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Biomedical subjects

F E Cuppage

Publications and source records attributed to F E Cuppage.

At least 37 records · Page 2Linked to original sources
PubMed1976

Gold nephropathy. Ultrastructural, fluorescence, and microanalytic studies of two patients.

Renal biopsy specimens from two patients with gold nephropathy showed two distinctly different types of alterations. The first demonstrated lesions suggestive of immunologic injury primarily to the glomerulus and identical with membranous glomerulonephritis. The second had no evidence of immunologic injury, but contained extensive vacuolar degeneration of proximal tubular epithelial cells. Ultrastructurally, the vacuoles contained lipid materials and occupied the basal portion of the cells. Other tubular cells contained numerous "gold-containing" cytosegresomes. In this second specimen, it appeared that the filtered gold had a direct toxic effect on the tubular epithelium and perhaps also on the glomerular capillary wall. These findings suggest that gold nephropathy may indeed be a spectrum of a combination of both direct toxic and immunologic injury to glomeruli and tubules.

Aurothioglucose↗
PubMed1975

Gentamicin nephrotoxicity in rats. I. Acute biochemical and ultrastructural effects.

This investigation characterizes the acute biochemical and ultrastructural alterations within the rat kidney following the single injection of 10, 40, 80, or 160 mg. of gentamicin per kilogram of rat weight. Gentamicin was given intraperitoneally and rats were killed 80 minutes later. To assess a possible inhibitory effect upon protein synthesis 3H-leucine was injected 20 minutes postantibiotic and renal cortex was assayed for whole tissue and the protein fraction amino acid uptake. To exclude the possibility of gentamicin-induced lysosomal membrane instability with subsequent release of acid hydrolases, the activity of acid phosphatase was assayed in the supernatant and the residue of cortical homogenates containing the lysosomal fraction. Ultrastructural changes were concomitantly studied. To determine the intracellular localization of gentamicin, levels of the antibiotic were measured in subcellular fractions of cortical homogenates obtained from rats 2 hours following a single subcutaneous injection of 20 mg. of gentamicin per kilogram of rat weight. No gentamicin-induced alterations either of protein synthesis or of acid phosphatase distribution were demonstrated. Ultrastructural changes were most marked at 160 mg. per kg. consisting mainly of dilation of the endoplasmic reticulum, altered mitochondria, and increased cytosegresomes. Significant quantities of gentamicin were distributed within the nuclear, mitochondrial, and microsomal fractions. These studies indicate that although cytoplasmic alterations are prominent within the proximal tubular epithelial cells, they are not likely the result of either inhibition of protein synthesis or release of acid phosphatase from lysosomes.

Acid Phosphatase↗
PubMed1973

Mitochondrial proliferation within the nephron. I. Comparison of mitochondrial hyperplasia of tubular regeneration with compensatory hypertrophy.

MITOCHONDRIAL PROLIFERATION IN THE RENAL PROXIMAL TUBULAR EPITHELIUM IN RESPONSE TO TISSUE LOSS HAS BEEN QUANTITATED BY TWO DIVERSE MODELS: acute tubular necrosis induced by mercuric chloride and unilateral nephrectomy. The increased work demand on the remaining tubular mass in both models has probably stimulated both cell hyperplasia and hypertrophy. In both instances, cell hyperplasia preceeds hypertrophy. During the cellular hypertrophy, mitochondria first proliferate in number and then increase in size; presumably to satisfy the greater need for energy metabolism necessary during increased active transtubular solute transport.

Animals↗