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Academic literature on the topic 'YC 5824'
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Journal articles on the topic "YC 5824"
Yu, S. M., Z. J. Cheng, J. H. Guh, F. Y. Lee, and S. C. Kuo. "Mechanism of anti-proliferation caused by YC-1, an indazole derivative, in cultured rat A10 vascular smooth-muscle cells." Biochemical Journal 306, no. 3 (March 15, 1995): 787–92. http://dx.doi.org/10.1042/bj3060787.
Full textHayes, J. D., D. J. Judah, L. I. McLellan, L. A. Kerr, S. D. Peacock, and G. E. Neal. "Ethoxyquin-induced resistance to aflatoxin B1 in the rat is associated with the expression of a novel Alpha-class glutathione S-transferase subunit, Yc2, which possesses high catalytic activity for aflatoxin B1-8,9-epoxide." Biochemical Journal 279, no. 2 (October 15, 1991): 385–98. http://dx.doi.org/10.1042/bj2790385.
Full textFrigolet, María E., Garry Thomas, Kristin Beard, Huogen Lu, Lijiang Liu, and I. George Fantus. "The bradykinin-cGMP-PKG pathway augments insulin sensitivity via upregulation of MAPK phosphatase-5 and inhibition of JNK." American Journal of Physiology-Endocrinology and Metabolism 313, no. 3 (September 1, 2017): E321—E334. http://dx.doi.org/10.1152/ajpendo.00298.2016.
Full textXu, Zhelong, Xiang Ji, and Philip G. Boysen. "Exogenous nitric oxide generates ROS and induces cardioprotection: involvement of PKG, mitochondrial KATP channels, and ERK." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 4 (April 2004): H1433—H1440. http://dx.doi.org/10.1152/ajpheart.00882.2003.
Full textCuevas, Santiago, Yu Yang, Laureano Assico, Jun Feranil, John Jones, Ines Armando, and Pedro A. Jose. "Abstract 75: Nrf2 Mediates the Antioxidant Effect of D2r Via Dj-1 in the Kidney." Hypertension 62, suppl_1 (September 2013). http://dx.doi.org/10.1161/hyp.62.suppl_1.a75.
Full textRocha, Layla Louise de Amorim, Matheus Francisco Barros Rodrigues, Rimsky Coelho Lopes da Rocha, Rodrigo da Franca Acioly, Daniel do Carmo Carvalho, Dennis Dinelly de Souza, and Cristofe Coelho Lopes da Rocha. "Recomendações em cirurgias bucomaxilofaciais de urgência e emergência em tempos de COVID-19." ARCHIVES OF HEALTH INVESTIGATION 9, no. 4 (October 6, 2020). http://dx.doi.org/10.21270/archi.v9i4.5031.
Full textDissertations / Theses on the topic "YC 5824"
Witt, Heiko. "Genetische Grundlagen der chronischen Pankreatitis." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/13963.
Full textThe recent discoveries of trypsinogen (PRSS1) and trypsin inhibitor (SPINK1) mutations in patients with hereditary and idiopathic chronic pancreatitis support the hypothesis that an inappropriate activation of pancreatic zymogens to active enzymes within the pancreatic parenchyma initiates the inflammatory process. Thus, pancreatitis may be the result of an imbalance of proteases and their inhibitors within the pancreatic parenchyma. Since the first description of inherited pancreatitis reported an autosomal dominant trait, hereditary CP was defined as an rare dominant inherited disease. Subsequently, the fact of familial clustering in one generation only, which indicates other inheritance pattern such as recessive or complex trait, was blinded out in the disease concept of hereditary CP for a long time. The Identification of PRSS1, SPINK1 and CFTR mutations in patients with so-called idiopathic chronic pancreatitis, however, shows that inherited cases of CP are much more frequent and that different mutations in different genes might lead to different inheritance pattern. Evaluation of patients with CP without an obvious predisposing factor should include genetic testing for mutations in the above mentioned genes even in the absence of a family history of pancreatitis. The finding of SPINK1 mutations in alcohol-induced pancreatitis indicates that genetic factors genetic factors may increase disease susceptibility to primary non-hereditary CP types. This work summarises the significance of genetic factors in the pathogenesis of hereditary and idiopathic as well as alcoholic chronic pancreatitis. Thus, the identification of further genes involved into the pathogenesis of inherited CP probably will also enhance our knowledge about more common types of CP such as alcoholic or tropical CP.