Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have compared the effect of two inhalational anesthetics, halothane and xenon, on Ca(2+)-ATPase (PMCA) pumping activity in plasma membrane vesicles prepared from cultured rat C6 glioma cells. Halothane, at concentrations ranging from 0.5 to 1.75 vol% (equivalent to 0.5 to 1.6 MAC), significantly inhibited Ca2+ uptake (transport) by plasma membrane vesicles in a dose-related fashion. Xenon, at partial pressures ranging from 0.5 to 1.5 atm (equivalent to 0.5 to 1.6 MAC), similarly inhibited PMCA pumping activity. Additive effects on suppression of PMCA pump activity were observed when C6 cell plasma membrane vesicles were exposed to increasing partial pressures of xenon in the presence of halothane (1 vol%). Halothane also inhibited PMCA pumping in cells from two other lines of neural origin, B104 (rat neuroblastoma) and PC12 (rat pheochromocytoma). Studies described in this report support the thesis that PMCA in cells of neural origin is inhibited by quite different inhalational anesthetics at clinically relevant concentrations.
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PMID:Inhibition of plasma membrane Ca(2+)-ATPase pump activity in cultured C6 glioma cells by halothane and xenon. 788 85

Little is known about the influence of infiltrating gliomas on the responsivity of the cerebral circulation to anesthetic agents. Therefore we designed a study to address this issue. Male Fischer 344 rats were assigned to two tumor groups and one sham group. In the two tumor groups, glioma cells were stereotactically injected into the right striatum; animals in the sham group were injected with sterile culture medium only. Either 12 or 16 days after injection, the rats were anesthetized with 1 MAC halothane in 40% O2/balance N2. Local and remote regional cerebral blood flow was then determined using 14C-iodoantipyrine autoradiography. Physiologic values (PaCO2, PaO2, pHa, mean arterial pressure, and rectal temperature) were similar for both tumor and sham groups. Tumor volume was relatively small (cross-sectional diameter = 2-3 mm), and there was no evidence of midline shift in coronal tissue sections. Blood flow within the tumor was substantially reduced relative to adjacent structures (e.g., tumor = 88 +/- 10 ml/100 g/min; adjacent caudate = 161 +/- 23 ml/100 g/min). There were no significant differences between the tumor and sham groups for regional blood flow values in histologically normal tissue in either the injected or contralateral hemispheres. We conclude that this model of brain neoplasia shows no evidence of either local or remote changes in the cerebrovascular responsibility of normal tissue to volatile anesthesia.
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PMID:Cerebral blood flow in a rat glioma model during halothane anesthesia. 840 Jul 58

Cyclooxygenases (cox) are potent mediators of inflammation and two cox-isoenzymes, cox-1, cox-2, are described to date. Cox-2 is cytokine-inducible in inflammatory cells and enhanced cox-2 expression has been attributed a key role in the development of edema and immunomodulation in pathologically altered brain tissues. In normal cerebral cortex cox-2 is present only in neurons, but not in the glial or vascular endothelial cells. The function of microglia in glioma biology is unclear. Microglia have both neurotrophic and neurotoxic functions and have been shown to release a variety of cytokines. Our preliminary results showed that the expression pattern of cox-2 is predominantly neuronal although glial expression was observed with the correlation of high malignancy. In this study we aimed to assess the phenotypes (astrocyte, microglia) of the cox-2-expressing glial cells in various types of human gliomas and to compare their expression patterns. For this purpose we employed dual immunohistochemistry for cox-2 and GFAP (astrocyte) or LCA-MAC (microglia-macrophage) in archival formalin-fixed, paraffin embedded human tissue diagnosed as oligodendroglioma and/or astrocytoma. The results showed that cox-2 immunoreactivity is up-regulated in the neurons according to the tumor grade. Most of the cox-2 immunoreactive glia were GFAP-positive in anaplastic oligodendrogliomas and at lesser extend in glioblastomas. Cox-2 and LCA co-localization was detected in more glial cells in glioblastomas. It may be speculated that the induction of cox-2 in microglia may contribute to the deleterious effects of prostanoids in cerebral edema formation during the progression of oligodendrogliomas. The detection of cox-2 in astrocytes surrounding the necrotic areas might be important to develop new strategies, such as the usage of cox-2 inhibitors combine with chemotherapy and radiotherapy in the treatment of glioma patients.
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PMID:Cyclooxygenase-2 expression in astrocytes and microglia in human oligodendroglioma and astrocytoma. 2005 22