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S Sandler

Publications and source records attributed to S Sandler.

189 records · Page 11Linked to original sources
PubMed1981

A gas chromatographic--mass spectrometric study of profiles of volatile metabolites in hepatic encephalopathy.

Volatile organic substances present in blood plasma and cerebrospinal fluids of certain control groups of human subjects and cirrhotic patients some of whom were suffering from hepatic encephalopathy were quantitatively analysed and identified. A rapid, reproducible, direct injection capillary column gas chromatographic method was developed for the concentration and detection of such volatiles at mg/l and lower concentrations. Of at least forty volatiles detected, twenty-one were identified. The mean concentration of one of these, 3-methylbutanal, was found to be significantly elevated (p less than 0.01) in chronic encephalopathics (2.37 +/- 0.79 mg/l, n = 18), when compared to the controls (0.30 +/- 0.08 mg/l, n = 20). Furthermore, the concentration of this component increased with the clinically diagnosed severity of the encephalopathic state. The presence of 3-methylbutanal is related to leucine, a branched-chain amino acid linked with hepatic encephalopathy.

Aldehydes↗
PubMed1981

Islet implantation into diabetic mice with pancreatic insulitis.

Repeated injections of small doses of streptozotocin (s.z.) lead to a slowly-developing hyperglycemia with a concomitant infiltration of lymphocytes into the pancreatic islets. Similarly, intrasplenically islet-implanted but otherwise normal mice became diabetic when given the multi-s.z.-treatment, suggesting that the splenic location of the islets does not protect them from the toxic effects of s.z. or immune-reactions. Intrasplenic, syngeneic islet implantation normalized the elevated blood sugars of multi-s.z.-treated mice, irrespective of whether the transplantation was performed 8 or 15 days after the first injection of s.z. These findings suggest that s.z. has to be present in order to trigger the auto-immune process of this insulitis model. In support of this suggestion, we observed that hyperglycemic, multi-s.z.-treated mice cured by islet implantation reverted to a hyperglycemic state when treated repeatedly with small doses of s.z., suggesting the presence of a booster-dose phenomenon.

Animals↗
PubMedDate not supplied

The protective effect of glucose, but not 3-O-methyl glucose, against alloxan-induced diabetes depends upon the route of hexose administration.

It is well established that pretreatment with glucose prevents the development of alloxan-induced diabetes in rodents. This was confirmed in the present study, and a protective effect against the development of hyperglycemia, after alloxan administration (75 mg/kg body weight), in male NMRI mice was observed when glucose was injected i.v. 10 or 20 min before alloxan injection. However, when glucose was administered i.p., a protective effect was only observed when glucose was given 20 min before alloxan, despite the fact that the serum glucose concentrations at the time of the alloxan injection were similar in the i.v.- and i.p.-injected animals. Administration of 3-O-methyl glucose by i.v. and i.p. routes protected against the effects of alloxan to the same extent. When alloxan was administered at a lower dose (65 mg/kg body weight) both i.v. and i.p. administration of glucose 10 min before alloxan, protected against the development of hyperglycemia. It is concluded that the route of administration of glucose, but not of 3-O-methyl glucose, affects its protective action against alloxan-induced diabetes. The present findings suggest that an important feature of the glucose mediated protection against alloxan-induced diabetes is the metabolism of glucose within the B-cells, rather than via extracellular effects on the B-cell plasma membrane.

3-O-Methylglucose↗
PubMedDate not supplied

Experimental pancreatic transplantation in diabetes.

Although transplantations of vascularized pancreas in diabetic patients show steadily improving results, the immediate operative risks and life-long immunosuppressive medication involved represent considerable disadvantages. Efforts are being made to develop simpler and safer methods of transplantation with isolated pancreatic islet grafts, e.g., isolated islets, fetal pancreas, or dispersed adult pancreas. Iso-, allo-, and xenografts of such preparations have been shown to reverse diabetes in animals. However, attempts to apply these techniques in clinical practice have remained largely unsuccessful, and major technical advances are needed before success is achieved. Attempts to use whole, segmented, or isolated islets from pancreatic grafts as a cure for diabetes in animals and in diabetic patients are reviewed. The importance to the graft's permanent function, of adequate preparation and storage of the graft, and of beta-cell growth and vascularization are reviewed. Various forms of immunomodulation by pretreatment of grafts in vitro have been employed in animal models of diabetes, but none of these have yet been employed with long-term success in humans. Recurrence of a specific autoimmune response toward the beta-cell in a spontaneously diabetic recipient is a potential mechanism for destruction of transplanted islet tissue.

Animals↗