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Biomedical subjects

E Friedman

Publications and source records attributed to E Friedman.

At least 541 records · Page 30Linked to original sources
PubMed1982

Ureteral replacement with a new synthetic material: Gore-Tex.

There are no currently accepted synthetic ureteral substitutes. When faced with the need for ureteral replacement, the urologist must resort to pedicle grafts of intestine or bladder. Based on encouraging preliminary work in Europe, we have used a new synthetic vascular substitute, Gore-Tex, to replace segments of ureter in the dog. This material is made of expanded (microporous) polytetrafluoroethylene. In vascular surgery it is currently the preferred material due to its non-wetting and non-clotting surface when used in the arterial and venous beds. Adult mongrel dogs underwent segmental replacement of the right ureter and subtotal replacement of the left ureter with segments of 5-mm. tubed Gore-Tex. All anastomoses were performed with running 6--0 prolene. Antibiotics were given routinely perioperatively. Data on 7 dogs are available. Results indicate that Gore-Tex is well tolerated as a ureteral substitute to bridge gaps between segments of ureter. Anastomoses of Gore-Tex to bladder were not successful, resulting in infection and migration of the prosthesis. Under proper circumstances, Gore-Tex can be a useful potential addition to the urologic armamentarium.

Animals↗
PubMed1982

Differential response of familial polyposis fibroblasts to two bifunctional alkylating agents.

Skin fibroblasts from three subjects with familial polyposis coli, a hereditary disorder predisposing to colon cancer, exhibited an unexpected insensitivity to mitomycin C (MMC). Sister chromatid exchanges (SCEs) were either reduced or unchanged after exposure to MMC, while another bi-functional alkylating agent, diepoxybutane (DEB), induced an increase in SCE level at a low, equitoxic dosage in parallel experiments. Increased sensitivity to MMC as assayed by colony formation was, however, shown by one of the subjects with polyposis. These cells with the familial polyposis genotype may have a deficiency in the DNA repair system handling MMC-induced alkylation damage yet remain capable of repairing damage induced by DEB alkylation. This deficiency may contribute to the increased frequency of neoplastic transformation known to occur in these cells in vivo.

Alkylating Agents↗