Association of air pollutants and hospital admissions for respiratory diseases in Lanzhou, China, 2014-2019.

The aim of this study was to assess the effects of air pollutants on hospital admissions for respiratory disease (RD) by using distributed lag nonlinear model (DLNM) in Lanzhou during 2014-2019. In this study, the dataset of air pollutants, meteorological, and daily hospital admissions for RD in Lanzhou, from January 1st, 2014 to December 31st, 2019, were collected from three national environmental monitoring stations, China meteorological data service center, and three large general hospitals, respectively. A time-series analysis with DLNM was used to estimate the associations between air pollutants and hospital admissions for RD including the stratified analysis of age, gender, and season. The key findings were expressed as the relative risk (RR) with a 95% confidence interval (CI) for single-day and cumulative lag effects (0-7). A total of 90, 942 RD hospitalization cases were identified during the study period. The highest association (RR, 95% CI) of hospital admissions for RD and PM2.5 (1.030, 1.012-1.049), and PM10 (1.009, 1.001-1.015), and NO2 (1.047, 1.024-1.071) were observed at lag 07 for an increase of 10 µg/m3 in the concentrations, and CO at lag07 (1.140, 1.052-1.236) for an increase of 1 mg/m3 in the concentration. We observed that the RR estimates for gaseous pollutants (e.g., CO and NO2) were larger than those of particulate matter (e.g., PM2.5 and PM10). The harmful effects of PM2.5, PM10, NO2, and CO were greater in male, people aged 0-14 group and in the cold season. However, no significant association was observed for SO2, O38h, and total hospital admissions for RD. Therefore, some effective intervention strategies should be taken to strengthen the treatment of the ambient air pollutants, especially gaseous pollutants (e.g., CO and NO2), thereby, reducing the burden of respiratory diseases.

Mesenchymal Stem Cell-Derived Exosomal Long Noncoding RNA MALAT1-201 Regulated the Proliferation, Apoptosis and Migration of Trophoblast Cells via Targeting miR-141.

OBJECTIVE: MALAT1 has been confirmed to play a vital role in the progression of preeclampsia (PE). However, as one of the spliceosomes of MALAT1, the role and mechanism of MALAT1-201 in the progression of PE remain elusive. Mesenchymal stem cells (MSCs) correlate with angiogenesis and trophoblast formation and could maintain successful pregnancy, while the molecular mechanisms are still unclear. The aim of the study was to investigate the role and potential mechanism of MALAT1-201 in PE. METHODS: We isolated MSCs from bone marrow and cultured in vitro. We overexpressed MALAT1-201 in MSCs and collected exosomes released by MSCs to treat trophoblast cells. Then, the proliferation, apoptosis and migration of MALAT1-201 elevated trophoblast cells were detected by CCK-8, flow cytometer and transwell assay, respectively. The binding site between MALAT1-201 and miR-141 was detected by dual-luciferase assays. The location of MALAT1-201 was detected by cytoplasmic and nuclear RNA fractionation. RESULTS: We successfully cultured bone marrow derived MSCs in vitro. MSC-Ex carrying MALAT1-201 promoted proliferation and migration, while suppressed apoptosis of trophoblast cells, which is similar to the effects of MALAT1-201 gene on trophoblast cells. In addition, MALAT1-201 was mainly localized in the nucleus and miR-141 was the target of MALAT1-201. CONCLUSIONS: MALAT1-201 derived from MSC-Ex regulated the proliferation, apoptosis and migration of HTR8-Svneo cells by targeting miR-141, which indicated a promising therapeutic target for PE.