Effects of ambient air pollution on the hospitalization risk and economic burden of mental disorders in Qingdao, China.

OBJECTIVE: The aim of this study was to examine the impacts of short-term exposure to air pollutants on hospitalizations for mental disorders (MDs) in Qingdao, a Chinese coastal city, and to assess the corresponding hospitalization risk and economic cost. METHODS: Daily data on MD hospitalizations and environmental variables were collected from January 1, 2015, to December 31, 2019. An overdispersed generalized additive model was used to estimate the association between air pollution and MD hospitalizations. The cost of illness method was applied to calculate the corresponding economic burden. RESULTS: With each 10 µg/m3 increase in the concentration of fine particulate matter (PM2.5) at lag05, inhalable particulate matter (PM10) at lag0, sulfur dioxide (SO2) at lag06 and ozone (O3) at lag0, the corresponding relative risks (RRs) and 95% confidence intervals (CIs) were 1.0182 (1.0035-1.0332), 1.0063 (1.0001-1.0126), 1.0997 (1.0200-1.1885) and 1.0099 (1.0005-1.0194), respectively. However, no significant effects of nitrogen dioxide (NO2) or carbon monoxide (CO) were found. Stratified analysis showed that males were susceptible to SO2 and O3, while females were susceptible to PM2.5. Older individuals (≥ 45 years) were more vulnerable to air pollutants (PM2.5, PM10, SO2 and O3) than younger individuals (< 45 years). Taking the Global Air Quality Guidelines 2021 as a reference, 8.71% (2,168 cases) of MD hospitalizations were attributable to air pollutant exposure, with a total economic burden of 154.36 million RMB. CONCLUSION: Short-term exposure to air pollution was associated with an increased risk of hospitalization for MDs. The economic advantages of further reducing air pollution are enormous.

Graph Neural Network and Spatiotemporal Transformer Attention for 3D Video Object Detection From Point Clouds.

Previous works for LiDAR-based 3D object detection mainly focus on the single-frame paradigm. In this paper, we propose to detect 3D objects by exploiting temporal information in multiple frames, i.e., point cloud videos. We empirically categorize the temporal information into short-term and long-term patterns. To encode the short-term data, we present a Grid Message Passing Network (GMPNet), which considers each grid (i.e., the grouped points) as a node and constructs a k-NN graph with the neighbor grids. To update features for a grid, GMPNet iteratively collects information from its neighbors, thus mining the motion cues in grids from nearby frames. To further aggregate long-term frames, we propose an Attentive Spatiotemporal Transformer GRU (AST-GRU), which contains a Spatial Transformer Attention (STA) module and a Temporal Transformer Attention (TTA) module. STA and TTA enhance the vanilla GRU to focus on small objects and better align moving objects. Our overall framework supports both online and offline video object detection in point clouds. We implement our algorithm based on prevalent anchor-based and anchor-free detectors. Evaluation results on the challenging nuScenes benchmark show superior performance of our method, achieving first on the leaderboard (at the time of paper submission) without any "bells and whistles." Our source code is available at https://github.com/shenjianbing/GMP3D.

Relationship between intestinal flora, inflammation, BDNF gene polymorphism and generalized anxiety disorder: A clinical investigation.

INTRODUCTION: Understanding factors related to generalized anxiety disorder pathogenesis is critical for elucidating the mechanism and preventing its establishment. Intestinal flora and hereditary factors such as brain-derived neurotrophic factor (BDNF) gene polymorphism may have a role in the development of generalized anxiety disorder. This work explored the relationship between intestinal flora, inflammatory changes and BDNF gene polymorphisms and the occurrence of generalized anxiety disorder. METHODS: Forty-eight patients with generalized anxiety disorder and 57 healthy people were included in the study. As the disease group and control group, the polymorphisms of rs10767664 and rs7124442 of the BDNF gene, differences in the distribution of intestinal flora, and changes in inflammatory and immune indicators were analyzed. RESULTS: The distribution of BDNF gene alleles, genotypes and haplotypes in the disease group were different from those in the control group. The levels of TNF-α (P = .000), interleukin-4 (P = .000), interleukin-10 (P = .043) and IgG (P = .008) in patients with generalized anxiety disorder in the disease group were different from those in the control group. The distribution of gut microbes in patients with generalized anxiety disorder in the disease group was different from that in the control group. CONCLUSION: The onset of generalized anxiety disorder is related to BDNF gene polymorphism, and is accompanied by changes in intestinal flora and inflammatory immune status in the body.

RasGRF1 participates in the protective effect of tanshinone IIA on depressive like behaviors of a chronic unpredictable mild stress induced mouse model.

Tanshinone IIA (Tan IIA) is reported to have neuroprotective effects to suppress cell apoptosis of cortical neurons induced by Aß25-35 through inhibiting oxidative stress. Nevertheless, few studies have investigated the effects of Tan IIA on depressive disorder. Here, we aimed to measure the effects of Tan IIA on chronic unpredictable mild stress (CUMS) induced mouse model and its underlying mechanism. For 28 days, mice were subjected to CUMS while Tan IIA was administered once daily at doses of 0, 1, 2.5, 5, or 10 mg/kg. CUMS exposure increased depressive-like behaviors, as indicated by increased immobility time in the forced swim and tail suspension tests, decreased sucrose preference in the sucrose preference test, and reduced exploratory behavior in the open field test. All of these behaviors were reversed dose-dependently by Tan IIA treatment. Oxidative stress was determined by measuring malondialdehyde, glutathione peroxidase, and superoxide dismutase activity and total antioxidant capacity. Levels of pro-inflammatory factors IL-1ß and IL-18, cAMP response element binding protein and brain derived neurotrophic factor were detected by ELISA and western blot assay, respectively. The results showed that CUMS increased oxidative stress and pro-inflammatory factors and decreased levels of cAMP response element binding protein and brain-derived neurotrophic factor. Tan IIA treatment again reversed these effects. Importantly, RasGRF1 expression increased in CUMS-exposed mice but decreased after Tan IIA administration. Using RasGRF1-/- mice to determine the role of RasGRF1 in mice exposed to CUMS, we found that knockdown of RasGRF1 reversed the effects of CUMS on mice, just like Tan IIA. These results indicate that Tan IIA may reverse depressive-like behaviors in CUMS-exposed mice by regulating RasGRF1.

Protective role of Dihydromyricetin in Alzheimer's disease rat model associated with activating AMPK/SIRT1 signaling pathway.

The aim of the present study was to understand the possible role of the Dihydromyricetin (DHM) in Alzheimer's disease (AD) rat model through regulation of the AMPK/SIRT1 signaling pathway. Rats were divided into Sham group, AD group, AD + DHM (100 mg/kg) group and AD + DHM (200 mg/kg) group. The spatial learning and memory abilities of rats were assessed by Morris Water Maze. Then, the inflammatory cytokines expressions were determined by radioimmunoassay while expressions of AMPK/SIRT1 pathway-related proteins by Western blot; and the apoptosis of hippocampal cells was detected by TdT-mediated dUTP nick end labeling assay. AD rats had an extended escape latency with decreases in the number of platform crossings, the target quadrant residence time, as well as swimming speed, and the inflammatory cytokines in serum and hippocampus were significantly elevated but AMPK/SIRT1 pathway-related proteins were reduced. Meanwhile, the apoptosis of hippocampal cells was significantly up-regulated with decreased Bcl-2 and increased Bax, as compared with Sham rats (all P<0.05). After AD rats treated with 100 or 200 mg/kg of DHM, the above effects were significantly reversed, resulting in a completely opposite tendency, and especially with 200 mg/kg DHM treatment, the improvement of AD rats was more obvious. DHM exerts protective role in AD via up-regulation of AMPK/SIRT1 pathway to inhibit inflammatory responses and hippocampal cell apoptosis and ameliorate cognitive function.