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

Two-week-old broiler chickens were experimentally infected with either eastern equine encephalitis (EEE) virus or Highland J (HJ) virus. Mortality rates were 24/30 (80%) in EEE-virus-inoculated chickens and 2/30 (7%) in HJ-virus-inoculated chickens. Chickens inoculated with EEE virus exhibited severe depression and somnolence on days 1-6 postexposure (PE), with 17/30 birds dying during this period. After day 6 PE, EEE-virus-inoculated chickens exhibited abdominal distention, depression, and growth retardation, and an additional seven chickens died. Pathologic changes in EE-virus-inoculated chickens dying on days 1-6 PE consisted of multifocal necrosis in the heart and liver, as well as lymphoid depletion and necrosis in the thymus, spleen, and bursa of Fabricius. Ascites, pericardial effusion, and right ventricular dilatation of the heart were the predominant lesions in chickens dying after day 6 PE. No clinical signs were observed in sham-inoculated controls or in most HJ-virus-inoculated chickens. Ascites, pericardial effusion, and multifocal myocardial necrosis were observed in 2/30 HJ-virus-inoculated chickens that died or were euthanatized after development of clinical signs. These findings indicate that both EEE virus and HJ virus are pathogenic for young chickens.
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PMID:Experimental infection of young broiler chickens with eastern equine encephalitis virus and Highlands J virus. 783 11

A 30-year-old nulliparous woman was seen for a detailed ultrasound scan at 20 weeks of gestation. The scan revealed a male fetus with truncus arteriosus, membranous ventricular septal defect, absent thymus and sacral meningomyelocele. A 46,XY karyotype with a 22q11 deletion was detected. The parents chose to terminate the pregnancy. The pathological autopsy showed normal facial structures, minimal ventricular dilatation in the brain and a sacral meningomyelocele. Overlapping toes and a left claw-hand were also noted. An aplastic thymus with absent parathyroid glands was detected. The cardiac examination was consistent with the ultrasound diagnosis. The parental karyotypes were both normal. Kousseff syndrome is caused by a chromosome 22q11 deletion. It includes sacral meningomyelocele and conotruncal heart defects, unlike DiGeorge syndrome. Obstetricians should consider this a not so rare entity when they detect conotruncal abnormalities and a meningomyelocele as part of a 22q11.2 deletion syndrome.
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PMID:Prenatal diagnosis of a 22q11 deletion in a second-trimester fetus with conotruncal anomaly, absent thymus and meningomyelocele: Kousseff syndrome. 2238 Jun 55