Renal damage in hemorrhagic fever with renal syndrome. Measurements of urine and serum lysozyme and urine IgG.
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Adolescent↗
Biomedical subjects
Q Su
Publications and source records attributed to Q Su.
[Antispasmodic effect of acetagastrodine on vascular smooth muscle].
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Animals↗
Uncomplicated selenium deficiency produced in chicks fed a corn-soy-based diet.
Day-old chicks were fed a practical-type diet based on corn- and soybean meal produced in a severely Se-deficient area of northeastern China. The diet contained 0.007 ppm Se and resulted in marked decreases in the activities of Se-dependent glutathione peroxidase in plasma and pancreas within 6 days of feeding. Chicks fed this basal diet showed histological signs of acinar atrophy of the pancreas, hyaline body formation, vacuolation and cytoplasmic shrinkage by 18 days and significantly elevated activities of amylase in plasma by 30 days. Each of these changes was prevented by supplementing the basal diet with Se to bring it to a level of 0.20 ppm. Chicks fed a Se-deficient purified diet based on crystalline amino acids also showed decreased Se-dependent glutathione peroxidase activities in plasma and pancreas, pancreatic damage as evidenced by histological examination and increases in plasma amylase activities. However, these signs of nutritionally induced pancreatic atrophy occurred sooner and were of greater magnitude than those observed in Se-deficient chicks fed the practical diet within the 30-day experimental period. These results, therefore, constitute the first report of nutritionally induced pancreatic atrophy in Se-deficient chicks fed a diet containing intact protein, and we suggest that a factor(s) associated with the practical diet acts to partially protect the chicks from this pathological consequence of severe Se deficiency.
Amylases↗
Nephrotoxicity of cyclosporin A and FK506: inhibition of calcineurin phosphatase.
Cyclosporin A (CsA; 50 mg/kg) and Fujimycine (FK506; 5 mg/kg), but not the related macrolide immunosuppressant rapamycin (5 mg/kg), caused a reduction of glomerular filtration rate, degenerative changes of proximal tubular epithelium, and hypertrophy of the juxtaglomerular apparatus in male Wistar rats when given for 10 days. The molecular mechanisms of CsA and FK506 toxicity were investigated. Cyclophilin A and FK506-binding protein, the main intracytoplasmic receptors for CsA and FK506, respectively, were each detected in renal tissue extract. In the kidney, high levels of immunoreactive and enzymatically active calcineurin were found which were inhibited by the immunosuppressants CsA and FK506, but not by rapamycin. Finally, specific immunophilin-drug-calcineurin complexes formed only in the presence of CsA and FK506, but not rapamycin. These results suggest that the nephrotoxic effects of CsA and FK506 is likely mediated through binding to renal immunophilin and inhibiting calcineurin phosphatase.
Animals↗