Gotowe bibliografie tematyczne / Calpain 2

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Gotowa bibliografia na temat „Calpain 2”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 13 lutego 2022

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Artykuły w czasopismach na temat "Calpain 2"

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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Wang, Yubin, Yan Liu, Xiaoning Bi, and Michel Baudry. "Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death." Cells 9, no. 12 (December 16, 2020): 2698. http://dx.doi.org/10.3390/cells9122698.

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Calpains are a family of soluble calcium-dependent proteases that are involved in multiple regulatory pathways. Our laboratory has focused on the understanding of the functions of two ubiquitous calpain isoforms, calpain-1 and calpain-2, in the brain. Results obtained over the last 30 years led to the remarkable conclusion that these two calpain isoforms exhibit opposite functions in the brain. Calpain-1 activation is required for certain forms of synaptic plasticity and corresponding types of learning and memory, while calpain-2 activation limits the extent of plasticity and learning. Calpain

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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 &#181;-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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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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Muniappan, Latha, Michihiro Okuyama, Aida Javidan, Devi Thiagarajan, Weihua Jiang, Jessica J. Moorleghen, Lihua Yang, et al. "Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice." Arteriosclerosis, Thrombosis, and Vascular Biology 41, no. 5 (May 5, 2021): 1694–709. http://dx.doi.org/10.1161/atvbaha.120.315546.

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Objective: Cytoskeletal structural proteins maintain cell structural integrity by bridging extracellular matrix with contractile filaments. During abdominal aortic aneurysm (AAA) development, (1) aortic medial degeneration is associated with loss of smooth muscle cell integrity and (2) fibrogenic mesenchymal cells mediate extracellular matrix remodeling. Calpains cleave cytoskeletal proteins that maintain cell structural integrity. Pharmacological inhibition of calpains exert beneficial effects on Ang II (angiotensin II)–induced AAAs in LDLR −/− (low-density receptor deficient) mice. Here, we

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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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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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Theopold, U., M. Pintér, S. Daffre, Y. Tryselius, P. Friedrich, D. R. Nässel, and D. Hultmark. "CalpA, a Drosophila calpain homolog specifically expressed in a small set of nerve, midgut, and blood cells." Molecular and Cellular Biology 15, no. 2 (February 1995): 824–34. http://dx.doi.org/10.1128/mcb.15.2.824.

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Calpains are calcium-dependent proteases believed to participate in calcium-regulated signal pathways in cells. Ubiquitous calpains as well as tissue-specific calpains have been found in vertebrates. We isolated cDNA clones for a highly tissue-specific calpain gene from Drosophila melanogaster, CalpA, at 56C-D on the second chromosome. The expression of the CalpA gene product was monitored by using a specific antiserum directed against the product expressed by one cDNA clone. The encoded protein is found in a few neurons in the central nervous system, in scattered endocrine cells in the midgut

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Rozprawy doktorskie na temat "Calpain 2"

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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Breiden, Maike [Verfasser], Michael [Akademischer Betreuer] Ehrmann, and Markus [Akademischer Betreuer] Kaiser. "Charakterisierung der Interaktion von HTRA1 und Calpain 2 / Maike Breiden. Gutachter: Markus Kaiser. Betreuer: Michael Ehrmann." Duisburg, 2014. http://d-nb.info/1058323385/34.

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Howells, Anwen. "The impact of innate immune cells on immunopathology in dengue." Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:0a251372-4d0e-416d-ad3c-8e07e6729e1b.

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Dengue virus (DENV) is an arthropod-borne virus and has become a worldwide problem with steadily rising annual infection rates. Patients present with a range of symptoms from mild fever to, in some cases, life-threatening hemorrhagic fever and shock syndrome. The most severe cases require emergency hospital care and currently, there is no effective drug treatment or vaccine for dengue. As severe symptoms appear post-peak viremia, immuno-pathology is thought to be the cause and a potential trigger of this is differential activation of the immune response upon recognition of DENV. This could be

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Liu, Tongzheng. "Regulation of Inflammtory Activation in Endothelial Cells by PIN1." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1242756227.

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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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Sanchez, Brualla Irene. "The potassium-chloride cotransporter KCC2 : a new therapeutic target for spasticity and neuropathic pain." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0677.

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La spasticité et la douleur neuropathique sont deux symptômes apparaissant fréquemment après une lésion médullaire. La spasticité est définie comme une augmentation du tonus musculaire qui provoque des contractures, tandis que la douleur neuropathique se caractérise par des sensations douloureuses survenant suite à une lésion du système nerveux.Ces deux symptômes résultent en partie d’une désinhibition des réseaux neuronaux sous-lésionnels lié à une diminution de l’expression du cotransporteur potassium-chlorure type 2 (KCC2). Pour être efficace,l’inhibition nécessite l’action de cette protéin

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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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Ruppert, Anne-Marie. "Rôle des calpaïnes extracellulaires dans la progression des adénocarcinomes lépidiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066317/document.

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La calpaïne 1 est une protéase à cystéine activée par le calcium, qui peut être partiellement externalisée. Les calpaines extracellulaires favorisent la résolution de l'inflammation et la réparation des tissus, à travers la prolifération et la migration cellulaire. Le récepteur Toll like (TLR) 2 a été identifié comme une cible des calpaïnes extracellulaires dans les lymphocytes. L'objectif est d'étudier le rôle de la calpaïne extracellulaire 1 dans la progression tumorale de l'adénocarcinome pulmonaire lepidique (ADL). La calpaïne extracellulaire, le fragment soluble de TLR2, le versican et le

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Hanna, Rachel. "REGULATION OF CALPAIN 2 BY CALPASTATIN." Thesis, 2010. http://hdl.handle.net/1974/5639.

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Calpains are a family of intracellular cysteine proteases activated by calcium. They participate in many processes including cell motility, cell cycle progression and cell death, in response to calcium signaling. Because calpain over-activation as a result of calcium dysregulation is a contributing factor to many disease states, these enzymes are important therapeutic targets. Within the cell, calpains 1 and 2 are regulated by the protein inhibitor calpastatin. This unstructured protein is specific for calpain, binds tightly, and recognizes only the activated form of the enzyme. Detailed

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Lal, Sangeet Kumar. "Calpain 2 proteolysis regulates glioblastoma cell invasion." Thesis, 2010. http://hdl.handle.net/1957/19988.

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Glioblastoma is the most malignant primary brain tumor with the average patients surviving only one year after diagnosis, even with aggressive therapy. The formation of numerous micro-tumors dispersed into the brain due to rapid invasion of tumor cells, presents the primary challenge to the surgical removal of tumors and limits the effectiveness of current treatments. This dissertation presents studies aimed at understanding the molecular mechanisms regulating invasion of human glioblastoma cells. Transplantation of human glioblastoma cells in the zebrafish brain showed that the knockdown of c

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Części książek na temat "Calpain 2"

Carragher, Neil O. "Calpain." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_782-2.

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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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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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Pénisson-Besnier, I., I. Richard, F. Dubas, J. S. Beckmann, and M. Fardeau. "Exercise Intolerance in Calpain Deficiency and in α-Sarcoglycanopathy." In Exercise Intolerance and Muscle Contracture, 63–66. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0855-0_6.

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Sorimachi, Hiroyuki, Shoji Hata, and Yasuko Ono. "Calpain-2/m-Calpain." In Handbook of Proteolytic Enzymes, 2007–11. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-382219-2.00454-3.

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"Calpain-2." In Class 3 Hydrolases, 61–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-85705-1_7.

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Randriamboavonjy, Voahanginirina, and Ingrid Fleming. "The Role of Calpain in Diabetes-Associated Platelet Hyperactivation." In Cardiovascular Pharmacology - Heart and Circulation, 235–57. Elsevier, 2010. http://dx.doi.org/10.1016/s1054-3589(10)59008-2.

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Streszczenia konferencji na temat "Calpain 2"

Singh, Vinay K., Jacqueline C. Kelly, R. John MacLeod, and Zongchao Jia. "Abstract 4226: Curcumin induced CaSR stimulates calpain autolysis in colon cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4226.

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Supinski, Gerald S., Alexander Alimov, Lin Wang, Xiao-Hong Song, and Leigh Ann P. Callahan. "NSmase 2 Is Required For Infection Induced Skeletal Muscle Calpain Activation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2716.

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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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Puri, R. N., F. Zhou, H. Bradford, E. J. Gustafson, R. F. Colman, and R. W. Colman. "HIGH MOLECULAR WEIGHT KININOGEN SPECIFICALLY BLOCKS THROMBIN-INDUCED AGGREGATION BY INHIBITING PLATELET CALPAIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643860.

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We have previously shown that platelet-aggregation induced by alpha-thrombin (1.7 nM) involves complete cleavage of the surface membrane polypeptide, Mr = 100 kDa (MP 100) labeled by FSBA in intact platelets. The failure to cleave MP100 in membrane preparations or in platelets treated with metabolic inhibitors or leupeptin, suggested that thrombin was acting by activating platelet calpain. Since high molecular weight kininogen (HMWK) is the most potent plasma inhibitor of calpain(s), we now report that HMWK inhibited thrombin-induced aggregation in a dose-dependent manner over a range of plasm

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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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Landowski, Terry H., Aluvia M. Escalante, Ryan McGrath, Matthew R. Karolak, Meredith Henderson, Georgia O. Perrian, and Ron Lynch. "Abstract 2643: Inhibition of calpain disrupts the autophagic response initiated by bortezomib resulting in increased death of myeloma cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2643.

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Wallace, Robert W., E. Ann Tallant, and Lynn M. Brumley. "POSSIBLE ROLE FOR THE CA2+-DEPENDENT PROTEASE (CALPAIN I) AS AN IRREVERSIBLE ACTIVATOR OF CA2+/CALMODULIN-MEDIATED REACTIONS IN THE HUMAN PLATELET." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644528.

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Calmodulin (CaM)-binding proteins have been identified in human platelets using Western blotting techniques and 125I-CaM. Ten proteins of 245, 225. 175, 150, 90. 82(2), 60 and 41(2) kilodaltons (kDa) bind 125I-CaM in a Ca2+-dependent manner; the binding is blocked by both trifluoperazine and nonradiolabeled CaM. The 225 and 90 kDa proteins are labeled by antisera against myosin light chain kinase (MLCK); the 60 kDa and one of the 82 kDa proteins have been identified as the CaM-dependent phosphatase (calcineurin) and caldesmon. The other proteins are presumed to be other Ca2+/CaM regulated enzy

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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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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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