Men presented with higher Hcy levels than women in the MS group; however, age, disease subtype, disease duration, relapse rate, and Expanded Disability Status Scale score/Multiple Sclerosis Severity Score did

not significantly affect Hcy levels in MS patients.

Conclusion: The preliminary data suggest that Hcy levels were not elevated in our sample of Greek MS patients, which does not support previous findings of a significant correlation between elevated serum Hcy levels and MS. Further studies to establish a possible association between MS and Hcy levels in the context of different ethnic groups with different habits are needed. Copyright (C) 2013 Elsevier Taiwan LLC Selleckchem PLX-4720 and the Chinese Medical Association. All rights reserved.”
“Slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized

by the delayed passage of contrast in the absence of obstructive epicardial coronary disease, and is an important clinical entity because it may be the cause of precordial pain when the body is at rest and/or during exercise. Although clinical and pathological features of SCF have been previously described, its etiopathogenesis remains unclear. The present study aims to investigate the risk factors of slow coronary flow, in order to provide the foundation for further exploration of potential mechanisms of SCF. A total of 47 consecutive patients with documented beta-catenin inhibitor slow coronary flow, and 33 patients with normal coronary flow-as defined by TIMI frame count (TFC)-were recruited for this study. Clinical

information was collected, and biochemical indicators including high-sensitivity C-reactive protein (hs-CRP), and a marker of systemic inflammation were Pictilisib mw detected. Logistic regression analysis was performed for statistical analysis. SCF patients had a higher level of serum uric acid (323.2 +/- 79.3 vs. 282.8 +/- 82.4 mu mol/l, p = 0.03), 2-h postprandial blood glucose (8.6 +/- 2.7 vs. 7.5 +/- 1.8 mmol/l, p = 0.04), platelet count (165.9 +/- 51.6 x 10(3) vs. 127.0 +/- 32.0 x 10(3) cells/mu l, p = 0.0003) and hs-CRP (3.4 +/- 0.8 vs. 2.0 +/- 0.9 mg/l, p < 0.0001) than those of patients in the control group. No marked differences in other variables were observed between the two groups. Logistic regression showed serum uric acid level (chi(2) = 3.84, beta = 0.007, p = 0.049), 2-h postprandial blood glucose (chi(2) = 5.02, beta = 0.277, p = 0.025) and blood platelet count (chi(2) = 12.16, beta = 0.026, p = 0.001) were independent predictors of SCF. When hs-CRP was included in the multivariate model, hs-CRP (chi(2) = 21.19, beta = 1.90, p < 0.0001) was the only independent predictor of SCF. These findings suggested that an elevation of serum uric acid level, 2-h postprandial blood glucose, and blood platelet count might be the causes of SCF, and inflammation was likely to be implicated in the causal pathway leading to SCF.