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Objective Physical inactivity is recognized as a pandemic health problem. The association of pain with physical activity, particularly when measured objectively, in older adults is unclear. This study investigates the association of number of chronic musculoskeletal pain sites and pain severity with objectively measured physical activity in community-dwelling older adults. Design Observational study. Setting Community. Subjects We analyzed 267 community-dwelling older adults (mean age = 75.3 years, 67.0% women). Methods Number of chronic musculoskeletal pain sites and pain severity were measured using a self-reported questionnaire. Mean steps per day and mean minutes of light physical activity per day and moderate to vigorous physical activity per day were measured using an accelerometer. Linear regression models were applied to analyze the association of number of chronic musculoskeletal pain sites and pain severity with physical activity. Results The results suggest that a higher number of chronic musculoskeletal pain sites is associated with lower step count (beta = −333.5, 95% confidence interval = −655.9 to −11.0, P  < 0.05) and moderate to vigorous physical activity (beta = −2.5, 95% confidence interval = −4.7 to −0.4, P  < 0.05) even after adjustment for age, gender, years of schooling, obesity, alcohol habits, smoking status, number of comorbidities, recent surgery, and depressive symptoms. Conclusions Our results suggest that the number of chronic musculoskeletal pain sites is associated with low physical activity in older adults. Therefore, low physical activity due to chronic musculoskeletal pain should not be overlooked. [ABSTRACT FROM AUTHOR]

Many factors contribute to palatability. In order to evaluate the palatability of Japanese alcohol sake paired with certain dishes by integrating multiple factors, here we applied an evaluation method previously reported for palatability of cheese by multiple regression analysis based on 3 subdomain factors (rewarding, cultural, and informational). We asked 94 Japanese participants/subjects to evaluate the palatability of sake (1st evaluation/E1 for the first cup, 2nd/E2 and 3rd/E3 for the palatability with aftertaste/afterglow of certain dishes) and to respond to a questionnaire related to 3 subdomains. In E1, 3 factors were extracted by a factor analysis, and the subsequent multiple regression analyses indicated that the palatability of sake was interpreted by mainly the rewarding. Further, the results of attribution-dissections in E1 indicated that 2 factors (rewarding and informational) contributed to the palatability. Finally, our results indicated that the palatability of sake was influenced by the dish eaten just before drinking. The palatability of sake paired with certain dishes is evaluated by multiple regression analysis based on 3 subdomain factors (rewarding, cultural, and informational). [ABSTRACT FROM PUBLISHER]

In high-quality sake brewing, the cerulenin-resistant sake yeast K1801 with high ethyl caproate-producing ability has been used widely; however, K1801 has a defective spindle assembly checkpoint (SAC). To identify the mutation causing this defect, we first searched for sake yeasts with a SAC-defect like K1801 and found that K13 had such a defect. Then, we searched for a common SNP in only K1801 and K13 by examining 15 checkpoint-related genes in 23 sake yeasts, and found 1 mutation, R48P of Cdc55, the PP2A regulatory B subunit that is important for the SAC. Furthermore, we confirmed that the Cdc55-R48P mutation was responsible for the SAC-defect in K1801 by molecular genetic analyses. Morphological analysis indicated that this mutation caused a high cell morphological variation. But this mutation did not affect the excellent brewing properties of K1801. Thus, this mutation is a target for breeding of a new risk-free K1801 with normal checkpoint integrity. K1801 (triploid) having 2 copies of R48P-typecdc55and 1 copy of R48-typecdc55showed a defective spindle assembly checkpoint (SAC). Cdc55-R48P is semidominant mutation in the SAC function. [ABSTRACT FROM PUBLISHER]

Investigates the immunological influences of orally administrated fructooligosaccharides (FOS) in mice. Increase of intestinal immunoglobulin A (IgA)secretion and IgA production of Peyer's patch (PP) after FOS administration; Cytokine production patterns of CD4+ PP cells in response to FOS administration; Suppression of Th2 type antibody in the sera.

Objective: Oxygen-derived free radicals can produce myocardial cellular damage, which might contribute to the ischemia-reperfusion injury and to heart failure (HF). However, the effects of oxygen radicals on myocyte structure have not been examined in the failing heart. Methods: We examined the susceptibility of intact cardiac myocytes isolated from control (n = 16) and rapid pacing (240 bpm, 4 wks)-induced HF (n = 8) dog hearts to an exogenous hydroxyl radical (·OH), generated from H2O2 and Fe3+-nitrilotriacetate. The production of ·OH was monitored by electron spin resonance with 5,5′-dimethyl-1-pyroline-N-oxide (DMPO) as a spin trap. Results: The magnitude of DMPO-OH signals was not attenuated in the presence of either control or HF myocytes. ·OH induced a time-dependent decrease in myocyte length (i.e. hypercontracture). The time to the onset of hypercontracture and that to the submaximal hypercontracture after exposure was significantly shortened in HF. Activities of superoxide dismutase, catalase, and glutathione peroxidase was not decreased in HF. Conclusions: HF myocytes were more susceptible to oxidative stress-induced cellular injury, which was not due to decreased antioxidant defense, but to the intrinsic properties of cells. [ABSTRACT FROM PUBLISHER]

Objective: The acute administration of growth hormone (GH) or insulin-like growth factor-1 (IGF-1) improves cardiac performance, possibly contributing to the beneficial effects of GH therapy on heart failure (HF). GH can induce the production of IGF-1 and thus the actions of GH may be mediated through its IGF-1 induction. However, these effects have not yet been demonstrated in failing hearts and the cellular basis of GH or IGF-1-induced inotropic effects remains unknown. We examined the direct effects of GH and IGF-1 on the contractile function and intracellular calcium ([Ca2+]i) homeostasis in normal and failing myocytes. Methods: To determine whether GH and IGF-1 have a direct effect on myocardial contractility and whether the GH/IGF-1-induced effect was the results of changes in Ca2+ activation, cell shortening and [Ca2+]i transient were simultaneously measured in the left ventricular myocyte preparations, isolated from normal and rapid pacing-induced HF dogs. Results: Basal shortening of HF myocytes was reduced by 64% (p<0.01). In normal and HF myocytes, GH (0.4–40×10−3 IU/ml) had no effect on either cell shortening or [Ca2+]i transients. In normal myocytes, IGF-1 exerted a positive inotropic effect in a time- and dose-dependent manner (25–500 ng/ml), associated with a parallel increase of [Ca2+]i transient amplitude. IGF-1 increased the shortening magnitude in normal (121±5% increase from baseline, p<0.05) and HF (118±4% increase from baseline, p<0.05) myocytes. It also increased [Ca2+]i transient amplitude in normal and HF cells by 124±4 and 125±7%, respectively. The percent increase of cell shortening and [Ca2+]i transient amplitude was comparable between normal and HF myocytes. Furthermore, IGF-1 did not shift the trajectory of the relaxation phase in the phase-plane plots of cell length vs. [Ca2+]i, indicating that it did not change myofilament Ca2+ sensitivity. Conclusions: In both normal and HF conditions, IGF-1 exerted an acute direct positive inotropic effect in adult cardiac myocytes by increasing the availability of [Ca2+]i to the myofilaments, possibly explaining the beneficial effect of GH on HF. [ABSTRACT FROM PUBLISHER]