Betel Nut Consumption and the Reasons for Its Rise among Chinese Migrant Workers.

Background: In China, betel nut users were initially concentrated in specific regions and ethnic groups. However, in recent years, public health concerns have been raised because betel nuts, addictive substances, have become largely used by Chinese migrant workers. Methods: This study adopts an anthropological fieldwork research methodology to investigate the rise in betel nut consumption among Chinese migrant workers. We observe the everyday lives of migrant workers in the rural-urban area of Wuhan. We use in-depth interviews to understand their psychology and behaviors toward betel nut consumption. Discussion: The study's results indicate that the observed increase in betel nut consumption among migrant workers is not only the result of the spread of betel nuts across regions and groups, but more importantly, it is related to the working and living conditions, social interaction, consumption culture, and masculinity image of migrant workers. The consumption of betel nuts reflects the political-economic structure and socio-cultural background to which Chinese migrant workers belong. Conclusion: The increasing consumption of betel nuts is a social issue that requires thorough research and government engagement. We contend that anthropology research may help identify the social mechanisms incentivizing betel nut consumption and solve the related public health issues among Chinese migrant workers from public policy and social governance perspectives.

sFgl2-Treg Positive Feedback Pathway Protects against Atherosclerosis.

Soluble fibrinogen-like protein 2 (sFgl2), a novel effector of regulatory T cells (Tregs), has been demonstrated to have potent immunosuppressive functions. Multiple studies indicate that Tregs could exert important atheroprotective effects, but their numbers gradually decrease during atherogenesis. The receptor of sFgl2 can be expressed on Treg precursor cells, while the role of sFgl2 on Treg differentiation and atherosclerosis progression remains unclear. Firstly, we detected that the sFgl2 was decreased in humans and mice with atherosclerotic diseases and was especially lower in their vulnerable plaques. Then, we used both Adeno-associated virus-sFgl2 (AAV-sFgl2)-injected ApoE-/- mice, which is systemic overexpression of sFgl2, and sFgl2TgApoE-/- bone marrow cells (BMC)-transplanted ApoE-/- mice, which is almost immune-system-specific overexpression of sFgl2, to explore the role of sFgl2 in atherosclerosis. Our experiment data showed that AAV-sFgl2 and BMT-sFgl2 could reduce atherosclerotic area and enhance plaque stability. Mechanistically, sFgl2 increases the abundance and immunosuppressive function of Tregs, which is partly mediated by binding to FcγRIIB receptors and phosphorylating Smad2/3. Collectively, sFgl2 has an atheroprotective effect that is mainly achieved by forming a positive feedback pathway with Treg. sFgl2 and Treg could synergistically protect against atherosclerosis.

Identification of key genes and immune infiltration modulated by CPAP in obstructive sleep apnea by integrated bioinformatics analysis.

Patients with obstructive sleep apnea (OSA) experience partial or complete upper airway collapses during sleep resulting in nocturnal hypoxia-normoxia cycling, and continuous positive airway pressure (CPAP) is the golden treatment for OSA. Nevertheless, the exact mechanisms of action, especially the transcriptome effect of CPAP on OSA patients, remain elusive. The goal of this study was to evaluate the longitudinal alterations in peripheral blood mononuclear cells transcriptome profiles of OSA patients in order to identify the hub gene and immune response. GSE133601 was downloaded from Gene Expression Omnibus (GEO). We identified black module via weighted gene co-expression network analysis (WGCNA), the genes in which were correlated significantly with the clinical trait of CPAP treatment. Finally, eleven hub genes (TRAV10, SNORA36A, RPL10, OBP2B, IGLV1-40, H2BC8, ESAM, DNASE1L3, CD22, ANK3, ACP3) were traced and used to construct a random forest model to predict therapeutic efficacy of CPAP in OSA with a good performance with AUC of 0.92. We further studied the immune cells infiltration in OSA patients with CIBERSORT, and monocytes were found to be related with the remission of OSA and partially correlated with the hub genes identified. In conclusion, these key genes and immune infiltration may be of great importance in the remission of OSA and related research of these genes may provide a new therapeutic target for OSA in the future.

Heterostructured SnO2-SnS2@C Embedded in Nitrogen-Doped Graphene as a Robust Anode Material for Lithium-Ion Batteries.

Tin-based anode materials with high capacity attract wide attention of researchers and become a strong competitor for the next generation of lithium-ion battery anode materials. However, the poor electrical conductivity and severe volume expansion retard the commercialization of tin-based anode materials. Here, SnO2-SnS2@C nanoparticles with heterostructure embedded in a carbon matrix of nitrogen-doped graphene (SnO2-SnS2@C/NG) is ingeniously designed in this work. The composite was synthesized by a two-step method. Firstly, the SnO2@C/rGO with a nano-layer structure was synthesized by hydrothermal method as the precursor, and then the SnO2-SnS2@C/NG composite was obtained by further vulcanizing the above precursor. It should be noted that a carbon matrix with nitrogen-doped graphene can inhibit the volume expansion of SnO2-SnS2 nanoparticles and promote the transport of lithium ions during continuous cycling. Benefiting from the synergistic effect between nanoparticles and carbon matrix with nitrogen-doped graphene, the heterostructured SnO2-SnS2@C/NG further fundamentally confer improved structural stability and reaction kinetics for lithium storage. As expected, the SnO2-SnS2@C/NG composite exhibited high reversible capacity (1201.2 mA h g-1 at the current rate of 0.1 A g-1), superior rate capability and exceptional long-life stability (944.3 mAh g-1 after 950 cycles at the current rate of 1.0 A g-1). The results demonstrate that the SnO2-SnS2@C/NG composite is a highly competitive anode material for LIBs.

Non-HDL-cholesterol to HDL-cholesterol ratio is an independent risk factor for liver function tests abnormalities in geriatric population.

BACKGROUND: Excessive lipid depositing in liver cells could induce pathophysiological development of liver. Our study aimed to assess whether non-HDL cholesterol to HDL-cholesterol ratio (NonHDLc/HDLc) is an independent risk factor for liver function tests (LFTs) abnormalities in geriatric population. METHODS: We enrolled 1745 eligible subjects (714 males, 1031 females) with normal liver function tests at baseline who participated in annual health checkup for liver disease in 2015. Logistic regression models were used to examine the independent relationship between NonHDLc/HDLc ratio and LFTs abnormalities. RESULTS: After one year follow-up, there were 6.1% (n = 107) participants developed new-onset LFTs abnormalities in 2016. Equally dividing participants into tertiles according to their baseline NonHDLc/HDLc ratio levels, we found compared with tertile 1, the multivariable-adjusted ORs (95% CIs) for new-onset LFTs abnormalities of tertile 3 were 2.85 (1.18-6.93), P = 0.021. In stratified analysis, compared with controls, the correlation between NonHDLc/HDLc ratio and incidence of LFTs abnormalities was more remarkable in female individuals, BMI > 24 individuals and free of diabetes individuals. CONCLUSION: Our study suggests that NonHDLc/HDLc ratio is an independent risk factor for LFTs abnormalities in geriatric population, and assessment of NonHDLc/HDLc ratio may help early identify high risk people of liver diseases. TRIAL REGISTRATION: Trial registration in the Ethics Committee of Tongji Medical College, Huazhong University of Science and Technology (IORG No: IORG0003571 ). Registered 3 March 2015.

MiR-181b Antagonizes Atherosclerotic Plaque Vulnerability Through Modulating Macrophage Polarization by Directly Targeting Notch1.

Atherosclerotic plaque vulnerability is the major cause for acute stroke and could be regulated by macrophage polarization. MicroRNA-181b (miR-181b) was involved in macrophage differential. Here, we explore whether miR-181b could regulate atherosclerotic plaque vulnerability by modulating macrophage polarization and the underline mechanisms. In acute stroke patients with atherosclerotic plaque, we found that the serum level of miR-181b was decreased. Eight-week apolipoprotein E knockout (ApoE-/-) mice were randomly divided into three groups (N = 10): mice fed with normal saline (Ctrl), mice fed with high-fat diet, and tail vein injection with miRNA agomir negative control (AG-NC)/miR-181b agomir (181b-AG, a synthetic miR-181b agonist). We found that the serum level of miR-181b in AG-NC group was lower than that in Ctrl group. Moreover, 181b-AG could upregulate miR-181b expression, reduce artery burden and attenuate atherosclerotic plaque vulnerability by modulating macrophage polarization. In RAW264.7 cells treated with oxidized low-density lipoprotein (ox-LDL), we found miR-181b could reverse the function of ox-LDL on M1/M2 markers at both mRNA and protein levels. Furthermore, by employing luciferase reporter assay, we found that Notch1 was a direct target of miR-181b and could be regulated by miR-181b in vivo and in vitro. Finally, inhibition of Notch1 could abolish the function of downregulating miR-181b on increasing M2 phenotype macrophages. Our study demonstrates that administration of miR-181b could reduce atherosclerotic plaque vulnerability partially through modulating macrophage phenotype by directly targeting Notch1.

MicroRNA-493 regulates angiogenesis in a rat model of ischemic stroke by targeting MIF.

MicroRNA-493 (miR-493) is known to suppress tumour metastasis and angiogenesis and its expression is decreased in stroke patients. In the present study, we investigated a role for miR-493 in regulating post-stroke angiogenesis. We found decreased expression of miR-493 in the ischemic boundary zone (IBZ) of rats subjected to middle cerebral artery occlusion (MCAO), and in rat brain microvascular endothelial cells (RBMECs) exposed to oxygen glucose deprivation. Down-regulating miR-493 with a lateral ventricular injection of antagomir-493, a synthetic miR-493 inhibitor, increased capillary density in the IBZ, decreased focal infarct volume and ameliorated neurologic deficits in rats subjected to MCAO. Intriguingly, MCAO also increased the expression of macrophage migration inhibitory factor (MIF) in the IBZ of rats; MIF expression was also increased in RBMECs exposed to oxygen glucose deprivation. We found that miR-493 directly targeted MIF, and that the protective effect of miR-493 inhibition in angiogenesis was attenuated by knocking down MIF. This effect could then be rescued by administration of recombinant MIF. Our findings highlight the importance of miR-493 in regulating angiogenesis after MCAO, and indicate that miR-493 is a potential therapeutic target in the treatment of stroke.