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Biomedical subjects

Russell W Chesney

Publications and source records attributed to Russell W Chesney.

12 recordsLinked to original sources
PubMed2003

Pamidronate in a girl with chronic renal insufficiency dependent on parenteral nutrition.

A 10-year-old 40-kg African-American female with megacystis microcolon hypoperistalsis syndrome maintained on total parenteral nutrition (TPN), with a history of metabolic bone disease and renal insufficiency, was admitted with a Candida parapsilosis central venous line infection. During her 280-day hospital stay, she had multiple episodes of bacteremia and recurrent candidemia. Furthermore, she developed pathological fractures and hip displacement with osteomyelitis due to Enterobacter. Hypercalcemia and a history of nephrocalcinosis had prevented appropriate dosing of calcium prior to and during the first months of her hospital stay. Pamidronate and chlorothiazide were added to her regimen. The urinary calcium to creatinine ratio and ionized calcium decreased. The pamidronate dose was increased to 60 mg once a week and was well tolerated. Daily calcium was added to her TPN solution and was increased to 10 mEq/day by the time of discharge. We conclude that relatively large doses of pamidronate may be required in certain cases of refractory hypercalcemia and are well tolerated in children.

Anti-Inflammatory Agents↗
PubMed2003

Regulation of taurine transporter gene (TauT) by WT1.

In the present study we have demonstrated that WT1 (Wilms tumor suppressor gene) enhances the expression of TauT (taurine transporter gene) in human embryonic kidney 293 cells in a dose-dependent manner. TauT promoter activity was increased five-fold by cotransfection of a full-length TauT promoter-reporter construct with WT1. Electrophoretic mobility shift assays (EMSAs) using nuclear extracts from WT1-overexpressing 293 cells showed a putative WT1-binding site in the basal promoter region of TauT, which bound to WT1 in EMSAs. Mutation of this WT1 consensus sequence abolished binding of WT1. These results demonstrate that TauT may represent a downstream target gene of WT1 during renal development.

Base Sequence↗
PubMed2002

Transcriptional repression of taurine transporter gene (TauT) by p53 in renal cells.

Taurine, an intracellular osmolyte whose body pool size is adaptively regulated by the kidney, is required for normal renal development. Overexpression of the p53 tumor suppressor gene in p53 transgenic mice results in renal malformation, suggesting that altered expression of certain p53 target gene(s) involved in renal development may be responsible. This study shows that the taurine transporter gene (TauT) is a transcriptional target of p53. Expression of TauT was decreased after activation of p53 by doxorubicin, a DNA-damaging drug, in 293 and NRK-52E renal cells. TauT promoter activity was decreased 5-10-fold by cotransfection of a full-length TauT promoter-reporter construct with p53, which was reversed by cotransfection with a mutant p53 (p53-281). Electrophoretic mobility shift assays using nuclear extracts from p53-expressing (10)1val cells showed a putative p53-binding site in the TauT promoter region, which bound to the p53 in electrophoretic mobility shift assays. Mutation of this p53 consensus sequence abolished binding of p53. These results demonstrate that TauT may represent a downstream target gene of p53 that could link the roles of p53 in renal development and apoptosis.

Animals↗
PubMed2002

The development of pediatric nephrology.

Pediatric nephrology, as a discipline, arose from descriptive studies of childhood glomerulonephritis in Europe and the field of pediatric metabolism in the United States. While pediatric scientists before 1950 were concerned with fluid and electrolyte metabolism, regulation of intracellular and extracellular fluid, acid-base homeostasis, and parenteral fluid therapy, the defined field of nephrology developed after the Second World War around six major advances: ACTH and glucocorticoid therapy for nephrotic syndrome; renal biopsy to diagnose glomerular disease; the role of immunologic factors in glomerular injury; the use of dialysis as renal replacement therapy; renal transplantation as the optimal form of therapy in children with end stage renal failure; and recognition of renal disease in the etiology of 80% of cases of childhood hypertension. These discoveries led to focused research, the definition of specific training in nephrology, establishment of an American, European, and an International Society of Pediatric Nephrology, as well as an American Sub-Board of Pediatric Nephrology, and the inception of a journal, Pediatric Nephrology, now in its 15th year. Major research themes have included developmental nephrology, transplantation immunology, and concerns about growth in children with renal disease. Many clinical entities have been described in detail, some of which are almost confined to children. The scientific basis of pediatric nephrology, ongoing patient care needs, and its technical aspects - renal biopsy, dialysis and transplantation - assure its continuing future as a major pediatric discipline on all continents.

Child↗