14 research outputs found
The Determinants of Planned Retirement Age of Informal Worker in Chiang Mai Province, Thailand
Increased permeability and tight junction alterations in the intestine of patients with non-alcoholic fatty liver disease (NAFLD)
Increased Intestinal Permeability and Tight Junction Alterations in Nonalcoholic Fatty Liver Disease
Involvement of resistin-like molecule β in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice
Resistin-like molecule β (RELMβ) reportedly has multiple functions including local immune responses in the gut. In this study, we investigated the possible contribution of RELMβ to non-alcoholic steatohepatitis (NASH) development. First, RELMβ knock-out (KO) mice were shown to be resistant to methionine-choline deficient (MCD) diet-induced NASH development. Since it was newly revealed that Kupffer cells in the liver express RELMβ and that RELMβ expression levels in the colon and the numbers of RELMβ-positive Kupffer cells were both increased in this model, we carried out further experiments using radiation chimeras between wild-type and RELMβ-KO mice to distinguish between the contributions of RELMβ in these two organs. These experiments revealed the requirement of RELMβ in both organs for full manifestation of NASH, while deletion of each one alone attenuated the development of NASH with reduced serum lipopolysaccharide (LPS) levels. The higher proportion of lactic acid bacteria in the gut microbiota of RELMβ-KO than in that of wild-type mice may be one of the mechanisms underlying the lower serum LPS level the former. These data suggest the contribution of increases in RELMβ in the gut and Kupffer cells to NASH development, raising the possibility of RELMβ being a novel therapeutic target for NASH
How Retired Households and Households Approaching Retirement Handle Their Equity Investments in the United States
Equity holdings, Elderly, Retirement,
Elevated levels of faecal calprotectin in primary Sjögren’s syndrome is common and associated with concomitant organic gastrointestinal disease
Etiology and diagnosis of acute biliary pancreatitis
Establishing a biliary etiology in acute pancreatitis is clinically important because of the potential need for invasive treatment, such as endoscopic retrograde cholangiopancreatography. The etiology of acute biliary pancreatitis (ABP) is multifactorial and complex. Passage of small gallbladder stones or biliary sludge through the ampulla of Vater seems to be important in the pathogenesis of ABP. Other factors, such as anatomical variations associated with an increased biliopancreatic reflux, bile and pancreatic juice exclusion from the duodenum, and genetic factors might contribute to the development of ABP. A diagnosis of a biliary etiology in acute pancreatitis is supported by both laboratory and imaging investigations. An increased serum level of alanine aminotransferase (>1.0 mu kat/l) is associated with a high probability of gallstone pancreatitis (positive predictive value 80-90%). Confirmation of choledocholithiasis is most accurately obtained using endoscopic ultrasonography or magnetic resonance cholangiopancreatography. This Review discusses the pathogenesis of ABP and the clinical techniques used to predict and establish a biliary origin in patients with suspected ABP
