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)

The Epstein-Barr virus nuclear antigen-leader protein (EBNA-LP) is required for high efficiency B lymphocyte growth transformation by the virus. To test the potential contribution of EBNA-LP to tumorigenesis in vivo, we produced transgenic mice carrying an EBNA-LP cDNA construct, using the widely expressed metallothionein promoter. Expression of EBNA-LP was detected in liver, kidney, heart, lung and spleen. There were no apparent oncogenic consequences of EBNA-LP expression. Unexpectedly however, at ages ranging from about 4 months to over a year, transgenic mice developed symptoms of congestive heart failure, including left ventricular dilatation, right ventricular hypertrophy, left atrial thrombosis, pulmonary oedema and hydrothorax. Fibrillation was not apparent in the electrocardiograph; however a reduction in T-wave amplitude suggested that the development of an abnormality of ventricular repolarization may precede the manifestation of overt symptoms. The highly predictable development of dilated heart failure in these transgenic mice suggests they may be a useful model for the pathophysiological changes associated with human dilated cardiomyopathy.
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PMID:Dilated heart failure in transgenic mice expressing the Epstein-Barr virus nuclear antigen-leader protein. 839 79

We report a case of non communicating hydrocephalus due to membranous obstruction of Magendie's foramen. A 37-year-old woman presented with intracranial hypertension symptoms caused by the occlusion of Magendie's foramen by a membrane probably due to arachnoiditis. As far as the patient's past medical history is concerned, an Epstein-Barr virus infectious mononucleosis was described. Fundoscopic examination revealed bilateral papilledema. Brain magnetic resonance imaging demonstrated a significant ventricular dilatation of all ventricles and turbulent flow of cerebelospinal fluid (CSF) in the fourth ventricle as well as back flow of CSF through the Monro's foramen to the lateral ventricles. The patient underwent a suboccipital craniotomy with C1 laminectomy. An occlusion of Magendie's foramen by a thickened membrane was recognized and it was incised and removed. We confirm the existence of hydrocephalus caused by fourth ventricle outflow obstruction by a membrane. The nature of this rare entity is difficult to demonstrate because of the complex morphology of the fourth ventricle. Treatment with surgical exploration and incision of the thickened membrane proved to be a reliable method of treatment without the necessity of endoscopic third ventriculostomy or catheter placement.
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PMID:Hydrocephalus due to Membranous Obstruction of Magendie's Foramen. 2567 49