Search PubMed⌕ Search

Biomedical subjects

P Raskin

Publications and source records attributed to P Raskin.

At least 145 records · Page 8Linked to original sources
PubMed1974

Mevalonate metabolism by renal tissue in vitro.

Previous studies from this laboratory have demonstrated that the kidneys rather than the liver play the major role in the in vivo metabolism of circulating mevalonic acid. Kidneys, however, convert mevalonic acid primarily to the precursors of cholesterol, squalene and lanosterol, rather than to cholesterol. This study was designed to define the specific tissue site within the kidney responsible for mevalonic acid metabolism. Tissue slices from rat and dog renal cortex and medulla and glomeruli and tubules were isolated, and the incorporation of (14)C-labeled mevalonic acid into the nonsaponifiable lipids squalene, lanosterol, and cholesterol was determined in these tissues. The results demonstrate that the renal cortex is the primary site of mevalonic acid metabolism within the kidney and that the glomerulus is responsible for 95% of the mevalonic acid metabolized by the renal cortex. As was the case for the whole kidney, the major metabolites of mevalonate in the glomeruli are squalene and lanosterol.

Acetates↗
PubMed1966

Arterial constrictor response in a diving mammal.

Angiograms were obtained in the harbor seal, Phoca vitulina, in air and during diving. During diving there is arterial constriction of the vascular beds of muscle, skin, kidney, liver, spleen, and presumably of all vascular beds except those perfusing the brain and heart. There is sudden constriction and narrowing of muscular arteries close to their origin from the aorta. Constriction of small arterial branches is so intense that blood flow is essentially lost in all involved organs.

Angiography↗
PubMedDate not supplied

Personality traits as predictors of good diabetic control.

To identify personality characteristics that might contribute to overall good control of type I diabetes mellitus, we used a biological correlate of control, glycosylated hemoglobin A1c values, as a means of selecting patients. Patients with evidence of good control (HbA1c less than 7.5%) were compared with patients with evidence of poor control (HbA1c greater than 10.4%). All patients were administered the Personality Research Form E. Need for achievement and a socially desirable response style were associated with good glycemic control. This finding is placed in the context of the complexity of health care behaviors required for adequate self-management.

Adult↗
PubMedDate not supplied

No correlation between glycemic control and an increase in erythrocyte aldose reductase activity in type I and type II diabetic patients.

Aldose reductase, the first enzyme of the polyol pathway, has been related to the pathogenesis of diabetic complications. The regulation of the enzyme in diabetes patients, however, has not yet been clarified. We recently reported that the activity of aldose reductase was increased in erythrocytes of insulin-dependent diabetes mellitus patients but short-term hyperglycemia did not affect the enzyme activity. It is still unclear, however, whether or not the increase in the enzyme activity is caused by long-term hyperglycemia and thus would be seen equally in both type I (insulin-dependent diabetes mellitus) and type 2 (non-insulin-dependent diabetes mellitus) individuals. To further clarify these issues we measured erythrocyte aldose reductase activity in 46 type I patients and 30 type II patients who had variable glucose control and in 16 nondiabetic subjects. We compared the enzyme activity with plasma glucose levels and hemoglobin A1c levels. The results show that erythrocyte aldose reductase activity is increased in both type I and type II patients as compared with nondiabetic subjects (7.1 +/- 0.3 U/L and 6.8 +/- 0.4 U/L erythrocytes versus 5.6 +/- 0.2 U/L erythrocytes, p less than 0.001 and p less than 0.01, respectively), but there were no significant differences between the two groups of diabetic patients. The enzyme activity varied by approximately four times among the diabetic individuals but there was no correlation between the enzyme activity and plasma glucose or hemoglobin A1c levels. We conclude that the increased activity of erythrocyte aldose reductase seen in diabetes is not related to hyperglycemia.

Adult↗
PubMedDate not supplied

The effect of the aldose reductase inhibitor, ponalrestat, on the progression of diabetic retinopathy.

The objective of this study was to evaluate the effects of ponalrestat, an aldose reductase inhibitor, on the progression of diabetic retinopathy. In this study, 62 patients with diabetes mellitus underwent a double-masked placebo-controlled clinical trial comparing the effect of ponalrestat 600 mg per day with a placebo on the progression of diabetic retinopathy. Both groups were comparable in terms of age, gender distribution, diabetes duration, metabolic control, and presence and severity of diabetic retinopathy. Seven-field stereo fundus photographs were performed at 0 (baseline), 12, and 18 months; 49 patients completed the study (26 in the ponalrestat group and 23 in the placebo group). In both treatment groups, a significant progression of diabetic retinopathy as evaluated by the Early Treatment Diabetic Retinopathy Study classification was observed (Wilcoxon Rank-Sum Test, p less than 0.05). No difference was observed in the progression of retinopathy between the two treatment groups (p = 0.96). The number of microaneurysms increased in the two study groups (from 5.6 +/- 1.2 to 10.5 +/- 1.3 in the placebo group and from 10.3 +/- 1.4 to 12.7 +/- 1.4 in the ponalrestat group); however, the increase was statistically significant only in the placebo group (p less than 0.05). When the increase in the number of microaneurysms was evaluated by change of category of microaneurysm count, no significant difference was observed. We conclude that ponalrestat at a dose of 600 mg per day has no clinically significant effect on the progression of diabetic retinopathy.

Aneurysm↗