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Biomedical subjects

E F Gilbert

Publications and source records attributed to E F Gilbert.

At least 37 records · Page 2Linked to original sources
PubMed1987

Mesenteric cyst-ovarian implant syndrome.

Primary tumors and cysts of the mesentery are quite rare. The cysts are said to be from embryonic, traumatic, or neoplastic origin. Mesenteric cysts of ovarian tissue origin, which, to our knowledge, have been reported only three times, appear under the term ovarian remnant syndrome, and involved patients with previous oophorectomies. It appears that the incidental implantation and growth of the minute portions of the ovarian tissue in the pelvis or lower abdomen is the origin of the syndrome. We describe two cases of the mesenteric cyst-ovarian implant syndrome with a brief review of the literature.

Adult↗
PubMed1986

Carnitine protection against adriamycin-induced cardiomyopathy in rats.

The effects of chronic adriamycin toxicity on myocardial carnitine content and contractile function were studied in rats, along with potential protective effects of L-carnitine administration. Cardiomyopathy was induced over a 6- to 7-week period by weekly intravenous injections of adriamycin, 2 mg/kg. In vivo myocardial tissue levels of carnitine were not significantly changed by adriamycin, but plasma levels were elevated. Cardiac output was depressed in isolated perfused hearts from adriamycin-treated rats perfused with 11 mM glucose. In a second experiment, 4-week-old male rats were divided into four groups: saline-treated control, L-carnitine-treated control, saline-treated adriamycin, and L-carnitine-treated adriamycin. L-Carnitine was given intraperitoneally each day at a dose of 500 mg/kg. Myocardial histology and ultrastructure were analyzed. Cardiac performance was determined in hearts perfused with 1.2 mM palmitate and 5.5 mM glucose. Hearts from saline-treated adriamycin rats showed histopathological changes and a significantly diminished cardiac output at various preloads when compared to saline-treated controls. Daily intraperitoneal L-carnitine reduced histopathological alterations and improved cardiac performance.

Animals↗
PubMed1986

Familial lung disease associated with proliferation and desquamation of type II pneumonocytes.

A family is described in which certain infants presented with a diffuse parenchymal pulmonary disorder characterized by proliferation and desquamation of alveolar epithelial cells that progressed to severe pulmonary fibrosis and cystic dysplasia, resulting in "honeycomb" lung typical of chronic pulmonary interstitial disease (idiopathic pulmonary fibrosis) at death. Electron microscopic examination of a lung biopsy specimen from one infant revealed that the proliferating/desquamating cells were ultrastructurally normal-appearing type II pneumonocytes with osmiophilic lamellar bodies. This patient did not respond to prednisone therapy, but she showed great improvement with chloroquine therapy, which was confirmed by a repeated lung biopsy. Possible mechanisms that might account for the effect of chloroquine, such as inhibition of DNA synthesis, as well as the cellular pathobiology of type II pneumonocyte proliferation in this disease, are discussed.

Cell Division↗
PubMed1986

The teratogenic effect of phenobarbital on the embryonic chick heart.

Phenobarbital was observed to produce cardiovascular malformations in embryonic chicks. Malformations included simple ventricular septal defect, ventricular septal defect associated with dextroposition of the aorta, double outlet right ventricle, and several types of aortic arch anomalies. Embryos were exposed to phenobarbital at doses of 1-25 mumol on day 4 of incubation (Hamburger-Hamilton developmental stage 24). Doses equal to and greater than 5 mumol phenobarbital (26 mg/kg egg) significantly increased the frequency of embryos with cardiovascular malformations compared with lesser doses and with saline. A significant reduction in heart rate and abnormal rhythm of the heart were observed in embryos treated with teratogenic doses of phenobarbital. No arrhythmia nor significant changes in heart rate were observed in embryos exposed to subteratogenic doses of phenobarbital or to saline.

Abnormalities, Drug-Induced↗
PubMed1986

Pulmonary stenosis with ventricular septal defect, common aorticopulmonary trunk, and dextroposition of the aorta: morphologic and qualitative physiologic effects in caffeine-treated chick embryos.

Effects of caffeine administration to Hamburger-Hamilton stage 19 chick embryos (3 days of incubation) were investigated. A morphologic study of the effect of caffeine on cardiogenesis showed that caffeine produced total cardiac malformations in the chick in a dose-related fashion. A maximum frequency of 70.6% was observed with 4.7 mg caffeine. Major malformations included common aorticopulmonary trunk and dextroposition of the aorta accompanied by ventricular septal defect with/without pulmonary stenosis. Qualitative analysis of cinegraphs following exposure of embryos to a single teratogenic dose of caffeine (3.5 mg/egg) produced marked alterations in cardiac function when compared with chick Ringer's controls. Within 3 minutes after exposure to caffeine, dilation of the common ventricle and weak ventricular contractility were observed and persisted for 1 hour. Dose-response data and microcinematographic observations suggest that caffeine induced cardiac anomalies by a direct toxic effect on the embryo rather than by altering cardiac cell function. Our data also suggest that pathophysiologic changes in cardiac function may play an important role in the pathogenesis of caffeine-induced cardiac anomalies in the chick embryo.

Abnormalities, Drug-Induced↗