PubMed · 5572684
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
L S Levy. 1971. Physiological changes during electrical asphyxiation.. https://doi.org/10.1136/oem.28.2.164
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The kidney-specific chromatin structure of the phosphoenolpyruvate carboxykinase (PEPCK) gene was examined and compared to that of the liver. Kidney nuclear extracts were found to lack a liver-enriched factor, pepA, that binds to HSS A, a distal enhancer of the PEPCK gene that may be involved in opening the chromatin domain of the PEPCK gene in the liver. To begin the characterization of the kidney-specific chromatin structure of the PEPCK gene, nuclease hypersensitive sites (HSS) were mapped by indirect end-labeling analysis in proximal tubules from control rats, proximal tubules from acidotic rats which express induced levels of PEPCK, and NRK52E cells, a rat kidney epithelial cell line which does not express the PEPCK gene. A subset of HSS, at -400/+1 over the proximal promoter and at +1900 within the coding region, correlate with kidney-specific PEPCK expression. Two other HSS, at -3.1 kb and +6.2 kb, are detected in kidney cells regardless of PEPCK expression. The HSS at -4800, -1240, and +4650, previously identified in PEPCK-expressing liver cells, were not observed in the kidney. As in the liver, the pattern of hypersensitivity in the kidney does not change by altering the rate of transcription.
Explore the source record for details and available documents.
A 7-day-old Jersey calf was evaluated because of diarrhea and pneumonia. The calf was hypernatremic, hypoproteinemic, and acidemic, and was treated initially with i.v. administration of fluids with sodium concentration (175 mEq/L) similar to the calf's serum sodium concentration. Sodium concentration of the administered fluids was gradually decreased over the following days, but the calf's serum sodium concentration decreased too rapidly, and the calf developed neurologic signs attributed to cerebral edema. Treatment with mannitol and i.v. administration of fluids with a higher concentration of sodium resulted in abatement of clinical signs. In calves, hypernatremia may develop over several days. Prescribing traditional isotonic or hypotonic fluids in such cases will be harmful, because during chronic hypernatremia, the brain's adaptive mechanisms involve accumulation of organic osmoles that may take several days to equilibrate across cell membranes, and cerebral edema may result. Administration of fluids containing sodium concentration approximately equal to the patient's measured serum sodium concentration is required to decrease serum sodium concentration more slowly than is possible with traditional isotonic fluids.