Data_Sheet_1_Biomass fuel usage for cooking and frailty among older adults in China: a population-based cohort study.pdf

BackgroundAlthough outdoor air pollution is reported to have a negative effect on frailty, evidence involving household air pollution is sparse.MethodsA cohort study on older participants aged ≥65 years from the Chinese Longitudinal Healthy Longevity Survey was conducted between 2011/2012 and 2014. Household cooking fuel types were determined by self-reported questionaries, and were dichotomized into clean or biomass fuels. The frailty status was evaluated via a 46-item frailty index (FI) and the FRAIL scale, respectively. Frailty was identified if FI >0.21 or FRAIL score ≥3. Cox proportional hazards models were employed to examine the relationship between cooking fuels and incident frailty. And the effects of swapping cooking fuels on frailty risk were also explored.ResultsAmong 4,643 participants (mean age at baseline 80.9 ± 9.6 years, 53.7% male) totaling 11,340 person-years, 923 (19.9%) incident frailty was identified using FI. Compared to clean fuels, cooking with biomass fuels was intricately linked to a 23% rise in frailty risk (hazard ratio [HR] 1.23, 95% confidence interval [CI] 1.06–1.43). A similar association was detected between biomass cooking fuels and frailty measured by the FRAIL scale (HR 1.24, 95% CI 1.04–1.50). Sensitive analyses supported the independent relationship between biomass fuels and frailty. Stratified analyses revealed that the frailty risk was higher among town residents (HR 1.44, 95% CI 1.13–1.84) and participants not exercising regularly (HR 1.35, 95% CI 1.11–1.64). In comparison with persistent biomass fuels usage, switching to clean fuels had a trend to reduce the frailty risk, and the opposite effect was observed when swapping from clean to biomass fuels.ConclusionCooking with biomass fuels was associated with an increased frailty risk in older adults, especially amongst those living in town and those lacking regular exercise. More studies are needed to confirm our findings and to evaluate the potential benefits of reducing indoor biomass fuel usage.</p

Table_1_Tooth loss, denture use, and all-cause and cause-specific mortality in older adults: a community cohort study.pdf

ObjectivesThe available evidence on the connections between tooth loss, denture use, and mortality from all causes or specific causes among older adults is inconclusive. Therefore, we aimed to investigate the association between tooth loss, denture use, and all-cause and cause-specific mortality in older adults.MethodsA cohort of 5,403 participants aged 65 and older were recruited in the 2014 Chinese Longitudinal Healthy Longevity Survey wave and followed up in the 2018 wave. Cox proportional hazard models were used to examine the association between the number of natural teeth, denture use, and all-cause and cause-specific mortality.ResultsDuring a mean (SD) follow-up of 3.1  years (1.3), 2,126 deaths (39.3%) occurred. Individuals with 0 and 1–9 teeth had higher mortality due to all-cause, cardiovascular disease (CVD), cancer, and other causes (all p-trend ConclusionHaving fewer natural teeth, particularly less than 10 teeth, is linked to an increased risk of mortality from all causes, including CVD, cancer, and other causes, but not respiratory disease. The use of dentures would mitigate the adverse impact of tooth loss on all-cause and some cause-specific mortality.</p

Discovery of Potent and Selective Allosteric Inhibitors of Protein Arginine Methyltransferase 3 (PRMT3)

PRMT3 catalyzes the asymmetric dimethylation of arginine residues of various proteins. It is crucial for maturation of ribosomes and has been implicated in several diseases. We recently disclosed a highly potent, selective, and cell-active allosteric inhibitor of PRMT3, compound <b>4</b>. Here, we report comprehensive structure–activity relationship studies that target the allosteric binding site of PRMT3. We conducted design, synthesis, and evaluation of novel compounds in biochemical, selectivity, and cellular assays that culminated in the discovery of <b>4</b> and other highly potent (IC₅₀ values: ∼10–36 nM), selective, and cell-active allosteric inhibitors of PRMT3 (compounds <b>29</b>, <b>30</b>, <b>36</b>, and <b>37</b>). In addition, we generated compounds that are very close analogs of these potent inhibitors but displayed drastically reduced potency as negative controls (compounds <b>49</b>–<b>51</b>). These inhibitors and negative controls are valuable chemical tools for the biomedical community to further investigate biological functions and disease associations of PRMT3