Relevant bibliographies by topics / Calpain 1

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Calpain 1'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Calpain 1"

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Upla, Paula, Varpu Marjomäki, Liisa Nissinen, Camilla Nylund, Matti Waris, Timo Hyypiä, and Jyrki Heino. "Calpain 1 and 2 Are Required for RNA Replication of Echovirus 1." Journal of Virology 82, no. 3 (November 21, 2007): 1581–90. http://dx.doi.org/10.1128/jvi.01375-07.

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ABSTRACT Calpains are calcium-dependent cysteine proteases that degrade cytoskeletal and cytoplasmic proteins. We have studied the role of calpains in the life cycle of human echovirus 1 (EV1). The calpain inhibitors, including calpeptin, calpain inhibitor 1, and calpain inhibitor 2 as well as calpain 1 and calpain 2 short interfering RNAs, completely blocked EV1 infection in the host cells. The effect of the inhibitors was not specific for EV1, because they also inhibited infection by other picornaviruses, namely, human parechovirus 1 and coxsackievirus B3. The importance of the calpains in E
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Weber, Jonasz J., Eva Haas, Yacine Maringer, Stefan Hauser, Nicolas L. P. Casadei, Athar H. Chishti, Olaf Riess, and Jeannette Hübener-Schmid. "Calpain-1 ablation partially rescues disease-associated hallmarks in models of Machado-Joseph disease." Human Molecular Genetics 29, no. 6 (January 21, 2020): 892–906. http://dx.doi.org/10.1093/hmg/ddaa010.

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Abstract Proteolytic fragmentation of polyglutamine-expanded ataxin-3 is a concomitant and modifier of the molecular pathogenesis of Machado–Joseph disease (MJD), the most common autosomal dominant cerebellar ataxia. Calpains, a group of calcium-dependent cysteine proteases, are important mediators of ataxin-3 cleavage and implicated in multiple neurodegenerative conditions. Pharmacologic and genetic approaches lowering calpain activity showed beneficial effects on molecular and behavioural disease characteristics in MJD model organisms. However, specifically targeting one of the calpain isofo
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Ben-Aharon, Irit, Paula R. Brown, Nir Etkovitz, Edward M. Eddy, and Ruth Shalgi. "The expression of calpain 1 and calpain 2 in spermatogenic cells and spermatozoa of the mouse." Reproduction 129, no. 4 (April 2005): 435–42. http://dx.doi.org/10.1530/rep.1.00255.

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There is some evidence suggesting that Ca2+is involved in processes that occur during the development and function of spermatozoa. Calcium-dependent proteins, such as calmodulin, are expressed during mammalian spermatogenesis further suggesting that Ca2+takes part in its regulation. However, the precise roles of Ca2+in spermatogenesis remain to be elucidated. Calpains are a family of Ca2+-dependent cysteine proteases whose members are expressed ubiquitously or in a tissue-specific manner. Calpain has been demonstrated to mediate specific Ca2+-dependent processes including cell fusion, mitosis
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Baudry, Michel. "Calpain-1 and Calpain-2 in the Brain: Dr. Jekill and Mr Hyde?" Current Neuropharmacology 17, no. 9 (August 22, 2019): 823–29. http://dx.doi.org/10.2174/1570159x17666190228112451.

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While the calpain system has now been discovered for over 50 years, there is still a paucity of information regarding the organization and functions of the signaling pathways regulated by these proteases, although calpains play critical roles in many cell functions. Moreover, calpain overactivation has been shown to be involved in numerous diseases. Among the 15 calpain isoforms identified, calpain-1 (aka µ-calpain) and calpain-2 (aka m-calpain) are ubiquitously distributed in most tissues and organs, including the brain. We have recently proposed that calpain-1 and calpain- 2 play op
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Murphy, Robyn M., Rodney J. Snow та Graham D. Lamb. "μ-Calpain and calpain-3 are not autolyzed with exhaustive exercise in humans". American Journal of Physiology-Cell Physiology 290, № 1 (січень 2006): C116—C122. http://dx.doi.org/10.1152/ajpcell.00291.2005.

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μ-calpain and calpain-3 are Ca2+-dependent proteases found in skeletal muscle. Autolysis of calpains is observed using Western blot analysis as the cleaving of the full-length proteins to shorter products. Biochemical assays suggest that μ-calpain becomes proteolytically active in the presence of 2–200 μM Ca2+. Although calpain-3 is poorly understood, autolysis is thought to result in its activation, which is widely thought to occur at lower intracellular Ca2+ concentration levels ([Ca2+]i; ∼1 μM) than the levels at which μ-calpain activation occurs. We have demonstrated the Ca2+-dependent aut
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McCartney, Christian-Scott E., Qilu Ye, Robert L. Campbell, and Peter L. Davies. "Insertion sequence 1 from calpain-3 is functional in calpain-2 as an internal propeptide." Journal of Biological Chemistry 293, no. 46 (September 25, 2018): 17716–30. http://dx.doi.org/10.1074/jbc.ra118.004803.

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Calpains are intracellular, calcium-activated cysteine proteases. Calpain-3 is abundant in skeletal muscle, where its mutation-induced loss of function causes limb-girdle muscular dystrophy type 2A. Unlike the small subunit–containing calpain-1 and -2, the calpain-3 isoform homodimerizes through pairing of its C-terminal penta-EF-hand domain. It also has two unique insertion sequences (ISs) not found in the other calpains: IS1 within calpain-3's protease core and IS2 just prior to the penta-EF-hand domain. Production of either native or recombinant full-length calpain-3 to characterize the fun
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Covington, Marisa D., David D. Arrington, and Rick G. Schnellmann. "Calpain 10 is required for cell viability and is decreased in the aging kidney." American Journal of Physiology-Renal Physiology 296, no. 3 (March 2009): F478—F486. http://dx.doi.org/10.1152/ajprenal.90477.2008.

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Aging is associated with abnormalities in kidney function, but the exact mechanisms are unknown. We examined calpains 1, 2, and 10 protein levels in kidneys from rats, mice, and humans of various ages and determined whether calpain 10 is required for cell viability. Calpain 10 protein expression decreased in the kidney, but not in the liver, of aging Fischer 344 rats, and this decrease was attenuated with caloric restriction. There was no change in calpains 1 or 2 levels in the kidney or liver in control and caloric-restricted aging rats. Aging mice also exhibited decreased calpain 10 protein
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Piper, Ann-Katrin, Reece A. Sophocleous, Samuel E. Ross, Frances J. Evesson, Omar Saleh, Adam Bournazos, Joe Yasa, et al. "Loss of calpains-1 and -2 prevents repair of plasma membrane scrape injuries, but not small pores, and induces a severe muscular dystrophy." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1226—C1237. http://dx.doi.org/10.1152/ajpcell.00408.2019.

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The ubiquitous calpains, calpain-1 and -2, play important roles in Ca2+-dependent membrane repair. Mechanically active tissues like skeletal muscle are particularly reliant on mechanisms to repair and remodel membrane injury, such as those caused by eccentric damage. We demonstrate that calpain-1 and -2 are master effectors of Ca2+-dependent repair of mechanical plasma membrane scrape injuries, although they are dispensable for repair/removal of small wounds caused by pore-forming agents. Using CRISPR gene-edited human embryonic kidney 293 (HEK293) cell lines, we established that loss of both
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Pánico, Pablo, Marcia Hiriart, Patricia Ostrosky-Wegman, and Ana María Salazar. "TUG is a calpain-10 substrate involved in the translocation of GLUT4 in adipocytes." Journal of Molecular Endocrinology 65, no. 3 (October 2020): 45–57. http://dx.doi.org/10.1530/jme-19-0253.

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The calpain-10 (CAPN10) protease is implicated in the translocation of the glucose transporter 4 (GLUT4), which is retained in the Golgi matrix via the Tether containing a UBX domain for GLUT4 (TUG) protein. Insulin stimulation induces the proteolytic processing of TUG, which leads to the translocation of GLUT4 to the cell membrane. We tested whether TUG is a CAPN10 substrate. Proteolysis of TUG by calpains was assessed using a cell-free system containing calpain-1 and TUG. In situ proteolysis of TUG by calpains was demonstrated in 3T3-L1 adipocytes in the presence of insulin or calpain inhibi
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Ou, B. R., and N. E. Forsberg. "Determination of skeletal muscle calpain and calpastatin activities during maturation." American Journal of Physiology-Endocrinology and Metabolism 261, no. 6 (December 1, 1991): E677—E683. http://dx.doi.org/10.1152/ajpendo.1991.261.6.e677.

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Our objectives were to characterize events underlying changes in skeletal muscle calpain and calpastatin activities, using maturation as a model. Muscle samples were taken from rabbits of four ages (newborn and 1, 2, and 5 mo old). Concentrations of RNA and protein and activities of calpains I and II and calpastatin were determined. Steady-state concentrations of mRNAs encoding calpain I, calpain II, calpastatin, alpha- and beta-tubulin, and beta-actin were determined using Northern blot analysis. Calpain and calpastatin activities declined markedly between birth and 1 mo of age and remained u
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Dissertations / Theses on the topic "Calpain 1"

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Ishak, Reezal. "Calpain-1 : investigating its role in murine neutrophils." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/37448/.

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Neutrophils are phagocytic white blood cells which act as the first line of defence against entry of foreign microorganisms. Neutrophils are recruited to their target site through the process of spreading, extravasation and phagocytosis involving complex signal transduction within the cells, which might include the activation of the cytosolic Ca2+ activated protease, calpain-1. The work described here investigates the role of calpain-1 in regulating neutrophil functions such as spreading, trans-endothelial migration, chemotaxis, phagocytosis and Ca2+ signalling. Through the work done at Europe
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Hanouna, Guillaume. "Rôle des calpaïnes dans le vieillissement et la réponse anti-tumorale." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066385/document.

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Les calpaïnes 1 et 2 sont des protéases à cystéine ubiquitaires et la calpastatine est leur inhibiteur naturel, également ubiquitaire. Les calpaïnes sont impliquées dans le développement de la réponse inflammatoire via l’activation par protéolyse partielle de plusieurs substrats (activation de NF-κB par le clivage de I-κBα, remodelage du cytosquelette des cellules inflammatoires, clivage de la protéine chaperonne HSP 90…).Il a été précédemment démontré que les calpaïnes favorisent le vieillissement neuronal. Nous avons pu montrer dans un modèle murin que l’inhibition in vivo des calpaïnes par
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Mendes, Atlante Silva. "Verapamil diminui a expressão proteica de calpaína-1 e metaloproteinase de matriz-2 na hipertrofia cardíaca induzida por hipertensão renovascular." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-08112018-150232/.

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Introdução: A hipertrofia cardíaca induzida por sobrecarga hemodinâmica crônica (HC) é caracterizada por espessamento das paredes do ventrículo esquerdo e do tecido intersticial. As atividades aumentadas de calpaína-1 e metaloproteinase de matriz(MMP)-2 são observadas em diferentes modelos de hipertensão arterial e estão relacionadas com as mudanças fisiopatológicas na HC. Por outro lado, a atividade de MMP-2 parece ser modulada positivamente por ativação de calpaína-1 em diferentes modelos. O objetivo deste trabalho é analizar se a calpaína-1 contribui para o aumento da atividade de MMP-2 no
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Marion, Allison. "La calpaïne - 6 : une nouvelle cible thérapeutique dans les ostéosarcomes." Paris 7, 2011. http://www.theses.fr/2011PA077134.

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Les ostéosarcomes sont des tumeurs fortement résistantes à la chimiothérapie, qui récidivent et métastasent de façon fréquente. L'objectif de ce travail est d'identifier de nouveaux mécanismes régulant la réponse aux agents cytotoxiques. Précédemment, nous avons mis en évidence le rôle du syndécan-2 dans le contrôle de l'apoptose et la réponse aux agents cytotoxiques des cellules d'ostéosarcome. Ici, nous nous sommes intéressés à la calpaïne-6, l'un des gènes modulés par le syndécan-2. Nous avons montré que le syndécan-2 diminue l'expression de la calpaïne-6 en inhibant les voies de signalisat
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Peltier, Julie. "Implication du TGF-BETA1 et des calpaïnes dans la glomérulopathie induite par les anticorps anti-membrane basale glomérulaire." Paris 7, 2006. http://www.theses.fr/2006PA077129.

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La réaction inflammatoire au cours des glomérulonéphrites est régulée par de nombreux médiateurs. Parmi eux, le transforming growth factor-beta1 (TGF-β1) peut jouer un rôle anti-inflammatoire, tandis que les calpaïnes, cystéines proteases activées par le calcium, favorisent la réaction inflammatoire. Nous montrons d'abord que le TGF-β1 augmente la synthèse du récepteur des glucocorticoïdes, par le biais des protéines Srnad 2/3 et AP-1. Et qu'il contribue à l'inhibition de la réaction macrophagique. Ensuite, nous montrons que l'activité calpaïne est augmentée dans le cortex rénal au cours des g
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Stroop, Davis M. "The Epidemiology of Early Type 2 Diabetes Mellitus in Black and White Females: Genetic and Environmental Factors." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1377870493.

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Muir, Matthew Stewart. "Proteomics of the ovine cataract." Diss., Lincoln University, 2008. http://hdl.handle.net/10182/792.

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The lens of the eye needs to be completely transparent in order to allow all light entering the eye to reach the retina. This transparency is maintained by the highly ordered structure of the lens proteins the crystallins. Any disruption to the lens proteins can cause an opacity to develop which is known as cataract. During cortical cataract formation there is increased truncation of the lens crystallins. It is believed that overactivation of calcium-dependent cysteine proteases, the calpains, is responsible for the increased proteolysis of the crystallins seen during cataractogenesis. Within
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Kriegel, Christian. "Untersuchungen zur kapazitationsassoziierten Signaltransduktion in humanen Spermatozoen und Evaluation des MACS-Verfahrens zur Ejakulataufbereitung." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-114339.

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Als Kapazitation bezeichnet man den im weiblichen Reproduktionstrakt stattfindenden Reifungsschritt, der Spermien das volle Fertilisierungspotential verleiht. Die molekularbiologischen Grundlagen dieses für eine erfolgreiche natürliche oder auch artifizielle Befruchtung essenziellen Prozesses sind bis heute nur unvollständig verstanden. Im Rahmen der vorliegenden Dissertation wurden die mit der Kapazitation einhergehenden funktionellen und strukturellen spermalen Veränderungen untersucht. Die kapazitative Stimulation führte zu einer gesteigerten Motilität bis hin zur Hyperaktivierung, zu eine
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Moubarak, Rana. "Caractérisation de la voie de mort cellulaire programmée induite par le dommage à l'ADN : rôles de PARP-1, calpaine, Bax et AIF." Paris 6, 2007. http://www.theses.fr/2007PA066045.

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Le dommage à l’ADN induit une mort cellulaire programmée de type nécrotique à travers les poly(ADP-ribose) polymerases (PARP) et Apoptosis-Inducing Factor (AIF). Suite à l’activation de PARP, AIF est relargué de la mitochondrie et transloque au noyau où il cause la condensation de la chromatine et la fragmentation de l’ADN. Nous avons identifié deux liens moléculaires entre PARP et AIF: les calpaines et Bax. Le dommage à l’ADN induit une mort indépendante de p53 mais impliquant PARP-1 et pas PARP-2. La nécrose due à la sortie d’AIF de la mitochondrie est dépendante des calpaines, mais pas des
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Fromberg, Iris [Verfasser]. "Immunhistochemische Untersuchungen zur Expression von Calpain 1, Calpain 2 und Calpastatin in Endometrium- und Ovarialkarzinom / vorgelegt von Iris Fromberg." 2009. http://d-nb.info/1006602755/34.

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Books on the topic "Calpain 1"

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Messer, Jeannette S., ed. Calpain. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1.

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Book chapters on the topic "Calpain 1"

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Calpain." In Encyclopedia of Signaling Molecules, 225–28. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_23.

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Carragher, Neil O. "Assaying Calpain Activity." In Adhesion Protein Protocols, 109–19. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-353-0_9.

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Biswas, Ashim Kumar, and Samarth Tandon. "Casein Zymography for Analysis of Calpain-1 and Calpain-2 Activity." In Methods in Molecular Biology, 31–38. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_3.

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Nguyen, Anh T. H., Matthew Campbell, Paul F. Kenna, Anna-Sophia Kiang, Lawrence Tam, Marian M. Humphries, and Peter Humphries. "Calpain and Photoreceptor Apoptosis." In Retinal Degenerative Diseases, 547–52. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_69.

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Biswas, Ashim Kumar, and Samarth Tandon. "Single-Step Purification of Calpain-1, Calpain-2, and Calpastatin Using Anion-Exchange Chromatography." In Methods in Molecular Biology, 3–11. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_1.

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Wang, Kevin K. W. "Calpain Zymography: General Methodology and Protocol." In Zymography, 279–85. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7111-4_26.

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del Carmen Lafita-Navarro, Maria, and Maralice Conacci-Sorrell. "Identification of Calpain-Activated Protein Functions." In Methods in Molecular Biology, 149–60. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_12.

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Samanta, Krishna, Pulak Kar, Tapati Chakraborti, and Sajal Chakraborti. "An Overview of Endoplasmic Reticulum Calpain System." In Proteases in Health and Disease, 3–19. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9233-7_1.

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duVerle, David A., and Hiroshi Mamitsuka. "CalCleaveMKL: a Tool for Calpain Cleavage Prediction." In Methods in Molecular Biology, 121–47. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_11.

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Kitagawa, Seiichi. "Experimental Manipulation of Calpain Activity In Vitro." In Methods in Molecular Biology, 209–18. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8988-1_16.

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Conference papers on the topic "Calpain 1"

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Colman, Robert W., Harlan Bradford, and Anjanayaki Annamalai. "FACTOR V IS ACTIVATED AND CLEAVED BY PLATELET CALPAIN: COMPARISON WITH THROMBIN PROTEOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643884.

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Platelets are known to process human and bovine factor V during secretion and/or membrane binding. We therefore studied the functional and structural changes produced in human factor V and Va by purified platelet calpain. A maximum increase in factor V coagulant activity of 2.5-fold over control incubations was observed for calpain (0.6 u/ml) at 25°C in comparison with a 10-fold increment for a thrombin (1 u/ml). Thrombin addition to reactions initiated by calpain resulted in further activation comparable to that of thrombin alone, while subsequent addition of calpain had no effect on the exte
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verhallen, P. F. J., E. M. Bevers, P. Comfurius, W. M. A. Linkskens, and R. F. A. Zwaal. "CALPAIN-MEDIATED CYTOSKELETAL DEGRADATION CORRELATES WITH STIMULATION OF PLATELET PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642821.

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We have shown earlier that the negatively charged phospholipid phosphatidylserine (PS), which becomes translocated from the inner surface to the outer surface of the plasma membrane upon platelet activation, is responsible for platelet procoagulant activity. Studies with erythrocytes have suggested a role for cytoskeletal proteins in the regulation of transmembrane asymmetry of PS. The possibility that platelet cytoskeletal proteins are involved in the loss of transmembrane asymmetry of PS, was explored by correlative investigations of both platelet prooagulant activity and activity of calpain
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Oh, Eunhye, Daeil Sung, Youngkwan Cho, Ji Young Kim, Nahyun Lee, Yoon-Jae Kim, Tae-Min Cho, and Jae Hong Seo. "Abstract 5463: Disulfiram suppresses metastasis via induction of anoikis and calpain activation in triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5463.

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Okita, J. R., M. M. Frojmovic, S. Kristopeit, T. Wong, and T. J. Kunicki. "MONTREAL PLATELET SYNDROME: DECREASED ACTIVITY OF PLATELET CALPAINS ASSOCIATED WITH AGGREGATION ABNORMALITIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642822.

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The Montreal platelet syndrome (MPS) is an inherited disorder of platelet function characterized by a) severe thrombocytopenia, b) formation of "giant" platelets upon physical or biochemical stimulation, c) spontaneous aggregation (stir-induced microaggregate formation) and d) a lack of aggregation in response to thrombin. The Bernard-Soulier syndrome (BSS) is similar to MPS in that both syndromes are characterized by "giant" platelets and an abnormal aggregation response to thrombin. BSS patients have a deficiency of specific platelet glycoproteins (GPs). From our investigations we conclude M
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Choo, Y., T. Sakai, R. Ikebe, A. Jeffers, S. Idell, T. A. Tucker, and M. Ikebe. "Calponin 1 Promotes Myofibroblast Differentiation of Human Pleural Mesothelial Cells During Mesothelial Mesenchymal Transition." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4420.

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Berndt, M. "STRUCTURE AND FUNCTION OF THE GLYCOPROTEIN Ib-IX COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643729.

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At high shear flow, the adhesion of platelets to the exposed vascular subendothelium requires von Willebrand factor (vWF) and is dependent upon a specific platelet membrane adhesion receptor, the human platelet membrane glycoprotein (GP) Ib-IX complex. Recent evidence suggests that vWFbinding to the GP Ib-IX complex plays an important role in other key aspects of hemostasis and thrombosis such as shear-induced platelet aggregation and the interaction of platelets with fibrin.Studies in our laboratory with a seriesof murine monoclonal antibodies directed against epitopes on GP lb, GP IX, or aga
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Driscoll, Tristan P., Su-Jin Heo, and Robert L. Mauck. "Dynamic Tensile Loading and Altered Cell Contractility Modulate Nuclear Deformation and Cytoskeletal Connectivity." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80550.

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Effective use of progenitor cells in orthopaedic tissue engineering will require a thorough understanding of the mechanisms by which forces are transmitted and sensed, and how these change with differentiation. Nesprins are a family of structural proteins that partially localize to the nuclear envelope where they interact with both cytoskeletal and nucleoskeletal proteins [1]. At their C-terminus, nesprins interact through a KASH domain with proteins of the nuclear membrane, including SUN and Lamin A/C [1]. Multiple isoforms of the 4 nesprin genes are produced by alternative transcriptional in
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Lavenne-Pardonge, E., C. Col-De Beys, R. Dion, R. Ponlot, and M. Moriau. "EFFECT OF ANTIAGGREGANT ON OCCLUSION OF SAPHENOUS GRAFT CORONARY BYPASS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644823.

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Double blind study on 49 patients, 24receiving aspirine-dipyri-damole, 25 a placebo. In both groups 20 patients were followed during one year. The two groupsdid not differ according to age, sex and number of coronary bypass. In all the patients, Calparin (3 x 5000 U/day) was injected subcutanously the day before andthe 7 days after surgery. In the first group dipyridamole (25 mg/ kg) was injected during the same period. The second group received a placebo IV injection. Thereafter long acting dipyridamole (400 mg/day) and aspirin (200 mg/day) were given orally in the first group, placebo in the
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9

Ishiguro, H., S. Higashiyama, C. Namikawa, I. Ohkubo, and M. Sasaki. "MAPPING OF FUNCTIONAL DOMAINS OF HUMAN HIGH MOLECULAR WEIGHT (HMW) AND LOW MOLECULAR WEIGHT (LMW) KININOGENS BY USING MURINE MONOCLONAL ANTIBODIES (MAbs)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642849.

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It has been widely known that HMW and LMW kininogens are the large potential sources of kinin in human blood, and that HMW kininogen also functions as a cofactor in the contact activation of blood coagulation. Recently, it has been demonstrated that the heavy chains of kininogens strongly inhibited a number of cysteine proteinases such as calpains, cathepsins, papain and ficin. We made an attempt at mapping of functional domains on the molecules of both kininogens by using MAbs.Thirty four MAbs raised against human HMW and LMW kininogens were screened by ELISA. By using HMW kininogen, kinin-fr
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10

McCarrick, Michael T., and Robert K. Rosencrance. "World’s First LM5000 to LM6000 Cogeneration Plant Repowering." In ASME Turbo Expo 2000: Power for Land, Sea, and Air. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/2000-gt-0190.

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With the introduction of GE’s latest and most efficient gas turbine, the LM6000 in 1992, and the end of production of GE’s LM5000 gas turbine in 1997, the concept of repowering aging LM5000 gas turbine powered cogeneration plants with LM6000 gas turbines was an idea that most LM5000 owners and operators dreamed about. The LM6000 is an ideal replacement for the LM5000 as they both have nearly the same mass flow and exhaust gas temperature (critical for Heat Recovery Steam Generator (HRSG) compatibility), are about the same physical weight and dimensions, and can be operated in the same power ra
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