Search PubMed⌕ Search

Biomedical subjects

F Elling

Publications and source records attributed to F Elling.

At least 37 records · Page 2Linked to original sources
PubMed1986

The effect of bromhexine on the kidney lesions in NZB-NZW-F1 mice.

The NZB-NZW-F1 mice develop a clinical picture resembling SLE and an exocrinopathy resembling Sjögren's syndrome. Three groups of hybrids were treated from their 20th week of age for 10, 17 and 20 weeks (groups 1, 2, 3) with Bromhexine in two different concentrations--6 & 60 mg/kg and placebo. NMRJ mice treated with placebo acted as healthy controls. After the treatment the kidneys were examined by light microscopy. The kidneys exhibited lupus-like lesions. Animals treated with 60 mg/kg Bromhexine for 17 weeks had a significantly lower degree of changes than had the other hybrids.

Animals↗
PubMed1985

Ochratoxin A-induced porcine nephropathy: enzyme and ultrastructure changes after short-term exposure.

Four pigs were treated with ochratoxin A (800 micrograms/kg) for five consecutive days. Subsequently, urine and bile were collected and kidneys were perfusion fixed unilaterally. Liver and kidney samples were examined for the distribution of ochratoxin A and metabolites in subcellular fractions and the effects of the toxin on protein synthesis and enzyme activities. Ochratoxin A and the hydrolytic product, ochratoxin alpha, were found in urine. Elevated levels of toxin accumulation in kidney (283 ng/g) compared with liver (189 ng/g) and toxin-mediated reductions in protein synthesis and enzyme activities in kidney identified it as a target organ of ochratoxin toxicity. Ultrastructural investigations of kidney in toxin-exposed animals identified a process of condensation of cellular material with disappearance of membranes and continuous desquamation in the lower part of the proximal convoluted tubules. In target cells peroxisomes appeared to have lost membrane integrity and the organelles were leaking materials into the cytosol. Reduction of structural integrity was associated with an increase in the presence of catalase and cyanide insensitive fatty acid oxidase activity in the soluble kidney fractions.

Animals↗
PubMed1985

Characterization of the T61 human breast carcinoma established in nude mice.

This paper gives a biological characterization of the T61 human breast carcinoma established in nude mice. The human origin of the tumour was verified by the demonstration of the presence of human chromosomes exclusively in the tumour cells. The tumour cells were found by chromosome analysis and flow cytometric DNA analysis to be aneuploid. By electron microscopy, the tumour cells were shown to display the characteristics of glandular epithelium; a light microscopic examination revealed morphological characteristics similar to those of an axillary metastasis of the patient from whom the T61 tumour was derived. Furthermore, the tumour was shown to contain classical receptors for oestrogen and progesterone. The growth of the tumour was characterized by gompertzian growth curves. Since the T61 tumour has a response pattern to endocrine treatment which differs from that described for other human breast tumours grown in nude mice, this tumour may provide a valuable supplement in the study of human breast cancer and endocrine treatment.

Animals↗
PubMed1985

Metabolism of ochratoxin B and its possible effects upon the metabolism and toxicity of ochratoxin A in rats.

A metabolic product was formed from ochratoxin B by rat liver microsomal fractions in the presence of NADPH. It was isolated from the incubation mixture by extraction, thin-layer chromatography, high-pressure liquid chromatography, and crystallization. On the basis of mass and nuclear magnetic resonance spectroscopy, the structure is suggested to be 4-hydroxyochratoxin B. The Km for the formation of 4-hydroxyochratoxin B was determined, and the hydroxylation of ochratoxin A was not altered by the presence of ochratoxin B. Rats were given ochratoxin A or B, or a mixture of both intraperitoneally. The ratios of the three metabolites, ochratoxin A, (4R)-4-hydroxyochratoxin A, and ochratoxin alpha, excreted in the urine did not change in the presence of ochratoxin B. Ochratoxin B was metabolized to 4-hydroxyochratoxin B and ochratoxin beta, but in a different ratio than for the ochratoxin A metabolites. When given intraperitoneally, ochratoxin beta was excreted within 24 h. In rats treated with ochratoxin A alone, the food intake was reduced by 50%, and histologically severe lesions, degeneration, and necrosis were observed in the proximal tubules. When ochratoxin A and B given in combination, the animals were clinically unaffected and histologically there was only slight damage of proximal tubules. These observations indicate that ochratoxin B considerably reduces the toxic effects of ochratoxin A.

Animals↗
PubMed1985

The pathogenesis of persistent turbinate atrophy induced by toxigenic Pasteurella multocida in pigs.

Six one-week-old piglets were pretreated with a 1% acetic acid solution for two days in one or both nostrils. Three piglets were not treated with acetic acid. Three days after treatment all nine piglets were inoculated in both nostrils with a toxigenic type D strain of Pasteurella multocida. Three piglets were killed seven days after inoculation; one died spontaneously 13 days after inoculation and the remaining pigs were killed at approximately 90 kg body weight, i.e., five to six months of age. All acetic acid-treated animals developed severe atrophy of the turbinates in the treated nostrils. Untreated nostrils were normal. The present results showed that toxigenic P. multocida can induce turbinate atrophy that persisted until 90 kg body weight when the lesions were similar to spontaneous atrophic rhinitis in pigs. The turbinate atrophy was not accompanied by inflammatory reaction, atrophy of other bone structures, or lesions in other organs. The experiment showed furthermore that toxigenic P. multocida may be present in the tonsils of control animals without causing turbinate atrophy. A pathogenesis for atrophic rhinitis in pigs is proposed.

Acetates↗
PubMed1984

The pathogenesis of atrophic rhinitis in pigs induced by toxigenic Pasteurella multocida.

The pathogenesis of atrophic rhinitis was studied in an experiment in which piglets were infected with a toxigenic type D Pasteurella multocida strain in the right half of the nasal cavity. Two days before inoculation the nasal mucosa on the right side had been subjected to mild irritation by intranasal instillation of a weak solution of acetic acid. The untreated (left) half of the nasal cavity served as an intrinsic control. Macroscopically, changes in the turbinates were already appreciable at 3 days p.i., and pronounced turbinate atrophy was noted at 7 days p.i. At 14 days p.i. deviation of the snout and almost complete turbinate atrophy was observed. The turbinates in the untreated half of the nasal cavity developed normally. Histologically, the changes were initially characterized by bone resorption mediated by an increased number of osteoclasts. Later osteoclasts were sparse, and there was an apparent disruption of osteoid synthesis. Ultrastructurally, the osteoblasts showed nuclear indentations and dilatation of the endoplasmic reticulum. Since no inflammatory reaction was observed, the hypothesis is advanced that atrophic rhinitis in pigs is caused by a P. multocida-produced factor which will stimulate bone resorption and suppress osteoid synthesis.

Animals↗
PubMed1983

A Danish adult case of EBV-positive Burkitt's lymphoma.

A 50-year-old Danish male presenting with swelling in fossa supraclavicularis and slight swelling of axillary and inguinal lymphnodes was diagnosed histologically as having malignant, non-Hodgkin, blast lymphoma. The EBV association was established by demonstration of EBV-DNA-positive tumor cells and the presence of high titers of antibodies of the IgG class to VCA, EA (D) and EBNA. The unique finding in this case was the high titers of IgA antibodies to VCA and to EA (D). This latter serological picture is characteristic of nasopharyngeal carcinoma (NPC) but has not previously been observed in Burkitt's lymphoma.

Burkitt Lymphoma↗
PubMed1979

Tissue distribution of radioactivity from ochratoxin A-14C in rats.

Examination of the distribution of radioactivity in rat tissues during the first 24 hr after administration of ochratoxin A-14C demonstrated maximum accumulation in stomach and kidney. The highest counts were observed in stomach, lung, kidney, thymus, spleen and heart during the first 6 hr after treatment, whereas the brain, liver muscle, duodenum, jejunum, ileum, and cecum exhibited the greatest counts at 18 hr after toxin exposure.

Animals↗
PubMed1979

Ochratoxin A-induced mycotoxic porcine nephropathy: alterations in enzyme activity in tubular cells.

Mycotoxic porcine nephropathy was induced by p.o. administration of crystalline ochratoxin A for periods of 5 days, 3 months and 2 years. Enzyme activities of the renal tissue were studied histochemically. These were NADH-tetrazolium reductase, NADPH-tetrazolium reductase, lactate dehydrogenase, isocitrate dehydrogenase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, alpha-glycerophosphate dehydrogenase, unspecific acid phosphatase and unspecific alkaline phosphatase. The activity of NADH-tetrazolium reductase and succinate dehydrogenase was reduced in the proximal tubule of all nephrons after 5 days ochratoxin A exposure and remained reduced after 3 months and 2 years exposure. The effect of ochratoxin A on these enzymes would appear to cause the impairment of proximal tubular function and the morphological changes observed in the proximal tubule in ochratoxin A-induced mycotoxic porcine nephropathy. The localization of alterations in enzyme activity corresponds to the localization of ochratoxin A previously demonstrated in the kidney. The activities of NADPH-tetrazolium reductase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and unspecific alkaline phosphatase were reduced focally corresponding to the areas with focal tubular atrophy and the degree of reduction was roughly parallel to the degree of atrophy.

Acid Phosphatase↗
PubMed1979

Nutritionally induced necrotizing glomerulonephritis and polyarteritis nodosa in pigs.

A florid necrotizing glomerulonephritis was found in all 48 pigs that were fed a waste product from the industrial production of the proteolytic enzyme Alcalase NOVO. In addition, three of the animals developed a lesion identical to polyarteritis nodosa. Focal necrosis of the glomeruli was observed in all animals. Electron microscopy showed electron dense deposits at the subendothelial and subepithelial side of the basement membrane of the glomerular capillary wall and in the mesangium. Immunofluorescence microscopy showed IgM in a fine granular pattern in the glomeruli of all 48 pigs. This appears to be the first report on nutritionally induced glomerulonephritis and polyarteritis nodosa in pigs.

Animal Feed↗
PubMed1979

Porcine nephropathy induced by long-term ingestion of ochratoxin A.

Nine pigs were fed crystalline ochratoxin A in their feed at a concentration of about 1 mg/kg. Three pigs and their controls were killed after 3 months and 6 pigs and controls were killed after 2 years. A decrease of the ratio TmPAH/CIn, increased urinary glucose excretion and decreased ability to concentrate urine, occurred within a few weeks and aggravated slightly during the 2-year period. Changes in renal structure, characterized by degeneration and atrophy of proximal tubules, interstitial fibrosis and hyalinization of glomeruli, were progressive during time of exposure, but terminal renal failure was not reached. The kidney, liver, muscular and adipose tissue contained 3 to 27 microgram ochratoxin A/kg after 3 months of exposure. No further accumulation of ochratoxin A residue was found after 2 years of exposure.

Animals↗
PubMed1978

Structural changes in kidneys of patients with oliguric extracapillary glomerulonephritis during immunosuppressive therapy.

Structural changes in kidney biopsies were investigated from five patients with primary oliguric extracapillary glomerulonephritis in whom the renal function was adequately maintained during extended combined immunosuppressive treatment. The most important structural change was a pronounced decrease in the number of crescents. Reduction in numbers of crescents in the late biopsies was significantly greater than the increase in the number of hyalinized glomeruli. Tubular parenchyma showed only slight diffuse atrophy, and a moderate interstitial fibrosis was always present during the latter stages of treatment. Disappearance of crescents in the glomeruli was not accompanied by disappearance of immunoglobulins. Successfull immunosuppressive treatment of extracapillary glomerulonephritis causes the disappearance of structural characteristics of the kidney that are diagnostic for this disease.

Adult↗
PubMed1977

Demonstration of ochratoxin A in kidneys of pigs and rats by immunofluorescence microscopy.

Ochratoxin A was localized in the kidney of pigs and rats by means of immunofluorescence microscopy after short-time exposure. Antibody against ochratoxin A was obtained from rabbits after repeated injections of bovine serum albumin-ochratoxin A conjugate. Ochratoxin A was localized exclusively in the proximal tubule. Light microscopically, necrosis and desquamation of epithelial cells in the pig kidneys were restricted to the proximal tubule where the toxin was found. The investigation had demonstrated conclusively that the proximal tubule is the target part of the nephron in ochratoxin A-induced mycotoxic nephropathy.

Animals↗
PubMed1977

Perfusion fixation of kidneys in adult pigs for electron microscopy.

In five female pigs, weighing approximately 100 kg, laparotomy was made under surgical anesthesia. One kidney was removed for immersion fixation and enzyme histochemistry, while the other kidney was fixed by vascular perfusion without prior interruption of the blood flow. A step-by-step description is given of the perfusion procedure, which requires three assistant. Prior to perfusion, heparin was given in order to prevent intravascular coagulation. 1% glutaraldehyde in Tyrode's solution was used as perfusion fluid. Polyvinylpyrrolidone 2.5% was added in order to adjust the colloid osmotic pressure of the perfusion fluid to that of the blood. Perfusion was maintained for 5 min. The tubules appeared with open lumina, and the proximal tubular cells had evenly arranged brush borders and both lateral and intercellular spaces were narrow and of constant width.

Animals↗
PubMed1976

Experimental avian nephropathy. Changes of renal function and structure induced by ochratoxin A-contaminated feed.

One-day-old chickens were fed ochratoxin A-contaminated diets at 2 levels: 0.3 and 1 mg ochratoxin A per kg feed, for 341 days. The only observable lesion to develop was a kidney damage comparable with the naturally occurring avian nephropathy. The changes in renal function were characterized by impairment of glomerular and tubular function, indicated by a decreased inulin clearance, TmPAH and decreased urine concentrating capacity. The changes of renal structure included degeneration of the tubular epithelium accompanied by regeneration. At slaughter, the kidneys, liver and muscular tissue of the birds contained residues of ochratoxin A (up to 50 mug per kg). As all the birds would have passed the meat inspection because no macroscopical lesions were present, this represents a possible health problem.

Animal Feed↗