Association of dietary fiber intake with subsequent fasting glucose levels and indicators of adiposity in school-age Japanese children

Abstract Objective: To evaluate the relationships of fiber intake with subsequent body mass index SD-score, waist-to-height ratio, and serum fasting glucose levels among school-age Japanese children. Design: A prospective study of school-age Japanese children. Participants were followed from 6–7 to 9–10 years of age (follow-up rate: 92.0%). Fiber intake was assessed using a validated food frequency questionnaire. Serum fasting glucose was measured by a hexokinase enzymatic method. Using a general linear model, the associations between dietary fiber intake at baseline and body mass index SD-score, waist-to-height ratio, and serum levels of fasting glucose at follow-up were evaluated after considering potential confounding factors. Setting: Public elementary schools in a city in Japan Participants: A total of 2,784 students. Results: The estimated means for fasting glucose at 9–10 years of age were 86.45, 85.68, 85.88, and 85.58 mg/dl in the lowest, second, third, and highest quartile of fiber intake at 6–7 years of age, respectively (p= 0.033, trend p= 0.018). Higher fiber intake at 6–7 years of age was associated with lower waist-to-height ratio at 9–10 years of age (trend p= 0.023). The change in fiber intake was inversely associated with concurrent change of body mass index SD-score (trend p= 0.044). Conclusion: These results suggest that dietary fiber intake may be potentially effective to limit excess weight gain and lower glucose levels during childhood

Recent comparability of oceanographic nutrients data: Results of a 2003 intercomparison exercise using reference materials

An intercomparison exercise was conducted using the recently developed Reference Material for Nutrients in Seawater (RMNS). Discrepancies of reported values among laboratories were greater than the homogeneity of RMNS samples and the reported analytical precision of nutrients. The variability of in-house standards of the participating laboratories might be the most likely source of interlaboratory discrepancies. Therefore, the use of common reference materials, i.e. certified RM, is essential to establish and improve the comparability of nutrient data of the world's oceans

Long-term culture following ES-like gene-induced reprogramming elicits an aggressive phenotype in mutated cholangiocellular carcinoma cells.

BACKGROUND: We recently reported that gastrointestinal (GI) cancer cells can be reprogrammed to a pluripotent state by the ectopic expression of defined embryonic stem (ES)-like transcriptional factors. The induced pluripotent cancer (iPC) cells from GI cancer were sensitized to chemotherapeutic agents and differentiation-inducing treatment during a short-term culture, although a phenotype induced by long-term culture needs to be studied. METHODS: A long-term cultured (Lc)-iPC cells were produced in GI cancer cell lines by virus-mediated introduction of four ES-like genes-c-MYC, SOX2, OCT3/4, and KLF4-followed by a culture more than three months after iPC cells induction. An acquired state was studied by expression of immature-related surface antigens, Tra-1-60, Tra-1-81, Tra-2-49, and Ssea-4; and epigenetic trimethyl modification at lysine 4 of histone H3. Sensitivity to chemotherapeutic agents and tumorigenicity were studied in Lc-iPC cells. RESULTS: Whereas the introduction of defined factors of iPC cells once induced an immature state and sensitized cells to therapeutic reagents, the endogenous expression of the ES-like genes except for activated endogenous c-MYC was down-regulated in a long-term culture, suggesting a high magnitude of the reprogramming induction by defined factors and the requirement of therapeutic maintenance in Lc-iPC cells from cholangiocellular carcinoma HuCC-T1 cells, which harbor TP53(R175H) and KRAS(G12D). The Lc-iPC cells showed resistance to 5-fluorouracil in culture, and high tumorigenic ability with activated endogenous c-MYC in immunodeficient mice. CONCLUSION: The Lc-iPC cells from HuCC-T1 might be prone to an undesirable therapeutic response because of an association with the activated endogenous c-MYC. To consider the possible therapeutic approach in GI cancer, it would be necessary to develop a predictive method for evaluating the improper reprogramming-associated aggressive phenotype of iPC cells

Presence of increased inflammatory infiltrates accompanied by activated dendritic cells in the left atrium in rheumatic heart disease.

AIMS:Left atrial (LA) structural remodelling develops in rheumatic heart disease (RHD) according to the disease severity of the mitral valve and the presence of atrial fibrillation. Sustained active inflammation has been previously reported in the LA of patients with RHD, suggesting a direct role of cell-mediated immunity in the pathogenesis of LA remodelling. Dendritic cells (DCs) have a major antigen-presenting role, and are known as crucial modulators of innate and adaptive immunity. We investigated whether DCs are involved in the pathogenesis of LA remodelling in RHD. METHODS AND RESULTS:Immunohistochemical analyses were performed using antibodies to CD11c, CD209 and CD80 as markers of myeloid DCs, migratory-active DCs, mature DCs and infiltrated inflammatory cells including T lymphocytes (CD3) and M1 (CD68; pro-inflammatory profile) and M2 (CD163; pro-resolution profile) macrophages. Furthermore, tenascin-C, an extracellular matrix (ECM) protein that appears during ECM remodelling and inflammatory response, was examined. Infiltrated myeloid DCs, migratory-active DCs, mature DCs and other inflammatory infiltrates including T lymphocytes and M1 and M2 macrophages, were significantly higher in the RHD group than the non-RHD group. The positive area fraction for tenascin-C was significantly higher in the RHD group than in the non-RHD group. CONCLUSION:Our histological findings suggest that inflammation may persist long after a bout of rheumatic fever, ultimately leading to ECM remodelling. We identified and quantitatively assessed several subsets of DCs and other immunocompetent cells, and our results indicated that activation of DCs has some role in persistence of LA inflammation in patients with chronic RHD