Background and Purpose-Hemorrhagic transformation (HT) is a major complication of intra-arterial (IA) thrombolytic therapy. Identifying significant predictors of hemorrhage after thrombolysis would be useful in guiding patient selection for IA treatment. Methods-Data were collected retrospectively on consecutive patients with acute focal cerebral ischemia within the anterior or posterior circulation who were treated with combined intravenous (IV)-IA or pure IA thrombolysis over an 8-year period at the UCLA Medical Center. Results-Eighty-nine patients were treated. Median baseline National Institutes of Health Stroke Scale (NIHSS) score was 16, and mean age was 69 years. Twenty-six patients received IA tissue plasminogen activator (tPA) only, 22 received IV-IA tPA, and 41 received IA urokinase only. Asymptomatic HT occurred in 29 patients (33%), minor symptomatic HT (1-to 3-point worsening in NIHSS score) occurred in 10 patients (11%), and major symptomatic HT (Ն4-point worsening in NIHSS score) occurred in 6 patients (7%). The rate of any HT was similar in patients treated with pure IA thrombolysis (39%) versus combined IV-IA thrombolysis (41%). In pure IA cases, the rate of any HT was 50% with tPA versus 32% with urokinase (Pϭ0.2). Eighty-six percent of the patients with HT versus 39% of the patients without HT were dead or disabled (modified Rankin score Ͼ2) at day 7 (PϽ0.0001). On multivariate analysis, independent predictors of any HT were higher NIHSS score, longer time to recanalization, lower platelet count, and higher glucose level. A model using these variables correctly predicted HT with positive predictive value 70% and overall accuracy 78%. Conclusions-In

Simvastatin promotes intracellular antioxidant systems, fundamentally SOD, restoring endothelial function but not having any effect on blood pressure.

We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids (19.0% +/- 2.2 vs 24.6% +/- 1.4, p < 0.0001) mainly at the expense of docosahexaenoic acid C22:6(n3) (2.9% +/- 1.1 vs 5.3% +/- 1.3, p < 0.001), and arachidonic acid C20:4n6 (12.0% +/- 1.6 vs 15.1% +/- 0.6, p < 0.0005). Conversely, the total amount of saturated fatty acids was significantly increased (p < 0.05) and the polyunsaturated/saturated ratio was decreased in the Type 1 diabetic patients (p < 0.00 005). Neither the time from diagnosis, nor C-peptide levels, correlated with parameters indicating a poor metabolic control of Type 1 diabetes. However, C22:6(n-3) and total n-3 content significantly correlated with HbA1c (r = -0.79 and r = -0.88, respectively, p < 0.01), fructosamine (r = -0.71 and r = -0.74, respectively, p < 0.05), and Na+-K+ ATPase activity (maximal rate/Km quotient) (r = 0.78 and r = 0.71, respectively, p < 0.05). In conclusion we have found marked alterations of cell membrane lipid composition in Type 1 diabetic patients. These cell membrane abnormalities in lipid content were related to sodium transport systems and to poor metabolic control. Either diet, or the diabetic state, might be responsible for the observed cell membrane abnormalities. A dietary intervention study might differentiate the role of diet and diabetes in the reported cell membrane alterations.

Background: A decreased content of n–3 fatty acids in erythrocyte membrane of type 1 diabetic patients, which is inversely related to plasma levels of HbA_1c, has been reported previously. Our aim in this study was to observe the changes after a low-dose n–3 fatty acid (330 mg/day docosahexaenoic acid and 630 mg/day eicosapentanoic acid) dietary intervention in the lipid composition of cell membrane and metabolic control (measured according to plasma HbA_1c levels). Since changes in both parameters may alter transmembrane sodium transport or influence parameters measuring target organ damage, we also studied the neural conduction quality and activity of four sodium transporters. Methods: Eighteen type 1 diabetic patients were randomly assigned to continue their usual diet (control group) or to supplement their diet with a daily low dose of n–3 fatty acids (supplemented group). The changes between baseline and end values of the following parameters were compared: HbA_1c, lipid and phospholipid composition of cell membrane, activity of four ion carriers and neural conduction quality. Results: The dietary supplementation caused statistically significant changes in membrane lipid composition, particularly an increase of C22:6 (n–3) and the total n–3 fatty acid (respectively +0.90 ± 1.14% vs. –0.44 ± 1.23% and +1.36 ± 1.62% vs. –0.5 ± 1.80%, p < 0.05). After the dietary supplementation, we also observed a significant decrease of HbA_1c (–2.00 ± 1.9% vs. –0.13 ± 0.48%, p < 0.05), without significant changes in the dose of insulin required, an increase in the motor conduction velocity by the median nerve (+2.12 ± 1.35 m/s vs. –0.8 ± 2.34 m/s, p < 0.05) and a decrease of the V_max of the Na⁺-Li⁺ countertransport (–96.6 ± 111.2 vs. +58.1 ± 81.3 μmol/l cell/h^–1, p < 0.01). Conclusion: A low-dose omega–3 fatty acid dietary supplementation may change the fatty acid composition of the cell membrane and improve the metabolic control of diabetes. Using this dose, we also observed a decrease of the maximal rate of Na⁺-Li⁺ countertransport and a slight improvement of neural conduction.

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In this sample of nonobese and glucose-tolerant subjects with an early stage of hypertension, SG but not SI was related to LVM.

We hypothesized that in nonectopic Cushing syndrome there is an insufficient activity of type II (renal) 11beta-hydroxysteroid dehydrogenase (11beta-HSD2) that is related to cortisol excess, rather than to corticotropin (adrenocorticotropic hormone [ACTH]) levels. We measured plasma ACTH and urinary-free cortisol (UFF), urinary-free cortisone (UFE), tetrahydrocortisol (UTHF), and tetrahydrocortisone (UTHE) in 24-h urine samples of 24 healthy subjects and 15 patients diagnosed with nonectopic Cushing syndrome. Then, in the group of patients, a new 24-h urine sample was collected after treatment with 800 mg daily of ketoconazole. The UFF/UFE and UTHF/UTHE ratios were calculated as an estimation of 11beta-HSD2 activity. The patients had an increase in both the UFF/UFE (19.95 +/- 10.3 vs 5.78 +/- 4.72 nmol/24 h; p < 0.0001) and UTHF/UTHE ratios (5.36 +/- 5.23 vs 1.39 +/- 0.95 nmol/24 h; p < 0.001). Both UFF/UFE and UTHF/UTHE ratios decreased after ketoconazole treatment (19.95 +/- 10.3 vs 12.2 +/- 6.9 nmol/24 h; p < 0.005; and 5.36 +/- 5.23 vs 1.62 vs 1.21 nmol/24 h; p < 0.001, respectively). The control subjects had a significant relationship between UFF and UFE (r = 0.70, p < 0.0001), and between UTHF and UTHE (r = 0.75, p < 0.0001) that did not exist in the patient group. After ketoconazole treatment, the decrease in cortisol excretion in the patient group allowed a positive and significant relation between UFF and UFE (r = 0.64, p < 0.01) and between UTHF and UTHE (r = 0.56, p < 0.05) to appear. There was not any significant relationship between either UFF/UFE or UTHF/UTHE ratios and plasma levels of ACTH.