Готові списки джерел за темами / Phosphate gla

Добірка наукової літератури з теми "Phosphate gla"

Автор: Grafiati
Опубліковано: 14 березня 2023

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Статті в журналах з теми "Phosphate gla"

1

Davis-Harrison, Rebecca L., Narjes Tavoosi, Mary Clay, John M. Boettcher, Chad M. Rienstra, and James H. Morrissey. "Structural Insights Into How Clotting Proteins with GLA Domains Bind to Membrane Surfaces." Blood 116, no. 21 (November 19, 2010): 1141. http://dx.doi.org/10.1182/blood.v116.21.1141.1141.

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Abstract Abstract 1141 Most steps in the blood coagulation cascade obligatorily take place on membrane surfaces and are dependent on the exposure of phosphatidylserine (PS). Many coagulation proteins bind to PS-containing membrane bilayers in a calcium-dependent manner via gamma-carboxyglutamate-rich (GLA) domains. In spite of their importance, a clear picture of how GLA domains bind to the membrane interface has yet to emerge. A further intriguing aspect of the membrane's role in blood coagulation is that certain phospholipids, most notably phosphatidylethanolamine (PE), strongly synergize with PS to promote clotting reactions. The mechanisms of this synergy, and of PE's contribution to GLA domain binding, are poorly understood – although a number of hypotheses have been put forward. We now propose a new hypothesis to explain GLA domain binding to membranes, which we term the ABC (Anything But Choline) hypothesis; it invokes two main types of protein-phospholipid interactions: a single L-serine-specific binding site in each GLA domain; and multiple “phosphate-specific” interactions in which the phosphate groups of non-phosphatidylcholine phospholipids form coordination complexes with the tightly bound calcium ions in GLA domains. We have utilized liposomes and nanoscale phospholipid bilayers (Nanodiscs) in studies employing a series of techniques including solid-state NMR (SSNMR) and surface plasmon resonance (SPR) to address the mechanism of GLA domain-membrane interactions. We provide direct evidence in favor of the ABC hypothesis for GLA domain binding to membrane surfaces. Using SSNMR, we demonstrate that two distinct PS headgroup conformations are induced by binding of calcium ions, and that a third, novel PS headgroup conformation is induced when the prothrombin GLA domain engages the membrane. SPR studies have allowed for the determination of thermodynamic profiles of GLA domains interacting with phospholipid bilayers containing PS and/or PE, providing further insights to the mechanisms of GLA domain-membrane interactions. Disclosures: No relevant conflicts of interest to declare.
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2

Rabkin, Simon W. "Endothelin but Not Angiotensin II May Mediate Hypertension-Induced Coronary Vascular Calcification in Chronic Kidney Disease." International Journal of Nephrology 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/516237.

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To understand the relationship between putative neurohormonal factors operative in hypertension and coronary artery calcification (CAC), the relevant cellular actions of angiotensin (Ang II) and endothelin-1 (ET-1) are reviewed. There is compelling evidence to implicate ET-1 in CAC. ET-1 increases phosphate transport with a 42 to 73% increase inVmax. Increased cellular phosphate may induce CAC through increased Ca x phosphate product, transformation of vascular smooth muscle cells into a bone-producing phenotype or cell apoptosis that releases procalcific substances. ET-1 is increased in several models of vascular calcification. ET-1 inhibits inhibitors of calcification, matrix Gla and osteoprotegerin, while enhancing pro-calcific factors such as BMP-2 and osteopontin. In contrast, Ang II inhibits phosphate transport decreasingVmaxby 38% and increases matrix Gla. Ang II also stimulates bone resorption. Vascular calcification is reduced by ET-1 A receptor antagonists and to a greater extent than angiotensin receptor blockade although both agents reduce blood pressure.
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3

Frustaci, Andrea, Behzad Najafian, Giuseppe Donato, Romina Verardo, Cristina Chimenti, Luigi Sansone, Manuel Belli, Enza Vernucci, and Matteo Antonio Russo. "Divergent Impact of Enzyme Replacement Therapy on Human Cardiomyocytes and Enterocytes Affected by Fabry Disease: Correlation with Mannose-6-phosphate Receptor Expression." Journal of Clinical Medicine 11, no. 5 (February 28, 2022): 1344. http://dx.doi.org/10.3390/jcm11051344.

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Background: The impact of enzyme replacement therapy (ERT) on cardiomyocytes and intestinal cells, affected by Fabry disease (FD), is still unclear. Methods: Six patients with FD, including five family members with GLA mutation c.666delC and one with GLA mutation c.658C > T, manifesting cardiomyopathy and intestinal symptoms (abdominal pain, diarrhea and malabsorption) were included in the study. Clinical outcome, cardiac magnetic resonance (CMR), endomyocardial and gastro-intestinal biopsies were evaluated before and after 2 years of treatment with agalsidase-α (0.2 mg/kg every other week). Immunohistochemistry and Western blot assessments of mannose-6-phosphate receptors (IGF-II-R) on intestinal and myocardial frozen tissue were obtained at diagnosis and after 2 years of ERT. Results: After ERT left ventricular maximal wall thickness, ranging from pre (<10.5 mm) to mild (<15 mm) and moderate hypertrophy (16 mm), was not associated with significant changes at CMR. Degree of dyspnea, mean cardiomyocyte diameter and % vacuolated areas of cardiomyocytes, representing intracellular GL3, remained unmodified. In contrast, intestinal symptoms improved with disappearance of diarrhea, recovery of anemia and weight gain, correlating with near complete clearance of the enterocytes from GL3 inclusions. IGF-II-R expression was remarkably higher even at histochemistry in intestinal tissue compared with myocardium (p < 0.001) either at baseline and after ERT, thus justifying intestinal recovery. Conclusions: Human cells affected by FD may respond differently to ERT: while cardiomyocytes retain their GL3 content after 2 years of treatment, gastro-intestinal cells show GL3 removal with recovery of function. This divergent response may be related to differences in cellular turnover, as well as tissue IGF-II-R expression.
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4

Madjid, Armeida Dwi Ridhowati, Merpiseldin Nitsae, and Akhmad Sabarudin. "Perbandingan Butiran Kitosan dengan Pengikat Silang Epiklorohidrin (ECH) dan Glutaraldehid (GLA): Karakterisasi dan Kemampuan Adsorpsi Timbal (Pb)." ALCHEMY 6, no. 1 (March 30, 2018): 29. http://dx.doi.org/10.18860/al.v6i1.6790.

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<table width="661" border="1" cellspacing="0" cellpadding="0"><tbody><tr><td valign="top" width="408"><p class="BodyAbstract">Chitosan was an abundantly available source but it has a drawback which unstable in acid or base. So, it must be added with a crosslinker. In this article, we would compare the using of 2 crosslinkers, glutaraldehyde (GLA) and epichlorohydrin (ECH). Chitosan was formed as bead using tripolyphosphate (TPP). Chitosan beads crosslinked with GLA became browny beads and chitosan beads crosslinked with ECH became pearly white. IR characterization showed peaks in 1640 and 1540 cm<sup>-1</sup> represent phosphate contained TPP. There is no significant or unique peak differ GLA chitosan bead from ECH chitosan bead. Adsorption capacity of lead (Pb) in ECH chitosan bead was higher than in GLA chitosan bead. Morphology in SEM characterization exhibited a crinkle GLA chitosan bead then ECH chitosan bead.</p><p class="BodyAbstract"> </p><p class="BodyAbstract">Kitosan merupakan polimer alam dengan ketersediaan yang meruah tetapi memiliki kelemahan yaitu kurang stabil dalam asam maupun basa sehingga diperlukan pengikat silang. Dalam artikel ini akan dibandingkan dengan penggunaan 2 agen pengikatsilang yang dapat mengatasi permasalahan tersebut yaitu epiklorohidrin (ECH) dan glutaraldehid (GLA). Untuk pembuatan butiran kitosan digunakan tripolyphosphate (TPP). Setelah menjadi butiran kitosan diikatsilangkan dengan GLA menjadi butiran kitosan yang berwarna kecoklatan dan diikatsilangkan dengan ECH menjadi butiran kitosan bening. Karakterisasi spektrofotometri Infra Merah menunjukkan puncak pada daerah 1640 dan 1540 cm<sup>-1</sup> yang merupakan serapan khas dari tripolyphospate sedangkan tidak nampak perbedaan puncak spektra yang signifikan dari butiran kitosan GLA maupun ECH. Kemampuan adsorpsi butiran logam timbal (Pb) butiran kitosan ECH lebih tinggi jika dibandingkan dengan butiran kitosan GLA. Morfologi butiran kitosan dianalisis menggunakan Scanning Electron Morphology (SEM) dan menunjukkan bahwa morfologi untuk butiran GLA memiliki morfologi yang lebih berkerut jika dibandingkan dengan butiran ECH.</p></td></tr></tbody></table>
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5

Davis-Harrison, Rebecca L., Narjes Tavoosi, Vincent S. Pureza, and James H. Morrissey. "Phospholipid Synergy in Prothrombinase Activity." Blood 118, no. 21 (November 18, 2011): 1175. http://dx.doi.org/10.1182/blood.v118.21.1175.1175.

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Abstract Abstract 1175 Most steps in the blood coagulation cascade obligatorily take place on membrane surfaces and are dependent on the exposure of phosphatidylserine (PS). Previous studies from our lab and others have shown that phosphatidylethanolamine (PE) poorly supports clotting reactions by itself, but strongly synergizes with PS to promote several membrane-dependent steps in the blood clotting cascade, although the mechanism for PE-PS synergy has been unclear. We recently put forward a new mechanistic explanation – which we termed the ABC or Anything But Choline hypothesis – for how PS and PE synergize to enhance factor X (fX) activation by the factor VIIa-tissue factor complex (Tavoosi et al., J. Biol. Chem. 286:23247–53, 2011). The membrane contribution to this reaction is dominated by the affinity of fX for the membrane surface; since fX binds to membranes via its gamma-carboxyglutamate-rich (GLA) domain, the ABC hypothesis therefore focuses on the mechanisms by which GLA domains engage the phospholipid bilayer. We identified two main types of GLA domain-phospholipid interactions: a single phospho-L-serine-specific binding site in each GLA domain; and multiple ”phosphate-specific” interactions in which the phosphate groups of non-phosphatidylcholine phospholipids form coordination complexes with the tightly bound calcium ions in GLA domains. In the current study, we test the ABC hypothesis in the context of the prothrombinase complex – i.e., activation of prothrombin by the membrane-bound complex of fXa and factor Va (fVa). Using a variety of approaches including surface plasmon resonance analyses, we measured the contributions of varying phospholipid compositions to the membrane binding affinities of fXa, fVa and prothrombin, as well as to the enzymatic activity of prothrombinase. Our results suggest that phospholipid synergy in prothrombinase activity differs in certain respects from that observed for the factor VIIa-tissue factor complex. Not only did PS synergize with PE for enhancing the activity of prothrombinase, but phosphatidylglycerol (PG) and phosphatidylacid (PA) also synergized with PE, albeit more weakly than with PS (i.e., significantly higher levels of PG or PA in the presence of PE were required to achieve prothrombinase activities comparable to mixtures of PS and PE). In contrast, PE failed to synergize with either PG or PA to support fX activation by the factor VIIa-tissue factor complex. These differences primarily arise from differential membrane binding of the substrates for these two complexes (fX for factor VIIa-tissue factor and prothrombin for prothrombinase). The data suggest that the phospho-L-serine-specific binding site in the GLA domain of prothrombin may not be as stringent as that of fX, as high levels of PG or PA can substitute for PS in membrane binding of prothrombin but not for fX. This study provides further insights into the membrane's role in regulating blood clotting reactions, specifically the binding interactions between GLA domains and membrane surfaces. Disclosures: No relevant conflicts of interest to declare.
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6

Pisani, Antonio, Bianca Visciano, Roberta Russo, Giusi R. Mozzillo, Caterina Porto, Ilaria De Maggio, Roberta Russo, et al. "A novel GLA mutation in a Fabry family with glucose-6-phosphate dehydrogenase deficiency." Journal of Nephrology 25, no. 4 (2012): 582–85. http://dx.doi.org/10.5301/jn.5000073.

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7

Ciceri, Paola, Francesca Elli, Irene Brenna, Elisa Volpi, Diego Brancaccio, and Mario Cozzolino. "The Calcimimetic Calindol Prevents High Phosphate-Induced Vascular Calcification by Upregulating Matrix GLA Protein." Nephron Experimental Nephrology 122, no. 3-4 (2012): 75–82. http://dx.doi.org/10.1159/000349935.

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8

Bjørklund, Geir, Erik Svanberg, Maryam Dadar, David J. Card, Salvatore Chirumbolo, Dominic J. Harrington, and Jan Aaseth. "The Role of Matrix Gla Protein (MGP) in Vascular Calcification." Current Medicinal Chemistry 27, no. 10 (March 27, 2020): 1647–60. http://dx.doi.org/10.2174/0929867325666180716104159.

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Matrix Gla protein (MGP) is a vitamin K-dependent protein, which is synthesized in bone and many other mesenchymal cells, which is also highly expressed by vascular smooth muscle cells (VSMCs) and chondrocytes. Numerous studies have confirmed that MGP acts as a calcification-inhibitor although the mechanism of action is still not fully understood. The modulation of tissue calcification by MGP is potentially regulated in several ways including direct inhibition of calcium-phosphate precipitation, the formation of matrix vesicles (MVs), the formation of apoptotic bodies (ABs), and trans-differentiation of VSMCs. MGP occurs as four species, i.e. fully carboxylated (cMGP), under-carboxylated, i.e. poorly carboxylated (ucMGP), phosphorylated (pMGP), and non-phosphorylated (desphospho, dpMGP). ELISA methods are currently available that can detect the different species of MGP. The expression of the MGP gene can be regulated via various mechanisms that have the potential to become genomic biomarkers for the prediction of vascular calcification (VC) progression. VC is an established risk factor for cardiovascular disease and is particularly prevalent in those with chronic kidney disease (CKD). The specific action of MGP is not yet clearly understood but could be involved with the functional inhibition of BMP-2 and BMP-4, by blocking calcium crystal deposition and shielding the nidus from calcification.
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9

Lee, Ju-Young, Kwang-Hyeon Liu, Yunhi Cho, and Kun-Pyo Kim. "Enhanced Triacylglycerol Content and Gene Expression for Triacylglycerol Metabolism, Acyl-Ceramide Synthesis, and Corneocyte Lipid Formation in the Epidermis of Borage Oil Fed Guinea Pigs." Nutrients 11, no. 11 (November 18, 2019): 2818. http://dx.doi.org/10.3390/nu11112818.

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Triacylglycerol (TAG) metabolism is related to the acyl-ceramide (Cer) synthesis and corneocyte lipid envelope (CLE) formation involved in maintaining the epidermal barrier. Prompted by the recovery of a disrupted epidermal barrier with dietary borage oil (BO: 40.9% linoleic acid (LNA) and 24.0% γ-linolenic acid (GLA)) in essential fatty acid (EFA) deficiency, lipidomic and transcriptome analyses and subsequent quantitative RT-PCR were performed to determine the effects of borage oil (BO) on TAG content and species, and the gene expression related to overall lipid metabolism. Dietary BO for 2 weeks in EFA-deficient guinea pigs increased the total TAG content, including the TAG species esterified LNA, GLA, and their C20 metabolized fatty acids. Moreover, the expression levels of genes in the monoacylglycerol and glycerol-3-phosphate pathways, two major pathways of TAG synthesis, increased, along with those of TAG lipase, acyl-Cer synthesis, and CLE formation. Dietary BO enhanced TAG content, the gene expression of TAG metabolism, acyl-Cer synthesis, and CLE formation.
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10

Julien, M., D. Magne, M. Masson, M. Rolli-Derkinderen, O. Chassande, C. Cario-Toumaniantz, Y. Cherel, P. Weiss, and J. Guicheux. "Phosphate Stimulates Matrix Gla Protein Expression in Chondrocytes through the Extracellular Signal Regulated Kinase Signaling Pathway." Endocrinology 148, no. 2 (February 1, 2007): 530–37. http://dx.doi.org/10.1210/en.2006-0763.

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Whereas increasing evidence suggests that inorganic phosphate (Pi) may act as a signaling molecule in mineralization-competent cells, its mechanisms of action remain largely unknown. The aims of the present work were to determine whether Pi regulates expression of matrix Gla protein (MGP), a mineralization inhibitor, in growth plate chondrocytes and to identify the involved signaling pathways. Chondrogenic ATDC5 cells and primary growth plate chondrocytes were used. Messenger RNA and protein analyses were performed by quantitative PCR and Western blotting, respectively. The activation and role of MAPKs were, respectively, determined by Western blotting and the use of specific inhibitors. Immunohistological detection of ERK1/2 was performed in rib organ cultures from newborn mice. The results indicate that Pi markedly stimulates expression of MGP in ATDC5 cells and primary growth plate chondrocytes. Investigation of the involved intracellular signaling pathways reveals that Pi activates ERK1/2 in a cell-specific manner, because the stimulation was observed in ATDC5 and primary chondrocytes, MC3T3-E1 osteoblasts, and ST2 stromal cells, but not in L929 fibroblasts or C2C12 myogenic cells. Accordingly, immunohistological detection of ERK1/2 phosphorylation in rib growth plates revealed a marked signal in chondrocytes. Finally, a specific ERK1/2 inhibitor, UO126, blocks Pi-stimulated MGP expression in ATDC5 cells, indicating that ERK1/2 mediates, mainly, the effects of Pi. These data demonstrate, for the first time, that Pi regulates MGP expression in growth plate chondrocytes, thereby suggesting a key role for Pi and ERK1/2 in the regulation of bone formation.
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Більше джерел

Дисертації з теми "Phosphate gla"

1

Tabcheh, Lina. "Tracheal mineralization : cellular and molecular mechanisms in mice." Thesis, Université de Lorraine, 2014. http://www.theses.fr/2014LORR0239/document.

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La trachée est une structure très complexe des voies respiratoires, qui est composée d'anneaux cartilagineux, fait de cartilage hyalin, et de bandes musculaires, formées de cellules musculaires lisses, dont l'architecture confère à la fois rigidité et souplesse au canal trachéen. Contrairement à d'autres cartilages, tels que ceux trouvés dans la plaque de croissance en développement et dans les articulations adultes, ou aux cellules musculaires lisses des vaisseaux, très peu d'informations sont disponibles sur le développement du cartilage et du tissu musculaire trachéal et sur leur capacité à se minéraliser, bien que la calcification de la trachée soit un événement commun dans la population âgée et plus rare dans certaines pathologies. Dans ce contexte, ce travail de thèse a cherché dans le modèle souris à mieux caractériser le cartilage et le tissu musculaire lisse de la trachée et également comprendre les mécanismes moléculaires jusqu'alors inexplorés, régulant la minéralisation de la trachée. Grâce à une nouvelle technique de culture de cellules provenant de la trachée, nous avons démontré que les chondrocytes et les cellules musculaires lisses trachéaux sont tous deux capables de minéraliser lorsqu'ils sont traités avec un haut niveau de Pi, mais via des mécanismes moléculaires différents. En parallèle, une étude in vivo nous a permis de démontrer que la minéralisation de la trachée se produit uniquement dans les anneaux cartilagineux dès 30 jours après la naissance. Des analyses histologiques et moléculaires ont permis d'affiner ces résultats et de proposer un modèle de minéralisation de la trachée via une progression rostro-caudale dépendante de BMP2
The trachea is a very complex structure of the respiratory tract, composed of C-shaped cartilaginous rings, made of hyaline cartilage, and muscular bands, made of smooth muscle cells, conferring rigidity and compliance to the windpipe, respectively. In contrast to other intensely studied cartilages such as the ones found in the developing growth plate and in the adult joints or smooth muscle cells from the vasculature, very little information is available on the development of the tracheal cartilage and smooth muscle tissues and on their innate propensity to mineralize, although calcification of the trachea is a common finding in the elderly population and also a rare manifestation of pathologic conditions. In this context, this PhD work sought to better characterized the poorly studied tracheal cartilage and smooth muscle tissue and understand the molecular mechanisms regulating tracheal mineralization that has been unexplored so far. We tackle these questions in the mouse model. Setting up a novel in-vitro culture of tracheal cells, we demonstrated that tracheal chondrocytes and smooth muscles cells are prone to mineralize when treated with high level of Pi, through different molecular mechanisms. In parallel, we found that in vivo mineralization of the trachea only happens in the cartilaginous rings, as early as 30 days after birth. Histological and molecular evidence suggest that tracheal mineralization occurs through a BMP-dependent rostro-caudal progression
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2

Moon, Jean. "Role of Sphingosine-1-phosphate Receptors in Cytokine and Chemokine Production by Glia." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5535.

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About 1 in 10 newly diagnosed HIV cases in the United States are attributed to injection drug abuse. Opiate abuse exacerbates HIV disease progression in the central nervous system by disrupting glial function and significantly augmenting glial-derived pro-inflammatory mediators. Astroglia and microglia exposed to viral proteins, such as transactivator of transcription (Tat), become activated leading to release of a large number of cytokines and chemokines and a positive loop of neuro-inflammation. Despite effective antiretroviral therapy, persistent inflammation and immune activation affect HIV-infected individuals. A potential alternative target is sphingosine 1-phosphate receptor 1 (S1PR1) which is known to play a role in proliferation and trafficking of immune cells. In addition, the S1P-S1PR1 ligand-receptor axis induces NF-κB activation and pro-inflammatory cytokine production in astrocytes. The drug FTY720 (fingolimod) acts at S1PR1,3,4,5 and its therapeutic effects are thought to result from the drug’s ability to cause receptor internalization and degradation thereby acting as a functional antagonist. The purpose of this study was to assess if S1PR1 modulation by FTY720 regulates cytokine levels in the context of downstream astroglial activation induced by HIV-1 Tat ± morphine. Pretreatment of primary murine glial cultures with FTY720 results in dose-dependent inhibition of Tat±morphine induced increases in IL-6, CCL2, CCL3, and CCL4 levels. A selective 1 antagonist, W146, blocked these increases providing evidence that indeed the significant reduction in cytokine levels was mediated through S1PR1. In comparison SEW 2871, a S1PR1 agonist that leads to receptor recycling upon internalization instead of ubiquitination/degradation, was used to examine if receptor downregulation is responsible for attenuated cytokine release. Glia that were pretreated with SEW 2871 for a shorter duration prior to treatment with Tat or morphine displayed time-dependent reduction in cytokine secretion. Contrastingly, cells pre-exposed to SEW 2871 for a longer period demonstrated elevated protein levels, suggesting the differential fate of receptor after internalization is involved in regulating the inflammatory response.
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3

Assari, Tracy Louise. "Regulation of α₁-adrenoceptor-linked phosphoinositide breakdown in cultured glia : role of protein phosphates." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270236.

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4

Castets, Aurore. "RMN de matériaux paramagnétiques : mesures et modélisation." Phd thesis, Université Sciences et Technologies - Bordeaux I, 2011. http://tel.archives-ouvertes.fr/tel-00664817.

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Ce travail consiste en l'étude par RMN multinoyaux de matériaux paramagnétiques d'électrodes positives pour batteries au Li. La RMN du solide permet une caractérisation de l'environnement local du noyau sondé grâce à l'exploitation des interactions hyperfines dues à la présence d'une certaine densité d'électrons célibataires (déplacement de contact de Fermi) ou de conduction (déplacement de Knight) sur ce noyau (densité transférée selon des mécanismes plus ou moins complexes). Les matériaux étudiés sont des phosphates de métaux de transition tels que Li3M2(PO4)3 (M = Fe, V), la famille des tavorites LiMPO4X (M = Fe, Mn; X = OH, F) ou encore les phases homéotypiques MPO4.H2O (M = Fe, Mn, V). Pour tous ces matériaux, caractérisés par RMN du 7Li, 31P et 1H, l'environnement local de ces noyaux a été étudié afin d'envisager les mécanismes de transfert de spin possibles. Des calculs ab initio ont été effectués pour reproduir les déplacements de RMN, puis établir des cartes de densité de spin afin d'étayer ou compléter la compréhension de ces mécanismes.
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5

Antflick, Jordan. "More than a Metabolite: An Evaluation of the Potential Role of L-serine-O-phosphate as the Endogenous Agonist for the Group III Metabotropic Glutamate Receptors." Thesis, 2012. http://hdl.handle.net/1807/32651.

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The Group III metabotropic glutamate receptors (mGluR) are located presynaptically on axon terminals and act as autoreceptors and heteroreceptors by inhibiting neurotransmitter release. Much has been learned about these receptors through exogenous application of L-serine-O-phosphate (L-SOP), an endogenous amino acid derivative and known activator of the Group III mGluRs. We hypothesized that L-SOP is the endogenous co-agonist at the high affinity Group III mGluR, mGluR4. We found the EC50 of L-SOP at mGluR4 was 0.5 μM, and determined that the concentration of L-SOP in whole brain was approximately 5 μM. An immunocytochemical survey revealed that cells containing the enzymatic machinery necessary for L-SOP synthesis and metabolism were observed in two brain regions known to express mGluR4, namely, cerebellum and hippocampus. In the cerebellum, the L-SOP synthetic and metabolic enzymes were found in Bergmann glia and Purkinje cells, two cells which form a tripartite synapse with parallel fiber axon terminals where the mGluR4 subtype is exclusively expressed at high levels. In the hippocampus, the L-SOP metabolic enzyme was detected in young neurons emanating from the neurogenic subventricular zone. Attempts to raise endogenous levels of L-SOP by crippling the L-SOP metabolizing enzyme (phosphoserine phosphatase), over-expressing the L-SOP synthesizing enzyme (phosphoserine aminotransferase), or through dietary protein restriction, to study the effects on neurotransmission and neurodevelopment in the central nervous system (CNS) were unsuccessful, suggesting that the production of L-SOP remains stable despite manipulation of the synthetic and metabolic enzymes. Finally, the ability of L-SOP to modulate glutamate release from presynaptic terminals was examined in cerebellar synaptosomes. Co-incident activation of presynaptic mGluR4 and presynaptic GABAA receptors facilitated glutamate release, suggesting that simultaneous activation of parallel fibers and Bergmann glia may serve to enhance synaptic transmission. This observation expands the traditional view of Group III mGluRs acting solely as inhibitory autoreceptors. Taken together, these results provide compelling evidence to support the hypothesis that L-SOP is the endogenous agonist at mGluR4, and possibly other Group III mGluRs.
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6

Rossignoli, Giada. "Aromatic amino acids decarboxylase and histidine decarboxylase: deep functional investigations give insights into pathophysiological mechanisms with possible therapeutic implications." Doctoral thesis, 2019. http://hdl.handle.net/11562/995224.

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Aromatic amino acids decarboxylase and histidine decarboxylase (AADC and HDC) are two homologous enzymes responsible for the synthesis of dopamine/serotonin and histamine, respectively, and other minor signalling aromatic amines. All these molecules are main protagonists or regulators of several physiological pathways, which are fundamental both in central nervous system and in peripheral tissues. Alterations of their homeostasis, indeed, as well as of AADC and HDC functioning or expression, cause and/or participate in the development and progression of several often severe and disabling pathological conditions, such as AADC Deficiency and cholangiocarcinoma. Consequently, AADC and HDC characterization might be useful in the pathophysiological understanding of several diseases and in improving/developing new therapeutic strategies. However, the knowledge of the biochemical features of these two crucial enzymes is still rather limited. Thus, the aim of this thesis is to biochemically characterise human HDC, mostly unknown, and to individuate some possible regulative mechanisms for both HDC and AADC. In addition, a neuronal AADC Deficiency cell model, derived from patient induced pluripotent stem cells (iPSCs), was used to evaluate endogenous AADC features, as well as to research further alterations in dopaminergic pathway. Investigations on human recombinant HDC allowed to discover that, surprisingly, its conformation and catalytic efficiency are influenced by redox state: increasing oxidizing conditions, indeed, favour a more stable and active form of the dimeric enzyme, due to the presence of an intermolecular reversible disulphide bridge involving residue Cys180 of both subunits. Then, in solution analyses of a possible phosphorylation of AADC identified Ser193 as protein kinase A target site, and allowed the detection of an effect on enzyme kinetic parameters, in particular an increased affinity for its substrates. Finally, endogenous AADC levels analyses in dopaminergic neurons derived from AADC Deficiency patients suggested a possible positive feedback mechanism that could tend to increase AADC expression, and the same cell model showed alterations in other cell types besides neurons, in particular glia cells, suggesting that variations in neurons-glia cells Abstract 5 interplay could participate in the pathophysiology mechanisms of AADC Deficiency. Altogether, data and information obtained from the performed experiments have increased AADC and HDC knowledge, as well as paved the way for new hypothesis regarding possible efforts in the development of new disease treatments.
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Книги з теми "Phosphate gla"

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Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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Частини книг з теми "Phosphate gla"

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Charhon, Sam A., Pierre D. Delmas, Luc Malaval, Pascale M. Chavassieux, Marie Claire Chapuy, and Pierre J. Meunier. "Serum Bone Gla-Protein Compared to Bone Histomorphometry in Hemodialyzed Patients." In Phosphate and Mineral Homeostasis, 291–96. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_37.

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Coen, Giorgio, Sandro Mazzaferro, Giuseppe Donato, Carlo Massimetti, Paola Ballanti, Franco Bondatti, Carlo Della Rocca, Antonella Smacchi, Flavia Mantazzoli, and Giulio A. Cinotti. "Effects of 1,25(OH)2D3 Administration on Serum Bone GLA Protein in Predialysis Chronic Renal Failure." In Phosphate and Mineral Homeostasis, 297–303. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_38.

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Yanagisawa, A. "With Allylic Phosphates." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00739.

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Ooi, T., and K. Maruoka. "Transformation of Allyl Phosphate Esters." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00158.

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Yanagisawa, A. "Displacement Reactions with Allylic Phosphates." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00531.

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Yanagisawa, A. "Cross Coupling of Allylic Halides with Allylic Phosphates." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00710.

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Takahashi, T., and Y. Liu. "Coupling Reactions Using Nickel–Phosphine Catalysts." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00565.

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Boessenecker, Robert W., and Sarah J. Boessenecker. "Paleontology of the “Ashley Phosphate Beds” of Charleston: Insights from Northbridge Park, Charleston, South Carolina." In Field Excursions in the Carolinas: Guides for the 2019 GSA Southeastern Section Meeting. Geological Society of America, 2019. http://dx.doi.org/10.1130/2019.0053(01).

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Cox, Morgan A., Aaron J. Cavosie, Michael Poelchau, Thomas Kenkmann, Phil A. Bland, and Katarina Miljković. "Shock deformation microstructures in xenotime from the Spider impact structure, Western Australia." In Large Meteorite Impacts and Planetary Evolution VI. Geological Society of America, 2021. http://dx.doi.org/10.1130/2021.2550(19).

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ABSTRACT The rare earth element–bearing phosphate xenotime (YPO4) is isostructural with zircon, and therefore it has been predicted that xenotime forms similar shock deformation microstructures. However, systematic characterization of the range of micro structures that form in xenotime has not been conducted previously. Here, we report a study of 25 xenotime grains from 10 shatter cones in silicified sandstone from the Spider impact structure in Western Australia. We used electron backscatter diffrac tion (EBSD) in order to characterize deformation and microstructures within xenotime. The studied grains preserve multiple sets of planar fractures, lamellar {112} deformation twins, high-angle planar deformation bands (PDBs), partially recrystallized domains, and pre-impact polycrystalline grains. Pressure estimates from micro structures in coexisting minerals (quartz and zircon) allow some broad empirical constraints on formation conditions of ~10–20 GPa to be placed on the observed microstructures in xenotime; at present, more precise formation conditions are unavailable due to the absence of experimental constraints. Results from this study indicate that the most promising microstructures in xenotime for recording shock deformation are lamellar {112} twins, polycrystalline grains, and high-angle PDBs. The {112} deformation twins in xenotime are likely to be a diagnostic shock indicator, but they may require a different stress regime than that of {112} twinning in zircon. Likewise, polycrystalline grains are suggestive of impact-induced thermal recrystallization; however, in contrast to zircon, the impact-generated polycrystalline xenotime grains here appear to have formed in the solid state, and, in some cases, they may be difficult to distinguish from diagenetic xenotime with broadly similar textures.
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Takahashi, T., and Y. Liu. "Grignard Reagents with Catalytic Dichlorobis(phosphine)nickel(II)." In Compounds of Groups 13 and 2 (Al, Ga, In, Tl, Be...Ba), 1. Georg Thieme Verlag KG, 2004. http://dx.doi.org/10.1055/sos-sd-007-00564.

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Тези доповідей конференцій з теми "Phosphate gla"

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Van Haarlem, L. J. M., H. C. Hemker, B. A. M. Soute, and C. Vermeer. "GLA-CONTAINING PROTEINS FROM CALCIFIED HUMAN ATHEROSCLEROTIC PLAQUES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643747.

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Vitamin K-dependent carboxylase activity has been detected in human andbovine vessel wall. Studies comparingthe carboxylases from liver and vessel wall revealed that the enzyme systems may be regarded as isoenzymes withwidely different substrate specificities. The carboxylated product of vessel wall carboxylase has not yet been identified, but it seems plausible that it will be found amongst the Gla-containing proteins which are abundantly present in calcified atherosclerotic plaques (Gla= gammacarboxyglutamicacid, the abnormal amino acid formed by vitamin K-dependent carboxylase). Therefore we have started to characterize the protein constituents of hardened atherosclerotic plaques.The calcified areas from human aortae were solubilized in EDTA and the proteins extracted were partly purified by batch-wise adsorption onto QAE and elution with high salt. The crudeplaque-extract did not contain prothrombin, factor X or protein C. This excludes the possibility that Gla-containing coagulation factors are bound non-specifically from blood. Osteocalcin accounted for 20% of the total amount of protein-bound Gla-residues.Another Gla-containing protein waspurified from the crude plaque-extract by employing high performance liquid chromatography (HPLC). Gel filtration yielded a Gla-rich protein with anapparent Mr of 25 kD. In vitro boththe crude plaque-extract and the purified Gla-containing protein strongly inhibited the precipitation of calcium phosphate and calcium carbonate. A similar effect was not found with humanserum albumin nor with a thermallydecarboxylated plaque-extract. If also in vivo the Gla-containing proteinsproduced by vessel wall carboxylase prevent the precipitation of calcium salts remains to be investigated.
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Komvopoulos, K., V. Do, E. S. Yamaguchi, and P. R. Ryason. "Nanomechanical and Nanotribological Properties of an Antiwear Tribofilm Produced From Phosphorus-Containing Additives on Boundary-Lubricated Steel Surfaces." In ASME/STLE 2004 International Joint Tribology Conference. ASMEDC, 2004. http://dx.doi.org/10.1115/trib2004-64284.

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Nanoindentation and nanotribological experiments were performed on an antiwear tribofilm produced from a blend consisting of gear base oil and phosphorus-containing additive. Electrical contact resistance measurements were used to determine in situ the formation of the tribofilm on AISI steel surfaces at 100 °C under conditions favoring sliding in the boundary lubrication regime. Nanoindentation experiments were carried out with a surface force microscope on a small sector of a disk specimen that contained part of the wear track. A Berkovich diamond tip with a nominal radius of curvature equal to 100 mm was used to perform indentations on and off the wear track under a normal load between 100 and 600 μN. The phosphate tribofilm exhibited an average hardness of 6.0 GPa and reduced elastic modulus of 122.7 GPa compared to 12.5 GPa and 217.6 GPa of the steel substrate, respectively. In addition to the nanomechanical properties, the nanotribological properties of the tribofilm were evaluated in light of nanofriction tests performed with a 20 μm radius of curvature conical diamond tip under a normal load in the range of 100–200 μN. The original steel surfaces exhibited constant friction, whereas the wear track covered by the phosphate tribofilm, whereas the wear track covered by the phosphate tribofilm revealed a higher and more fluctuating coefficient of friction, which is attributed to the roughness of the wear track and the greater plasticity of the tribofilm than the substrate.
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Schilling, Keith E. "DISSOLVED PHOSPHATE CONCENTRATIONS IN IOWA SHALLOW GROUNDWATER." In 54th Annual GSA North-Central Section Meeting - 2020. Geological Society of America, 2020. http://dx.doi.org/10.1130/abs/2020nc-347858.

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Emsbo, Poul, Patrick I. McLaughlin, Thijs R. A. Vandenbroucke, Edward A. du Bray, and Eric D. Anderson. "A GLOBAL ASSESSMENT OF REE’S IN SEDIMENTARY PHOSPHATE DEPOSITS." In GSA Annual Meeting in Denver, Colorado, USA - 2016. Geological Society of America, 2016. http://dx.doi.org/10.1130/abs/2016am-286523.

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Tosca, Nicholas, Matthew P. Brady, and Rosalie Tostevin. "MARINE PHOSPHATE AVAILABILITY AND THE CHEMICAL ORIGINS OF LIFE ON EARTH." In GSA Connects 2021 in Portland, Oregon. Geological Society of America, 2021. http://dx.doi.org/10.1130/abs/2021am-367609.

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Kane, Tyler J., Kate M. Campbell, and Michael Hay. "MECHANISMS OF URANIUM ORE PASSIVATION DURING IN SITU PHOSPHATE INJECTIONS." In GSA Annual Meeting in Phoenix, Arizona, USA - 2019. Geological Society of America, 2019. http://dx.doi.org/10.1130/abs/2019am-341312.

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Slabic, Ane, and Daniel Imrecke. "GEOCHEMICAL SIGNATURES OF MARTIAN SHOCKED CALCIUM PHOSPHATE MINERALS: IMPACTS AND IMPLICATIONS." In GSA Connects 2022 meeting in Denver, Colorado. Geological Society of America, 2022. http://dx.doi.org/10.1130/abs/2022am-383185.

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Kane, Tyler, Kate M. Campbell, and Michael Hay. "IN SITU PASSIVATION OF URANIUM ORE MATERIAL SURFACES WITH URANYL PHOSPHATE PRECIPITATION." In GSA Annual Meeting in Denver, Colorado, USA - 2016. Geological Society of America, 2016. http://dx.doi.org/10.1130/abs/2016am-285382.

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Kubicki, James D., Jiye Guo, Lin Ma, T. Ohno, and Patrick Hatcher. "MODELING COMPETITIVE ADSORPTION OF PHOSPHATE AND SALICYLATE ON THE GOETHITE (210) SURFACE." In GSA Annual Meeting in Indianapolis, Indiana, USA - 2018. Geological Society of America, 2018. http://dx.doi.org/10.1130/abs/2018am-316231.

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Hagni, Richard D., and Ann M. Hagni. "KARST OCCURRENCE, CHARACTER, AND PHOSPHATE MINERALOGY OF JAMAICA BAUXITES ORES." In Joint 53rd Annual South-Central/53rd North-Central/71st Rocky Mtn GSA Section Meeting - 2019. Geological Society of America, 2019. http://dx.doi.org/10.1130/abs/2019sc-326347.

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