In patients with HCV, alterations in the liver tissue as reflected by ALT elevation are mainly associated with periportal bridging/necrosis, viral load and duration of disease. A cut-off value < 23 IU/L distinguished with high diagnostic accuracy healthy controls from patients with HCV.

The aim of this study was to determine reference values for serum cystatin C at, and 3 days after, birth, and to determine if the concentration was influenced by gender, gestational age or bilirubin level. Umbilical cord and peripheral venous blood was taken, and serum cystatin C, creatinine, and total and direct bilirubin levels were measured. The mean concentration of cystatin C was not significantly different between cord blood and blood taken on day 3 (1.36 ± 0.35 mg/l and 1.35 ± 0.33mg/l, respectively). Comparison of subgroups, divided by gender, duration of gestation and bilirubin levels, using the Mann-Whitney U-test and Wilcoxon analysis, showed no effect of these parameters on cystatin C levels.

Autophagy is a major clearance mechanism that degrades organelles and large protein aggregates to maintain cell survival and protein homeostasis. Although induction of autophagy can promote longevity in experimental models, the question as to whether increased basal levels of autophagy can be associated with human longevity remains open. In this pilot study, we investigated the association between serum concentrations of beclin-1, a key regulator of autophagy, and human exceptional longevity (EL). Serum beclin-1 was measured in three study groups: 79 healthy centenarians (39 males, aged 100-104 years); 178 non-diabetic patients who had experienced an acute myocardial infarction at a young age (101 males, 28-39 years); and 180 age- and sex-matched healthy young volunteers (103 males, 27-39 years) using an enzyme-linked immunosorbent assay. Healthy centenarians had significantly higher beclin-1 levels (2.2±0.8 ng/mL) compared with both young patients with myocardial infarction (1.5±0.7 ng/mL; p<0.001) and healthy controls (1.4±0.9 ng/mL; p<0.001), whereas no significant difference was observed between the two groups of young subjects. The multivariate-adjusted odds ratio for having serum beclin-1 levels >1.5 ng/mL (i.e., 75th percentile of the young controls' levels) was 3.4 (95% confidence interval 1.8-5.7; p<0.001) for healthy centenarians. Our preliminary data suggest that elevated basal levels of autophagy as reflected by high serum beclin-1 levels may be a biomarker of healthy human EL.

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A systemic inflammatory reaction is a common feature of both sarcoidosis and atherosclerosis. Endothelial-cell specific molecule 1 (endocan) is a marker of vascular pathology which also shows a correlation with inflammation, endothelial dysfunction, and atherosclerosis. The objective of this study was to evaluate the vascular involvement in sarcoidosis using serum endocan levels and brachial artery flow-mediated dilation (FMD), a marker of endothelial dysfunction. We included 53 patients with sarcoidosis without conventional cardiovascular risk factors and 40 healthy controls. Endothelial function was assessed using FMD. Endocan concentrations were measured using a commercially available enzyme-linked immunoassay. Patients with sarcoidosis had significantly higher endocan levels (306 [68] ng/mL vs 269 [73] ng/mL; P = .039) and lower FMD (2.7% [2.3%-3.2%] vs 8% [5%-13%]; P < .001) compared with the healthy group. A negative correlation was found between endocan levels and FMD in the sarcoidosis group ( r = -.325, P < .007). We conclude that sarcoidosis is associated with high levels of endocan and lower FMD values, which may indicate endothelial dysfunction and an early stage of atherosclerosis.