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Biomedical subjects

D Roth

Publications and source records attributed to D Roth.

At least 271 records · Page 15Linked to original sources
PubMed1968

Regulation of histidine catabolism by succinate in Pseudomonas putida.

The regulation of the histidine-degrading pathway is known to involve induction and repression. Our studies have shown that succinate may control the histidine-degrading pathway by sequential negative feedback inhibition. Succinate inhibited urocanase, and urocanate in turn inhibited histidase. Crude preparations of the two enzymes were made from Pseudomonas putida grown on l-histidine. Succinate was a competitive inhibitor of urocanase (K(i), 1.8 mm). Lactate, pyruvate, alpha-ketoglutarate, and glutamate did not inhibit urocanase. Urocanate inhibited histidase competitively (K(i), 0.13 mm). A multienzyme system (histidine to glutamate), when incubated with histidine and succinate, exhibited the combined effect. Succinate caused the level of accumulated urocanate to increase and indirectly blocked histidine disappearance. Growth of cells on urocanate as a nitrogen source was inhibited by 1% succinate. Succinate may play a physiological role in the biological regulation of histidine metabolism.

Acetates↗
PubMedDate not supplied

Selective percutaneous "biopsy" of atheromatous plaque tissue for cell culture.

The combination of percutaneous atherectomy and angioscopy enabled a selective "biopsy" of protruding atheromatous plaque material from 11 patients with arterial occlusive disease. The removed specimens were cultivated as adhering explants or single cells were obtained by enzymatic disintegration. The vast majority of the cultivated cells resembled fibroblasts, but could be identified as smooth muscle cells by their smooth muscle alpha-actin content. Proliferation rate was slow with 0.1 doublings per day. Endothelial cells were not observed by immunologic criteria. The described biopsy technique and in vitro evaluation of cultured human atheromatous plaque material may be useful for a better understanding of atherogenesis.

Actins↗
PubMedDate not supplied

Gastric and oesophageal carcinogenesis: models for the identification of risk and protective factors.

Male weanling rats of the Charles River Sprague-Dawley strain were exposed to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the water for 3 months at the concentration of 75 ml/litre. Other real or potential risk factors were administered, alone or in combination with MNNG. When MNNG was administered in combination with NaCl, bile acids, aspirin or BHA, forestomach tumours were enhanced. MNNG-induced tumours were inhibited by selenium or by difluoromethylornithine, an ornithine decarboxylase inhibitor. BHA alone caused forestomach tumours. When BHA was administered by dietary means or by gavage, alone or in combination with MNNG, the gavage method resulted in greater tumorigenesis than dietary exposure. This increase was associated with increased [3H]thymidine labelling of forestomach epithelium and increased hyperplasia. Oesophageal carcinogenesis induced by methylbenzylnitrosamine (MBN) was enhanced by zinc deficiency, alcohol and 13-cis-retinoic acid. Zinc deficiency also resulted in oesophageal tumours in rats exposed to the hepatocarcinogen dimethylnitrosamine. Riboflavin deficiency injured oral and oesophageal epithelium and increased sensitivity to MBN-induced oesophageal tumours.

Administration, Oral↗
PubMedDate not supplied

The new immunosuppressive era.

Immunosuppression, although necessary to enable the graft to escape the consequence of immune surveillance carries some risks for the patients. There is an associated increase in neoplasm, opportunistic infections, and end-organ toxicity. In addition, even with excellent patient compliance, rejection (acute and chronic) remain a major limitation that contributes to the loss or decrease in the function of the allograft. New drugs have been added to the armamentarium of immunosuppressive agents to suppress allograft rejection and to rescue graft from cyclosporine-resistant. Most of the immunosuppressive agents in use today are direct at the T lymphocyte, non-specifically inhibiting T-cell activation and proliferation. The authors described here an update of these new immunosuppressive agents and new strategies used in solid organ transplantation.

Bone Marrow Transplantation↗