[Analysis of the Jumping Characteristics and Influencing Factors of Ozone Pollution in Beijing].

Based on environmental monitoring data and meteorological observation data from 2016 to 2022 in Beijing, combined with backward trajectory clustering and potential source area contribution analysis, the characteristics, meteorological impacts, and potential source areas of ozone (O3) pollution were analyzed. The results showed that there was a total of 41 O3 pollution processes with jumping characteristics in Beijing from 2016 to 2022, with an average of 5.9 times a year. The occurrence time was concentrated in May to July, and the day of the jump (OJD2) was higher than the day before the jump (OJD1). The average value of ρ(O3-8h) was 78.3% higher, and the peak concentration was 78.9% higher. The high O3 concentration zone in the OJD2 region exhibited a characteristic of advancing from south to north. The main reasons for the occurrence of jumped O3 pollution in Beijing could be summarized as local accumulation caused by unfavorable meteorological conditions and regional transmission impact. The occurrence of jump-type ozone pollution was characterized by an increase in southerly wind frequency, temperature rise, pressure decrease, and precipitation decrease. The increase in southerly wind frequency provided conditions for the transport of O3 and its precursors, and rapid photochemical reactions occurred under local high temperatures, with less superimposed precipitation, comprehensively pushing up the ozone concentration level of OJD2. Six air mass transporting pathways were identified through clustering analysis; the air mass from the direction north of OJD2 decreased by 11.2%, whereas the air mass from the south and east directions increased by 6.7% and 4.4%, respectively, with the air masses mainly transmitting over short distances. The ozone concentration corresponding to the south and east directions was relatively high, making a significant contribution to Beijing's pollution. The analysis of potential source areas revealed that the main potential source areas of OJD2 ozone pollution were the central, southern, and eastern parts of Beijing-Tianjin-Hebei, which contributed 82.6% to the pollution trajectory. There was a significant contribution of regional transport during jump-type ozone pollution, and it is necessary to strengthen joint prevention and control in the Beijing-Tianjin-Hebei Region.

Platelet-rich plasma inhibits osteoblast apoptosis and actin cytoskeleton disruption induced by gingipains through upregulating integrin ß1.

The aim of this study was to explore the effects of platelet-rich plasma on gingipain-caused changes in cell morphology and apoptosis of osteoblasts. Mouse osteoblasts MC3T3-E1 cells were treated with gingipain extracts from Porphyromonas gingivalis in the presence or absence of platelet-rich plasma. Apoptosis was detected with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. F-actin was determined by phalloidin-fluorescent staining and observed under confocal microscopy. Western blot analysis was used to detect integrin ß1, F-actin, and G-actin protein expressions. A knocking down approach was used to determine the role of integrin ß1. The platelet-rich plasma protected osteoblasts from gingipain-induced apoptosis in a dose-dependent manner, accompanied by upregulation of integrin ß1. Platelet-rich plasma reversed the loss of F-actin integrity and decrease of F-actin/G-actin ratio in osteoblasts in the presence of gingipains. By contrast, the effects of platelet-rich plasma were abrogated by knockdown of integrin ß1. The platelet-rich plasma failed to reduce cell apoptosis and reorganize the cytoskeleton after knockdown of integrin ß1. In conclusion, platelet-rich plasma inhibits gingipain-induced osteoblast apoptosis and actin cytoskeleton disruption by upregulating integrin ß1 expression.

Gingipains promote RANKL-induced osteoclastogenesis through the enhancement of integrin ß3 in RAW264.7 cells.

As a crucial virulence factor of Porphyromonas gingivalis, gingipains play an important role in periodontal destruction. This study aimed to investigate the effect of gingipains on osteoclastogenesis. We used RAW264.7 cells as osteoclast precursors in our study. In experimental groups, cells were treated with gingipains and/or receptor activator of nuclear factor-κB ligand (RANKL). Tartrate-resistant acid phosphatase (TRAP) activity staining assay showed osteoclast precursors and RANKL-induced mature osteoclasts were increased in a gingipains dose-dependent manner. Real-time reverse transcription polymerase chain reaction analysis demonstrated that gingipains upregulated osteoclastic genes including the protease cathepsin K (Ctsk), matrix metalloprotein 9 (Mmp9), nuclear factor of activated T cells 1 (Nfatc1) and acid phosphatase 5, tartrate resistant (Acp5) in a time-dependent manner. Western blotting assays presented upregulated expressions of TNF receptor-activating factor 6 (TRAF6) and integrin ß3 induced by gingipains and RANKL compared to RANKL alone. Enhanced integrin-related signaling was also demonstrated by elevated phosphorylations of FAK and paxillin compared to control. Moreover, the pit resorption assays showed that gingipains augmented bone resorptive function of osteoclasts induced by RANKL. When we used Cilengitide to block integrin αvß3, gingipains reversed the reduction of formation and resorptive function in RANKL-induced osteoclasts, as they enhanced integrin αvß3 levels more than RANKL treatment alone. In conclusion, our data suggest that gingipains augmented the differentiation and function of mature osteoclasts induced by RANKL through the increase in integrin αvß3.

High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1.

OBJECTIVE: This research is aimed at investigating how high glucose affects the proliferation and apoptosis in periodontal ligament stem cells (PDLSCs) in the presence of TNF-α. METHODS: PDLSCs obtained from periodontal healthy permanent teeth were treated under either high-glucose condition (30 mmol/L, G30 group) or normal glucose condition (5.6 mmol/L, G5.6 group) in the presence or absence of TNF-α. α. α. RESULTS: CCK-8 assay showed that high glucose exacerbated TNF-α. α. α. α. α. α. CONCLUSION: High glucose exacerbates TNF-α-induced proliferative inhibition in human periodontal ligament stem cells through the upregulation and activation of TNF receptor 1. Inhibition of intracellular ROS expression by vitamin C partially rescues PDLSCs in terms of cell proliferation.α.

Comparisons of two serious air pollution episodes in winter and summer in Beijing.

Characteristics of two serious air pollution episodes (9-15 January, as the winter case; and 30 June to 1 July, as the summer case), which occurred in Beijing in 2013 were investigated and compared using multi-method observations and numerical simulations. During these two air pollution episodes, PM2.5 concentrations varied significantly within Beijing, with PM2.5 concentrations in southern parts of Beijing being significantly higher than in northern areas. Typically, heavy air pollution episodes begin in the southern parts and disperse towards the northern parts of Beijing. Clearly, synoptic patterns and the stability of atmospheric circulation patterns were the main factors controlling air pollution in Beijing. During the winter case, a warm center above 900hPa occurred over Beijing. Meanwhile, in the summer case, although there was only a weak inversion, the convective inhibition energy was strong (over 200J/kG). This clearly influenced the duration of the air pollution event. Except for the local accumulation and secondary atmospheric reactions in both cases, regional straw burnings contributed a lot to the PM2.5 concentrations in summer case. Using the CAMx model, we established that regional transport contributed almost 59% to the PM2.5 averaged concentration in Beijing in the winter case, but only 31% in the summer case. Thus, the winter case was a typical regional air pollution episode, while the summer case resulted from local accumulation straw burnings transportation and strong secondary atmospheric reactions. Given that air pollution is a regional problem in China, consistent and simultaneous implementation of regional prevention and control strategies is necessary to improve regional air quality.

Signal-Regulated Protein Kinases/Protein Kinase B-p53-BH3-Interacting Domain Death Agonist Pathway Regulates Gingipain-Induced Apoptosis in Osteoblasts.

BACKGROUND: Gingipains are cysteine proteases produced by Porphyromonas gingivalis, the predominant pathogen in chronic periodontitis. The present study aims to examine the role of gingipains in promoting apoptosis in osteoblasts. METHODS: Human calvarial osteoblasts and osteoblast MC3T3-E1 cells were treated with 8.348 U/L gingipains. Flow cytometry analysis and terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling staining were used to detect cell apoptosis. Protein expression was examined by Western blotting, and gene expression was detected by real-time polymerase chain reaction. Small interfering (si)RNA transfection was used to knock down BH3-interacting domain death agonist (Bid) expression. RESULTS: Treatment with 8.348 U/L gingipains from 4 to 72 hours increased apoptosis, accompanied by elevated cleaved caspase-3 levels. Notably, gingipain-induced apoptosis was associated with increase of Bid and its truncated form, tBid, as well as p53. Transfection with Bid siRNA resulted in suppression of gingipain-induced apoptosis. The p53 inhibitor, Pifithrin-α, blocked the gingipain-induced Bid. The ability of gingipains to stimulate p53 and Bid expression was mimicked by PD-0325901 and MK-2206, the specific extracellular signal-regulated protein kinases (ERK) and protein kinase B (PKB) inhibitors, respectively. Furthermore, treatment with gingipains reduced phospho-ERK and phospho-PKB levels, an effect correlated to gingipain-induced increase in p53 and tBid expression. CONCLUSION: The present findings suggest that Bid plays an essential role in gingipain-induced osteoblast apoptosis, which is dependent on inhibition of ERK and PKB phosphorylation, followed by the activation of p53.

Copper in Diabetes Mellitus: a Meta-Analysis and Systematic Review of Plasma and Serum Studies.

Copper (Cu) is an important trace element involved in oxidative stress, which is associated with the onset and progression of diabetes mellitus (DM). However, clinical studies comparing plasma or serum Cu levels in patients with DM and in healthy individuals report conflicting findings. Therefore, in this meta-analysis, we analyzed the circulating levels of Cu associated with DM (including type 1 diabetes mellitus [T1DM] and type 2 diabetes mellitus [T2DM]). We searched the articles indexed in PubMed, OVID, and Cochrane databases, published through January 2016 and meeting our predefined criteria. Requisite data were extracted, and a random-effect model or a fixed-effect model was used to conduct the meta-analysis. Fifteen eligible studies involving a total of 1079 DM patients and 561 healthy controls were identified. Overall, the DM patients showed higher Cu levels than the healthy controls (plasma Cu mean difference [MD] = 1.69 µmol/L, p < 0.0001; serum Cu MD = 4.06 µmol/L, p = 0.005; plasma and serum Cu MD = 2.67 µmol/L, p = 0.006). Stratification based on the type of diabetes also indicated higher levels of Cu in the plasma and serum of DM patients than in healthy controls, respectively. Stratification of DM patients associated with and without complications also revealed similar results. This meta-analysis suggests that DM patients carried higher levels of Cu than healthy individuals. However, international cohort studies are needed to corroborate our findings.

Design of Friction Stir Spot Welding Tools by Using a Novel Thermal-Mechanical Approach.

A simple thermal-mechanical model for friction stir spot welding (FSSW) was developed to obtain similar weld performance for different weld tools. Use of the thermal-mechanical model and a combined approach enabled the design of weld tools for various sizes but similar qualities. Three weld tools for weld radii of 4, 5, and 6 mm were made to join 6061-T6 aluminum sheets. Performance evaluations of the three weld tools compared fracture behavior, microstructure, micro-hardness distribution, and welding temperature of welds in lap-shear specimens. For welds made by the three weld tools under identical processing conditions, failure loads were approximately proportional to tool size. Failure modes, microstructures, and micro-hardness distributions were similar. Welding temperatures correlated with frictional heat generation rate densities. Because the three weld tools sufficiently met all design objectives, the proposed approach is considered a simple and feasible guideline for preliminary tool design.

[Formation Mechanism of a Serious Pollution Event in January 2013 in Beijing].

The weather conditions, atmospheric environmental background and formation mechanism of a heavy air pollution episode in Beijing City from January 9th to 15th, 2013 was preliminarily investigated by combining observed data and the WRF meteorology model. The results showed that the average concentration of PM2.5 was 323 µg x m(-3) from January 10th to 14th; the heavy pollution episode was closely related to the local meteorological conditions; the stable atmospheric circulation pattern provided favorable environmental field for the lasting of this heavy air pollution; small wind speed, high humidity, low PBL, and lasting temperature inversion were the main reasons for this heavy air pollution incident; further analysis showed that contributions of regional transmission to the receptor sites in Beijing were between 53% - 69% and there were obvious secondary conversions and transformations; overall regional transportation played a more important role during this serious air pollution incident; the meteorological conditions played a key role in the formation and destruction of the heavy air pollution, therefore we need to strengthen the study on early warning of heavy air pollution, in order to prevent and control the air heavy pollution effectively.

Comparison of the properties of human CD146+ and CD146- periodontal ligament cells in response to stimulation with tumour necrosis factor α.

OBJECTIVES: Periodontal ligament stem cells (PDLSCs) can be used in periodontal regeneration. Tumour necrosis factor-alpha (TNF-α) participates in the regulation of cell proliferation, apoptosis, differentiation, and migration. However, whether TNF-α can affect the biological features of PDLSCs is still unclear. The objective of this study was to illustrate the biological effects (proliferation, apoptosis, osteogenesis and migration) of TNF-α on human CD146 positive periodontal ligament cells (CD146+PLDCs) and CD146 negative periodontal ligament cells (CD146-PDLCs). METHODS: CD146±PDLCs were isolated from human PDLCs and analyzed using a fluorescence-activated cell sorter. The biological effects of TNF-α on CD146±PDLCs were evaluated by CCK-8 assay (proliferation), DAPI staining (apoptosis), alizarin red staining and alkaline phosphatase activities assay (osteogenesis), and wounding assay and transwell assay (migration). RESULTS: CD146+PDLCs, which expressed MSC surface markers CD105, CD90, CD73, CD44, and Stro-1, showed higher proliferative and osteogenic potential than CD146-PDLCs. TNF-α at a dose of 2.5ng/ml was found to enhance both proliferation and osteogenesis in CD146+PDLCs. At 5ng/ml, TNF-α promoted proliferation, osteogenesis, and apoptosis in CD146+PDLCs and enhanced osteogenesis in CD146-PDLCs. At 10ng/ml, TNF-α only aggravated apoptosis in CD146+PDLCs. The migratory ability of both CD146+PDLCs and CD146-PDLCs was not altered by TNF-α. CONCLUSIONS: CD146+PDLCs were subpopulation of MSC. It showed greater proliferative and osteogenic potential than CD146-PDLCs. At low concentration, TNF-α was beneficial to CD146+PDLCs on proliferation and osteogenesis, and at high concentration it was detrimental. CD146-PDLCs were found to be less sensitive to TNF-α.