Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(1) The concentrations of various anticonvulsants (PB, PHT, CBZ, VPA) were measured in brain specimens from 7 patients who had undergone neurosurgery for a therapy resistant epilepsy of tumoral origin (astrocytoma) in 6 cases, glioblastoma in 1 case). (2) Great interindividual variability of the mean brain/plasma concentration ratios was observed for PB in 5 patients (range: 0.4-1.0). A mean brain/plasma ratio of 1.0 was recorded for PHT and CBZ (one patient each). (3) In the different tissue specimens (7-14) from the same patient AED concentrations varied greatly, even in neighboring areas. (4) Intraindividual variations were more marked in the present group of patients than in previously studied non-tumoral epileptics. (5) No correlation was found between the localization of the lesions and the variations in AED concentrations. (6) Brain AED concentration appeared to be higher in the few samples of non-tumoral tissue and lower in the 'epileptogenic' areas as defined by stereo-EEG seconding. (7) On the basis of these data, the hypothesis can be formulated that the therapy resistance of these patients may be at least partly explained by the presence of low AED concentration (even in presence of 'therapeutic' AED plasma levels) in the epileptogenic areas.
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PMID:[Cerebral concentrations of anticonvulsants in patients with epilepsy of tumoral origin (author's transl)]. 704 45

The plexiform lesion in primary pulmonary hypertension is a glomeruloid structure forming channels in branches of the pulmonary artery. These lesions have been considered an abnormal growth of modified smooth muscle cells. We present immunohistochemical evidence in 10 cases of plexogenic pulmonary hypertension that the plexiform channels and the concentric obliterative arteriopathy associated with these channels represent abnormal growth of factor VIII-related antigen-positive endothelial cells. In addition, these cells strongly expressed vimentin, a growth- and differentiation-related intermediate filament. Morphologically and immunohistochemically, the lesions resembled the neovascularization associated with the brain tumor glioblastoma multiform. Furthermore, we noted an exclusively perivascular inflammatory cell infiltrate (but no vasculitis) in seven of the 10 cases with plexogenic arteriopathy composed of T cells, B cells, and macrophages. Our findings indicate that the plexiform lesion may result from a deregulated growth of endothelial cells. The presence of perivascular inflammatory cells suggested that cytokines and growth factors may further influence the development of the plexiform lesion.
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PMID:Exuberant endothelial cell growth and elements of inflammation are present in plexiform lesions of pulmonary hypertension. 1143 86