観音 隆幸

Background/Objectives: Macronutrients (protein, fat, and carbohydrate) provide sources of energy and play crucial roles in various physiological functions. However, sex differences in the relationships between protein, fat, and carbohydrate intakes and all-cause mortality remain unclear. The present study investigated sex differences in the relationships between protein, fat, and carbohydrate intakes and all-cause mortality using longitudinal epidemiological data. Methods: A total of 3743 healthy residents (1666 men and 2077 women) aged 40 years or older were followed up (men: 6.64 ± 1.51 years, women: 6.76 ± 1.28 years from 2013) in Shika Town, Ishikawa Prefecture, Japan. Nutrient intake was assessed at the baseline survey using the Brief Self-Administered Dietary History Questionnaire. The prospective relationship between baseline nutrient intake and all-cause mortality during the follow-up period, stratified by sex, was evaluated using two-way analysis of covariance and multiple logistic regression analysis, adjusted for age and BMI. Results: We documented 330 deaths (179 men and 151 women) during the 10-year follow-up period. Significant interactions between death and sex were observed for the intake of total protein (p < 0.001), animal protein (p < 0.001), vegetable protein (p = 0.033), total fat (p = 0.012), and animal fat (p = 0.024). Multiple logistic regression analysis demonstrated that total protein (p = 0.004), and animal protein (p = 0.010) decreased the all-cause mortality and increased carbohydrates (p = 0.046) in women. In men, total fat (p = 0.017) decreased the all-cause mortality. Conclusions: The present study revealed distinct sex differences in the effects of total protein, animal protein, and carbohydrate intakes on all-cause mortality. This sex difference may be due to the sex differences in nutrients intake themselves.

Abstract Context Oxytocin supplementation improves obstructive sleep apnea (OSA), and animal studies suggest involvement of oxytocin in respiratory control. However, the relationship between endogenous oxytocin signaling and human sleep status remains undetermined. Objective In this study, we approached the contribution of the intrinsic oxytocin-oxytocin receptor (OXTR) system to OSA by genetic association analysis. Methods We analyzed the relationship between OXTR gene polymorphisms and sleep parameters using questionnaire data and sleep measurements in 305 Japanese participants. OSA symptoms were assessed in 225 of these individuals. Results The OXTR rs2254298 A allele was more frequent in those with OSA symptoms than in those without (P = .0087). Although total scores on the Pittsburgh Sleep Quality Index questionnaire did not differ between the genotypes, breathlessness and snoring symptoms associated with OSA were significantly more frequent in individuals with rs2254298 A genotype (P = .00045 and P = .0089 for recessive models, respectively) than the G genotype. A multivariable analysis confirmed these genotype-phenotype associations even after adjusting for age, sex, and body mass index in a sensitivity analysis. Furthermore, objective sleep efficiency measured by actigraph was not significantly different between genotypes; however, subjective sleep efficiency was significantly lower in the rs2254298 A genotype (P = .013) compared with the G genotype. The frequency of the A allele is higher in East Asians, which may contribute to their lean OSA phenotype. Conclusion The OXTR gene may contribute to OSA symptoms via the respiratory control system, although it could be in linkage disequilibrium with a true causal gene.

BACKGROUND: Low-grade systemic inflammation may be a key player in the immune activation that has been reported for mental health deterioration. We hypothesised that elevated serum levels of inflammatory cytokines increase neuroinflammation and exacerbate depressive symptoms. METHODS: The participants were part of a cohort study for whom data was available for both 2015 and 2019. In 2015, blood samples were collected from 232 participants. Their depressive symptoms were assessed both 2015 and 2019 using the Centre for Epidemiologic Studies Depression Scale (CES-D) (n = 33). The multiplex immunoassay system (Luminex® 200) was used to measure the serum concentrations of IL-6, IL-10, IL-12, IL-17A and TNFα. Data were analysed using linear models with the level of significance considered to be p < 0.05. RESULTS: After controlling for age, BMI, smoking and alcohol consumption, in 2015 the serum concentrations of IL-17A and TNFα in 2015 were significantly positively associated with the CES-D scores of women (standardised β (B) = .027, p < 0.01 and B = 0.26, p < 0.01, respectively). The serum concentrations of IL-17A and TNFα of men were significantly positively associated with the CES-D scores of 2019 (B = 0.62, p = 0.02 and B = 0.59, p = 0.02, respectively). CONCLUSIONS: In this cross-sectional study, we found a significant positive correlation between the depressive symptoms and serum TNFα and IL-17A levels of women. In addition, our longitudinal findings suggest the possibility that TNFα and IL-17A could elevate the depressive symptoms of men.

Abstract Although the relationship between dyslipidaemia (DL) and coronary artery disease (CAD) or between trace minerals intake and CAD is well known separately, the exact nature of this relationship remains unknown. We hypothesize that the relationship between trace mineral intake and CAD may differ depending on whether or not the individual has DL. The present study analysed the relationships among trace mineral intake, DL, and CAD in middle-aged and older adults living in Shika town, Ishikawa prefecture, Japan. This study included 895 residents following the exclusion of those with genetic risk carriers for familial hypercholesterolemia. Trace mineral intake was evaluated using the brief-type self-administered diet history questionnaire. Interactions were observed between DL and CAD with zinc (p = 0.004), copper (p = 0.010), and manganese intake (p &lt; 0.001) in a two-way analysis of covariance adjusted for covariates such as sex, age, body mass index, and current smokers and drinkers. Multiple logistic regression analysis showed that zinc (odds ratio (OR): 0.752; 95% confidence interval (CI): 0.606, 0.934; p = 0.010), copper (OR: 0.175; 95% CI: 0.042, 0.726; p = 0.016), and manganese (OR: 0.494; 95% CI: 0.291, 0.839; p = 0.009) were significant independent variables for CAD in the dyslipidaemic group. The present results suggest that DL with a low trace mineral intake is associated with CAD. Further longitudinal studies are required to confirm this relationship.

Protein phosphorylation, a key regulator of cellular processes, plays a central role in brain function and is implicated in neurological disorders. Information on protein phosphorylation is expected to be a clue for understanding various neuropsychiatric disorders and developing therapeutic strategies. Nonetheless, existing databases lack a specific focus on phosphorylation events in the brain, which are crucial for investigating the downstream pathway regulated by neurotransmitters. To overcome the gap, we have developed a web-based database named “Kinase-Associated Neural PHOspho-Signaling (KANPHOS).” This paper presents the design concept, detailed features, and a series of improvements for KANPHOS. KANPHOS is designed to support data-driven research by fulfilling three key objectives: (1) enabling the search for protein kinases and their substrates related to extracellular signals or diseases; (2) facilitating a consolidated search for information encompassing phosphorylated substrate genes, proteins, mutant mice, diseases, and more; and (3) offering integrated functionalities to support pathway and network analysis. KANPHOS is also equipped with API functionality to interact with external databases and analysis tools, enhancing its utility in data-driven investigations. Those key features represent a critical step toward unraveling the complex landscape of protein phosphorylation in the brain, with implications for elucidating the molecular mechanisms underlying neurological disorders. KANPHOS is freely accessible to all researchers at https://kanphos.jp.