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Biomedical subjects

A S Mia

Publications and source records attributed to A S Mia.

18 recordsLinked to original sources

Rapid turbidimetric determination of serum pancreatic lipase in the dog.

A rapid and highly reproducible turbidimetric method for the determination of serum pancreatic lipase activity in the dog is described. Values of 0 to 50 IU/L of serum were obtained in 35 healthy mature dogs, and the maximum values of 325 to 800 IU/L were observed in 8 dogs with induced pancreatitis.

Animals

Serum values of amylase and pancreatic lipase in healthy mature dogs and dogs with experimental pancreatitis.

Serum values of amylase and pancreatic lipase were determined by the iodometric and the turbidimetric methods, respectively, in 44 mature healthy dogs and in 8 dogs with experimentally induced pancreatitis (plus 1 sham-operated control). Serum value of amylase in mature healthy dogs varied from 250 to 1,500 Caraway units/dl and that of pancreatic lipase varied from 0 to 50 IU/L. Maximal serum values of amylase and pancreatic lipase in the dogs with experimentally induced pancreatitis varied from 4,540 to 14,000 Caraway units/dl and 325 to 810 IU/L, respectively. Following pancreatic damage, serum values of amylase and pancreatic lipase increased rapidly in the 8 dogs and ran parallel to each other in 6 of the 8 dogs studied. However, the serum value of amylase returned to within normal range earlier than the serum value of pancreatic lipase in 2 dogs; the reverse was true in 2 other dogs.

Amylases

Direct colorimetric determination of serum arginase in various domestic animals.

A direct colorimetric method for the determination of serum arginase activity in various domestic animals is described. Serum arginase activity in healthy mature dogs, cats, horses, cattle, sheep, and pigs ranged from 0 to 14 IU/L. Serum arginase activity increased considerably in these animals during experimental hepatic damage induced by oral administration of carbon tetrachloride.

Animals

Renal radial fibrosis in mutant Southdown sheep with congenital hyperbilirubinemia.

Kidneys from 7 mutant Southdown sheep with congenital hyperbilirubinemia, aged from 1 to 5 years were examined. Renal biopsies were taken from another mutant at 3 months and 12 months of age. At 3 months, lesions consisted of thin radial bands of myxomatous tissue in the medullary rays and atrophy of the adjacent collecting tubules. By 1 year collagen had replaced myxomatous tissue. Grossly, the kidneys were normal until 2 years when they became red and gray mottled and stained with bilirubin. The capsules stripped readily to reveal fine granular surfaces in sheep over 2 years of age. On the cut surface of the cortex were 0.5 mm wide radial gray streaks of fibrous tissue. Progressive fibrosis in sheep 2 to 5 years old resulted in a thinning of the cortex. With increasing fibrosis, the number of cystic tubules increased progressively. Protein casts and hyaline droplet degeneration were numerous in sheep over 2 years of age. Plasma cells and lymphocytes were frequently seen in the fibrous bands, and bile pigment was visible in the macrophages in the fibrous tissue and in the epithelium of the proximal tubule cells. Polyuria, low specific gravity urine and reduced effective renal plasma flow and glomerular filtration rates resulted from the replacement of specialized proximal tubule cells by low cuboidal cells, fibrous tissue separating the capillaries from the loops of Henle, destruction of glomeruli and segregation of glomeruli in fibrous bands. The kidney lesions may be determined by the same gene responsible for the hepatic excretion defect for bilirubin.

Age Factors