Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The calpains form a growing family of structurally related intracellular multidomain cysteine proteinases containing a papain-related catalytic domain, whose activity depends on calcium. The calpains are believed to play important roles in cytoskeletal remodeling processes, cell differentiation, apoptosis and signal transduction, but are also implicated in muscular dystrophy, cardiac and cerebral ischemia, platelet aggregation, restenosis, neurodegenerative diseases, rheumatoid arthritis and cataract formation. The best characterized calpains, the ubiquitously expressed mu- and m-calpains, are heterodimers consisting of a common 30-kDa small and a variable 80-kDa subunit. The recently determined crystal structures of human and rat m-calpain crystallized in the absence of calcium essentially explain the inactivity of the apoform by catalytic domain disruption, indicate several sites where calcium could bind causing reformation of a papain-like catalytic domain, and additionally reveal modes by which phospholipid membranes could reduce the calcium requirement. Current evidence points to a cooperative interaction of several sites, which, upon calcium binding, trigger the reformation of a papain-similar catalytic domain.
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PMID:The structure of calcium-free human m-calpain: implications for calcium activation and function. 1167 52

Autonomic regulation of the heart was examined in 5 groups of rats: intact, sham-operated, experimental chronic obstructive pulmonary disease, acute cerebral ischemia, and acute cerebral ischemia modeled against the background of chronic obstructive pulmonary disease. The latter was provoked by combination of inhaled papain and intraperitoneal bacterial LPS, whereas acute cerebral ischemia was modeled by single-stage bilateral occlusion of the common carotid arteries. Chronic obstructive pulmonary disease was verified by X-ray computed microtomography. The disturbances in autonomic control of the heart during comorbid pathologies were most prominent; they were manifested by overstrain and decompensation of the mechanisms implicated in the heart control and systolic-diastolic arterial hypotension. The correlations were established between blood oxygenation, respiration rate, and some parameters of autonomic cardiac regulation. The data attest to relevance and usefulness of the developed model of respiratory and cerebrovascular comorbidity in assessment of pathophysiological mechanisms underlying dysregulation of the heart and the development of personalized approaches for its pharmacological correction.
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PMID:Autonomic Cardiac Regulation in Experimental Comorbidity of Chronic Obstructive Pulmonary Disease and Acute Cerebral Ischemia. 3102 May 85