Internet use and physical activity of older adults during the COVID-19 pandemic: a cross-sectional study in a northern Japanese City.

BACKGROUND: Little is known of whether Internet use is associated with physical activity among socially isolated older adults during the coronavirus disease 2019 (COVID-19) pandemic. This study investigated the association between Internet use and physical activity, and whether this association differs depending on social isolation among community-dwelling Japanese older adults. METHODS: A cross-sectional study was conducted with 1048 community-dwelling residents aged 65-90 years. Data were obtained using a self-reported questionnaire in August 2020. Physical activity was assessed using the International Physical Activity Questionnaire-Short Form. Multivariable logistic regression analyses were used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between Internet use and moderate-to-vigorous physical activity (MVPA). RESULTS: Internet use showed a significant association with MVPA (OR = 1.42, 95% CI: 1.06-1.90) after adjusting for age, sex, self-reported socioeconomic status, and other health-related characteristics. When the results were stratified by social participation and living status, Internet use was associated with a significantly higher likelihood of MVPA among participants with no social participation (OR = 1.81, 95% CI: 1.03-3.17) and living with family (OR = 1.40, 95% CI: 1.02-1.93). CONCLUSION: Internet use was associated with sufficient physical activity, and this association may differ depending on the social isolation among community-dwelling older adults in Japan.

Associations between Socioeconomic Status, Social Participation, and Physical Activity in Older People during the COVID-19 Pandemic: A Cross-Sectional Study in a Northern Japanese City.

Physical activity (PA) is a key determinant of health in older adults. However, little is known about the effect of social factors on PA among older adults during the coronavirus disease 2019 (COVID-19) pandemic. Therefore, we aimed to clarify the association between socioeconomic status, social participation, and PA during the pandemic. A cross-sectional study was conducted on 999 community-dwelling residents aged 65-90 years. A self-administered questionnaire was used to collect socioeconomic status, social participation, and PA data in August 2020. Multivariable logistic regression analyses were used to calculate the odds ratios (ORs) for the associations between socioeconomic status, social participation, and maintaining PA. For both sexes, PA was reduced by approximately 5%-10% after the onset of COVID-19-related distancing restrictions. Men with a low socioeconomic status were less physically active (OR = 0.49, 95% CI: 0.30-0.82). Women who reported social participation had higher odds of maintaining PA (OR = 1.67, 95% CI: 1.13-2.45) during the restrictions. Higher socioeconomic status and social participation levels before the COVID-19 pandemic may have helped older adults to maintain PA during the COVID-19 pandemic. Further research is needed to clarify the potential effects of these factors on the health of older adults.

Autophagy induction under carbon starvation conditions is negatively regulated by carbon catabolite repression.

Autophagy is a conserved process in which cytoplasmic components are sequestered for degradation in the vacuole/lysosomes in eukaryotic cells. Autophagy is induced under a variety of starvation conditions, such as the depletion of nitrogen, carbon, phosphorus, zinc, and others. However, apart from nitrogen starvation, it remains unclear how these stimuli induce autophagy. In yeast, for example, it remains contentious whether autophagy is induced under carbon starvation conditions, with reports variously suggesting both induction and lack of induction upon depletion of carbon. We therefore undertook an analysis to account for these inconsistencies, concluding that autophagy is induced in response to abrupt carbon starvation when cells are grown with glycerol but not glucose as the carbon source. We found that autophagy under these conditions is mediated by nonselective degradation that is highly dependent on the autophagosome-associated scaffold proteins Atg11 and Atg17. We also found that the extent of carbon starvation-induced autophagy is positively correlated with cells' oxygen consumption rate, drawing a link between autophagy induction and respiratory metabolism. Further biochemical analyses indicated that maintenance of intracellular ATP levels is also required for carbon starvation-induced autophagy and that autophagy plays an important role in cell viability during prolonged carbon starvation. Our findings suggest that carbon starvation-induced autophagy is negatively regulated by carbon catabolite repression.

PKCδ and ε regulate the morphological integrity of the ER-Golgi intermediate compartment (ERGIC) but not the anterograde and retrograde transports via the Golgi apparatus.

The ER-Golgi intermediate compartment (ERGIC) is an organelle through which cargo proteins pass and are being transferred by either anterograde or retrograde transport between the endoplasmic reticulum (ER) and the Golgi apparatus. We examined the effect of 80 different kinase inhibitors on ERGIC morphology and found that rottlerin, a PKCδ inhibitor, induced the dispersion of the perinuclear ERGIC into punctate structures. Rottlerin also delayed anterograde transport of vesicular stomatitis virus G protein (VSVG) from the ER to the Golgi and retrograde transport of cholera toxin from cell surface to the ER via the Golgi. RNA interference revealed that knockdown of PKCδ or ε resulted in the dispersion of the ERGIC, but unexpectedly did not inhibit VSVG and cholera toxin transport. We also found that rottlerin depolarized the mitochondrial membrane potential, as does carbonylcyanide-p-trifluoromethoxyphenylhydrazone (FCCP), an uncoupler, and demonstrated that a decrease in the intracellular adenosine triphosphate (ATP) levels by rottlerin might underlie the block in transports. These results suggest that PKCδ and ε specifically regulate the morphology of the ERGIC and that the maintenance of ERGIC structure is not necessarily required for anterograde and retrograde transports.

Golgi-associated GSK3beta regulates the sorting process of post-Golgi membrane trafficking.

Glycogen synthase kinase ß (GSK3ß) phosphorylates many substrates in mammalian cells, and functions in many physiological processes. We observed that GSK3ß knockdown by siRNA perturbed both Golgi morphology in HeLa cells and the anterograde transport of cation-independent mannose 6-phosphate receptor (CI-M6PR) from the trans-Golgi network (TGN) to prelysosomal compartments (PLC), diverting it to the exocytic pathway. Moreover, we demonstrate that a portion of GSK3ß was localized to the TGN through the Golgi peripheral protein p230 and that this localization regulated CLASP2 phosphorylation. Our results also show that GSK3ß knockdown resulted in accumulation of CLASP2 at microtubule plus ends at the cell periphery. Our findings support the hypothesis that GSK3ß at the TGN acts as a guide, activates exocytic transport, and redirects CI-M6PR from transport to the PLC into the exocytic pathway by regulating the affinity of CLASPs for microtubules.

Visual screening and analysis for kinase-regulated membrane trafficking pathways that are involved in extensive beta-amyloid secretion.

Membrane trafficking is an important cellular process that enables the precise localization of membrane proteins. The disturbance of membrane trafficking results in various disease states. To explore systematically the defects in trafficking pathways that cause these disturbances or disease states, we developed an automated high-throughput fluorescence-based imaging system and carried out visual screening for kinase-regulated trafficking pathways of the cation-independent mannose 6-phosphate receptor (CI-M6PR) in HeLa cells. As the result of our visual screening, which examined the effect of kinase inhibitors and a kinase siRNA library, we identified five kinases (CDC42BPB, PRKACA, PRKACG, GSK3 beta and CSNK2A1) that regulate CI-M6PR trafficking. Moreover, we focused on Alzheimer's disease (AD) to study the relationship between the five kinases and a disease state. Notably, two trafficking pathways, which were regulated by PRKACG and GSK3 beta, respectively, induced high levels of secretion of Abeta, the hallmark of AD. In addition, we found that the modulation of GSK3 beta activity affected the microtubule plus end tracking function of cytoplasmic linker protein-associating protein 2 and resulted in the perturbation of BACE1 localization/trafficking and extensive A beta secretion. Our systems provide new approaches for the analysis of spatially-regulated membrane trafficking and related disease states.