Factors that dynamically affect provincial incidences of catastrophic health expenditure among middle-aged and elderly Chinese population-transition of disease financial risk protection from global to local.

BACKGROUND: The high incidence of catastrophic health expenditure (ICHE) among middle-aged and elderly population is a major deterrent for reducing the financial risk of disease. Current research is predominantly based on the assumption of spatial homogeneity of nationwide population characteristics, ignoring the differences in regional characteristics. Thus, our study aimed to explore the impact of various influencing factors on the ICHE from a spatiotemporal perspective. METHODS: We used data from the China Health and Retirement Longitudinal Study (waves 1 to 4), to conduct a retrospective cohort study across 28 provinces, from 2011 to 2018. We measured regional incidences of catastrophic health expenditure using methods recommended by the World Health Organization. Ordinary least squares (OLS) and geographical and temporal weighted regression (GTWR) were used as the global and local estimation models, respectively. The Fortheringham method was used to test the spatiotemporal non-stationarity. RESULTS: National ICHE showed a gradual increase from 2011 to 2015, but suddenly decreased from 2015 to 2018, also showing the spatial heterogeneity. And the southwest area and Hebei showed persistently high ICHE (Qinghai even reached the highest value of 27.5% in 2015). Out-of-pocket payment, gross domestic product, PM2.5, ageing, incidence of non-communicable diseases and disabilities, number of nurses, and health insurance coverage in the global estimation passed the significance test, and the GTWR model showed a better model fit (0.769) than the OLS model (0.388). Furthermore, except for health insurance coverage, all seven variables had spatiotemporal non-stationarity among their impacts on ICHE. CONCLUSION: In this longitudinal study, we found spatiotemporal non-stationarity among the variable relationships, supporting regional governments' adoption of regional-target policies. First, after the completion of universal health insurance coverage, the spatiotemporal non-stationarity of the prevalence of non-communicable diseases and disability and ageing should be the focus of the next phase of health insurance design, where improvements to compensation coverage and benefit packages are possible policy instruments. Second, the governance and causes of catastrophic health expenditure need to be laid out from a macro perspective rather than only from the individual/household perspective, especially for the potential impact of economic development, air pollution and nursing resources.

Alpha-1-antitrypsin suppresses oxidative stress in preeclampsia by inhibiting the p38MAPK signaling pathway: An in vivo and in vitro study.

This present study was designed to investigate the effects of alpha-1-antitrypsin (AAT) on oxidative stress in preeclampsia (PE) by regulating p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. HTR8/SVneo cells were randomly assigned into normal, hypoxia/reoxygenation (H/R), HR + AAT and HR + siRNA-AAT groups. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the mRNA and protein expressions of p-p38MAPK, AAT, signal transducer and activator of transcription 1 (STAT1) and activating transcription factor2 (ATF2). Flow cytometry, scratch test, cell counting kit-8 (CCK-8) assay and the 3-(4,5)-dimethylthiazol (-z-y1)-3,5-di- phenyltetrazolium bromide (MTT) assay were conducted to detect reactive oxygen species (ROS) and cell apoptosis, cell migration, proliferation and cytotoxicity, respectively. Mouse models in PE were established, which were divided into normal pregnancy (NP), PE and PE + AAT groups with blood pressure and urine protein measured. Chromatin immunoprecipitation (ChIP) and enzyme-linked immunosorbent assay (ELISA) were conducted to detect the activity of oxidative stress-related kinases and expressions of inflammatory cytokines and coagulation-related factors in cells and mice placenta. Immunohistochemistry, Western blotting and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect AAT and p38MAPK expressions, apoptosis-related protein expressions, and apoptosis rate in mice placenta. Compared with the normal group, the H/R group had decreased expression of AAT, activity of superoxide dismutase (SOD) and GSH-Px, cell proliferation and migration, but increased p38MAPK, STAT1, ATF2, MDA, H2O2, inflammatory cytokines, coagulation-related factors, cell cytotoxicity, ROS, apoptotic factors and apoptosis rate. Compared with the H/R group, the HR + ATT group had increased expressions of AAT, activity of SOD and GSH-Px, cell proliferation and migration but decreased p38MAPK, STAT1, ATF2, malonyldialdehyde (MDA), H2O2, inflammatory cytokines and coagulation-related factors, cell cytotoxicity, ROS, apoptotic factors and apoptosis rate, while opposite results were observed in the HR + siRNA-ATT group. Compared with the NP group, the PE group had decreased activity of SOD and GSH-Px but increased MDA, H2O2, AAT, p38MAPK, inflammatory cytokines, coagulation-related factors and apoptosis rate. The indexes in the PE + AAT group were between the NP and PE groups. Thus, we concluded that AAT suppressed oxidative stress in PE by inhibiting p38MAPK signaling pathway.