In the TOHO Lipid Intervention Trial Using Pitavastatin (TOHO-LIP), a multicenter randomized controlled trial, pitavastatin significantly reduced cardiovascular (CV) events compared to atorvastatin in patients with hypercholesterolemia. To investigate the mechanism by which pitavastatin preferentially prevents CV events, we investigated the relationship between CV events and cardio-ankle vascular index (CAVI) using the TOHO-LIP database.
 
  For the subgroup analysis, we selected patients from a single center, Toho University Sakura Medical Center. After excluding those who had CV events at baseline or during the first year, 254 patients were enrolled. The primary end point was the same as that of TOHO-LIP, and three-point major cardiac adverse events (3P-MACE) was added as secondary end point.
 
  The cumulative 5-year incidence of 3P-MACE (pitavastatin 1.6%, atorvastatin 6.1%, P=0.038) was significantly lower in pitavastatin group (2 mg/day) than in atorvastatin group (10 mg/day). CAVI significantly decreased only in pitavastatin group during the first year (9.50-9.34, P=0.042), while the change in low-density lipoprotein cholesterol (LDL-C) did not differ between the two groups. The change in CAVI during the first year positively correlated with 3P-MACE and tended to be an independent predictor of 3P-MACE in Cox proportional hazards model (hazard ratio, 1.736; P=0.079). The annual change in CAVI throughout the observation period was significantly higher in subjects with CV events compared to those without.
 
  In this subgroup analysis, the reduction in CV events tended to be associated with the CAVI-lowering effect of pitavastatin, which was independent of the LDL-C-lowering effect.
 In this subgroup analysis, the reduction in CV events tended to be associated with the CAVI-lowering effect of pitavastatin, which was independent of the LDL-C-lowering effect.
  Proprotein convertase subtilisin/kexin type 9 (PCSK9) degrades the low-density lipoprotein (LDL) receptor, leading to hypercholesterolemia and cardiovascular risk. Treatment with a statin leads to a compensatory increase in circulating PCSK9 level.  https://www.selleckchem.com/products/Nolvadex.html  Anagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, was shown to decrease LDL cholesterol (LDL-C) levels to a greater extent than that by sitagliptin, another DPP-4 inhibitor, in the Randomized Evaluation of Anagliptin versus Sitagliptin On low-density lipoproteiN cholesterol in diabetes (REASON) trial. We investigated PCSK9 concentration in type 2 diabetes mellitus (T2DM) and the impact of treatment with anagliptin or sitagliptin on PCSK9 level as a sub-analysis of the REASON trial.
 
  PCSK9 concentration was measured at baseline and after 52 weeks of treatment with anagliptin (n=122) or sitagliptin (n=128) in patients with T2DM who were receiving statin therapy. All of the included patients had been treated with a DPP-4 inhibitor prior to randomization.
 
  Ba-mediated PCSK9 induction and subsequent degradation of the LDL receptor.
  In 2012, the Korean National Health Insurance extended its coverage to include denture services for older adults. We examined whether the new policy resulted in improved chewing ability in the eligible population.
 
  We used interrupted time-series (ITS) analysis, a quasi-experimental design, to analyze the effect of the policy. We used data from the Korea National Health and Nutrition Examination Survey conducted from 2007 to 2016-2018. The study population consisted of two groups the treatment group, aged 65 years or older and eligible for the dental insurance benefit; and the control group, those younger than 65 years and ineligible. The main evaluated outcome was self-reported chewing difficulty.
 
  The ITS analysis showed that chewing difficulty decreased annually by 0.93% (95% CI -1.30 to -0.55) and 0.38% (95% CI -0.59 to -0.16) after the policy extension in the older than 65 and younger than 65 groups, respectively. However, we could not conclude that the insurance extension affected chewing difficulty because there was a decrease in the control group as well.
 
  Chewing ability improved in both older and younger adults regardless of dental insurance coverage for older adults. Other exogenous factors probably led to the improvements in chewing ability as well as dental insurance benefits.
 Chewing ability improved in both older and younger adults regardless of dental insurance coverage for older adults. Other exogenous factors probably led to the improvements in chewing ability as well as dental insurance benefits.
  The objective of this study is to describe the legislation regulating the use of electronic cigarettes (e-cigarettes) in various places in European countries.
 
  A survey among experts from all countries of the World Health Organization (WHO) European Region was conducted in 2018. We collected and described data on legislation regulating e-cigarette use indoors and outdoors in public and private places, the level of difficulties in adopting the legislation, and the public support and compliance. Factors associated with the legislation adoption were identified with Poisson and linear regression analyses.
 
  Out of 48 countries, 58.3% had legislation on e-cigarette use at the national level. Education facilities were the most regulated place (58.3% of countries), while private areas (homes, cars) were the least regulated ones (39.6%). A third of countries regulated e-cigarette use indoors. Difficulty and support in adopting the national legislation and its compliance were all at a moderate level. Countries' smoking prevalence and income levels were linked to legislation adoption.
 
  Although most WHO European Region countries had introduced e-cigarette use legislation at the national level, only a few of the legislation protect bystanders in indoor settings.
 Although most WHO European Region countries had introduced e-cigarette use legislation at the national level, only a few of the legislation protect bystanders in indoor settings.Renal tubular cell death is caused by various extracellular stresses including toxic amounts of cadmium, an occupational and environmental pollutant metal, and is responsible for renal dysfunction. While cadmium exposure disrupts many intracellular signaling pathways, the molecular mechanism underlying cadmium-induced renal tubular cell death has not yet been fully elucidated. We have recently identified two important intracellular signaling pathways that promote cadmium-induced renal tubular cell death the Notch1 signaling and activin receptor-like kinase (ALK) 4/5 signaling (also known as the activin-transforming growth factor β receptor pathways). In this review paper, we introduce our previous experimental findings, focusing on Notch1 and ALK4/5 signaling pathways, which may uncover the molecular mechanisms involved in cadmium-induced renal tubular cell death.