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Biomedical subjects

G Trautwein

Publications and source records attributed to G Trautwein.

At least 91 records · Page 5Linked to original sources
PubMed1980

The role of the pituitary gland in spontaneous canine mammary tumorigenesis.

The morphological changes of the pituitary gland of 29 female dogs with spontaneous mammary tumours or dysplasia or both were correlated with basal serum prolactin, growth hormone, adrenocorticotrophin, thyrotrophin, cortisol, total cholesterol, thyroxine and thyroid binding index as well as with lesions in other endocrine and genital organs. Spontaneous canine mammary tumorigenesis seemed to be associated with increased secretory activity of growth hormone rather than prolactin cells. Depressed secretory activity of follicle stimulating hormone-, luteinizing hormone- and thyrotrophin-producing cells, as well as signs of inhibition of ovarian (anovulation) and thyroid function, were also consistent findings in dogs with mammary tumours. There also was disturbance in pituitary-adrenal function associated with hyperplastic and neoplastic changes of the pituitary gland and adrenal cortex.

Animals↗
PubMed1980

Functional morphology of spontaneous hyperplastic and neoplastic lesions in the canine pituitary gland.

The pituitary glands of 10 male and 29 female dogs of different breeds had diffuse hyperplasia and hypertrophy of growth hormone or prolactin cells. Immunoreactive adrenocorticotrophin/melanotrophin was in the frequent focal hyperplastic lesions and micro- and macroadenomas of both pars distalis and pars intermedia of old female dogs. Pituitary tumours of other functional cell types were not found. Focal hyperplastic and neoplastic lesions usually were accompanied by spontaneous nodular hyperplasia or adenomas of the adrenal cortex as well as by changes in serum adrenocorticotrophic hormone and cortisol levels.

Adenoma↗
PubMed1980

[Potassium hydrogen phosphate induced nephropathy in the dog. I. Pathogenesis of tubular atrophy (author's transl)].

A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HPO4 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells. During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g K2HPO4/kg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and beta-glucuronidase were found on cryostat sections. Kidneys fixed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated. Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosomes into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane. The degradation process described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward the end of the experiment. So far, it is not clear whether the tubular basement membrane is synthesized by the tubular cells, by fibroblasts or by both cell types. The presence of basement membrane-like material in tubular epithelial cells and in parietal epithelial cells of the glomerulus favors the view that epithelial cells produce the basement membranes and that increased production of basement membrane-like material is a sign of loss of differentiation.

Animals↗
PubMed1980

[Potassium hydrogen phosphate induced nephropathy in the dog. II. Glomerular alterations (author's transl)].

A disseminated atrophy of the proximal tubule accompanies K2HPO4-induced nephropathy in dogs. These pathologic processes cause glomerular changes that pass through different inflammatory stages and terminate in glomerular sclerosis. Experimental animals, design of the experiment and methods have been described [15]. During the 14-week study we determined the amount of urine (24 hours), protein (mg/dl), protein excretion (mg protein/24 hr) and the macro- and microprotein fraction in the urine by SDS-polyacrylamide gel electrophoresis. Clinical examinations were at 15, 66, and 85 days. Beagle dogs treated with 0.8 g K2HPO4/kg body weight developed significant glomerular selective and unselective protienuria. During the experiment the macroproteins in the urine decreased markedly, and at the last examination (day 85) glomerular proteinuria was no longer detectable by electrophoresis. Morphologically, there were only slight glomerular changes in the biopsy material taken at four weeks. Widespread lesions at 14 and 38 weeks were dilatation of Bowman's space, thickening of the basement membrane, increase in mesangial matrix, interposition of non-argentophilic mesangial matrix into the glomerular basement membrane, protein deposits in the mesangium and parietal basement membrane, formation of crescents, shrinkage of the glomeruli with collapse of glomerular tufts, and finally glomerular sclerosis. The parietal epithelial cells contained cytoplasmic areas that were free of organelles and contained microfilamentous and fine-granular material. These areas were close to the capsular basement membrane. Bundles of filaments within parietal epithelial cells had contact with the basement membrane, thus resembling hemidesmosomes. The sequelae of tubular atrophy are retention of glomerular filtrate and dilatation of Bowman's space, followed by compression and shrinkage of the glomerular tufts, and inflammatory processes within the glomerulus. The latter may be characterized as mesangio-sclerosing, mesangio-proliferative, membrano-proliferative, and extra-capillary glomerulonephritis. The decrease of urinary protein excretion towards the end of the experiment may be related to intratubular lysosomal digestion of cellular and amorphous components.

Animals↗