Minorities and the medical profession: a historical perspective and analysis of current and future trends.
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Black or African American↗
Biomedical subjects
D E Wilson
Publications and source records attributed to D E Wilson.
Release of AMP and adenosine from rat heart mitochondria.
Release of AMP and adenosine from rat heart mitochondria was studied. The rate of appearance of extramitochondrial adenosine was independent of the extramitochondrial phosphate concentration between 5 and 20 mM. In the absence of exogenous, respiratory substrates or in the presence of glutamate/malate plus rotenone, the rate of appearance of adenosine was relatively low when phosphate was not added. The appearance of extramitochondrial AMP + adenosine was found to be directly proportional to the extra-mitochondrial phosphate concentration. Zn2+ (10 mM) decreased the rate of adenosine appearance by 90% and increased the rate of AMP appearance 6-fold. The mitochondrial preparations dephosphorylated exogenous AMP; this activity was inhibited by 10 mM Zn2+. We conclude that the adenosine appearing in the extramitochondrial space was not due to a direct release from the matrix, but instead was due to adenine nucleotide release with subsequent conversion to adenosine in the extramitochondrial space.
5'-Nucleotidase↗
Retinyl ester retention in chronic renal failure. Further evidence for a defect in chylomicron remnant metabolism.
The metabolic remnants of triglyceride-rich lipoproteins are atherogenic in man and experimental animals. Particles resembling lipoprotein remnants have been found in plasma from patients with chronic renal failure (CRF). In this study we took advantage of the observation that retinyl esters are transported only by lipoproteins that originate in the intestine, that is, by chylomicrons (CM) and their remnants. To investigate further remnant metabolism in CRF, plasma RE were measured by reverse-phase high performance liquid chromatography in 20 non-diabetic hemodialyzed patients with CRF and 20 hospitalized non-diabetic control subjects 12-15 h after the administration of retinyl ester, 25000 IU orally. Total plasma RE were increased 3-fold in the CRF patients (P less than 0.001). Quantitative analysis of retinoids and lipids in fractions separated by unit-gravity flotation and flocculation in 3% polyvinylpyrrolidone indicated that the plasma RE were not contained among intact CM. Mean plasma retinol in CRF was also elevated consistent with previous observations and the known role of the kidney in retinol-binding protein metabolism. Although postabsorptive RE concentration was correlated positively and significantly with plasma triglyceride concentration in both groups, RE were higher in CRF patients at comparable plasma triglyceride concentrations. These data support the proposal that atherogenic lipoprotein remnants accumulate in the plasma of patients with CRF.
Adult↗
Postchallenge plasma lipoprotein retinoids: chylomicron remnants in endogenous hypertriglyceridemia.
This study was conducted to determine whether chylomicron remnants accumulate in the plasma of patients with "endogenous" hypertriglyceridemia. Retinyl esters were used as markers of chylomicrons and chylomicron remnants since they are carried mainly if not exclusively by lipoproteins of intestinal origin. Seventy-six fasting normotriglyceridemic and hypertriglyceridemic patients were studied 12 to 15 hours after ingesting 25,000 IU of vitamin A. Plasma retinol and retinyl esters were measured by reversed-phase high-performance liquid chromatography. Chylomicronemia was assessed by flotation at unit gravity and by chylomicron flocculation in 3% polyvinylpyrrolidone. Plasma lipids, retinoids, lipoprotein cholesterol, and the electrophoretic mobility of very-low density lipoproteins were determined in a subset of 36 subjects. Progressively elevated plasma retinyl ester concentrations were observed among patients with mild, moderate, and severe hypertriglyceridemia. All subjects with fasting chylomicronemia had retinyl ester retention. The majority of subjects with mild or moderate hypertriglyceridemia (predominantly type IV hyperlipoproteinemia) also had elevated plasma concentrations of retinyl esters. Total plasma retinyl ester and plasma triglyceride concentrations correlated significantly (rs = 0.721, P less than 0.001) in nonchylomicronemic subjects. In addition, total plasma retinol concentrations were mildly elevated among hypertriglyceridemic subjects because retinol, as well as retinyl esters, is transported by triglyceride-rich lipoproteins. If lipoprotein remnants are atherogenic in man, then chylomicron remnant retention may accelerate atherogenesis in hypertriglyceridemic individuals.
Adult↗
The effect of neurotensin on the concentration of cholesterol and bile acids in the guinea pig.
In guinea pigs, total plasma cholesterol concentrations increased above the control values after single intravenous injections and after 3 days of continuous subcutaneous administration of neurotensin (NT). A high dose of NT (125 pmol/100 g body weight) induced tachycardia and severe respiratory distress; the lowest dose (1.25 pmol/100 g body weight) had the greatest hypercholesterolemic effect 15 min after the injections. The bulk of the total plasma cholesterol was in low density lipoprotein fractions. Cholesterol increased in the same fractions after intravenous administrations of NT. NT induced a decrease in the cholesterol content in the ileum but did not affect significantly the cholesterol content in the liver, kidneys or adrenals. In 48-hr fasted controls, plasma cholesterol concentration and cholesterol content in the liver, kidneys, adrenals and terminal ileum increased; after intravenous injections of NT, plasma cholesterol concentration further increased but cholesterol content of the liver, kidneys and ileum decreased. In fed animals, the concentration of the biliary taurochenodeoxycholic acid increased above the control values 5 and 35 min after the intravenous injections of NT. In fasted controls, the total concentration of bile acids was higher than in fed controls, but only the concentration of taurochenodeoxycholic acid further increased after the injections of NT. Proportionately more taurochenodeoxycholic acid than cholesterol was present in bile after the intravenous injections of NT. These data are consistent with the hypothesis that NT has a regulatory role in intestinal cholesterol transport.
Animals↗
The inheritance of high density lipoprotein cholesterol and apolipoproteins A-I and A-II.
A large pedigree was ascertained through cases of early myocardial infarction. High density lipoprotein cholesterol and apolipoproteins A-I and A-II were measured on family members. Likelihood analysis, using the polygenic/major gene mixed model, provided no evidence that major loci play a role in determining the levels of any of the three measurements. Heritability estimates, assuming polygenic inheritance, were 0.59 and 0.26 for HDL-C level and A-II level, respectively. No evidence of genetic transmission of A-I level was found.
Adult↗
Effects of prostaglandin E2, 16,16-dimethyl prostaglandin E2 and a prostaglandin endoperoxide analogue (U-46619) on gastric secretory volume, [H+] and mucus synthesis and secretion in the rat.
The effects of orally administered prostaglandin E2, 16,16-dimethyl prostaglandin E2 and U-46619, an analogue of the prostaglandin endoperoxide PGH2, on gastric secretory volume, acid and mucus were studied in the rat. All of the compounds significantly increased the volume of gastric secretion, mucus secretion, measured as N-acetylneuraminic acid and mucus synthesis measured as the incorporation of [3H]-glucosamine into mucosal glycoprotein; however, only PGE2 and 16,16-dimethyl PGE2 inhibited acid secretion. U-46619, 1.5 mg/kg provided significant protection against ethanol-induced gastric ulcers, an effect that has been previously shown for the other two compounds. These studies provide additional evidence that prostaglandin induced mucosal protection may be related to an effect on mucus and on stimulation of nonparietal cell gastric secretion. Further study of these parameters may be important in the development of antiulcer drugs for long term clinical use.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
A new PGE1 analogue (CL115,574) III. Effects on gastric acid and mucus secretion in man.
CL115,574, an analogue of PGE1, is a potent inhibitor of gastric acid secretion in animals. The effects of this compound on gastric acid and mucus secretion were studied in 8 male volunteers. The compound was well tolerated, and its maximally effective antisecretory dose (750 micrograms) inhibited pentagastrin stimulated acid secretion by approximately 40% over a 2-hour period, with stimulation beginning one hour after the drug was orally administered. CL115,574 proved to have a significant and sustained effect upon the stimulation of mucus secretion into gastric juice. Considering the possible role that mucus may play in mucosal cytoprotection, CL115,574 because of its antisecretory and mucogenic actions may prove to be an important clinical anti-ulcer compound.
Adult↗
Mortality and renal failure in the streptozocin-alloxan diabetic dog attributed to contamined alloxan preparations.
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Acute Kidney Injury↗
Tax reforms.
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Multi-Institutional Systems↗
In vitro transfer of chylomicron retinol and retinyl esters.
The redistribution of rat chylomicron retinoids following incubation with fasting- or postheparin human plasma was investigated. With fasting plasma, chylomicron retinol appeared among higher density lipoprotein acceptors and density greater than 1.21 gm/ml plasma proteins; only small amounts of retinyl ester were found therein. With postheparin plasma, retinyl ester-containing chylomicron remnants with densities spanning the low- and high density lipoprotein distributions were generated; appreciable quantities of retinyl esters appeared among rho greater than 1.019 lipoproteins only in the presence of postheparin plasma. These observations are consistent with the conservation of retinyl esters, but not retinol, among chylomicrons and their catabolic products.
Animals↗
The genetics of quantitative plasma Lp(a): analysis of a large pedigree.
Likelihood analysis using the mixed model of quantitative plasma Lp(a) measurements on members of a large pedigree provided evidence that high levels of Lp(a) are inherited as a dominant major gene with polygenic background. The dominant allele frequency was estimated as 0.10. The major gene and polygenic components together accounted for 95% of the variation seen in the measurements. The major gene index and OBP plots, methods that do not allow for the presence of both components, favored the polygenic model over the major gene model as the mode of inheritance. No association was found with any of the lipids, lipoproteins or apolipoproteins considered.
Female↗
Plasma lipoprotein retinoids after vitamin A feeding in normal man: minimal appearance of retinyl esters among low-density lipoproteins.
Retinyl esters have been thought to be carried solely by lipoproteins of intestinal origin (chylomicrons and their catabolic derivatives). Recent reports, however, have indicated that there may be significant transfer of retinyl esters from chylomicrons to low-density lipoproteins (LDL) in vitro, and that in other species, substantial amounts of retinyl esters may appear in LDL. Since in man lipoproteins of intestinal origin are not considered to contribute to a quantitatively significant extent to circulating LDL, we have examined this issue further. The distribution of retinol and retinyl esters within the plasma lipoproteins of eight normal human volunteers was measured following the ingestion of vitamin A along with a mixed meal. Retinyl esters appeared in the chylomicrons and very-low-density lipoproteins. Small amounts of retinyl esters were also detected in the intermediate- and low-density lipoprotein (LDL) classes. Estimates of the masses of retinyl esters, however, indicated that 5% or less of chylomicron retinyl esters appeared in the LDL. These observations are consistent with orderly chylomicron delipidation and provide further evidence that chylomicron-derived components do not contribute directly or to a quantitatively significant extent to circulating LDL.
Adult↗
Phenotypic heterogeneity in the extended pedigree of a proband with lipoprotein lipase deficiency.
We have studied the large nonconsanguineous pedigree of a proband with Type I hyperlipoproteinemia (HL) and lipoprotein lipase (LPL) deficiency. Within the nuclear family, the mother and two of the proband's five siblings had fasting hypertriglyceridemia or low-normal tissue adipose LPL activities or both. Retention of lipoprotein retinyl esters after vitamin A feeding was present only in the propositus. The maternal side of the extended pedigree contained individuals with Types IIA, IV, and V hyperlipoproteinemia, findings most consistent with autosomal dominant multiple lipoprotein-type hyperlipidemia (familial combined hyperlipidemia). This family and previously reported pedigrees of Type I HL probands have demonstrated phenotypic heterogeneity. Without specific genetic markers, homozygous LPL deficiency and complex multiple-gene mechanisms cannot be distinguished unambiguously. Parental hyperlipidemia in nuclear pedigrees of Type I HL probands should not be equated with heterozygous LPL deficiency in the absence of extended pedigree data or more informative markers. The possibility that the complex inheritance of two different genetic defects in lipoprotein transport can produce the Type I HL phenotype must be considered.
Adipose Tissue↗
Renal function in the neotropical bat, Artibeus jamaicensis.
1. When feeding on figs (Ficus insipida), the bat Artibeus jamaicensis increases dietary sodium density while decreasing potassium density by primarily extracting and ingesting pulp juices rather than other parts of the fruit. 2. Based on urine osmotic pressure, these bats are uniformly dehydrated when they leave day roosts and become rapidly rehydrated (0.5-1 hr) after initiation of feeding. 3. After 2000 hr, and throughout the night there is no difference in urine concentration of free-flying bats compared with bats held in the laboratory without food or water for the same time interval. 4. Mean maximum urine concentration in this species is 972 mOsm/kg.
Animals↗
Eucaloric substitution of medium chain triglycerides for dietary long chain fatty acids in acquired total lipodystrophy: effects on hyperlipoproteinemia and endogenous insulin resistance.
Previous studies have suggested that reduction of dietary fat intake, with or without caloric restriction, may lead to improvement in certain of the characteristic abnormalities that accompany total lipodystrophy (TLD). We have studied the effects of eucaloric medium chain triglyceride (MCT) substitution for dietary long chain fatty acids in a patient with acquired total lipodystrophy and unusual somatic and visceral anomalies. The patient exhibited insulin resistance, carbohydrate intolerance, striking fasting- and glucose-stimulated hyperinsulinemia, hyperglucagonemia, type V hyperlipoproteinemia, and lipoprotein lipase deficiency on a normal diet. Improvement in chylomicronemia, hypertriglyceridemia, and xanthomatosis occurred during eucaloric MCT substitution. Carbohydrate intolerance decreased and fasting immunoreactive glucagon and insulin concentrations fell 37% and 83%, respectively. Plasma triglyceride polyunsaturated fatty acid concentrations decreased to very low levels. With long term MCT feeding supplemented by polyunsaturated fatty acids, hepatomegaly has gradually decreased, while body weight has remained stable. The patient has not yet required insulin therapy. These observations suggest that the abnormalities in carbohydrate metabolism are closely linked to, and perhaps dependent on, the abnormalities in lipoprotein transport in TLD. Long chain triglyceride restriction and MCT supplementation should be attempted in additional patients with the features of TLD to determine whether this is a generally effective therapeutic approach.
Adolescent↗
Excessive insulin therapy: biochemical effects and clinical repercussions. Current concepts of counterregulation in type I diabetes.
Excessive doses of insulin cause unstable or "brittle" diabetes in many diabetic patients. Chronic insulin overtreatment can be very difficult to recognize because nocturnal hypoglycemia may be infrequent and asymptomatic. Recognition of subtle historical clues and informed interpretation of laboratory results facilitate diagnosis. Some insulin-treated diabetic patients fail to respond to severe nocturnal hypoglycemia with the acute secretion of counterregulatory hormones. "Rebound" morning hyperglycemia coincides with decreased plasma free insulin levels and the normal diurnal rise in plasma cortisol levels. Moreover, these patients show hyperresponsiveness to counterregulatory hormones (particularly cortisol and epinephrine), exaggerated hepatic glucose production, and prolonged impairment of peripheral and splanchnic glucose disposal. When chronic overtreatment is suspected, insulin therapy must be modified to better approximate physiologic needs for glucose disposal. Until fundamental problems of insulin replacement are solved, chronic insulin overtreatment should be considered as one cause of unstable diabetes.
Blood Glucose↗
Intraperitoneal insulin administration produces a positive portal-systemic blood insulin gradient in unanesthetized, unrestrained swine.
The present study was performed to evaluate the porto-systemic insulin gradient in response to (1) glucose feeding (2) intramuscular insulin administration, and (3) peritoneal insulin administration in unanesthetized swine. The experiment was designed to verify the hypothesis that intraperitoneal insulin administered might lead to a more physiologic portal vein insulin concentration than systemic administration of a similar insulin dose. Studies were performed in 4 domestic swine with chronic, indwelling catheters in the inferior vena cava and portal vein. Unpaired studied of the absolute portal venous and systemic venous insulin concentrations were performed in response to glucose prn(n = 4), 1 unit regular insulin/kg i.m.(n = 4), and 1 unit regular insulin/kg i.p.(n = 5). Timed blood samples were obtained and serum insulin concentrations determined by RIA. Portal and caval serum insulin concentrations following intramuscular insulin injection showed no significant difference. A significant portal vein insulin excess (p less than 0.001) was demonstrated following both feeding and intraperitoneal insulin.
Animals↗