion.The close-readings developed here are also close-listenings that take into account the phonetic dimension of texts, the study of the poetic voice being completed by an analysis of the poet’s physical voice. Considering the graphotext, the phonotext and the audiotext as three equally significant incarnations of one poem, aims at bringing a nuanced perspective on Heaney’s prosody as it is too often reduced to formal – if not formalist – versification
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.
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
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.
Full textGarrett, Jasmine Jay Tamara, and University of Lethbridge Faculty of Arts and Science. "Autobahn : a gene that has a role in auxin influx in Arabidopsis leaves." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2005, 2005. http://hdl.handle.net/10133/258.
Full textx, 69 leaves : ill. ; 28 cm.
Cryer, Nicholas Colin. "The cloning and characteristion of anion influx and efflux transports from higher plants." Thesis, Royal Holloway, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269798.
Full textOliver-Evans, Ceridwen. "The implications of the abolition of influx control legislation in the Western Cape." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/22412.
Full textInflux control legislation was formally abolished in South Africa in 1986. This thesis investigates the social processes set in motion with its abolition in the spheres of employment and urbanisation and argues that the way in which influx control has been defined is central to any analysis concerned with its abolition. In this regard, influx control has been viewed in two senses: a narrow one in which it has been equated with formal influx control legislation, 'the pass laws'; and, secondly and more broadly, through definitions which embrace all methods of control over African urbanisation and associated labour mobility. This thesis argues that, in the macro domain, while influx control in its narrow sense has been abolished, it has been replaced with far more complex and subtle forms of control. These ostensibly racially neutral measures, an 'orderly urbanisation' policy and a wide variety of laws existing on South African statute books continue to circumscribe African rights. The research focuses on a specific region, the Western Cape, an area where influx control has been more harshly implemented than elsewhere through the implementation of the Coloured Labour Preference Policy. This thesis investigates on a micro-level, via the medium of a company compound, how people at both an individual and institutional level have interpreted the legislative changes and acted upon them. The particular range of actors include government officials, employers and employer organisations, union representatives, and migrant workers and their families living in the company compound. The evidence I present was obtained primarily through interviews and ethnographic field-research conducted in 1988. A particular concern of the thesis has been to examine the disjunction between policy and practice as pursued by government officials and the effects and implications arising from this among the actors mentioned above. The main themes which have emerged from this research are those of confusion and a lack of knowledge among many of the informants. It was found that high-ranking government officials lack consensus on vital issues of citizenship and employment which affect the lives of thousands of Transkeian and Ciskeian citizens. Employers, confused by the confusion in government departments, and confronted by a new situation and new sets of rules have either ignored these or succumbed to government policy. Equally, unions have been slow to respond or systematically adopt a policy on the 1986 legislative changes. Finally, it was found that migrant workers and their families are availing themselves of opportunities presented by the abolition of influx control legislation in terms of freedom of movement, although as I argue, this takes the form of a complex range of fluid and dynamic movement patterns between the compound, the rural areas and urban townships. This complexity, as the thesis demonstrates, is reflected both in the attitudes and in the practical daily living arrangements of the workers as they respond to and interpret the macro-level forces which affect them.
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.
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
Iwakura, Toshio. "Sustained enhancement of Ca[2+] influx by glibenclamide induces apoptosis in RINm5F cells." Kyoto University, 2001. http://hdl.handle.net/2433/150204.
Full textSawamura, Seishirou. "Elucidation of signal regulation by interacting molecules and proteins of Ca2+ influx channels." 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/215579.
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
Parry, Geraint. "Investigating the mechanisms of auxin transport." Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391391.
Full textKortekaas, 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 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 textLundblad, Katarina. "Studies on Tropical Palaeo-variation in Climate and Cosmic Ray Influx : Geochemical data from stalagmites collected in Tanzania and northern South Africa." Doctoral thesis, Stockholm : Department of Physical Geography and Quaternary Geology, Stockholm university, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-982.
Full textReynders, Nadia. "Interface : altering architecture : transforming existing mono-functional buildings in the Pretoria CBD to adapt to changing social spatial conditions. The notion of ‘altering architecture’ aims to manipulate existing boundaries into INTERFACES to affect interior spaces and building skins as well extend into the urban context." Diss., University of Pretoria, 2010. http://hdl.handle.net/2263/30070.
Full textDissertation (MInt(Prof))--University of Pretoria, 2010.
Architecture
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Segato, Tommaso. "Time-series Database: progettazione e sviluppo di una libreria di supporto al tool Influx 2.0." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amslaurea.unibo.it/21555/.
Full textTolhurst, Gwen Rachel. "A study of cationic influx channels in the murine megakaryocyte : a model for platelet signalling." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614220.
Full textGunnarsson, Urban. "Vegetation changes on Swedish mires : Effects of raised temperature and increased nitrogen and sulphur influx." Doctoral thesis, Uppsala : Acta Universitatis Uppsaliensis, 2000. http://catalogue.bnf.fr/ark:/12148/cb40007342x.
Full textSilva, Petterson Costa ConceiÃÃo. "Role of glutamine in the regulation of nitrate influx in cowpea roots exposed to salinity." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16067.
Full textThere are many studies showing that the salinity may directly affect the nitrate uptake, from their osmotic effect, nature of the salt and its ionic composition. However, little is known about the mechanisms related to the salt ability to inhibit the nitrate acquisition indirectly. This study was carried with aim to induce inhibition of NO3- influx in cowpea roots of indirect form triggered by a negative feedback mechanism, caused by the increase in the pool of free amino acids in the tissue, induced by salt stress.For this, were done three isolated studies and continuous.The exogenous glutamine application promoted an increase in the free amino acids content.The presence of glutamine decreased significantly the nitrate acquisition.The free ammonium can also be listed as a key-compound in the role of nitrate influx regulation, since use of the MSX (Methionine sulfoximine) promoted the increase of NH4+ content and also reduced nitrate influx, but, in a lesser degree when compared to treatment with AZA (Azaserine). Salt stress caused a reduction in NO3- influx by decrease in the growth of plants induced by salt. The data indicated which this reduction in the influx is triggered by increase of amino acids content, mainly the glutamine, that is main likely compound to act as signal in the N-feedback regulation.
Existem muitos estudos mostrando que a salinidade pode afetar a absorÃÃo de nitrato de forma direta, a partir do seu efeito osmÃtico, da natureza do sal e de sua composiÃÃo iÃnica. Entretanto, pouco se sabe sobre os mecanismos relacionados com a capacidade do sal em inibir a aquisiÃÃo de nitrato de forma indireta. O presente estudo teve como objetivo induzir a inibiÃÃo do influxo de NO3- em raÃzes de feijÃo-caupà de forma indireta desencadeada por um mecanismo de feedback negativo, provocado pelo aumento no pool de aminoÃcidos livres no tecido, induzido por estresse salino. Para isso, foram realizados trÃs estudos isolados e contÃnuos. A aplicaÃÃo de glutamina exÃgena promoveu um aumento no conteÃdo de aminoÃcidos livres. A presenÃa de glutamina reduziu significativamente a aquisiÃÃo de nitrato. O amÃnio livre tambÃm pode ser listado como um composto-chave no papel da regulaÃÃo do influxo de nitrato, pois a utilizaÃÃo do MSO (Metionina sulfoximina) promoveu o aumento do conteÃdo de NH4+ e tambÃm reduziu o influxo de nitrato, porÃm em menor grau quando comparado ao o tratamento com AZA (Azaserina). O estresse salino causou uma reduÃÃo no influxo de NO3-, pela diminuiÃÃo no crescimento das plantas induzida pelo sal. Adicionalmente, estes dados indicaram que esta reduÃÃo no influxo està ligada ao aumento do teor de aminoÃcidos, principalmente a glutamina, que à o principal componente para atuar como sinal na regulaÃÃo por N-feedback.
Laloi, Maryse. "Caractérisation de transporteurs (efflux du saccharose, influx de peptides) impliqués dans la distribution des assimilats." Poitiers, 1995. http://www.theses.fr/1995POIT2283.
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
Hawley, Greer. "Diatoms : indicators of tidal influx in a hydraulically regulated estuary, Zandvlei, in the southern Cape." Bachelor's thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/26027.
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 textMathenge, Christine W. "Effects of migrant influx, occupance and land acquisition on changing land tenure patterns in southwest Uganda." [Bloomington, Ind.] : Indiana University, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3332470.
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