Environmental and Individual Correlates of Various Types of Physical Activity among Community-Dwelling Middle-Aged and Elderly Japanese

Recent studies have suggested the importance of the neighborhood environment in determining the specific type of physical activity. However, few studies on this topic have been undertaken in Japan. This study examined the association of three types of physical activity and their associations with individual and neighborhood environmental factors among middle-aged and elderly Japanese. Participants were 2,449 adults aged 40–69 living in Fujisawa city who had undergone health checkups and responded to our survey by mail. Individual factors, the International Physical Activity Questionnaire (long form), and its environmental module acted as inputs to the study. The adjusted odds ratios (ORs) of high levels of moderate-to-vigorous intensity leisure-time physical activity (LTPA), walking for active recreation, and transportation were calculated in relation to individual and neighborhood environmental factors through multiple logistic regression models. Not working and good self-rated health were significantly associated with a higher level of each physical activity outcome. According to the adjusted ORs, higher educational attainment, higher economic status, good access to exercise facilities, and owning motor vehicles were associated with longer LTPA time. However, different sets of factors were associated with longer walking times for recreation and transportation. The results suggest that diverse individual and neighborhood environmental characteristics are associated with different physical activity outcomes. Therefore, customizing environments to become activity-friendly is necessary to increase physical activity effectively among middle-aged and elderly Japanese

Phase Behavior and Structural Characterization of Ionic Clathrate Hydrate Formed with Tetra‑<i>n</i>‑butylphosphonium Hydroxide: Discovery of Primitive Crystal Structure

This paper reports phase equilibrium measurements and crystal structure analysis on the ionic clathrate hydrate formed from tetra-<i>n</i>-butylphosphonium hydroxide (TBPOH). Phase equilibrium temperatures were measured in the mole fraction range of TBPOH in aqueous solution from 0.0072 to 0.0416. The highest ionic clathrate hydrate–solution equilibrium temperature was determined to be 290.2 K at a TBPOH mole fraction of 0.0340, which corresponds to the congruent composition. Single-crystal X-ray diffraction measurements were performed on the crystal formed at 288.7 K, and the chemical composition of the TBPOH hydrate crystal was determined to be TBPOH·29.6H₂O, which is consistent with the congruent composition obtained by the phase equilibrium measurement. The crystal structure of the TBPOH hydrate has a superstructure identical with Jeffrey’s type I cubic structure, with an <i>I</i>4̅3<i>d</i> space group with a lattice constant of 24.5191(13) Å. The TBPOH hydrate structure is compared with the same hydrate structure formed by the tetra-<i>n</i>-butylammonium fluoride. We provide a comprehensive overview of the dissociation temperature, the counteranion, and the hydrate structure regarding TBP and TBA salt hydrates. The dissociation temperatures decrease linearly with the increase in the partial molal volume of anions for TBA and TBP salt hydrates, changing the hydrate structures from the primitive cubic one that has the minimum hydration number

Nitrosonifedipine Ameliorates the Progression of Type 2 Diabetic Nephropathy by Exerting Antioxidative Effects

<div><p>Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects.</p></div

Effects of NO-NIF on DN in KKAy mice.

<p>Changes in urinary total protein excretion (A) and urinary albumin excretion (B) of the C57BL/6 and KKAy mice with or without NO-NIF at 0, 2, and 4 weeks after the commencement of NO-NIF administration. Values are expressed as the means ± S.E., n = 8–10. *p<0.05 vs. C57BL/6 mice at 0 weeks, #p<0.05 vs. vehicle-treated KKAy mice at 4 weeks. (C) Histopathological analysis of diabetic kidneys at 0 and 4 weeks after the commencement of NO-NIF administration. Representative histological images of PAS staining. Quantitative analysis of the glomerular diameter (D) and glomerular tuft area (E) in the C57BL/6 and KKAy mice. Values are expressed as the means ± S.E., n = 8–10. *p<0.05 vs. C57BL/6 mice at 0 weeks, #p<0.05 vs. vehicle-treated C57BL/6 mice at 4 weeks, and †p<0.05 vs. vehicle-treated KKAy mice at 4 weeks. (F) The effect of NO-NIF on insulin-induced HMC proliferation. HMCs were treated with 10 μM NO-NIF for 6 h prior to treatment with 100 nM insulin for 48 h. Cell proliferation was determined using the MTT assay according to the manufacturer's instructions. *p<0.05 vs. control, #p<0.05 vs. insulin alone.</p