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עמוד בית
Mon, 25.11.24

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April 2000
March 2000
Joseph Meyerovitch MD, Trevor Waner BVSc PhD, Joseph Sack MD, Juri Kopolovic MD and Joshua Shemer MD

Background: Despite current treatment protocols, the long-term complications of insulin-dependent diabetes mellitus have prompted the investigation of strategies for the prevention of IDDM.

Objectives: To investigate the effect of oral vanadate in reducing diabetes type I in non-obese diabetic mice.

Methods: Sodium metavanadate, 3.92 mmol/L, was added to the drinking water of 8-week-old female NOD mice. Blood glucose levels, water consumption and body weight were measured, and the end point of the study was judged by the appearance of hyperglycemia in the mice.

Results: Treatment with vanadate did not significantly reduce the incidence of type I diabetes as compared to the control group. However, oral vanadate therapy significantly reduced the blood glucose levels after the fourth week of treatment compared to the control group (3.83±10.67 vs. 4.44±10.83 mmol/L, P<0.03). There was a consistent and significant increase in body weight of the vanadate-treated pre-diabetic NOD mice compared to the controls. Diabetic mice treated with vanadate had significantly lower levels of serum insulin as compared to control diabetic mice (104±27 vs. 151±36 mol/L, P<0.03). Histologically, no significant differences were found in inflammatory response of the islets of Langerhans between the control and treated groups.

Conclusions: This study suggests that the post-receptor insulin-like effect induced by vanadate is not sufficient to prevent the development of diabetes and insulitis in pre-diabetic NOD mice.

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IDDM= insulin-dependent diabetes mellitus

NOD= non-obese diabetic

December 1999
Haya Zaltzberg MSc, Yoram Kanter MD, PhD, Michael Aviram DSc and Yishai Levy MD
Background: Atherosclerosis and microvascular complications in patients with non-insulin-dependent diabetes have been linked to increased oxidative stress. The glutathione redox cycle is a major determinant of the antioxidative capacity of plasma and its constituents.

Methods: We attempted to investigate plasma oxidation and plasma and erythrocyte glutathione and glutathione enzymes in 20 patients with NIDDM, compared with euglycemic matched controls. Plasma oxidation was analyzed both basally (without) and as induced by 2,2'-azobis,2-amidopropane hydrochloride measured by the generation of thiobarbituric acid reactive substances and lipid peroxides.

Results: There was a significant increase in oxidation both basally (without) and as induced by AAPH. Plasma glutathione was lowered by 50% (P<0.01) and erythrocyte glutathione peroxidase, glutathione s-transferase and glutathione reductase activities were lower by 30%, 27% and 46%, respectively (P<0.01) in the patients with NIDDM.

Conclusions: Confronted by increased oxidation, patients with NIDDM show an abnormal plasma and erythrocyte antioxidative capacity, which may result in an accelerated rate of complications.

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NIDOM= non-insulin-dependent diabetes mellitus

October 1999
Shmuel Kivity MD, Amir Onn MD, Yoel Greif MD, Elizabeth Fireman PhD, Shmuel Pomeranz MD and Marcel Topilsky MD
 Background: Nedocromil sodium confers both acute and chronic protective effects in patients with bronchial asthma, the interactions of which are unknown.

Objective: To examine to what extent and for how long nedocromil sodium prevents exercise-induced asthma when given immediately before exertion compared to chronic administration.

Patients and Methods: Eighteen asthmatic patients were given 4 mg NS at 30 min or 3.5 hours before exertion. We compared the resultant effect with that of the same protocol measured after 2 and 4 weeks of continuous treatment with the drug.

Results: Nedocromil sodium decreased exercise-induced asthma similarly at both points when given acutely. Chronic treatment of up to 4 weeks did not improve this protective effect at either interval following the inhalation.

Conclusion: Nedocromil sodium most likely reaches its maximal effect on exercise-induced asthma upon the first administration, although treatment for longer than 4 weeks might be required to prove a chronic effect of the drug.

September 1999
Avishai Ziser, MD, Ludmila Guralnik, MD, Robert Markovits, MD, Yousif Matanis, MD, and Genia Mahamid, MD.
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