Готові списки джерел за темами / Mctp

Добірка наукової літератури з теми "Mctp"

Автор: Grafiati
Опубліковано: 28 вересня 2022
Оновлено: 25 жовтня 2022

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Статті в журналах з теми "Mctp":

1

Bonen, Arend, Miriam Heynen, and Hideo Hatta. "Distribution of monocarboxylate transporters MCT1-MCT8 in rat tissues and human skeletal muscle." Applied Physiology, Nutrition, and Metabolism 31, no. 1 (February 1, 2006): 31–39. http://dx.doi.org/10.1139/h05-002.

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In the past decade, a family of monocarboxylate transporters (MCTs) have been identified that can potentially transport lactate, pyruvate, ketone bodies, and branched-chain ketoacids. Currently, 14 such MCTs are known. However, many orphan transporters exist that have transport capacities that remain to be determined. In addition, the tissue distribution of many of these MCTs is not well defined. Such a cataloging can, at times, begin to suggest the metabolic role of a particular MCT. Recently, a number of antibodies against selected MCTs (MCT1, -2, -4, and -5 to -8) have become commercially available. Therefore, we examined the protein expression of these MCTs in a large number of rat tissues (heart, skeletal muscle, skin, brain, testes, vas deferens, adipose tissue, liver, kidney, spleen, and pancreas), as well as in human skeletal muscle. Unexpectedly, many tissues coexpressed 4-5 MCTs. In particular, in rat skeletal muscle MCT1, MCT2, MCT4, MCT5, and MCT6 were observed. In human muscle, these same MCTs were present. We also observed a pronounced MCT7 signal in human muscle, whereas a very faint signal occurred for MCT8. In rat heart, which is an important metabolic sink for lactate, we confirmed that MCT1 and -2 were expressed. In addition, MCT6 and -8 were also prominently expressed in this tissue, although it is known that MCT8 does not transport aromatic amino acids or lactate. This catalog of MCTs in skeletal muscle and other tissues has revealed an unexpected complexity of coexpression, which makes it difficult to associate changes in monocarboxylate transport with the expression of a particular MCT. The differences in transport kinetics for lactate and pyruvate are only known for MCT1, -2 and -4. Transport kinetics remain to be established for many other MCTs. In conclusion, this study suggests that in skeletal muscle, as well as other tissues, lactate and pyruvate transport rates may not only involve MCT1 and -4, as other monocarboxylate transporters are also expressed in rat (MCT2, -5, -6) and human skeletal muscle (MCT2, -5, -6, -7).Key words: muscle, lactate, pyruvate, human, rat.
2

Becker, Helen M., Nilufar Mohebbi, Angelica Perna, Vadivel Ganapathy, Giovambattista Capasso, and Carsten A. Wagner. "Localization of members of MCT monocarboxylate transporter family Slc16 in the kidney and regulation during metabolic acidosis." American Journal of Physiology-Renal Physiology 299, no. 1 (July 2010): F141—F154. http://dx.doi.org/10.1152/ajprenal.00488.2009.

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The monocarboxylate transporter family (MCT) comprises 14 members with distinct transport properties and tissue distribution. The kidney expresses several members of the MCT family, but only little is known about their exact distribution and function. Here, we investigated selected members of the MCT family in the mouse kidney. MCT1, MCT2, MCT7, and MCT8 localized to basolateral membranes of the epithelial cells lining the nephron. MCT1 and MCT8 were detected in proximal tubule cells whereas MCT7 and MCT2 were located in the thick ascending limb and the distal tubule. CD147, a β-subunit of MCT1 and MCT4, showed partially overlapping expression with MCT1 and MCT2. However, CD147 was also found in intercalated cells. We also detected SMCT1 and SMCT2, two Na+-dependent monocarboxylate cotransporters, on the luminal membrane of type A intercalated cells. Moreover, mice were given an acid load for 2 and 7 days. Acidotic animals showed a marked but transient increase in urinary lactate excretion. During acidosis, a downregulation of MCT1, MCT8, and SMCT2 was observed at the mRNA level, whereas MCT7 and SMCT1 showed increased mRNA abundance. Only MCT7 showed lower protein abundance whereas all other transporters remained unchanged. In summary, we describe for the first time the localization of various MCT transporters in mammalian kidney and demonstrate that metabolic acidosis induces a transient increase in urinary lactate excretion paralleled by lower MCT7 protein expression.
3

PRICE, T. Nigel, N. Vicky JACKSON, and P. Andrew HALESTRAP. "Cloning and sequencing of four new mammalian monocarboxylate transporter (MCT) homologues confirms the existence of a transporter family with an ancient past." Biochemical Journal 329, no. 2 (January 15, 1998): 321–28. http://dx.doi.org/10.1042/bj3290321.

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Measurement of monocarboxylate transport kinetics in a range of cell types has provided strong circumstantial evidence for a family of monocarboxylate transporters (MCTs). Two mammalian MCT isoforms (MCT1 and MCT2) and a chicken isoform (REMP or MCT3) have already been cloned, sequenced and expressed, and another MCT-like sequence (XPCT) has been identified. Here we report the identification of new human MCT homologues in the database of expression sequence tags and the cloning and sequencing of four new full-length MCT-like sequences from human cDNA libraries, which we have denoted MCT3, MCT4, MCT5 and MCT6. Northern blotting revealed a unique tissue distribution for the expression of mRNA for each of the seven putative MCT isoforms (MCT1-MCT6 and XPCT). All sequences were predicted to have 12 transmembrane (TM) helical domains with a large intracellular loop between TM6 and TM7. Multiple sequence alignments showed identities ranging from 20% to 55%, with the greatest conservation in the predicted TM regions and more variation in the C-terminal than the N-terminal region. Searching of additional sequence databases identified candidate MCT homologues from the yeast Saccharomyces cerevisiae, the nematode worm Caenorhabditis elegans and the archaebacterium Sulfolobus solfataricus. Together these sequences constitute a new family of transporters with some strongly conserved sequence motifs, the possible functions of which are discussed.
4

Chidlow, Glyn, John P. M. Wood, Mark Graham, and Neville N. Osborne. "Expression of monocarboxylate transporters in rat ocular tissues." American Journal of Physiology-Cell Physiology 288, no. 2 (February 2005): C416—C428. http://dx.doi.org/10.1152/ajpcell.00037.2004.

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The aim of the present study was to determine the distribution of monocarboxylate transporter (MCT) subtypes 1-4 in the various structures of the rat eye by using a combination of conventional and real-time RT-PCR, immunoblotting, and immunohistochemistry. Retinal samples expressed mRNAs encoding all four MCTs. MCT1 immunoreactivity was observed in photoreceptor inner segments, Müller cells, retinal capillaries, and the two plexiform layers. MCT2 labeling was concentrated in the inner and outer plexiform layers. MCT4 immunolabeling was present only in the inner retina, particularly in putative Müller cells, and the plexiform layers. No MCT3 labeling could be observed. The retinal pigment epithelium (RPE)/choroid expressed high levels of MCT1 and MCT3 mRNAs but lower levels of MCT2 and MCT4 mRNAs. MCT1 was localized to the apical and MCT3 to the basal membrane of the RPE, whereas MCT2 staining was faint. Although MCT1-MCT4 mRNAs were all detectable in iris and ciliary body samples, only MCT1 and MCT2 proteins were expressed. These were present in the iris epithelium and the nonpigmented epithelium of the ciliary processes. MCT4 was localized to the smooth muscle lining of large vessels in the iris-ciliary body and choroid. In the cornea, MCT1 and MCT2 mRNAs and proteins were detectable in the epithelium and endothelium, whereas evidence was found for the presence of MCT4 and, to a lesser extent, MCT1 in the lens epithelium. The unique distribution of MCT subtypes in the eye is indicative of the pivotal role that these transporters play in the maintenance of ocular function.
5

Hadjiagapiou, Christos, Larry Schmidt, Pradeep K. Dudeja, Thomas J. Layden, and Krishnamurthy Ramaswamy. "Mechanism(s) of butyrate transport in Caco-2 cells: role of monocarboxylate transporter 1." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 4 (October 1, 2000): G775—G780. http://dx.doi.org/10.1152/ajpgi.2000.279.4.g775.

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The short-chain fatty acid butyrate was readily taken up by Caco-2 cells. Transport exhibited saturation kinetics, was enhanced by low extracellular pH, and was Na+independent. Butyrate uptake was unaffected by DIDS; however, α-cyano-4-hydroxycinnamate and the butyrate analogs propionate and l-lactate significantly inhibited uptake. These results suggest that butyrate transport by Caco-2 cells is mediated by a transporter belonging to the monocarboxylate transporter family. We identified five isoforms of this transporter, MCT1, MCT3, MCT4, MCT5, and MCT6, in Caco-2 cells by PCR, and MCT1 was found to be the most abundant isoform by RNase protection assay. Transient transfection of MCT1, in the antisense orientation, resulted in significant inhibition of butyrate uptake. The cells fully recovered from this inhibition by 5 days after transfection. In conclusion, our data showed that the MCT1 transporter may play a major role in the transport of butyrate into Caco-2 cells.
6

Bruner, L. H., K. J. Johnson, G. O. Till, and R. A. Roth. "Complement is not involved in monocrotaline pyrrole-induced pulmonary injury." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 2 (February 1, 1988): H258—H264. http://dx.doi.org/10.1152/ajpheart.1988.254.2.h258.

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Monocrotaline pyrrole (MCTP) causes pulmonary vascular injury, pulmonary hypertension, and right ventricular hypertrophy in rats. The mechanisms by which MCTP causes lung injury are not known. After treatment with a moderate dose of MCTP, several days pass before major lung injury is detected, thus suggesting that the damage is caused indirectly. Since activation of the complement system can cause lung injury, it was of interest to test whether complement activation may be important in lung injury due to MCTP. Accordingly, rats were given a single dose of MCTP (3.5 mg/kg iv), and serum hemolytic complement activity was measured at several times after rats were treated. Neutrophil aggregometry also was used to determine whether complement activation products could be detected in serum after MCTP was given in vivo. The effect of complement depletion on MCTP-induced pulmonary injury was tested by cotreating rats with purified cobra venom factor and MCTP. MCTP treatment did not cause detectable complement activation in vivo, and complement depletion did not protect rats from lung injury. The direct effect of MCTP on serum complement also was tested by exposing fresh rat serum to MCTP in vitro and measuring serum complement activity. MCTP decreased serum hemolytic complement activity in vitro, but it did not interfere with subsequent zymosan-induced activation of complement. These results suggest that complement does not play a role in the development of major lung injury that occurs several days after treatment of rats with MCTP.
7

Ganey, P. E., K. H. Sprugel, S. M. White, J. G. Wagner, and R. A. Roth. "Pulmonary hypertension due to monocrotaline pyrrole is reduced by moderate thrombocytopenia." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 5 (November 1, 1988): H1165—H1172. http://dx.doi.org/10.1152/ajpheart.1988.255.5.h1165.

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To elucidate further the role of the platelet in the development of monocrotaline pyrrole (MCTP)-induced lung injury and pulmonary hypertension, MCTP-treated rats were made thrombocytopenic by cotreatment with an anti-rat platelet serum (PAS). Lung injury was assessed from increases in lung weight, lavage fluid protein concentration, and lactate dehydrogenase activity and from accumulation in lung tissue of 125I-labeled albumin. These indexes of injury were not different in MCTP-treated rats with normal or reduced platelet numbers at day 4,8, or 14. In MCTP-treated rats not receiving the PAS, pulmonary arterial pressure was elevated by day 8. However, pulmonary arterial pressure was the same as controls at both day 8 and day 14 in MCTP-treated rats made moderately thrombocytopenic by cotreatment with PAS. More marked reduction of platelet number abolished the protective effect of thrombocytopenia against pulmonary hypertension. In a separate series of experiments, treatment with antibodies to platelet-derived growth factor (PDGF), a potential mediator in the response to MCTP-induced injury, did not protect rats from the cardiopulmonary effects of MCTP. These data indicate that moderate reduction of the number of circulating platelets prevents MCTP-induced pulmonary hypertension but not MCTP-induced lung injury, suggesting that the platelet is involved in the pulmonary hypertensive response to MCTP-induced lung injury by unknown mechanisms.
8

Wagner, J. G., T. W. Petry, and R. A. Roth. "Characterization of monocrotaline pyrrole-induced DNA cross-linking in pulmonary artery endothelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 264, no. 5 (May 1, 1993): L517—L522. http://dx.doi.org/10.1152/ajplung.1993.264.5.l517.

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Monocrotaline pyrrole (MCTP) is a putative, toxic metabolite of the pyrrolizidine alkaloid, monocrotaline (MCT). When given intravenously to rats, it produces a delayed and progressive injury to the vasculature of the lungs that results in pulmonary hypertension and right heart hypertrophy. Dysfunctional endothelium and vascular leak are early signs of overt injury to the lung. When administered to endothelial cell cultures, MCTP causes cell enlargement, delayed and progressive cytotoxicity, and inhibition of proliferation in surviving cells. MCTP is a bifunctional alkylating agent which binds to DNA and other macromolecules. To examine DNA-MCTP interactions in endothelium, MCTP-induced DNA cross-linking was characterized in cultures of porcine endothelial cells (PECs) derived from pulmonary artery. MCTP caused DNA cross-linking in a dose-dependent manner that was consistent with its ability to inhibit cell proliferation. PECs exposed to MCTP for 48 h developed cross-linking that was maximal at 2 days and remained significant through 10 days. Increasing the duration of PEC exposure to the medium to which MCTP had been added was associated with increased DNA cross-linking. These results indicate that MCTP causes DNA cross-linking, which may explain the inhibition of cell proliferation observed in pulmonary endothelial cells in vitro. The long-lasting nature of DNA cross-linking and its dose relatedness are consistent with the delayed and progressive effects of MCTP on endothelial cells in vitro and on pulmonary vasculature in vivo.
9

Ganey, P. E., and R. A. Roth. "Thromboxane does not mediate pulmonary vascular response to monocrotaline pyrrole." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 4 (April 1, 1987): H743—H748. http://dx.doi.org/10.1152/ajpheart.1987.252.4.h743.

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The possible involvement of thromboxane (Tx) in the pulmonary hypertension caused by monocrotaline pyrrole (MCTP) administration to rats was investigated by pharmacological intervention of Tx synthesis and action. The cyclooxygenase inhibitor, ibuprofen, at doses that inhibited platelet function and suppressed plasma Tx levels, did not attenuate MCTP-induced right ventricular hypertrophy or increased lung weight. Dazmegrel, an inhibitor of Tx synthetase, did not affect the MCTP-induced increase in lung weight or the elevation of lactate dehydrogenase activity or protein concentration in bronchopulmonary lavage fluid, despite significant reduction of the plasma concentration of Tx. Dazmegrel also did not alter the vascular leak or right ventricular hypertrophy due to administration of MCTP to rats. Finally, the Tx receptor antagonist L-640,035 was tested using a dosing regimen that reduced the increase in right ventricular pressure caused by a stable endoperoxide analogue in MCTP-treated rats. Cotreatment with L-640,035 did not attenuate the increase in lung weight, lavage fluid lactate dehydrogenase activity or protein concentration, or the pulmonary hypertension caused by MCTP. These results indicate that interference with Tx synthesis or action does not attenuate the toxic effects of MCTP and suggest that Tx is not necessary for the cardiopulmonary response to MCTP.
10

Hoorn, C. M., and R. A. Roth. "Monocrotaline pyrrole alters DNA, RNA and protein synthesis in pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 6 (June 1, 1992): L740—L747. http://dx.doi.org/10.1152/ajplung.1992.262.6.l740.

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Administration of monocrotaline pyrrole (MCTP) to animals results in pulmonary vascular injury. Pulmonary vascular endothelium is a likely target for this pneumotoxicant. Cultured porcine pulmonary artery endothelial cells (PECs) treated with MCTP remain viable but are unable to divide and exhibit an altered morphology. Such responses raise a question about the extent to which affected cells carry out normal functions such as RNA and protein synthesis. Accordingly, the cellular activity of MCTP-treated PECs was examined in this study. PECs were treated with a single administration of MCTP or vehicle, and determinations of cell number, protein, and DNA content were made at times up to 7 days posttreatment. DNA, RNA, and protein synthesis were quantified by incorporation of [3H]thymidine, [3H]uridine, and [3H]leucine, respectively. Increases in cell number that occurred with time in the control cells were reduced in MCTP-treated cells. At 7 days posttreatment, both protein and DNA content increased above control levels. Synthesis of DNA, RNA, and protein continued in all treatment groups throughout the posttreatment period, but cells treated with high concentrations of MCTP showed less synthetic activity than controls during the initial 48 h posttreatment. By 7 days, MCTP-treated cells were producing significantly more DNA, RNA, and protein. These results indicate that cells treated with MCTP continue to synthesize DNA, resulting in an increased DNA content. In addition, treated cells continue to synthesize RNA and translate RNA into protein. Thus, cellular activity is maintained but altered substantially by MCTP exposure.
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Статті в журналах Дисертації Книги

Дисертації з теми "Mctp":

1

Ovens, Matthew James. "Further characterisation of substrate, inhibitor and ancillary protein specificity of MCT1, MCT2, MCT4 and MCT6." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528104.

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The MonoCarboxylate Transporter (MCT) family of transmembrane proteins contain 14 members of which 6 have been functionally characterized. Of these characterised MCTs only MCTs 1-4 have been shown to transport lactate. These MCTs also facilitate the movement of pyruvate and ketone bodies across the plasma membrane (PM) in cotransport with a proton. For trafficking to and function at the PM MCTl, MCT3 and MCT4 require association with the monotopic ancillary glycoprotein basigin whereas MCT2 prefers association with embigin. This thesis has investigated the sensitivity of MCTl, MCT2 and MCT4 to the highly potent and selective MCTI inhibitor, ARC155858, discovered by AstraZeneca. Chimeras of MCTI and MCT4 were constructed and expressed in Xenopus laevis oocytes for transport studies to determine their inhibitor sensitivity. These identified a region between transmembrane domains (TMs) 7 and 10 of MCTI with which AR-C155858 binds from the cytoplasmic side. ARC155858 was shown to inhibit MCT2 but sensitivity was found to be dependent on the ancillary protein with which it is associated. Co-expression with embigin decreased the sensitivity of MCT2, but not MCTl, to AR-CI55858. The MCT C-terminus was shown to playa role in the interaction between MCT and ancillary protein which is secondary to interactions between the TM of the ancillary protein and TMs3 and 6 of the MCT. Additional studies were performed to characterise the substrate specificity of the orphan transporter, MCT6. Initial work suggested that products of pyruvate decarboxylation or polymerisation will provide lead compounds in the continuing search for the physiological substrate of MCT6, with formate another potential substrate. During this work it was also discovered that MCTI can catalyse the transport of specific dicarboxylates at low pH.
2

Petit, Jules. "Membrane Tethering in Plant Intercellular Communication : Structure-Function of Multiple C2 domains and Transmembrane Region Proteins (MCTP) at Plasmodesmata ER-PM Membrane Contact Site." Thesis, Bordeaux, 2022. https://tel.archives-ouvertes.fr/tel-03789611.

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La multicellularité chez les plantes repose sur une communication intercellulaire qui permette le transfert d'informations à travers l'entièreté de l'organisme. Chez les plantes terrestres, la route principale de ces “conversations cellulaires” est assurée par les plasmodesmes (PD), des canaux nanoscopiques qui traversent la paroi pecto-cellulosique. En effet, ces pores sont impliqués dans la circulation d'une très grande variété de molécules, comme des facteurs de transcription, de l'ARN, des hormones et des métabolites et ceci à tous les stades de la vie végétale, permettant réponses et adaptations à l'environnement. Les PD sont particuliers dans le sens où ils forment une continuité du réticulum endoplasmic (RE), de la membrane plasmique (MP) et du cytoplasme entre les cellules adjacentes. Leur architecture est singulière et consiste en un filament de RE, appelé desmotubule, entouré d'un tube de MP qui, lui, longe la paroi. Les PD sont actuellement décrits comme des sites de contact membranaire, du fait du fort accolement des membranes du RE et de la MP (2 à 10 nm) et de la présence de protéines de jonction qui connectent les deux organelles. Dans la présente étude, nous décrivons au niveau structural et fonctionnel plusieurs membres de la famille des MCTPs (protéine avec de multiples domaines C2 et une région transmembranaire) comme protéines assurant la jonction du RE et de la MP dans les PD. Nous démontrons que ces protéines possèdent les caractéristiques moléculaires nécessaires à l'interaction transitoire avec les lipides anioniques de la MP, via leurs domaines C2, ainsi qu'à l'induction de courbure membranaire au RE, via la région transmembranaire qui agit comme un domaine homologue aux protéines réticulons. Ces données nous ont permis de corréler la fonction des MCTPs à l'architecture et la biogenèse des PD et de réfléchir au rôle du RE à l'intérieur des PD. En conclusion, ce travail a fourni des résultats originaux qui placent les MCTPs comme des protéines centrales dans l'établissement de la structure fine des PD et des fonctions qui y sont associées
Plant multicellularity relies on intercellular communication in order to transmit information from cell to cell and throughout the entire plant body. In land plants, the major line for such cellular conversations is through plasmodesmata (PD) pores, which are nanoscopic membranous tunnels spanning the pecto-cellulosic cell wall. These pores are indeed involved in the transfer of a wide variety of molecules such as transcription factors, RNAs, hormones and metabolites during all stages of plant life, adaptation and responses to their environment. PD are singular amongst other types of intercellular junctions as they provide a direct continuity of the endoplasmic reticulum (ER), the plasma membrane (PM) and the cytosol between neighboring cells. Their architectural organization can be summarized as followed: a thin strand of constricted ER, called desmotubule, is encased in a tube of PM lining the cell wall. PD are seen as a specialized ER-PM membrane contact sites from the very close apposition (2 to 10 nm) of the ER and PM membranes and the presence of tethering elements bridging the two organelles. In this study, we describe the structural organization and function of several members of the MCTP (Multiple C2 domains and Transmembrane region Protein) family which act as ER-PM tethering elements at PD. We show that these proteins possess molecular features capable of transient interaction with anionic lipids of the PM, through their C2 domains, as well as ER membrane shaping, through their transmembrane region which presents homology to a reticulon domain. We further correlate MCTP function with PD architecture and biogenesis, and investigate on the role of the ER inside PD. Altogether, this work provides original data placing MCTPs as core PD proteins that appear to be crucial in the establishment of PD ultrastructure and associated functions
3

Little, L. Nicole. "Characterization of Basigin and the Interaction Between Embigin and Monocarboxylate Transporter -1, -2, and -4 (MCT1, MCT2, MCT4) in the Mouse Brain." UNF Digital Commons, 2011. http://digitalcommons.unf.edu/etd/384.

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Basigin and Embigin are members of the immunoglobulin superfamily that function as cell adhesion molecules. Studies of Basigin null mice revealed reproductive sterility, increased pain sensitivity, and blindness. It is thought that the mechanism causing blindness involves misexpression of monocarboxylate transporter 1 (MCT1) in the absence of Basigin. It is known that the transmembrane domain of Basigin interacts with MCT1. In the absence of Basigin, MCT1 does not localize to the plasma membrane of expressing cells and photoreceptor function is disrupted. Studies of the Basigin null mouse brain suggest that MCT1 is properly expressed, which suggests a separate mechanism causes the increased pain sensitivity in these animals, and also that a different protein directs MCT1 to the plasma membrane of expressing cells in mouse brain. Embigin is known to interact with MCT2 in neurons and with MCT1 in erythrocytes. It is not known, however, if Embigin normally interacts with MCT1 in the mouse brain or if Embigin acts to compensate for the lack of Basigin in the Basigin null animals. Therefore, the purpose of this study was to determine if Embigin normally interacts with MCT1, 2, or 4 in the mouse brain and if so, whether the interaction is similar to that between Basigin and MCT1. Expression of Basigin, Embigin, MCT1, MCT2, and MCT4 in mouse brain was assessed via immunoblotting and immunohistochemical analyses. In addition, recombinant protein probes corresponding to the Embigin transmembrane domain were generated for ELISA binding assays using endogenous mouse brain MCTs. It was determined that the proteins in question are rather ubiquitously expressed throughout the mouse brain, and that the cell adhesion molecules Basigin and Embigin may be co-expressed in the same cells as the MCT2 and MCT4 transporter proteins. In addition, it was determined that the Embigin transmembrane domain does not interact with the MCTs. The data therefore suggest that MCTs do not require Basigin or Embigin for plasma membrane expression in mouse brain.
4

Richards, William. "The influence of aging and cardiovascular training status upon monocarboxylate transporters." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1133362045.

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5

Feringer, Júnior Walter Heinz [UNESP]. "Expressão dos transportadores de monocarboxilatos de equinos e cães." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/153171.

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O principal mecanismo de transporte dos íons lactato e H+ em equinos e cães é o complexo transportador formado pelos transportadores de monocarboxilatos, isoformas 1 (MCT1) e 4 (MCT4) juntamente com a proteína auxiliar CD147. Objetivando identificar diferenças entre equinos com desempenho distinto, 16 equinos da raça Brasileiro de Hipismo (BH) foram distribuídos em dois grupos, desempenho inferior (DI, n=8) e desempenho superior (DS, n=8) que foram submetidos a teste de salto incrementai (TSI). Realizou-se biópsia do músculo Gluteus medius para tipificação e análise das expressões das isoformas MCT1, MCT4 e CD147. Amostras sanguíneas foram colhidas para avaliar as expressões MCT1 e CD147 das hemácias. Aplicaram-se testes de normalidade de Shapiro Wilk e homogeneidade de Levene. As medidas morfométricas foram submetidas ao teste de Tukey. Teste “t” de Student não pareado para a comparação das médias dos grupos DI e DS. Aplicou-se correlação de Spearman para as expressões dos transportadores. Para todas as análises utilizou-se p≤0,05. Não houve diferença entre os grupos quanto à frequência de cada tipo de fibra e constatou-se maior quantidade das fibras tipo I em relação às fibras IIA e IIX em todos os equinos avaliados. Não houve diferença entre os pesos moleculares e a expressão das proteínas MCT1, MCT4, e CD147 musculares ou sanguíneas. Houve correlações positivas entre MCT1 vs. CD147 e MCT4 vs. CD147 musculares dos grupos DI e DS. As correlações encontradas foram esperadas uma vez que as isoformas estudadas dependem intimamente da proteína auxiliar CD147 para o transporte. Os equinos BH não apresentaram diferenças nas expressões dos MCT1,4 e CD147, musculares ou sanguíneos, mesmo com níveis de condicionamento diferentes. Com o objetivo de investigar as concentrações de lactato plasmático e das hemácias e avaliar as expressões eritrocitáras do complexo transportador MT1/CD147, 6 cães da raça American Pitbull Terrier (APBT) foram submetidos ao teste de esforço incremental (TEI) em esteira. No final de cada incremento de velocidade foi coletado sangue da veia cefálica. Foram mensuradas concentrações de lactato sanguíneo (LS), plasmático (LP), pH e hematócrito (Ht). A concentração do lactato dentro das hemácias (LH) foi estimada e estabeleceu-se a relação LH:LP. As expressões sanguíneas do complexo MCT1/CD147 foram avaliadas por Western Bloting. Aplicou-se análise de variância de uma via seguido pelo teste de Dunn’s. Para pH e Ht aplicou-se teste t de student para amostras pareadas e a correlação de Pearson foi utilizada para MCT1 e CD147, estabeleceu-se nível de significância P≤0,05. LS, LP e LH e pH não apresentaram diferenças entre si, a relação LH:LP foi próxima de 1 com tendência de aumento. MCT1 e CD147 apresentaram 48 e 59 kDa de peso molecular e 1,27 e 1,05 de unidades ópticas arbitrárias (UOA). Não foram encontradas correlações entre MCT1 e CD147. A grande velocidade de transporte do MCT1/CD147 explica a relação LP:LH próxima de 1, esta velocidade e o mecanismo de arquejo podem explicar os valores de pH constantes. A raça APBT, quando submetidos à atividade física apresentaram tendência de aumento da relação LH:LP e expressam de maneira homogênea o complexo MCT1/CD147.
The central transport mechanism of lactate and H+ ions in horses and dogs is the carrier complex formed by the monocarboxylate, isoform 1 (MCT1) and 4 (MCT4) associated with the ancillary protein CD147. This study aimed to identify possible differences between horses with different performances levels, 16 horses of the Brazilian Sport Horse breed (BH) were distributed in two groups, inferior performance (IP, n = 8) and superior performance (SP, n = 8). A Gluteus medius muscle biopsy was performed for cellular typing and analysis of MCT1, MCT4, and CD147 muscle expressions. By jugular venipuncture, blood samples were collected to evaluate MCT1 and CD147 expressions in the red blood cells (RBC). Normality Shapiro Wilk test and homogeneity of Levene were applied. The morphometric measurements were submitted to the Tukey test, and not paired Student's t-test were applied to compare the mean of the IP and SP groups for all variables and was used Spearman's correlation for isoform expressions, for all analyzes, p≤0.05. There were no differences between the groups regarding the frequency of each type of fiber and a higher number of type I fibers were observed about the IIA and IIX fibers in all groups. There was no difference between molecular weights and expressions of MCT1, MCT4, and CD147 in muscle or blood. There were positive correlations between muscles MCT1 vs CD147 and MCT4 vs CD147 in both groups. The relationships found were expected since the MCT1 and 4 depended on the CD147 ancillary protein for correct functioning. The BH horses do not present differences in the muscle or RBC expressions of MCT1, 4 and CD147, even with different conditioning levels. To investigate plasma and erythrocyte lactate concentrations and to evaluate erythrocyte expression of the MT1/CD147 transporter complex, six dogs of the American Pit Bull Terrier breed (APBT) were submitted to a treadmill incremental effort test (IET). At the end of each increment of speed, blood was collected from the cephalic vein. Concentrations of blood (BL) and plasma lactate (PL), pH and hematocrit (Ht) were measured. The concentration of lactate inside the red blood cells (LC) was estimated and the LC: PL ratio was established, the blood expressions of the MCT1/CD147 transporter complex were evaluated by western blot. Data were submitted to the Shapiro-Wilks normality test, one-way ANOVA and Dunn's test. For pH and Ht, paired Student's t-test was applied, and Pearson's correlation was used for MCT1 and CD147 analysis, for all analyzes, p≤0.05. BL, PL, LC, pH showed no differences, the LC: PL ratio was close to 1 with an increasing tendency. MCT1 and CD147 presented 48 and 59 kDa of molecular weight and 1.27 and 1.05 of arbitrary optical units (AOU). No correlations were found between MCT1 and CD147. The high transport velocity of the MCT1/CD147 could explain the LC: PL ratio close to 1, this velocity plus the grasping mechanism may explain the constant of pH values. The APBT submitted to intense physical activity showed a tendency to increase the LC: PL ratio, and homogeneously express the MCT1/CD147 complex
FAPESP: 11/11080-0
6

Feringer-Junior, Walter Heinz. "Expressão dos transportadores de monocarboxilatos de equinos e cães /." Jaboticabal, 2017. http://hdl.handle.net/11449/153171.

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Orientador: Guilherme de Camargo Ferraz
Resumo: O principal mecanismo de transporte dos íons lactato e H+ em equinos e cães é o complexo transportador formado pelos transportadores de monocarboxilatos, isoformas 1 (MCT1) e 4 (MCT4) juntamente com a proteína auxiliar CD147. Objetivando identificar diferenças entre equinos com desempenho distinto, 16 equinos da raça Brasileiro de Hipismo (BH) foram distribuídos em dois grupos, desempenho inferior (DI, n=8) e desempenho superior (DS, n=8) que foram submetidos a teste de salto incrementai (TSI). Realizou-se biópsia do músculo Gluteus medius para tipificação e análise das expressões das isoformas MCT1, MCT4 e CD147. Amostras sanguíneas foram colhidas para avaliar as expressões MCT1 e CD147 das hemácias. Aplicaram-se testes de normalidade de Shapiro Wilk e homogeneidade de Levene. As medidas morfométricas foram submetidas ao teste de Tukey. Teste “t” de Student não pareado para a comparação das médias dos grupos DI e DS. Aplicou-se correlação de Spearman para as expressões dos transportadores. Para todas as análises utilizou-se p≤0,05. Não houve diferença entre os grupos quanto à frequência de cada tipo de fibra e constatou-se maior quantidade das fibras tipo I em relação às fibras IIA e IIX em todos os equinos avaliados. Não houve diferença entre os pesos moleculares e a expressão das proteínas MCT1, MCT4, e CD147 musculares ou sanguíneas. Houve correlações positivas entre MCT1 vs. CD147 e MCT4 vs. CD147 musculares dos grupos DI e DS. As correlações encontradas foram esperadas ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The central transport mechanism of lactate and H+ ions in horses and dogs is the carrier complex formed by the monocarboxylate, isoform 1 (MCT1) and 4 (MCT4) associated with the ancillary protein CD147. This study aimed to identify possible differences between horses with different performances levels, 16 horses of the Brazilian Sport Horse breed (BH) were distributed in two groups, inferior performance (IP, n = 8) and superior performance (SP, n = 8). A Gluteus medius muscle biopsy was performed for cellular typing and analysis of MCT1, MCT4, and CD147 muscle expressions. By jugular venipuncture, blood samples were collected to evaluate MCT1 and CD147 expressions in the red blood cells (RBC). Normality Shapiro Wilk test and homogeneity of Levene were applied. The morphometric measurements were submitted to the Tukey test, and not paired Student's t-test were applied to compare the mean of the IP and SP groups for all variables and was used Spearman's correlation for isoform expressions, for all analyzes, p≤0.05. There were no differences between the groups regarding the frequency of each type of fiber and a higher number of type I fibers were observed about the IIA and IIX fibers in all groups. There was no difference between molecular weights and expressions of MCT1, MCT4, and CD147 in muscle or blood. There were positive correlations between muscles MCT1 vs CD147 and MCT4 vs CD147 in both groups. The relationships found were expected since the MCT1 and 4 depended on the CD... (Complete abstract click electronic access below)
Doutor
7

Benesch, Franziska. "Regulative Einflüsse auf die Monocarboxylattransporter 1 und 4 im Pansenepithel des Schafes." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-211226.

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Einleitung: Monocarboxylattransporter (MCT) 1 & 4 sind in zahlreichen Geweben als Kotransporter für Monocarboxylate und Protonen beschrieben. Auch im Pansenepithel werden MCT benötigt, um kurzkettige Fettsäuren (SCFA) aus dem Pansenlumen in die Pansenepithelzelle aufzunehmen (MCT4) und um SCFA und deren Metabolite aus der Pansenepithelzelle in das Blut auszuschleusen (MCT1). Die transepitheliale Permeation von SCFA über die Pansenwand ist von enormer Bedeutung, da sie die wichtigste Energiequelle der Wiederkäuer darstellen. Die beteiligten Transportprozesse müssen dementsprechend einer Anpassung an variierende Mengen von SCFA unterliegen. Bisherige Studien bei anderen Spezies deuten auf eine Regulation des MCT1 auf mRNA Ebene über den Peroxisom-Proliferator-aktivierten Rezeptor α (PPARα) hin. Ziele der Untersuchung: Das Ziel dieser Arbeit war herauszufinden, ob MCT1 in ovinen Pansenepithelzellen über PPARα reguliert wird und ob auch MCT4 dieser Regulation unterliegt. Eine gleichzeitige Regulation beider Transporter läge nahe, da sie gemeinsam an der transepithelialen Permeation beteiligt sind. Die Auswirkungen solch einer Regulation auf die Proteinexpression und die Transportleistung der MCT sollte charakterisiert werden. Ebenfalls war das Potenzial der bei erhöhter Kraftfutterfütterung vermehrt anfallenden SCFA Butyrat auf die MCT1 Expression zu untersuchen. Material & Methoden: Aus dem Vorhof von Schafen wurden Pansenepithelzellen gewonnen und entsprechend einer bereits etablierten Methode kultiviert. Nach einer Subkultivierung wurden die Zellen immunzytochemisch mit Antikörpern gegen MCT1, MCT4 und Na+/K+-ATPase untersucht, um deren Lokalisation in den kultivierten Pansenepithelzellen zu bestimmen. Weiterhin erfolgte eine Behandlung mit WY 14.643, einem spezifischen, synthetischen PPARα Agonisten, sowie mit GW 6471, einem Antagonisten des PPARα. Mittels qPCR wurden die relativen mRNA Mengen von MCT1, MCT4, ACO, CPT1A und CACT bestimmt und auf die Referenzgene GAPDH und Na+/K+-ATPase normalisiert. Die Proteinexpression von MCT1 und MCT4 wurde mittels Western Blot bestimmt. Zur funktionellen Quantifizierung wurde der intrazelluläre pH-Wert der Zellen mittels Spektrofluorometrie gemessen und der laktatabhängige Protonentransport als Vergleichswert zwischen den Behandlungen genutzt. Um den MCT-abhängigen Teil des Transportes zu bestimmen, wurde ein spezifischer MCT1 & 4 Inhibitor, die p-Hydroxymercuribenzensulfonsäure (pHMB) eingesetzt. Die Zellen wurden mit Butyrat über einen Zeitraum von 6 und 48 h induziert. Die Erfassung der MCT1 Expression erfolgte mittels semiquantitativer PCR. Ergebnisse: MCT1 & 4 sind sowohl in der Zellmembran als auch intrazellulär in den Pansenepithelzellen lokalisiert. Die mRNA Expressionsdaten konnten zeigen, dass MCT1 und die PPARα Zielgene durch WY 14.643 hochreguliert werden konnten, wohingegen die MCT4 Expression keine eindeutige Antwort auf die Stimulation zeigt. Die Behandlung mit den Antagonisten zeigt eine Abhängigkeit der MCT1 Expression von PPARα, die MCT4 Expression konnte dagegen nicht beeinflusst werden. Mittels pHMB gelang es, den laktatabhängigen Protonenexport fast vollständig zu blocken. Sowohl laktatabhängiger Protonenexport als auch die Proteinexpression zeigten keine Änderung durch WY 14.643 Stimulation. Die Butyratexposition veränderte die Morphologie der Pansenepithelzellen und schien nicht geeignet für Untersuchungen der mRNA Expression zu sein. Schlussfolgerungen: Es konnte in dieser Arbeit erstmals gezeigt werden, dass MCT1 in Pansenepithelzellen über PPARα reguliert wird, nicht aber MCT4. PPARα scheint demnach einer der entscheidenden Angriffspunkte für die Regulation des SCFA Transportes zu sein, dessen natürliche Liganden im Pansen aber noch nicht bekannt sind. Damit legt diese Arbeit den Grundstein für regulative Studien am intakten Pansenepithel
Introduction: Monocarboxylate transporters (MCT) 1 & 4 are cotransporters of monocarboxylates and protons in a variety of mammalian cell types. In the ruminal epithelium MCT are necessary to transport short-chain fatty acids (SCFA) from the lumen into the ruminal epithelial cell (MCT4) and to discharge SCFA and their metabolites from the cell into the blood (MCT1). Transepithelial permeation of SCFA is of great importance, because they are the main source of energy for ruminants. The regulation of appropriate transport proteins should thus be subject to the adaptation to varying SCFA amounts. Previous studies in other species suggested that gene expression of MCT1 is regulated by peroxisome proliferator-activated receptor α (PPARα), a ligand-activated nuclear receptor. Aims: The aim of the study was to examine if MCT1 in ruminal epithelial cells is regulated by PPARα and furthermore if MCT4 can be regulated by PPARα, as well. A simultaneous regulation seems likely, because both are acting jointly in the transepithelial transporting of SCFA. The implications of such a regulation on protein expression and transport capacity of MCT should be characterized. The effect of butyrate, a SCFA which increases under concentrate feeding, on MCT1 expression was determined. Materials & Methods: Ruminal epithelial cells of sheep were cultivated according to methods previously established. After subcultivation, immunocytochemistry with antibodies against MCT1, MCT4 and Na+/K+-ATPase was performed to determine their localization in ruminal epithelial cells. For studying the influence of PPARα, WY 14.643, a synthetic and selective ligand of PPARα, and GW 6471, a synthetic antagonist of PPARα, were applied to the culture medium of the cells. After processing the specimens, the relative amount of mRNA of MCT1, MCT4 and the target genes ACO, CPT1A and CACT were analyzed by qPCR and normalized on the reference genes GAPDH and Na+/K+-ATPase. Protein abundance of MCT1 & 4 was measured by using the Western Blot method. Functional quantification was measured by the intracellular pH (pHi) of cells using spectrofluorometry as well as comparing the effect of WY 14.643 treatment on lactate-dependent proton export. To determine the MCT-dependent part of the pHi recovery, p-hydroxymercuribenzoic acid (pHMB), a specific inhibitor of MCT1 & 4, was applied. Cells were also treated with butyrate for 6 h and 48 h and the mRNA abundance of MCT1 was analyzed by semiquantitative PCR. Results: Both MCT1 and MCT4 were localized in the cell membrane as well as in the cytoplasm of ruminal epithelial cells. By qPCR it could be demonstrated that the mRNA abundance of MCT1 and PPARα target genes in the ruminal epithelial cells was increased by WY 14.643 in comparison to untreated cells, whereas the response of MCT4 did not yield distinct results. Treatment with the PPARα antagonist pointed out, that MCT1 is influenced by PPARα, but not MCT4. Lactate-dependent proton export was blocked almost completely by pHMB. Both lactate-dependent proton export and protein expression were not altered by WY 14.643 treatment. Butyrate exposure changed the morphology of ruminal epithelial cells and seemed unsuitable for the analysis of mRNA expression. Conclusion: For the first time, it could be demonstrated, that MCT1 in ruminal epithelial cells is regulated by PPARα, but not MCT4. PPARα seems to be a vital target in the rumen for SCFA transport regulation, whose natural triggers have yet to be identified. Furthermore, this study provides the basis for regulative studies on intact ruminal epithelium
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Hutchinson, Laura. "The role and therapeutic significance of monocarboxylate transporters in prostate cancer." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/the-role-and-therapeutic-significance-of-monocarboxylate-transporters-in-prostate-cancer(280f6221-d12b-4ca9-9322-e0ba1f5511f6).html.

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It has been shown that tumour cells are capable of switching to glycolytic metabolism for the production of ATP even in the presence of oxygen, this is known as aerobic glycolysis or the 'Warburg effect'. The glycolytic phenotype has been associated with tumour aggressiveness and poor outcome in several cancer types. This makes the area of cancer metabolism an attractive area for the potential identification of new therapeutic targets. One key component, required for cells to maintain the glycolytic phenotype, is the presence of monocarboxylate transporters that are capable of exporting lactate. These transporters are vital for the maintenance of the intracellular pH of cells under these conditions. This study was centred around the hypothesis that altering expression of MCTs would impact on the metabolism of tumour cells and, therefore, other key characteristics of cells relating to metastatic capabilities and survival following treatment. For the purpose of this work, prostate cancer cell lines were transfected with lentiviral particles targeting overexpression of MCT1 or MCT4, or knockdown of MCT4. Following transfection, cellular metabolic profiles were assessed under normoxic and hypoxic conditions and the metastatic phenotype of each cell line was investigated. Additionally, the effect of MCT expression on response to chemotherapy and radiation therapy was explored, and a siRNA metabolome screen was performed to identify combinations of targets that may produce synthetic lethality in prostate cancer cell lines. It was shown that changes in the expression of MCT1 or MCT4 did not cause significant changes in the metastatic phenotypes of the prostate cancer cell lines investigated. Some differences were observed in the metabolic pathways used by these prostate cancer cells following alterations in MCT expression. For example, overexpression of MCT1 in DU145 cells resulted in an increase in intracellular lactate. Additionally, MCT4 knockdown in PC3 cells was able to reduce OXPHOS under reduced oxygen. MCT1 overexpression was able to sensitise androgen-independent prostate cancer cells to treatment with chemotherapy and radiation therapy. Furthermore, combinations of siRNA treatments were identified that may be capable of producing synthetic lethality. In summary, findings in this study indicated that targeting MCT1 and MCT4 expression could offer therapeutic benefit in prostate cancer. However, it was also highlighted that the roles of these transporters are specific to cancer type, and even cell line.
9

Manoharan, Christine. "The molecular basis for the interaction between MCT1 and MCT2 with the ancillary proteins CD147 and GP70." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417644.

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Py, Guillaume. "Étude du transport sarcolemmal du lactate et de l'expression des isoformes MCT1 et MCT4 chez le rat diabétique et Zucker fa/fa." Montpellier 1, 2001. http://www.theses.fr/2001MON1T014.

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Le lactate a longtemps ete considere comme un produit final de la glycolyse et le temoin d'une limitation de l'apport en oxygene au niveau des tissus. Durant les vingt dernieres annees, grace au developpement de nouvelles techniques, des travaux ont permis de montrer que le lactate etait produit en condition d'oxygenaton normale et que celui-ci etait le substrat neoglucogenique de choix au niveau hepatique. Associe aux anomalies du metabolisme du glucose, l'etat de diabete et d'insulinoresistance sont caracterises par des lactatemies basales anormalement elevees. L'origine de ces niveaux eleves de lactate est encore mal definie. Nous avons, dans ce travail, mis en evidence des alterations des echanges sarcolemmaux du lactate dans des modeles animaux de diabete et d'obesite, a l'aide d'un modele subcellulaire que sont les vesicules de sarcolemme. [. . . ] ainsi, meme si les alterations de l'activite de transport du lactate dans le diabete de type 1 ne trouvent pas leur explication dans l'expression des isoformes musculaires de mct, il semble aux vues de donnees recentes, que ceux-ci soient quand meme impliques dans la diminution de la clearance du lactate. A la difference, la perturbation musculaire des echanges et du metabolisme du lactate dans l'obesite pourrait participer a l'etat d'insulinoresistance.
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Книги з теми "Mctp":

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Mathematics Curriculum and Teaching Program. MCTP: Professional development package. Canberra: Curriculum Development Centre, 1988.

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Cattini, Roland. Windows 7: Microsoft Certified Technology Specialist und IT Professional ; [Vorbereitung auf die Pru fungen #70-680, #70-682 und #70-685]. Heidelberg: mitp, 2010.

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Alpern, Naomi. The real MCTS/MCITP exam 70-640: Active directory configuration ; prep kit. Burlington, MA: Syngress Media, 2008.

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Alpern, Naomi. The real MCTS/MCITP exam 70-640: Active directory configuration ; prep kit. Edited by Piltzecker Anthony and Shimonski Robert J. Burlington, MA: Syngress Media, 2008.

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Robb, Richard. Exchange server 2010 portable command guide: MCTS 70-662 and MCITP 70-663. Indianapolis, Ind: Pearson IT Certification, 2011.

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Miller-White, Marilyn. MCITP. Indianapolis, Ind: Wiley Pub., Inc., 2007.

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Gibson, Darril. Windows 7 portable command guide: MCTS 70-680, and MCITP 70-685 and 70-686. Indianapolis, Ind: Pearson Education, 2011.

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Piltzecker, Tony. The real MCTS/MCITP exam 70-647 prep kit: Independent and complete self-paced solutions. Burlington, Mass: Syngress, 2008.

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Gibson, Darril. Windows Server 2008 portable command guide: MCTS 70-640, 70-642, 70-643, and MCITP 70-646, 70-647. Indianapolis, Ind: Pearson IT Certifcation, 2011.

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Barry, Eileen. MCP science. Cleveland, Ohio: Modern Curriculum Press, 1987.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "MCTD." In Encyclopedia of Molecular Mechanisms of Disease, 1270. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6275.

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Hendricks, John S., Martyn T. Swinhoe, and Andrea Favalli. "Additional Topics." In Monte Carlo N-Particle Simulations for Nuclear Detection and Safeguards, 275–92. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04129-7_5.

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AbstractCareful scrutiny of MCNP output is required to ensure the results obtained are the results desired. The principal sources of error are examined with recommendations on how to detect them and avoid them. There are some situations where the MCNP default physics treatments are inadequate and different options should be selected. Most MCNP physics is very robust, but other physics is more approximate such as charged particle transport, secondary particle emission, and radioactive activation and decay. Differences between MCNP table and model physics are highlighted.
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Hendricks, John S., Martyn T. Swinhoe, and Andrea Favalli. "Basic Concepts." In Monte Carlo N-Particle Simulations for Nuclear Detection and Safeguards, 5–154. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04129-7_2.

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AbstractThis guide for MCNP students and practitioners begins with the simplest possible example: neutrons in a single spherical surface void sphere. Examples are provided for running MCNP and plotting its geometries. Modifications to the starting geometry demonstrate the full combinatorial solid geometry capability of MCNP. Further problem input examples explain materials capabilities and physics options. Standard source capabilities enable modeling of almost any radiation particle source. Output tally and plotting options provide a full description of physical processes in a problem and what detectors see. And every MCNP calculation automatically assesses the statistical convergence of the underlying Monte Carlo sampling.
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Shi, Yong, Yingjie Tian, Gang Kou, Yi Peng, and Jianping Li. "MCLP Extensions." In Advanced Information and Knowledge Processing, 133–56. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-504-0_8.

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Hutchins, Tiffany, Giacomo Vivanti, Natasa Mateljevic, Roger J. Jou, Frederick Shic, Lauren Cornew, Timothy P. L. Roberts, et al. "MCT." In Encyclopedia of Autism Spectrum Disorders, 1813. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_100859.

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Hendricks, John S., Martyn T. Swinhoe, and Andrea Favalli. "Introduction." In Monte Carlo N-Particle Simulations for Nuclear Detection and Safeguards, 1–4. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04129-7_1.

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AbstractThis book is intended to aid nuclear safeguard scientists and engineers in more effective use of the MCNP® radiation modeling computer code. It should also be of use to both beginning and advanced users of the MCNP software in other fields and to those interested in nuclear safeguard technology and computational modeling.
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Shi, Yong, Yingjie Tian, Gang Kou, Yi Peng, and Jianping Li. "Non-additive MCLP." In Advanced Information and Knowledge Processing, 171–81. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-504-0_10.

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8

Weiss, Arnold-Peter C. "MCP Arthroplasty." In Disorders of the Hand, 231–39. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6563-7_15.

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9

Baliga, B. Jayant. "Silicon MCT." In Advanced High Voltage Power Device Concepts, 385–436. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0269-5_8.

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10

Shahid, Azmeh, Kate Wilkinson, Shai Marcu, and Colin M. Shapiro. "Munich Chronotype Questionnaire (MCTQ)." In STOP, THAT and One Hundred Other Sleep Scales, 245–47. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9893-4_58.

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Тези доповідей конференцій з теми "Mctp":

1

Hernandez Lopez, Hector, and Javier Ortiz Villafuerte. "Projection of the Neutronic and Thermal Fuel Rod Behavior in a BWR." In 12th International Conference on Nuclear Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/icone12-49137.

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Currently, at the Instituto Nacional de Investigaciones Nucleares (National Institute for Nuclear Research) in Mexico, it is being developed a computational code for evaluating the neutronic, thermal and mechanical performance of a fuel element at several different operation conditions. The code is referred as to MCTP (Multigrupos con Temperaturas y Potencia), and is benchmarked against data from the Laguna Verde Nuclear Power Plant (LVNPP). In the code, the neutron flux is approximated by six groups of energy: one group in the thermal region (E < 0.625 eV), four in the resonances region (0.625 eV < E < 0.861 MeV), and one group in the fast region (E > 0.861 MeV). Thus, the code is able to determine the damage to the cladding due to fast neutrons. The temperature distribution is approximated in both axial and radial directions taking into account the changes in the coolant density, for both the single and two-phase regions in a BWR channel. It also considerate the changes in the thermal conductivity of all materials involved for the temperature calculations, as well as the temperature and density effects in the neutron cross sections. In the code, fuel rod burnup is evaluated. Also, plutonium production and poison production from fission. In this work, the neutronic and thermal performance of fuel rods in a 10×10 fuel assembly is evaluated. The fuel elements have a content of 235U. The fuel assembly was introduced to the unit 1 of LVNPP reactor core in the cycle 9 of operation, and will stay in during three cycles. In the analysis of fuel rod performance, the operating conditions are those for the cycle 9 and 10, whereas for the current cycle (cycle 11) the reactor is projected to operate during 460 days. The analysis for cycle 11 uses the actual location of the fuel assembly that will have in the core. The results show that the fuel rods analyzed did not reach the thermal limits during the cycles 9 and 10, as expected, and for cycle 11 the same thermal limits are not predicted to be reached.
2

Eilertsen, Marte, Sigve Andersen, Samer Al-Saad, Yury Kiselev, Tom Donnem, Helge Stenvold, Khalid Al-Shibli, Elin Richardsen, Lill-Tove Busund, and Roy Martin Bremnes. "Abstract 2377: MCT1 and MCT4 in NSCLC: Overexpression of MCT1 in tumor and stroma is an independent prognostic marker for NSCLC survival." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2377.

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3

Sharma, Sambad, Gregory Goreczny, Satish Kumar Noonepalle, Erica Palmer, Maria Garcia-Hernandez, Daliya Banerjee, Jaime Escobedo, Alejandro Villagra, and Vincent Sandanayaka. "Abstract 1268: A novel treatment approach for melanoma by dually targeting MCT1 and MCT4 lactate transporters." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1268.

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4

Adams, Kenneth J. "MCNP Monte Carlo: a precis of MCNP." In Fifth International Conference on Applications of Nuclear Techniques: Neutrons in Research and Industry, edited by George Vourvopoulos. SPIE, 1997. http://dx.doi.org/10.1117/12.267945.

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5

Floch, Renaud Le, Johanna Chiche, Ibtissam Marchiq, Tanesha Naiken, Karine Ilc, Marie-Pierre Simon, Danièle Roux, and Jacques Pouyssegur. "Abstract 3225: Growth inhibition of glycolytic tumors by targeting basigin/lactate-H+ symporters (MCTs): Metformin sensitizes MCT inhibition." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3225.

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6

Hu, Yong, Daniel Mueller-Gritschneder, and Ulf Schlichtmann. "Wavefront-MCTS." In ICCAD '18: IEEE/ACM INTERNATIONAL CONFERENCE ON COMPUTER-AIDED DESIGN. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3240765.3240863.

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7

Baier, Hendrik, and Michael Kaisers. "Novelty and MCTS." In GECCO '21: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3449726.3463217.

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8

Chaffin, Antoine, Vincent Claveau, and Ewa Kijak. "PPL-MCTS: Constrained Textual Generation Through Discriminator-Guided MCTS Decoding." In Proceedings of the 2022 Conference of the North American Chapter of the Association for Computational Linguistics: Human Language Technologies. Stroudsburg, PA, USA: Association for Computational Linguistics, 2022. http://dx.doi.org/10.18653/v1/2022.naacl-main.215.

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9

Lan, Li-Cheng, Wei Li, Ting-Han Wei, and I.-Chen Wu. "Multiple Policy Value Monte Carlo Tree Search." In Twenty-Eighth International Joint Conference on Artificial Intelligence {IJCAI-19}. California: International Joint Conferences on Artificial Intelligence Organization, 2019. http://dx.doi.org/10.24963/ijcai.2019/653.

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Many of the strongest game playing programs use a combination of Monte Carlo tree search (MCTS) and deep neural networks (DNN), where the DNNs are used as policy or value evaluators. Given a limited budget, such as online playing or during the self-play phase of AlphaZero (AZ) training, a balance needs to be reached between accurate state estimation and more MCTS simulations, both of which are critical for a strong game playing agent. Typically, larger DNNs are better at generalization and accurate evaluation, while smaller DNNs are less costly, and therefore can lead to more MCTS simulations and bigger search trees with the same budget. This paper introduces a new method called the multiple policy value MCTS (MPV-MCTS), which combines multiple policy value neural networks (PV-NNs) of various sizes to retain advantages of each network, where two PV-NNs f_S and f_L are used in this paper. We show through experiments on the game NoGo that a combined f_S and f_L MPV-MCTS outperforms single PV-NN with policy value MCTS, called PV-MCTS. Additionally, MPV-MCTS also outperforms PV-MCTS for AZ training.
10

Baier, Hendrik, and Michael Kaisers. "ME-MCTS: Online Generalization by Combining Multiple Value Estimators." In Thirtieth International Joint Conference on Artificial Intelligence {IJCAI-21}. California: International Joint Conferences on Artificial Intelligence Organization, 2021. http://dx.doi.org/10.24963/ijcai.2021/555.

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This paper addresses the challenge of online generalization in tree search. We propose Multiple Estimator Monte Carlo Tree Search (ME-MCTS), with a two-fold contribution: first, we introduce a formalization of online generalization that can represent existing techniques such as "history heuristics", "RAVE", or "OMA" -- contextual action value estimators or abstractors that generalize across specific contexts. Second, we incorporate recent advances in estimator averaging that enable guiding search by combining the online action value estimates of any number of such abstractors or similar types of action value estimators. Unlike previous work, which usually proposed a single abstractor for either the selection or the rollout phase of MCTS simulations, our approach focuses on the combination of multiple estimators and applies them to all move choices in MCTS simulations. As the MCTS tree itself is just another value estimator -- unbiased, but without abstraction -- this blurs the traditional distinction between action choices inside and outside of the MCTS tree. Experiments with three abstractors in four board games show significant improvements of ME-MCTS over MCTS using only a single abstractor, both for MCTS with random rollouts as well as for MCTS with static evaluation functions. While we used deterministic, fully observable games, ME-MCTS naturally extends to more challenging settings.

Звіти організацій з теми "Mctp":

1

Conlin, Jeremy Lloyd. NJOY and MCNP. Office of Scientific and Technical Information (OSTI), October 2016. http://dx.doi.org/10.2172/1329846.

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2

Trumble, E. F. MCNP certification package. Office of Scientific and Technical Information (OSTI), August 1992. http://dx.doi.org/10.2172/10145883.

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3

Valentine, T. E. MCNP-DSP users manual. Office of Scientific and Technical Information (OSTI), January 1997. http://dx.doi.org/10.2172/296719.

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4

Whalen, D. J., D. A. Cardon, J. L. Uhle, and J. S. Hendricks. MCNP: Neutron benchmark problems. Office of Scientific and Technical Information (OSTI), November 1991. http://dx.doi.org/10.2172/10103487.

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5

Klasky, Marc Louis, Steven Charles Myers, Michael R. James, and Douglas R. Mayo. MCNP and GADRAS Comparisons. Office of Scientific and Technical Information (OSTI), April 2016. http://dx.doi.org/10.2172/1248125.

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6

Galloway, Jack D. MCNP Coupling with BISON. Office of Scientific and Technical Information (OSTI), February 2016. http://dx.doi.org/10.2172/1239066.

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7

Bingamon, Brian Michael. Feynman Award Recipient MCNP. Office of Scientific and Technical Information (OSTI), April 2020. http://dx.doi.org/10.2172/1608666.

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8

Stevens, J. G. The REBUS-MCNP linkage. Office of Scientific and Technical Information (OSTI), April 2009. http://dx.doi.org/10.2172/964248.

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9

Whalen, D. J., D. E. Hollowell, and J. S. Hendricks. MCNP: Photon benchmark problems. Office of Scientific and Technical Information (OSTI), September 1991. http://dx.doi.org/10.2172/5217899.

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10

Harmony, S. C., and B. E. Boyack. 1994 MCAP annual report. Office of Scientific and Technical Information (OSTI), April 1995. http://dx.doi.org/10.2172/93476.

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