Сопротивление и твердость металлических винтовых спиральных пружин Ø 31 мм, предназначенных для подвесных тележек Y25LSDI, установленных на товарных вагонах

On the strength and reliability of Ø 31 mm metallic helical springs, used for Y25LSDI bogie suspension mounted at freight cars

Nonalcoholic fatty liver disease: a marker of adipose tissue distribution

Recent evidence has shifted the paradigm of white adipose tissue from simple energy storage to the body's major endocrine and paracrine organ synthesizing and releasing multiple signaling proteins, collectively termed adipokines. White adipose tissue is distributed in two large depots (subcutaneous and visceral) and many small depots associated with the heart, blood vessels, lymph nodes, ovaries, mammary glands, prostate gland, pancreas. Even in a lean person, adipose tissue represents about 15-20 % of body weight, including external (subcutaneous and visceral) and internal (organ-associated) adipose tissue, the latter being even more important than the former; however the internal fat distribution was beyond the scope of the present study. Nonalcoholic fatty liver disease (NAFLD) is a term used to describe the accumulation of fat in the liver of people in the absence of alcohol consumption or consumption of less than 20 g/day. It is a progressive, low-grade inflammatory disease related to obesity and metabolic syndrome. NAFLD represent a spectrum of disorders ranging from fat accumulation (steatosis) to nonalcoholic steatohepatitis (NASH) that can progress to fibrosis and cirrhosis. The aim of the present study was to evaluate the clinic and metabolic parameters in patients with type 2 diabetes and NAFLD depending on gender and BMI and to assess relation of adipose tissue distribution with insulin resistance. Total of 118 patients (mean age 55.93 years; male, 46, female, 72) with type 2 diabetes evaluated in an outpatient diabetes clinic were diagnosed with NAFLD by ultrasonography and were assessed by weight, body mass index (BMI), waist circumference, fasting plasma glucose, HbAlc, and fasting insulin level. We calculated the HOMA-IR index [FPG (mmol/l) x FI (μU/ml)]:22.5. Body adipose percentage and trunk adipose content were measured using bioelectrical impedance analysis (TANITA BC-418). Overall, the present results suggest that insulin resistance may be considered a pathogenic link between T2DM and NAFLD, also at the level of adipose tissue distribution. Evaluating the distribution of internal, organ-associated adipose tissue remains a challenge for future studies in patients with T2DM and NAFLD.Adipobiology 2012; 4: 97-101

Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease

BACKGROUND: The cholesteryl ester transfer protein inhibitor evacetrapib substantially raises the high-density lipoprotein (HDL) cholesterol level, reduces the low-density lipoprotein (LDL) cholesterol level, and enhances cellular cholesterol efflux capacity. We sought to determine the effect of evacetrapib on major adverse cardiovascular outcomes in patients with high-risk vascular disease. METHODS: In a multicenter, randomized, double-blind, placebo-controlled phase 3 trial, we enrolled 12,092 patients who had at least one of the following conditions: an acute coronary syndrome within the previous 30 to 365 days, cerebrovascular atherosclerotic disease, peripheral vascular arterial disease, or diabetes mellitus with coronary artery disease. Patients were randomly assigned to receive either evacetrapib at a dose of 130 mg or matching placebo, administered daily, in addition to standard medical therapy. The primary efficacy end point was the first occurrence of any component of the composite of death from cardiovascular causes, myocardial infarction, stroke, coronary revascularization, or hospitalization for unstable angina. RESULTS: At 3 months, a 31.1% decrease in the mean LDL cholesterol level was observed with evacetrapib versus a 6.0% increase with placebo, and a 133.2% increase in the mean HDL cholesterol level was seen with evacetrapib versus a 1.6% increase with placebo. After 1363 of the planned 1670 primary end-point events had occurred, the data and safety monitoring board recommended that the trial be terminated early because of a lack of efficacy. After a median of 26 months of evacetrapib or placebo, a primary end-point event occurred in 12.9% of the patients in the evacetrapib group and in 12.8% of those in the placebo group (hazard ratio, 1.01; 95% confidence interval, 0.91 to 1.11; P=0.91). CONCLUSIONS: Although the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease. (Funded by Eli Lilly; ACCELERATE ClinicalTrials.gov number, NCT01687998 .)