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)

Review of our experience in the diagnosis and treatment of 44 patients with inferior vena cava tumoral thrombosis (IVCTT), associated or not to other neoplastic processes: 34 hypernephroma, 2 cava leiomyosarcoma, 1 paratesticular rhabdomyosarcoma and 1 biphasic synovial sarcoma. Twenty-five patients with hypernephroma and tumor thrombi in the ipsilateral renal vein only were excluded from the analysis since this fact did not change the usual therapeutic approach. In the 19 remaining patients, concomitantly to the primary tumour exeresis a thrombectomy was performed, using cavotomy with proximal and distal clamping in 11 patients and cardiopulmonary by-pass, deep hypothermia and cardiocirculatory arrest in 8 patients. The paper analyzes the radiological investigations performed in order to reach a IVCTT diagnosis, and reviews the related literature.
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PMID:[Tumor thrombosis in inferior vena cava: diagnostic imaging and therapeutic approximation]. 150 99

In recent years, the phosphoinositide-3-kinase/Akt cell survival signaling pathway has been increasingly researched in the field of stroke. Akt activity is suggested to be upregulated by phosphorylation through the activation of receptor tyrosine kinases by growth factors. Although the upstream signaling components phosphoinositide-dependent protein kinase (PDK)1 and integrinlinked kinase enhance the activity of Akt, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) decreases it. Upon activation, Akt phosphorylates an array of molecules, including glycogen synthase kinase3beta (GSK3beta), forkhead homolog in rhabdomyosarcoma (FKHR), and Bcl-2-associated death protein, thereby blocking mitochondrial cytochrome c release and caspase activity. Generally, the level of Akt phosphorylation at site Ser 473 (P-Akt) transiently increases after focal ischemia, whereas the levels of phosphorylation of PTEN, PDK1, forkhead transcription factor, and GSK3beta decrease. Numerous compounds (such as growth factors, estrogen, free radical scavengers, and other neuroprotectants) reduce ischemic damage, possibly by upregulating P-Akt. However, preconditioning and hypothermia block ischemic damage by inhibiting an increase of P-Akt. Inhibition of the Akt pathway blocks the protective effect of preconditioning and hypothermia, suggesting the Akt pathway contributes to their protective effects and that the P-Akt level does not represent its true kinase activity. Together, attenuation of the Akt pathway dysfunction contributes to neuronal survival after stroke.
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PMID:Phosphoinositide-3-kinase/akt survival signal pathways are implicated in neuronal survival after stroke. 1730 56