Trends in health and health inequality during the Japanese economic stagnation: Implications for a healthy planet

Introduction: Human health and wellbeing may depend on economic growth, the implication being that policymakers need to choose between population health and the health of ecosystems. Over two decades of low economic growth, Japan's life expectancy grew. Here we assess the temporal changes of subjective health and health inequality during the long-term low economic growth period. Methods: Eight triennial cross-sectional nationally representative surveys in Japan over the period of economic stagnation from 1992 to 2013 were used (n = 625,262). Health is defined positively as wellbeing, and negatively as poor health, based on self-rated health. We used Slope and Relative Indices of Inequality to model inequalities in self-rated health based on household income. Temporal changes in health and health inequalities over time were examined separately for children/adolescents, working-age adults, young-old and old-old. Results: At the end of the period of economic stagnation (2013), compared to the beginning (1992), the overall prevalence of wellbeing declined slightly in all age groups. However, poor health was stable or declined in the young-old and old-old, respectively, and increased only in working-age adults (Prevalence ratio: 1.14, 95% CI 1.08, 1.20, <0.001). Over time, inequality in wellbeing and poor self-rated health were observed in adults but less consistently for children, but the inequalities did not widen in any age group between the start and end of the stagnation period. Conclusions: Although this study was a case study of one country, Japan, and inference to other countries cannot be made with certainty, the findings provide evidence that low economic growth over two decades did not inevitably translate to unfavourable population health. Japanese health inequalities according to income were stable during the study period. Therefore, this study highlighted the possibility that for high-income countries, low economic growth may be compatible with good population health

Identifying Frail-Related Biomarkers among Community-Dwelling Older Adults in Japan: A Research Example from the Japanese Gerontological Evaluation Study

We examined correlating clinical biomarkers for the physical aspect of frailty among community-dwelling older adults in Japan, using Japanese Gerontological Evaluation Study (JAGES). We used information from the JAGES participants (N = 3,128) who also participated in the community health screening in 2010. We grouped participants’ response to the Study of Osteoporotic Fracture (SOF) Frailty Index into robust (=0), intermediate frail (=1), and frail (=2+) ones to indicate physical aspect of frailty. Independent of sex and age, results from multinomial logistic regression showed above normal albumin and below normal HDL and haemoglobin levels were positively associated with intermediate frail (RRR = 1.99, 95% CI = 1.22–3.23; RRR = 1.36, 95% CI = 1.33–1.39; RRR = 1.36, 95% CI = 1.23–1.51, resp.) and frail cases (RRR = 2.27, 95% CI = 1.91–2.70; RRR = 1.59, 95% CI = 1.51–1.68; RRR = 1.40, 95% CI = 1.28–1.52, resp.). Limited to women, above normal Hb1Ac level was similarly associated with intermediate frail and frail cases (RRR = 1.18, 95% CI = 1.02, 1.38; RRR = 2.56, 95% CI = 2.23–2.95, resp.). Use of relevant clinical biomarkers can help in assessment of older adults’ physical aspect of frailty

Correction: Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory

Correction to: International Journal of Obesity https://doi.org/10.1038/s41366-020-00735-9 The original version of this article unfortunately contained a mistake in the ESM. The original article has been corrected

Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory

BACKGROUND/OBJECTIVES: The mediating role of eating behaviors in genetic susceptibility to weight gain during mid-adult life is not fully understood. This longitudinal study aims to help us understand contributions of genetic susceptibility and appetite to weight gain. SUBJECTS/METHODS: We followed the body-mass index (BMI) trajectories of 2464 adults from 45 to 65 years of age by measuring weight and height on four occasions at 5-year intervals. Genetic risk of obesity (gene risk score: GRS) was ascertained, comprising 92 BMI-associated single-nucleotide polymorphisms and split at a median (=high and low risk). At the baseline, the Eating Inventory was used to assess appetite-related traits of 'disinhibition', indicative of opportunistic eating or overeating and 'hunger' which is susceptibility to/ability to cope with the sensation of hunger. Roles of the GRS and two appetite-related scores for BMI trajectories were examined using a mixed model adjusted for the cohort effect and sex. RESULTS: Disinhibition was associated with higher BMI (β = 2.96; 95% CI: 2.66-3.25 kg/m2), and accounted for 34% of the genetically-linked BMI difference at age 45. Hunger was also associated with higher BMI (β = 1.20; 0.82-1.59 kg/m2) during mid-life and slightly steeper weight gain, but did not attenuate the effect of disinhibition. CONCLUSIONS: Appetite disinhibition is most likely to be a defining characteristic of genetic susceptibility to obesity. High levels of appetite disinhibition, rather than hunger, may underlie genetic vulnerability to obesogenic environments in two-thirds of the population of European ancestry

Bile Acid-Induced Virulence Gene Expression of Vibrio parahaemolyticus Reveals a Novel Therapeutic Potential for Bile Acid Sequestrants

Vibrio parahaemolyticus, a bacterial pathogen, causes human gastroenteritis. A type III secretion system (T3SS2) encoded in pathogenicity island (Vp-PAI) is the main contributor to enterotoxicity and expression of Vp-PAI encoded genes is regulated by two transcriptional regulators, VtrA and VtrB. However, a host-derived inducer for the Vp-PAI genes has not been identified. Here, we demonstrate that bile induces production of T3SS2-related proteins under osmotic conditions equivalent to those in the intestinal lumen. We also show that bile induces vtrA-mediated vtrB transcription. Transcriptome analysis of bile-responsive genes revealed that bile strongly induces expression of Vp-PAI genes in a vtrA-dependent manner. The inducing activity of bile was diminished by treatment with bile acid sequestrant cholestyramine. Finally, we demonstrate an in vivo protective effect of cholestyramine on enterotoxicity and show that similar protection is observed in infection with a different type of V. parahaemolyticus or with non-O1/non-O139 V. cholerae strains of vibrios carrying the same kind of T3SS. In summary, these results provide an insight into how bacteria, through the ingenious action of Vp-PAI genes, can take advantage of an otherwise hostile host environment. The results also reveal a new therapeutic potential for widely used bile acid sequestrants in enteric bacterial infections

Mechanisms and Kinetics for Sorption of CO2 on Bicontinuous Mesoporous Silica Modified with n-Propylamine

We studied equilibrium adsorption and uptake kinetics and identified molecular species that formed during sorption of carbon dioxide on amine-modified silica. Bicontinuous silicas (AMS-6 and MCM-48) were postsynthetically modified with (3-aminopropyl)triethoxysilane or (3-aminopropyl)methyldiethoxysilane, and amine-modified AMS-6 adsorbed more CO(2) than did amine-modified MCM-48. By in situ FTIR spectroscopy, we showed that the amine groups reacted with CO(2) and formed ammonium carbamate ion pairs as well as carbamic acids under both dry and moist conditions. The carbamic acid was stabilized by hydrogen bonds, and ammonium carbamate ion pairs formed preferably on sorbents with high densities of amine groups. Under dry conditions, silylpropylcarbamate formed, slowly, by condensing carbamic acid and silanol groups. The ratio of ammonium carbamate ion pairs to silylpropylcarbamate was higher for samples with high amine contents than samples with low amine contents. Bicarbonates or carbonates did not form under dry or moist conditions. The uptake of CO(2) was enhanced in the presence of water, which was rationalized by the observed release of additional amine groups under these conditions and related formation of ammonium carbamate ion pairs. Distinct evidence for a fourth and irreversibly formed moiety was observed under sorption of CO(2) under dry conditions. Significant amounts of physisorbed, linear CO(2) were detected at relatively high partial pressures of CO(2), such that they could adsorb only after the reactive amine groups were consumed.authorCount :7</p

MiR-218 Inhibits Invasion and Metastasis of Gastric Cancer by Targeting the Robo1 Receptor

MicroRNAs play key roles in tumor metastasis. Here, we describe the regulation and function of miR-218 in gastric cancer (GC) metastasis. miR-218 expression is decreased along with the expression of one of its host genes, Slit3 in metastatic GC. However, Robo1, one of several Slit receptors, is negatively regulated by miR-218, thus establishing a negative feedback loop. Decreased miR-218 levels eliminate Robo1 repression, which activates the Slit-Robo1 pathway through the interaction between Robo1 and Slit2, thus triggering tumor metastasis. The restoration of miR-218 suppresses Robo1 expression and inhibits tumor cell invasion and metastasis in vitro and in vivo. Taken together, our results describe a Slit-miR-218-Robo1 regulatory circuit whose disruption may contribute to GC metastasis. Targeting miR-218 may provide a strategy for blocking tumor metastasis