Impaired lung function is associated with morbidity and mortality in the elderly. However, there is a paucity of data regarding the long-term effects of particulate matter (PM) on lung function among the elderly. This study evaluated the exposure-response relationship between ambient PM and different lung function indices among the elderly in Taiwan. A cross-sectional survey of individuals aged ≥65 years was conducted in Taiwan from October 2015 to September 2016. Those who attended the annual health examination for the elderly in five hospitals of varying background PM concentrations were enrolled. The long-term (2015 annual mean concentration) exposure to air pollution was estimated by the Kriging method at the residence of each subject. The association between ambient PM exposure and lung function was evaluated by linear regression modeling, with adjustments for age, sex, height, weight, educational attainment, presence of asthma or chronic obstructive pulmonary disease, smoking status, season, and co-pollutants. There were 1241 subjects (mean age, 70.5 years). The mean residential PM_2.5 and PM_2.5–10 in 2015 was 26.02 and 18.01 μg/m³, respectively. After adjustments for confounders and co-pollutants, the FVC decrease was best associated with fine particles (PM_2.5), whereas the FEV₁, FEF_25–75%, FEF_25% and FEF_50% decreases were best associated with coarse particles (PM_2.5–10). An IQR (10 μg/m³) increase in PM_2.5 decreased FVC by 106.38 ml (4.47%), while an IQR (7.29 μg/m³) increase in PM_2.5–10 decreased FEV₁ and FEF_25–75% by 91.23 ml (4.85%) and 104.44 ml/s (5.58%), respectively. Among the Taiwanese elderly, long-term PM_2.5 exposure mainly decreases the vital capacity of lung function. Moreover, PM_2.5–10 has a stronger negative effect on the function of conductive airways than PM_2.5.

Background: Warfarin, a vitamin K antagonist, has been shown to affect bone mineral density and cause osteoporosis. However, studies investigating the relationship between non–vitamin K antagonist oral anticoagulants ( NOAC s) and osteoporosis are limited. We thus compared the risk of osteoporosis in patients with atrial fibrillation treated with either NOAC s or warfarin. Methods and Results: This nationwide, retrospective cohort study used Taiwan's National Health Insurance Research Database. All adult patients in Taiwan who were newly diagnosed with atrial fibrillation and treated with NOAC s or warfarin between January 2012 and December 2015 were included and classified into their respective cohorts. Patients who received NOAC s were subcategorized into the rivaroxaban, dabigatran, and apixaban subgroups. Propensity score matching was performed for each head‐to‐head comparison. Adjusted hazard ratios ( aHR s) for the risk of osteoporosis were calculated using Cox proportional hazards regression models, with adjustment for confounders. Overall, 17 008 patients were included, with 8504 in each cohort. NOAC s were associated with a lower osteoporosis risk than warfarin ( aHR =0.82; 95% CI=0.68–0.97). A subgroup effect of treatment duration was identified (namely, the lower osteoporosis risk with NOAC compared with warfarin became stronger in those with longer treatment duration [ P for interaction <0.001]). Furthermore, significantly lower risks of osteoporosis were observed in the rivaroxaban ( aHR =0.68; 95% CI =0.55–0.83) and apixaban ( aHR =0.38; 95% CI =0.22–0.66) subgroups, but not in the dabigatran subgroup ( aHR =1.04; 95% CI =0.85–1.27). Conclusions: Compared with warfarin, rivaroxaban and apixaban were associated with a significantly lower risk of osteoporosis in patients with atrial fibrillation.

Current evidence suggests that vitamin K improves insulin sensitivity and glucose tolerance by regulating vitamin K–dependent proteins, anti-inflammatory signaling, and lipid metabolism. In additio... Visual Oral Anticoagulants and Diabetes-Related Complications. Current evidence suggests that vitamin K improves insulin sensitivity and glucose tolerance by regulating vitamin K–dependent... Background: Evidence about the association between types of oral anticoagulants and hazards of diabetes complications is limited in patients with atrial fibrillation (AF) and diabetes mellitus (DM)...

3T3-L1 cells are widely used to study adipogenesis and insulin response. Their adipogenic potential decreases with time in the culture. Expressing exogenous genes in 3T3-L1 cells can be challenging. This work tries to establish and characterize an alternative model of cultured adipocytes that is easier to work with than the 3T3-L1 cells. Induced cells were identified as adipocytes based on the following three characteristics: (1) Accumulation of triglyceride droplets as demonstrated by oil red O stain. (2) Transport rate of 2-deoxyglucose increased after insulin stimulation. (3) Expression of fat specific genes such as Fabp4 (aP2), Slc2a4 (Glut4) and Pparg (PPARγ). Among the cell lines induced under different conditions in this study, only NIH/3T3 cells differentiated into adipocytes after prolonged incubation in 3T3-L1 induction medium containing 20% instead of 10% fetal bovine serum. Rosiglitazone added to the induction medium shortened the incubation period from 14 to 7 days. The PI3K/AKT pathway showed similar changes upon insulin stimulation in these two adipocytes. C/EBPα mRNA was barely detectable in NIH/3T3 adipocytes. NIH/3T3 adipocytes induced in the presence of rosiglitazone showed higher 2-deoxyglucose transport rate after insulin stimulation, expressed less Agt (angiotensinogen) and more PPARγ. Knockdown of C/EBPα using shRNA blocked 3T3-L1 but not NIH/3T3 cell differentiation. Mouse adipose tissues from various anatomical locations showed comparable levels of C/EBPα mRNA. NIH/3T3 cells were capable of differentiating into adipocytes without genetic engineering. They were an adipocyte model that did not require the reciprocal activation between C/EBPα and PPARγ to differentiate. Future studies in the C/EBPα independent pathways leading to insulin responsiveness may reveal new targets to diabetes treatment.