Objective This study aimed to evaluate the association between acute kidney injury (AKI) and bronchopulmonary dysplasia (BPD) in infants born <32 weeks of gestational age (GA). Study Design Present study is a secondary analysis of premature infants born at <32 weeks of GA in the Assessment of Worldwide Acute Kidney Injury Epidemiology in Neonates (AWAKEN) retrospective cohort (n = 546). We stratified by gestational age and used logistic regression to determine association between AKI and moderate or severe BPD/mortality. Results Moderate or severe BPD occurred in 214 of 546 (39%) infants, while death occurred in 32 of 546 (6%); the composite of moderate or severe BPD/death occurred in 246 of 546 (45%). For infants born ≤29 weeks of gestation, the adjusted odds ratio (OR) of AKI and the primary outcome was 1.15 (95% confidence interval [CI] = 0.47–2.86; p = 0.76). Infants born between 29 and 32 weeks of gestation with AKI had four-fold higher odds of moderate or severe BPD/death that remained after controlling for multiple factors (adjusted OR = 4.21, 95% CI: 2.07–8.61; p < 0.001). Conclusion Neonates born between 29 and 32 weeks who develop AKI had a higher likelihood of moderate or severe BPD/death than those without AKI. Further studies are needed to validate our findings and evaluate mechanisms of multiorgan injury.

Background: The high prevalence of type 2 diabetes mellitus (T2DM) in individuals over 65 years old and cognitive deficits caused by T2DM have attracted broad attention. The pathophysiological mechanism of T2DM induced cognitive impairments, however, remains poorly understood. Previous studies have suggested that the cognitive impairments can be attributed not merely to local functional and structural abnormalities but also to specific brain networks. Thus, we aimed to investigate the changes of global networks selectively affected by T2DM. Methods: A resting state functional network analysis was conducted to investigate the intrinsic functional connectivity in 37 patients with diabetes and 40 healthy controls which were recruited from local communities in Beijing, China. Results: We found that patients with T2DM exhibited cognitive function declines and functional connectivity disruptions within the default mode network, left frontal parietal network, and sensorimotor network. More importantly, the fasting glucose level was correlated with abnormal functional connectivity. Conclusions: These findings could help to understand the neural mechanisms of cognitive impairments in T2DM and provide potential neuroimaging biomarkers that may be used for early diagnosis and intervention in cognitive decline.

Objectives: to examine the associations of two common CRP gene polymorphisms with CRP levels, frailty and co-morbidity in an elderly Chinese population. Design: a population-based cohort study. Setting and participants: we obtained data on 1,723 elderly participants aged 70–84 from the ageing arm of the Rugao Longevity and Ageing study (RuLAS), a population-based observational cohort study conducted in Rugao, Jiangsu province, China. Measurements: the genotyping of two common CRP gene polymorphisms (rs1205 and rs3093059) was performed. Items concerning the frailty index and co-morbidity were collected. Results: the mean age of the study population was 75.3 ± 3.9 years, and 53.5% (n = 922) were women. The minor allele frequencies of rs1205 and rs3093059 were 42.4% (C allele) and 16.9% (C allele), respectively. The polymorphisms rs1205 and rs3093059 were significantly associated with CRP levels (β = 0.113 and 0.222, all P < 0.001). Non-significant association between rs1205 and rs3093059 and frailty, as well as between rs3093059 and co-morbidity was observed. However, SNP rs1205 CC genotype had an increased odds of co-morbidity compared with the TT genotype (odds ratio (OR):1.53; 95% confidence interval (CI): 1.16–2.02). Each additional copy of the C allele of SNP rs1205 was associated with 1.23 times (95% CI: 1.07–1.41) odds of co-morbidity. The significance remained after controlling for covariates such as education level, etc. Conclusions: among elderly Chinese individuals, two CRP gene polymorphisms were significantly associated with CRP levels. However, none of them was associated with frailty. The preliminary findings warrant further validations.

Rationale: Wildfires significantly affect air quality in the western United States. Although prior research has linked wildfire smoke fine particulate matter (i.e., aerodynamic diameter ≦2.5 μm [PM2.5]) to respiratory health outcomes, these studies typically have limited geographic and temporal coverage, lacking evidence from multiple states over extended periods. Objectives: To examine the differential acute effects of wildfire smoke and nonsmoke PM2.5 exposure on respiratory disease emergency department visits in the western United States. Methods: We obtained data on more than 6 million emergency department visits for respiratory diseases, including asthma, chronic obstructive pulmonary disease, upper respiratory infections (URIs), and bronchitis, from five states in the western United States during 2007–2018. Daily exposure to wildfire smoke and nonsmoke PM2.5 was estimated using a state-of-the-art model system. A time-stratified case cross-over design with conditional logistic regression models was used to assess the acute respiratory effects of smoke and nonsmoke PM2.5 exposure. Measurements and Main Results: The odds ratios associated with a 1-μg/m³ increase in the 3-day average wildfire smoke PM2.5 were 1.016 (95% confidence interval, 1.015–1.016) for asthma, 1.004 (1.003–1.005) for chronic obstructive pulmonary disease, 1.001 (1.000–1.011) for URIs, and 1.004 (1.004–1.004) for bronchitis. Wildfire smoke PM2.5 had stronger estimated effects than nonsmoke PM2.5, particularly for asthma (nonsmoke PM2.5: odds ratio, 1.002; 95% confidence interval, 1.001–1.004). Stratified analyses showed greater vulnerability among women and adults. Sensitivity analyses confirmed robust associations across exposure windows, and concentration–response functions suggested no clear threshold for adverse effects. Conclusions: Wildfire smoke PM2.5 was associated with increased risks of acute respiratory outcomes. Stronger effects were observed from smoke PM2.5 than nonsmoke PM2.5, particularly for asthma and URIs. These findings underscore the need for targeted public health interventions and further research into the unique toxicological properties of wildfire emissions.