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 present the case history of a 23-year-old man who underwent frontal craniotomy followed by radiotherapy for a Grade III anaplastic glioma. Magnetic resonance imaging (MRI) at the 3-month follow-up showed significant tumour response. He became unwell some weeks after the MRI with an upper respiratory tract infection, severe headache and mild right-sided weakness. A computed tomographic (CT) scan showed a very large volume of intracranial gas, thought to have entered via a defect in the frontal air sinus after craniotomy and brought to light by blowing his nose. Intracranial air is frequently present after craniotomy, but it is normally absorbed within 34 weeks. The presence of pneumocephalus on a delayed postoperative CT scan should raise the possibility of a cerebrospinal fluid (CSF) fistula, or infection with a gas-forming organism. Many CSF fistulae require surgical closure in order to prevent potentially life-threatening central nervous system infection and tension pneumocephalitis. Immediate neurosurgical review is advisable.
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PMID:Gas in the cranium: an unusual case of delayed pneumocephalus following craniotomy. 1085 52

Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC(50) value was 400 microM. The DNA fragment became evident after incubation of the cells with 300 microM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).
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PMID:Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells. 1546 37