ショクジ ト ウンドウ ニツイテ

Obesity is the principal risk factor of type 2 diabetes, and is developed when the energy intake exceeds the energy expenditure. Dietary and exercise intervention has been thought to play as important role in the treatment and prevention of type 2 diabetes. In this review, the balance of energy intake and energy expenditure is introduced. The amount of energy requirement was obtained by the calculation with ideal body weight and physical activity（low level : 25～30 kcal/kg, normal level : 30～35 kcal/kg）. Furthermore, both quantity and quality of the food are important. It has been reported that low-glycemic index diet is effective in the prevention and the treatment of type 2 diabetic patients. Exercise can also improve insulin sensitivity in muscle and liver. Recently, reference values for the quantity of physical activity（23MET・hours/week）and exercise （4MET・hours/week）for health promotion was established as the recommended exercise allowance for preventing lifestyle-related disease. It is important for us to understand an adequate and correct amount of individual energy requirement and expenditure

Functions of UPR in Campylobacter jejuni infection

Campylobacter jejuni is a major cause of bacterial foodborne illness in humans worldwide. Bacterial entry into a host eukaryotic cell involves the initial steps of adherence and invasion, which generally activate several cell-signaling pathways that induce the activation of innate defense systems, which leads to the release of proinflammatory cytokines and induction of apoptosis. Recent studies have reported that the unfolded protein response (UPR), a system to clear unfolded proteins from the endoplasmic reticulum (ER), also participates in the activation of cellular defense mechanisms in response to bacterial infection. However, no study has yet investigated the role of UPR in C. jejuni infection. Hence, the aim of this study was to deduce the role of UPR signaling via induction of ER stress in the process of C. jejuni infection. The results suggest that C. jejuni infection suppresses global protein translation. Also, 12 h of C. jejuni infection induced activation of the eIF2α pathway and expression of the transcription factor CHOP. Interestingly, bacterial invasion was facilitated by knockdown of UPR-associated signaling factors and treatment with the ER stress inducers, thapsigargin and tunicamycin, decreased the invasive ability of C. jejuni. An investigation into the mechanism of UPR-mediated inhibition of C. jejuni invasion showed that UPR signaling did not affect bacterial adhesion to or survival in the host cells. Further, Salmonella Enteritidis or FITC-dextran intake were not regulated by UPR signaling. These results indicated that the effect of UPR on intracellular intake was specifically found in C. jejuni infection. These findings are the first to describe the role of UPR in C. jejuni infection and revealed the participation of a new signaling pathway in C. jejuni invasion. UPR signaling is involved in defense against the early step of C. jejuni invasion and thus presents a potential therapeutic target for the treatment of C. jejuni infection

Campylobacter jejuni感染はT-84細胞におけるCFTR活性化によるCl⁻分泌亢進を抑制する

Campylobacter jejuni causes foodborne disease associated with abdominal pain, gastroenteritis, and diarrhea. These symptoms are induced by bacterial adherence and invasion of host epithelial cells. C. jejuni infection can occur with a low infective dose, suggesting that C. jejuni may have evolved strategies to cope with the bacterial clearance system in the gastrointestinal tract. The mucosa layer is the first line of defense against bacteria. Mucus conditions are maintained by water and anion (especially Cl-) movement. Cystic fibrosis transmembrane conductance regulator (CFTR) is the main Cl- channel transporting Cl- to the lumen. Mutations in CFTR result in dehydrated secreted mucus and bacterial accumulation in the lungs, and recent studies suggest that closely related pathogenic bacteria also may survive in the intestine. However, the relationship between C. jejuni infection and CFTR has been little studied. Here, we used an 125I- efflux assay and measurement of short-circuit current to measure Cl- secretion in C. jejuni-infected T-84 human intestinal epithelial cells. The basic state of Cl- secretion was unchanged by C. jejuni infection, but CFTR activator was observed to induce Cl- secretion suppressed in C. jejuniinfected T-84 cells. The suppression of activated Cl- secretion was bacterial dose-dependent and duration-dependent. A similar result was observed during infection with other C. jejuni strains. The mechanism of suppression may occur by affecting water movement or mucus condition in the intestinal tract. A failure of mucus barrier function may promote bacterial adhesion or invasion of host intestinal epithelial cells, thereby causing bacterial preservation in the host intestinal tract

タイトジャンクションは極性化上皮細胞においてCampylobacter jejuniの細胞側面からの効率的な侵入を妨げ炎症によるバリアの破綻は菌の侵入を促進する

Campylobacter jejuni invasion is closely related to C. jejuni pathogenicity. The intestinal epithelium contains polarized epithelial cells that form tight junctions (TJs) to provide a physical barrier against bacterial invasion. Previous studies indicated that C. jejuni invasion of non-polarized cells involves several cellular features, including lipid rafts. However, the dynamics of C. jejuni invasion of polarized epithelial cells are not fully understood. Here we investigated the interaction between C. jejuni invasion and TJ formation to characterize the mechanism of C. jejuni invasion in polarized epithelial cells. In contrast to non-polarized epithelial cells, C. jejuni invasion was not affected by depletion of lipid rafts in polarized epithelial cells. However, depletion of lipid rafts significantly decreased C. jejuni invasion in TJ disrupted cells or basolateral infection and repair of cellular TJs suppressed lipid raft-mediated C. jejuni invasion in polarized epithelial cells. In addition, pro-inflammatory cytokine, TNF-a treatment that induce TJ disruption promote C. jejuni invasion and lipid rafts depletion significantly reduced C. jejuni invasion in TNF-a treated cells. These data demonstrated that TJs prevent C. jejuni invasion from the lateral side of epithelial cells, where they play a main part in bacterial invasion and suggest that C. jejuni invasion could be increased in inflammatory condition. Therefore, maintenance of TJs integrity should be considered important in the development of novel therapies for C. jejuni infection

Research and development of exclusive equipment for cell-free and concentrated ascites reinfusion therapy (CART) by medical-industrial, hospital-university, and multifarious worker cooperation

Cell-free and concentrated ascites reinfusion therapy（CART）is an effective and safe therapy for patients with refractory ascites or pleural effusion. CART was initially indicated for cirrhotic ascites, and has come to be widely used for malignant ascites. Recently, cancer therapy that applies cancer cells obtained by filtration process is considered, and CART attracts attention as one of the important therapies to support future cancer therapy. However, the numbers of CART in Japan is not sufficient because the equipment for CART is high price and large. Additionally, the specialized medical staff such as clinical engineers is necessary for CART because of complicated operation. Therefore, we think that development of next-generation type equipment for CART that can be performed safely, easily, and reliably is necessary. We could develop the exclusive equipment for CART according to the project management by multifarious worker cooperation in five years