Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autonomic neuropathy in several neurodegenerative disorders results from disturbance in physiological functions of different cell types in the central and peripheral nervous systems. For a clearer understanding of the etiology and pathogenesis of the autonomic disorders it is necessary to create animal models in which degeneration of the causative neuronal types can be induced. Immunotoxin-mediated cell targeting (IMCT) is a novel transgenic mouse technology for eliminating selective cell types with the cytotoxic activity of a recombinant immunotoxin anti-Tac(Fv)-PE40. In this study we conditionally disrupted peripheral catecholaminergic cells with IMCT to generate a mouse model developing autonomic failure based on primary defects of the sympathetic nervous system. Transgenic mice expressing human interleukin-2 receptor alpha subunit under the control of the dopamine beta-hydroxylase gene promoter were intravenously treated with a proper dose of anti-Tac(Fv)-PE40. The immunotoxin induced a selective loss of the target cells in peripheral tissues of the transgenic mice and an impairment of catecholamine metabolism in the tissues. Targeting of the peripheral catecholaminergic cells resulted in severe and progressive phenotypic abnormalities mainly characterized by cardiac dysfunction, hypoactivity, and hypothermia, which explain development of autonomic neuropathy. Our IMCT strategy is useful for elucidating the involvement of different neuronal types and their interactions in the development and symptom of autonomic disorders.
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PMID:Autonomic neuropathy in transgenic mice caused by immunotoxin targeting of the peripheral nervous system. 946 70

In this study, soluble receptor of interleukin-2, interleukin-8, creatine kinase, and creatine kinase MB isoenzyme levels were determined serially before, during, and after cardiopulmonary bypass in blood samples of 24 patients. Interleukin-2 receptor levels were 683+/-80 U/ml in the preoperative period and 640+/-60 U/ml during hypothermia. Subsequently, these levels increased significantly at the end of the procedure (791+/-70 U/ml, P<0.01), remaining elevated 1 h after (882+/-92 U/ml, P<0.001) and reaching peak values 24 h postoperatively (1,752+/-200 U/ml, P<0.001). Preoperative plasma values of interleukin-8 were 230+/-43 pg/ml. Interleukin-8 concentrations were 185+/-25 pg/ml during hypothermia. The peak interleukin-8 levels were observed at the end of cardiopulmonary bypass (754+/-94 pg/ml, P<0.001) and tended to decrease 1 h after the procedure (643+/-76 pg/ml, P<0.001), declining to preoperative values, 24 h postoperatively (273+/-41 pg/ml). Interleukin-2 receptor levels correlated well with creatine kinase levels during the procedure. Furthermore, creatine kinase MB levels were correlated with interleukin-2 receptor values only at the end and 1 h after completion of cardiopulmonary bypass. We concluded that interleukin-8 and Interleukin-2 receptor levels are elevated after cardiopulmonary bypass and may contribute to myocardial injury as reflected by increased levels of creatine kinase and creatine kinase MB and correlations between interleukin-2 receptor and both creatine kinase and creatine kinase MB levels.
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PMID:Soluble interleukin-2 receptor and interleukin-8 plasma levels during and after cardiopulmonary bypass: correlations with creatine kinase and creatine kinase MB. 1146 97