Co-existing aldosterone-producing adrenal tumor (aldosteronoma) and bilateral renovascular lesions.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H C Gonick.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We sought to determine whether continuous low-level lead exposure (100 ppm lead acetate in drinking water) for periods of 1, 3, 6, 9, or 12 mo would produce adverse effects on kidney function or morphology in rats. Maximum blood lead levels in experimental animals were reached at 3 mo and averaged 29.4 +/- 4.1 micrograms/dl. Glomerular filtration rate, determined by single-injection 125I-iothalamate clearance, was found to be significantly increased above pair-fed controls at 1 and 3 mo, but it was normal at other time periods. Levels of urinary N-acetyl-beta-D-glucosaminidase exceeded levels found in controls at all time periods, except at 12 mo, when the normal increase with aging obscured differences between experimental animals and controls. In contrast, urinary ligandin (glutathione S transferase), a more specific marker of metal-associated proximal tubular injury, was normal at all time periods. Proximal tubular nuclear inclusion bodies were sparse and were observed only at 1 and 3 mo. There were no other pathological alterations in the kidneys, except at 12 mo, at which time mild tubular atrophy and interstitial fibrosis were seen. Therefore, low-level lead exposure in rats produced no significant changes in renal function and produced only mild alterations in renal morphology after 12 mo. The absence of changes in urinary ligandin accorded with the relative absence of morphological changes, whereas the observed increases in urinary N-acetyl-beta-D-glucosaminidase suggest that this enzyme may be an overly sensitive indicator of tubular injury.
Membrane Na+,K+-adenosinetriphosphatase in erythrocytes from three groups of industrially exposed Pb workers (without toxicity, with toxicity associated with high blood Pb levels, and with toxicity associated with low blood Pb levels) was inversely correlated with Pb in the membrane fraction but not significantly correlated with total erythrocyte Pb. This difference was attributable to the proportion of erythrocyte Pb bound to hemoglobin and a Pb-binding protein of molecular weight 10,000.
The purpose of the present study was to investigate bone changes in the adult rat exposed to low lead levels during intake of normal dietary calcium and to contrast these findings with data from our earlier studies performed with animals receiving low dietary calcium concurrent with lead exposure. The present study exposed adult rats to 100 ppm lead via drinking water for 12 weeks and assessed bone histology, 1,25-dihydroxyvitamin D, 25(OH)vitamin D and parathyroid hormone levels. No osteopenia was evident by quantitative bone histology, and circulating levels of 1,25-dihydroxyvitamin D, 25(OH) vitamin D and parathyroid hormone were normal. Bone ash findings documented incorporation of significant amounts of lead into bone mineral. These findings document absence of interference with vitamin D metabolism, absence of secondary hyperparathyroidism and absence of osteopenia following 12 weeks of low lead exposure in the adult rat maintained on normal calcium intake. Results stress the importance of adequate calcium intake in our elderly population who may be exposed to cumulative, low-level lead exposure.
Diabetes mellitus has been shown to develop as a consequence of chromium (Cr) deficiency in experimental animals and in humans sustained by prolonged total parenteral nutrition. Prior limited trials in humans had indicated that Cr supplements, in either inorganic or organic form, may improve carbohydrate utilization. We report here a clinical double-blind, random crossover trial of inorganic Cr trichloride, a brewer's yeast that contained Cr as glucose tolerance factor (GTF), a brewer's yeast extract without GTF, and a placebo. Forty-three outpatient diabetic men received three of these supplements for 4 mo each. Subgroups included 21 ketosis-prone men; 7 ketosis-resistant, nonobese men; and 15 ketosis-resistant obese men. Chromium levels were followed pre- and posttreatment in hair, red blood cells, plasma, and urine. Response of carbohydrate metabolism to treatment was assessed in terms of change in insulin requirements, fasting plasma glucose, plasma cholesterol, and triglycerides, as well as change in plasma glucose, glucagon, and insulin or C-peptide levels in response to a standard meal. In some men, these parameters were also measured after i.v. tolbutamide. Both the inorganic and organic oral Cr supplements increased measurable body pools of Cr in hair and red blood cells by about 25%. However, fasting plasma glucose and lipids and the glucose response to either the standard meal or to tolbutamide were not significantly altered by any of the treatments. Despite this lack of effect on carbohydrate levels, the ketosis-resistant subgroups demonstrated a significant increase in postprandial insulin after treatment with the brewer's yeast that contained GTF.
An international symposium on natriuretic and digitalis-like factors was convened for the first time since 1992. Topics discussed included structures and biosynthesis of endogenous digitalis-like factors (EDLF), biologic activities, physiology function and role of EDLF in hypertension, and novel natriuretic factors. Progress was reported in determining the exact structure of an isomer of ouabain isolated from bovine hypothalamus. Evidence was presented supporting the existence of a second mammalian EDLF that resembles steroids found in toads (bufodienolides). Support for endogenous synthesis of mammalian EDLF was also presented. Mammalian EDLF were reported to have effects which are different from those possessed by digitalis like steroids derived from plants. New evidence was presented implicating EDLF in various forms of hypertension in humans and animal models. Finally, several unique natriuretic factors that do not inhibit Na, K ATPase and that appear to play a role in mammalian volume regulation were discussed.