VTA-projecting cerebellar neurons mediate stress-dependent depression-like behaviors.

Although cerebellar alterations have been implicated in stress symptoms, the exact contribution of the cerebellum to stress symptoms remains to be elucidated. Here, we demonstrated the crucial role of cerebellar neurons projecting to the ventral tegmental area (VTA) in the development of chronic stress-induced behavioral alterations in mice. Chronic chemogenetic activation of inhibitory Purkinje cells in crus I suppressed c-Fos expression in the DN and an increase in immobility in the tail suspension test or forced swimming test, which were triggered by chronic stress application.

Recent Advances in the Understanding of Specific Efferent Pathways Emerging From the Cerebellum.

The cerebellum has a long history in terms of research on its network structures and motor functions, yet our understanding of them has further advanced in recent years owing to technical developments, such as viral tracers, optogenetic and chemogenetic manipulation, and single cell gene expression analyses. Specifically, it is now widely accepted that the cerebellum is also involved in non-motor functions, such as cognitive and psychological functions, mainly from studies that have clarified neuronal pathways from the cerebellum to other brain regions that are relevant to these functions. The techniques to manipulate specific neuronal pathways were effectively utilized to demonstrate the involvement of the cerebellum and its pathways in specific brain functions, without altering motor activity.

Direct pharmacological Akt activation rescues Alzheimer's disease like memory impairments and aberrant synaptic plasticity.

Amyloid β (Aβ) is a key mediator for synaptic dysfunction and cognitive impairment implicated in Alzheimer's disease (AD). However, the precise mechanism of the toxic effect of Aβ is still not completely understood. Moreover, there is currently no treatment for AD.

A coronary heart disease prediction model: the Korean Heart Study.

Objective: The objectives of this study were to develop a coronary heart disease (CHD) risk model among the Korean Heart Study (KHS) population and compare it with the Framingham CHD risk score.

Design: A prospective cohort study within a national insurance system.

Setting: 18 health promotion centres nationwide between 1996 and 2001 in Korea.

Hemoglobin concentration and risk of cardiovascular disease in Korean men and women - the Korean heart study.

This study investigated the relationship between hemoglobin concentration and the incidence of cardiovascular diseases (CVD). A total of 407,858 subjects (256,851 men, aged 30-94 yr), who underwent physical examination at 17 Korean nationwide health examination centers, was included in this study. Data regarding CVD incidence were obtained from the Korean National Health Insurance database.

The Korean Heart Study: rationale, objectives, protocol, and preliminary results for a new prospective cohort study of 430,920 men and women.

Background: To describe the rationale, objectives, protocol, and preliminary results for a new prospective cohort study of cardiovascular disease (CVD) risk factors in South Korea.

Methods: Study members were recruited from participants in routine health assessments at health promotion centres across South Korea. Established and emerging CVD risk factors were measured.

Fasting glucose level and the risk of incident atherosclerotic cardiovascular diseases.

Objective: Although diabetes increases the risk of cardiovascular disease (CVD) and mortality, the dose-response relationship between fasting glucose levels below those diagnostic of diabetes with cardiovascular events has not been well characterized.

Research Design And Methods: A prospective cohort study of more than one million Koreans was conducted with a mean follow-up of 16 years. A total of 1,197,384 Korean adults with no specific medical conditions diagnosed were classified by baseline fasting serum glucose level.

Adiponectin as predictor for diabetes among pre-diabetic groups.

Adiponectin is found to associate with diabetes in studies apart from cohort studies. This prospective cohort study is to evaluate the predictive role of adiponectin in diabetes among participants with impaired fasting glucose (IFG). A total of 42,845 participants who visited 7 health examination centers located in Seoul and Kyunggi province, South Korea, during 2004-2008 were first included.

Prevalence of antibodies in response to Legionella species, analysis of a healthy population from Jeollanam-do Province, Korea.

Seroepidemological investigation of antibodies to Legionella species in 500 healthy individuals from a single geographical location in Korea was conducted by indirect fluorescent antibody assay (IFA). Considering an antibody titer of > or =1:128 as positive reaction, 15.2% of total sera were positive.

zVAD-fmk, unlike BocD-fmk, does not inhibit caspase-6 acting on 14-3-3/Bad pathway in apoptosis of p815 mastocytoma cells.

In a preliminary study, we found that benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD- fmk), unlike Boc-aspartyl(OMe)-fluoromethylketone (BocD-fmk), at usual dosage could not prevent genistein-induced apoptosis of p815 mastocytoma cells. This study was undertaken to reveal the mechanism underlying the incapability of zVAD-fmk in preventing this type of apoptosis. We observed that 14-3-3 protein level was reduced in genistein-treated cells and that BocD-fmk but not zVAD-fmk prevented the reduction of 14-3-3 protein level and the release of Bad from 14-3-3.

Synthetic chenodeoxycholic acid derivatives inhibit glioblastoma multiform tumor growth in vitro and in vivo.

We previously reported that the synthetic chenodeoxycholic acid (CDCA) derivatives showed apoptosis-inducing activity on various cancer cells in vitro. This study was undertaken to explore whether synthetic CDCA derivatives, HS-1199 and HS-1200, had an anticancer effect on malignant glioblastoma cells. We administered them in culture to U-118MG, U-87MG, T98G, and U-373MG cells.

Trichostatin A induces apoptosis of p815 mastocytoma cells in histone acetylation- and mitochondria-dependent fashion.

Although inhibition of histone deacetylase has been demonstrated to induce apoptosis of various cancer cells, there is no report on its effect on mast cell demise to date. Here we studied whether a histone deacetylase inhibitor Trichostatin A (TSA) produces apoptosis in p815 mastocytoma cells. TSA prominently increased the amount of acetylated histones, H3, H4, H2A and H2B, in p815 mastocytoma cells.

Endoscopically observed lower esophageal capillary patterns.

Background: It has been reported that there are four zones of distinct venous patterns around the gastroesophageal junction (GEJ); i.e. truncal, perforating, palisade (PZ) and gastric zones.

[Viral breakthrough in HBeAg-negative chronic hepatitis B patients receiving lamivudine therapy].

Background/aims: Long-term efficacy and the rate of viral breakthrough in patients with HBeAg- negative chronic hepatitis B receiving lamivudine therapy is uncertain. This study was conducted to determine the rate of viral breakthrough according to the HBeAg status and the relation of viral breakthrough with YMDD mutants.

Methods: Two hundred and five patients with HBeAg-positive and 49 patients with HBeAg-negative chronic hepatitis B, who had received lamivudine for at least 9 months, were included.

[Clinical outcome in cases of viral breakthrough during lamivudine therapy in chronic hepatitis B patients].

Background/aims: Long-term lamivudine therapy can induce the emergence of lamivudine resistant hepatitis B virus (HBV) mutants. Clinically emergence of the mutant is expressed by the reappearance of disappeared HBV DNA in serum. Continued lamivudine treatment has been usually recommended in cases of viral breakthrough.

Genistein-induced apoptosis of p815 mastocytoma cells is mediated by Bax and augmented by a proteasome inhibitor, lactacystin.

Although genistein has been demonstrated to induce apoptosis of various cells, there is no report of its effect on mast cell proliferation. Here we show that genistein reduced the viability of mast cell tumor cell lines, p815 and RBL-2H, but not of a human mast cell line, HMC-1. Further investigation on its growth-inhibitory mechanism was undertaken on p815 mastocytoma cells.