Vasoactive intestinal polypeptide in algodystrophy.
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Biomedical subjects
Publications and source records attributed to S Bloom.
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Chorioretinal folds have been reported as a result of many intraocular and extraocular inflammatory processes or tumors. Visual loss is usually secondary to a combination of the underlying process and chorioretinal folds involving the macula. We report a patient who developed decreased vision, metamorphopsia, chorioretinal folds, and a lamellar macular hole secondary to global compression by a bone fragment. The chorioretinal folds regressed and his vision stabilized following surgical decompression. Chorioretinal folds and lamellar macular hold formation are previously unrecognized complications of reconstructive craniofacial surgery.
The increased vulnerability of animals fed a magnesium (Mg)-deficient (MD) diet to ischemia-induced myocardial necrosis has been attributed to changes in myocardial electrolyte metabolism. However, a variety of hematologic changes have also been reported in MD and some of these, such as an increase in platelet aggregability, may contribute to the increased myocardial vulnerability. In the present study, we quantified the effect of MD on platelet and megakaryocyte abundance as well as on platelet aggregability with and without an administered calcium channel blocker (nifedipine). Hamsters were fed either a "minimal Mg" diet, in which the level of Mg was kept just high enough to prevent seizures, or a "preset Mg" diet containing precisely known amounts of Mg. Animals fed the minimum Mg diet showed an initial increase in the platelet count, which returned to control range when the dietary Mg was increased to 9 mmoles/kg. Animals on the preset Mg diet showed an increased platelet count if the Mg level was 10 mmoles/kg or less. In addition to the increase in number, platelets from MD animals were less responsive to the aggregation-inhibiting effect of nifedipine than were platelets from control animals, although MD itself did not result in an increased aggregability under the conditions used here. Animals with an increase in circulating platelets showed decreased megakaryocyte abundance in the femoral marrow, but megakaryocytes that were present were larger than those in control animals. These results indicate a profound effect of dietary Mg deficiency on platelet biology. The observed changes could contribute to the increase in myocardial vulnerability to injury found in MD animals.
The Department of Family Practice, College of Medicine, in partnership with the University of Illinois at Chicago, was responsible for the reorganization of the Student Health Service into a health maintenance organization (HMO), Campus Care. Historically, the two campuses of the University of Illinois at Chicago operated student health as an infirmary model. Reorganization of student health into the Campus Care HMO provided expanded health care services to students, preserved more health care dollars in the university system, and provided a nonincremental increase in the size and responsibility of the Department of Family Practice. One year's experience showed that while the capitation was low compared with standard HMOs, the variable and less frequent use of services by the student population resulted in a fiscally viable operation. Numerous transition difficulties were encountered, including the need for rapid systems conversion within a complex university system, reeducation of students as well as traditional university-based practitioners for operation in a managed care system, and the rapid expansion of a small family practice department. The positive experience of the University of Illinois at Chicago supports the notion that family practice is better suited to providing student health care than other primary care disciplines. Three issues are paramount to success: (1) approval, support, and protection by higher level administration from university territorialism, (2) a core family practice faculty with strong leadership and experience in high-volume clinical activity, and (3) a close examination of financial resources in light of expected utilization.
The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal model for familial hypercholesterolemia, has a deficiency in low density lipoprotein (LDL) receptor binding and exhibits elevated plasma lipoprotein levels and spontaneous atherosclerosis. Since atherosclerotic plaque formation has a number of features in common with the inflammatory process, we have investigated the effect of dietary supplementation with an anti-inflammatory steroid (cortisone acetate, 5 mg daily for 3 months) on atherosclerosis using the WHHL rabbit as a model. Atherosclerotic plaque formation in cortisone-fed animals was reduced by about 60% compared to control WHHL rabbits. Steroid administration increased circulating cholesterol levels modestly and triglycerides were increased about 6-fold. While very low density lipoprotein (VLDL)-cholesterol was increased, LDL-cholesterol levels were decreased and the particle was more triglyceride-enriched as well as less dense. Steroid-fed animals also exhibited decreased platelet aggregation and increased aortic 15-lipoxygenase activity. The histological observations showed typical fibrous plaques in aortas of both control and cortisone-fed rabbits, with intima thickened by foamy macrophages and subcellular lipoproteinaceous debris covered by a fibrous cap. These findings thus indicate that steroids reduce the rate of plaque initiation or progression but do not significantly change the histological appearance of the lesion.
There is reason to believe that calcium influx into heart muscle during acute myocardial infarction (AMI) can aggravate myocyte injury. Furthermore, the degree of such influx might correlate with the occurrence of microscopic myocyte calcification observed at autopsy. We have searched for evidence of myocyte calcification in hearts of patients found to have AMI at autopsy at the Veterans Administration Medical Center in Salt Lake City (SLCVA), a region with a low myocardial infection death rate, and at the George Washington University Medical Center in Washington, DC (GWUMC), a region with a high myocardial infection death rate. Of 23 consecutive cases examined under "blind" conditions at the GWUMC in which AMI was found, there were 15 instances of cardiac myocyte calcification observed in von Kossa-stained sections. Not a single example of myocyte calcification was found in 23 comparable cases at the SLCVA. The basis of this difference in myocyte calcification is unknown, but may be related to the fact that the Salt Lake City drinking water contains a higher level of magnesium, which is known to protect against soft tissue calcification, than does that of Washington, DC. This may be the basis for the apparent protection that dietary magnesium exerts against myocardial infarction death.
Hamsters fed a Mg-deficient diet (MD) develop a cardiomyopathy (CM) with foci of myocardial necrosis, calcification, and modest mononuclear and giant cell infiltration. We hypothesize that the lesions are secondary to Ca overload following an increase in myocardial Na due to inhibition of (Na.K)-ATPase and secondary Na-Ca exchange. Nifedipine and digoxin were selected as agents to test this hypothesis. Hamsters were given nifedipine, digoxin, or placebo as sustained release subcutaneous pellets the same day they were started on the MD diet. Animals were killed after 14 days, and MD lesions were quantified in H&E stained slides. Regression analysis showed that nifedipine produced a dose-dependent reduction in lesion abundance (p less than .005) and diameter (p less than .05), while digoxin produced a dose-dependent increase in lesion abundance (p less than .005) and diameter (p less than .005). These results support the hypothesis that MDCM is secondary to Ca overload coupled to inhibition of (Na.K)-ATPase of cardiac myocytes.
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The alpha-glucosidase inhibitor acarbose has been successfully used in diabetic patients to decrease the postprandial rise in blood glucose. The aim of the present experiments was to investigate the fate and effects of acarbose along the small intestine using a slow-marker perfusion technique. In 8 healthy volunteers, jejunal and ileal loads of acarbose, glucose, and total carbohydrates were determined following a liquid, 400-kcal formula meal containing either 200 mg of acarbose or placebo. Preprandial and postprandial plasma concentrations of glucose and several polypeptide hormones were determined. Recovery of acarbose during 4 h was 65% +/- 9% (mean +/- SEM) of ingested dose in the ileum but 94% +/- 9% in the jejunum, indicating that the compound was neither degraded nor absorbed by the intestine to a major degree. After acarbose administration, ileal loads of glucose and total carbohydrates were considerably higher, whereas postprandial plasma concentrations of glucose, insulin, and gastric inhibitory polypeptide were lower when compared with placebo. The retardation of carbohydrate digestion to be inferred from these findings is confirmed by significantly elevated plasma concentrations of enteroglucagon after acarbose administration compared with placebo administration.
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A case of rupture of a sinus of Valsalva aneurysm in a middle-aged woman with an unusual assortment of associated conotruncal and other cardiac anomalies is reported. The anomalies included bicuspid aortic valve, aortic sinus aneurysm (ruptured), quadricuspid pulmonic valve, membranous coarctation of the aorta, subclavian and common carotid arteries arising directly from aorta, and atrial septal defect. Excluding the atrial septal defect, these anomalies may be explained by a single embryologic event affecting conobulbar septation and aortic arch development occurring at the level of neural crest development.
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Clinical and laboratory data for nine patients with hepatocellular fibrolamellar carcinoma treated at our institution have been summarized with emphasis on the relevance of plasma neurotensin levels as a tumor marker. The mean age of the patients was 22 years. Seven underwent hepatic resection, and two of these had later surgical removal of recurrent disease. Plasma neurotensin levels were initially elevated in five of the seven patients in whom it was measured. Neurotensin levels were within normal limits in three of four patients with recurrent disease, but were elevated in one patient who also had elevated plasma neurotensin levels preoperatively. In addition, a review of 80 patients reported since 1980 was performed. The mean age of these patients was 23 years, and only 6 percent were older than 50. The male to female ratio was 3:4. Eight percent were positive for hepatitis B antigen and 11 percent had elevated alpha-fetoprotein levels. Four percent had cirrhosis of the liver. The resectability rate was 58 percent. Five year survival for patients who underwent hepatic resection was 56 percent. Patients treated nonsurgically had a median survival of 13 months, and none of these patients lived for 5 years. Fibrolamellar hepatoma seems to be a distinct clinical entity that mainly occurs in young patients. The prognosis in patients treated with a curative resection is good. Plasma neurotensin levels may be of value as a tumor marker, but further studies are necessary to substantiate this theory.