Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five neonatal beagles were used for this study. Gliosarcoma was injected into the cerebral hemisphere of 7 neonatal beagles (Group I). These animals were then treated by boron neutron capture therapy. The response of the tumor to therapy was evaluated by serial CT scans and 3 times magnification of cerebral angiography. The animals were sacrificed at varying post-therapy periods for histological study. Fifteen neonatal beagles implanted gliosarcoma without therapy (Group II) and 3 normal controls without tumor (Group III) were subjected to the same follow-up studies. (Results) (1) Neonatal beagles with implanted tumor showed moderate degree of ventricular dilatation within a short period. The finding of communicating hydrocephalus was interpreted as initial growth of tumor. (2) Animals after therapy had variable cavitation in the hemisphere that had contained calcium deposit on CT. Moderate dilatation of the lateral ventricle was present without any significant midline shift and there was an area of porencephaly extending out from the right lateral ventricle on CT (Fig. 1, Case 2). Cerebral angiography demonstrated hydrocephalus with an avascular region in the right cerebral hemisphere, compatible with the previously described porencephalic cyst (Fig. 2, Case 2). (3) Three cases out of 7 showed neurological symptoms after tumor implantation (Cases 3, 5 and 6). Carotid angiography showed large temporal lobe tumor with some tumor stain and also some involvement of the right frontal lobe after therapy (Fig. 7, Case 3). In postmortem examination, there was tumor seen coating the right lateral ventricle as well as the left temporal horn. The right cerebral hemisphere was slightly smaller than the left. The left lateral ventricle was remarkably enlarged (Fig. 9). (4) Four out of 7 treated animals with injected gliosarcoma showed no evidence of tumor at postmortem examination. CT demonstrated moderate dilatation of the lateral ventricle without any significant midline shift, an area of porencephaly and definite decrease in size of the right cerebral hemisphere and calvarium (Fig. 4). (5) Fifteen neonatal beagles implanted gliosarcoma without therapy (Group II) developed symptomatic and died within two weeks. (6) Control animals showed no ventricular dilatation or other abnormalities. (7) Microscopic examinations showed no similarities between implanted gliosarcoma and human glioblastoma. (Conclusion) Serial CT scans and magnification cerebral angiography in this experimental model appear extremely helpful in following the effects of therapy and important tool for the evaluation of a tumor growth or regression.
 ...
PMID:[Neuroradiological Evaluation of an experimentally implanted tumor into cerebral hemisphere of neonatal beagles (author's transl)]. 709 78

Increased activity of matrix metalloproteinases (MMPs) has been implicated in numerous disease processes, including tumor growth and metastasis, arthritis, and periodontal disease. It is now becoming increasingly clear that extracellular matrix degradation by MMPs is also involved in the pathogenesis of cardiovascular disease, including atherosclerosis, restenosis, dilated cardiomyopathy, and myocardial infarction. Administration of synthetic MMP inhibitors in experimental animal models of these cardiovascular diseases significantly inhibits the progression of, respectively, atherosclerotic lesion formation, neointima formation, left ventricular remodeling, pump dysfunction, and infarct healing. This review focuses on the role of MMPs in cardiovascular disease, in particular myocardial infarction and the subsequent progression to heart failure. MMPs, which are present in the myocardium and capable of degrading all the matrix components of the heart, are the driving force behind myocardial matrix remodeling. The recent finding that acute pharmacological inhibition of MMPs or deficiency in MMP-9 attenuates left ventricular dilatation in the infarcted mouse heart led to the proposal that MMP inhibitors could be used as a potential therapy for patients at risk for the development of heart failure after myocardial infarction. Although these promising results encourage the design of clinical trials with MMP inhibitors, there are still several unresolved issues. This review describes the biology of MMPs and discusses new insights into the role of MMPs in several cardiovascular diseases. Attention will be paid to the central role of the plasminogen system as an important activator of MMPs in the remodeling process after myocardial infarction. Finally, we speculate on the use of MMP inhibitors as potential therapy for heart failure.
 ...
PMID:Matrix metalloproteinase inhibition after myocardial infarction: a new approach to prevent heart failure? 1148 70