Long-term nanoplastics exposure contributes to impaired steroidogenesis by disrupting the hypothalamic-testis axis: Evidence from integrated transcriptome and metabolome analysis.

Cumulative evidence suggested that nanoplastics (NPs) cause male toxicity, but the mechanisms of which are still misty. Steroidogenesis is a key biological event that responsible for maintaining reproductive health. However, whether dysregulated steroidogenesis is involved in NPs-induced impaired male reproductive function and the underlying mechanism remains unclear. In our study, Balb/c mice were continuously exposed to pristine-NPs or NH2-NPs for 12 weeks, spanning the puberty and adult stage. Upon the long-term NPs treatment, the hypothalamus and testis were subjected to transcriptome and metabolome analysis. And the results demonstrated that both primitive-NPs and NH2-NPs resulted in impaired spermatogenesis and steroidogenesis, as evidenced by a significant reduction in sperm quality, testosterone, FSH, and LH. The expression of genes involved in hypothalamic-pituitary-testis (HPT) axis, such as Kiss-1 and Cyp17a1 that encoded the key steroid hormone synthetase, was also diminished. Furthermore, the phosphatidylcholine and pantothenic acid that mainly enriched in glycerophospholipid metabolism were significantly reduced in the testis. Comprehensive analysis of the transcriptome and metabolome indicated that down-regulated Cyp17a1 was associated with decreased metabolites phosphatidylcholine and pantothenic acid. Overall, we speculate that the disturbed HPT axis induced by long-term NPs contributes to disordered glycerophospholipid metabolism and subsequently impaired steroidogenesis. Our findings deepen the understanding of the action of the mechanism responsible for NPs-induced male reproductive toxicology.

Gut microbiota combined with metabolome dissects long-term nanoplastics exposure-induced disturbed spermatogenesis.

As the concerned emerging pollutants, several lines of evidence have indicated that nanoplastics (NPs) lead to reproductive toxicity. However, the biological mechanism underlying NPs disturbed spermatogenesis remains largely unknown. Therefore, we aimed to reveal the potential mechanism of impaired spermatogenesis caused by long-term NPs exposure from the perspective of integrated metabolome and microbiome analysis. After 12 weeks of gavage of polystyrene nanoplastics (PS-NPs) and animo-modified polystyrene nanoplastics (Amino-NPs), a well-designed two-exposure stages experimental condition. We found that NPs exposure induced apparent abnormal spermatogenesis, which appeared more severe in the Amino-NPs group. Mechanistically, 14 floras associated with glucose and lipid metabolism were significantly altered, as evidenced by 16 S rRNA sequencing. Testicular metabolome revealed that the Top 50 changed metabolites were also enriched in lipid metabolism. Subsequently, the combined gut microbiome and metabolome analysis uncovered the strong correlations between Klebsiella, Blautia, Parabacteroides, and lipid metabolites (e.g., PC, LysoPC and GPCho). We speculate that the dysbiosis of gut microbiota-related disturbed lipid metabolism may be responsible for long-term NPs-induced damaged spermatogenesis, which provides new insights into NPs-induced dysregulated spermatogenesis.

Transport of microplastics in the body and interaction with biological barriers, and controlling of microplastics pollution.

Microplastics (MPs) are one novel environmental pollutant sized < 5 mm that is ubiquitously present in numerous environmental media and particularly susceptible to interact with various toxic chemicals. Importantly, MPs can enter the food chain, and are bio-enriched and bio-accumulated with trophic levels, eventually endangering ecosystems and human health. However, there need to be more understanding regarding the bio-interaction of MPs with the host, particularly for biological barriers. This review aimed to summarize the latest findings regarding the main exposure routes of MPs that generated health burdens on humans. Furthermore, their interactions with biological barriers that generate adverse health effects and the underlying mechanisms were also reviewed. Additionally, we provided a comprehensive overview of recent advances regarding the removing and controlling of MPs. Finally, we discussed the future directions for MPs hazard prevention to provide helpful information for regulating decision-making and guiding safer plastics applications.

Prevalence of workplace violence against general practitioners: A systematic review and meta-analysis.

Global Conference on Primary Health Care identified that promoting the primary healthcare system has become an important work. Workplace violence (WPV) against GPs is an important global problem. This study aimed to summarise the evidence on the prevalence of WPV against GPs. We systematically searched the PubMed, Embase, and Web of Science databases, and the references of retrieved articles to identify studies on reporting the prevalence of WPV against GPs. We included 15 eligible studies in this meta-analysis. 63.1% (95% confidence interval (CI): 55.6%-70.6%) experienced any form of WPV, 33.8% (95% CI: 25.3%-42.3%) encountered non-physical violence, and 8.5% (95% CI: 5.7%-11.4%) reported experiencing physical violence. The proportion of physical violence differed across study location, sex, and practice setting, and the prevalence of physical violence increased with study period. No significant differences in the prevalence of non-physical violence in sex and study location were found. The prevalence of WPV against GPs is high. A higher prevalence of physical violence was found in some Asian countries (such as China), male GPs, and primary care.

Clinical characteristics and risk factors of fatal patients with COVID-19: a retrospective cohort study in Wuhan, China.

BACKGROUND: The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable mortality. The risk factors, clinical treatments, especially comprehensive risk models for COVID-19 death are urgently warranted. METHODS: In this retrospective study, 281 non-survivors and 712 survivors with propensity score matching by age, sex, and comorbidities were enrolled from January 13, 2020 to March 31, 2020. RESULTS: Higher SOFA, qSOFA, APACHE II and SIRS scores, hypoxia, elevated inflammatory cytokines, multi-organ dysfunction, decreased immune cell subsets, and complications were significantly associated with the higher COVID-19 death risk. In addition to traditional predictors for death risk, including APACHE II (AUC = 0.83), SIRS (AUC = 0.75), SOFA (AUC = 0.70) and qSOFA scores (AUC = 0.61), another four prediction models that included immune cells subsets (AUC = 0.90), multiple organ damage biomarkers (AUC = 0.89), complications (AUC = 0.88) and inflammatory-related indexes (AUC = 0.75) were established. Additionally, the predictive accuracy of combining these risk factors (AUC = 0.950) was also significantly higher than that of each risk group alone, which was significant for early clinical management for COVID-19. CONCLUSIONS: The potential risk factors could help to predict the clinical prognosis of COVID-19 patients at an early stage. The combined model might be more suitable for the death risk evaluation of COVID-19.

Hepatic oxidative damage and Nrf2 pathway protein changes in rats following long-term manganese exposure.

This study investigated hepatic oxidative damage in rats following long-term manganese (Mn) exposure and clarified the underlying mechanisms. Forty-eight rats (SPF, male) were randomly assigned to receive low (10 mg/kg, n = 16) or high doses of Mn (50 mg/kg, n = 16) or sterilized distilled water (control group, n = 16). Rats were euthanized after 12 months, and liver Mn levels and histopathological changes were determined. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and liver malondialdehyde (MDA), glutathione peroxidase (GSH-PX), nuclear factor E2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinine oxidoreductase-1 (NQO1) levels were also determined. The Mn concentration and relative liver weights were significantly higher in the high-dose Mn group than in the control and low-dose Mn exposure groups. Low-dose Mn exposure resulted in mild expansion of hepatic sinuses and intact nuclei, whereas high-dose exposure led to pathological alterations in hepatocytes. High-dose Mn treatment significantly increased AST, ALT, and MDA activities and decreased GSH-PX activity. Additionally, liver Nrf2, HO-1, and NQO1 protein expression were markedly reduced by Mn exposure. Under the study conditions, long-term low-dose Mn exposure resulted in slight pathological changes in liver structure, but high-dose Mn exposure affected both liver structure and function, which might be related to the inhibition of Nrf2 expression, suppression of the transcription of its underlying antioxidant genes, and down regulation of the corresponding proteins. Consequently, the antioxidant capacity in the rat liver was weakened.

CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications.

PURPOSE OF REVIEW: Atherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein. RECENT FINDINGS: Animal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders. We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis.

Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor-ß1/Smad2 and nuclear factor-κB signaling pathways in human fetal lung fibroblasts.

Fibroblast-to-myofibroblast differentiation, which is characterized by increased expression of α-smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Sirtuin 6 (SIRT6), a member of the sirtuin family, has been proved to inhibit epithelial-to-mesenchymal transition during idiopathic pulmonary fibrosis. However, the function of SIRT6 in lung myofibroblast differentiation is still obscure. Transforming growth factor-ß1 (TGF-ß1) is one of the main factors that can powerfully promote myofibroblast differentiation. In the current study, we aimed to explore the role of SIRT6 in the cellular model of fibroblast-to-myofibroblast differentiation induced by TGF-ß1 using human fetal lung fibroblasts (HFL1). We demonstrated that the SIRT6 protein level is upregulated by TGF-ß1 in HFL1 cells. Overexpression of SIRT6 significantly suppresses TGF-ß1-induced myofibroblast differentiation in HFL1 cells. Mechanistically, SIRT6 decreases phosphorylation and nuclear translocation of Smad2 under TGF-ß1 stimulation. Nevertheless, mutant SIRT6 (H133Y) without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2. Meanwhile, SIRT6 interacts with the nuclear factor-κB (NF-κB) subunit p65 and represses TGF-ß1-induced NF-κB-dependent transcriptional activity, which is also dependent on its deacetylase activity. Overexpression of wild-type SIRT6 but not the H133Y mutant inhibits the expression of NF-κB-dependent genes including interleukin (IL)-1ß, IL-6 and matrix metalloproteinase-9 (MMP-9) induced by TGF-ß1, all of which have been demonstrated to promote myofibroblast differentiation. Collectively, our study reveals that SIRT6 prevents TGF-ß1-induced lung myofibroblast differentiation through inhibiting TGF-ß1/Smad2 and NF-κB signaling pathways.

Sirtuin 6 inhibits MWCNTs-induced epithelial-mesenchymal transition in human bronchial epithelial cells via inactivating TGF-ß1/Smad2 signaling pathway.

Multi-walled carbon nanotubes (MWCNTs) have been developed with numerous beneficial applications. However, rodent models demonstrate that exposure to MWCNTs via respiratory pathways results in pulmonary fibrosis. Therefore, they could elicit a potential risk of pulmonary fibrosis in humans due to occupational or consumer exposure. Sirtuin 6 (SIRT6), a nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, has been proved to prevent fibrosis in the liver, renal and myocardial tissues. In this present study, we aimed to explore the role of SIRT6 in MWCNTs-induced epithelial-mesenchymal transition (EMT), one of the major contributor of lung fibrogenesis in human bronchial epithelial BEAS-2B cells. We found that the protein level of SIRT6 was elevated after exposure to MWCNTs in BEAS-2B cells. Overexpression of SIRT6 significantly inhibited MWCNTs-induced EMT and EMT-like cell behaviors in BEAS-2B cells. Moreover, wild-type SIRT6 was found to decrease MWCNTs-induced phosphorylation of Smad2, but not mutant SIRT6 (H133Y) without histone deacetylase activity. In conclusion, our study demonstrated that SIRT6 inhibited MWCNTs-induced EMT in BEAS-2B cells through TGF-ß1/Smad2 signaling pathway, which depended on its deacetylase activity, and provided evidences that targeting SIRT6 could be a potential novel therapeutic strategy for MWCNTs-induced pulmonary fibrosis.

Rutaecarpine: A promising cardiovascular protective alkaloid from Evodia rutaecarpa (Wu Zhu Yu).

Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Wu Zhu Yu, Family: Rutaceae), a versatile medicinal herb which is clinically used to treat headache, abdominal pain, postpartum hemorrhage, dysentery, and amenorrhea in China. As one of the most representative indolopyridoquinazoline alkaloids of Evodia rutaecarpa, rutaecarpine has broad pharmacological actions in treating various cardiovascular, cerebrovascular, and metabolic diseases. The cardiovascular actions of rutaecarpine have aroused intense research interest due to its purported inotropic and chronotropic, vasodilatory, anti-platelet activation, anti-oxidant, anti-inflammatory, and lipid-lowering effects. Biochemical and pharmacological studies have illustrated the molecular targets of rutaecarpine, such as TRPV1, CGRP, AMPK, ABCA1, and ß1-AR. Furthermore, several rutaecarpine derivatives (such as bromorutaecarpine and fluororutaecarpine) have been shown to possess cardioprotective and vasculoprotective effects with improved safety profile. Hereby, we provide a systematic overview of pharmacological actions, toxicological effects, and molecular targets of rutaecarpine in cardiovascular disease prevention/treatment, aiming to exploit the therapeutic potential of rutaecarpine and its derivatives in treating cardiovascular diseases.

Tanshinone IIA suppresses cholesterol accumulation in human macrophages: role of heme oxygenase-1.

Accumulation of foam cells in the neointima represents a key event in atherosclerosis. We previously demonstrated that Tanshinone IIA (Tan), a lipophilic bioactive compound extracted from Salvia miltiorrhiza Bunge, inhibits experimental atherogenesis, yet the detailed mechanisms are not fully understood. In this study, we sought to explore the potential effects of Tan on lipid accumulation in macrophage foam cells and the underlying molecular mechanisms. Our data indicate that Tan treatment reduced the content of macrophages, cholesterol accumulation, and the development of atherosclerotic plaque in apolipoprotein E-deficient mice. In human macrophages, Tan ameliorated oxidized low density lipoporotein (oxLDL)-elicited foam cell formation by inhibiting oxLDL uptake and promoting cholesterol efflux. Mechanistically, Tan markedly reduced the expression of scavenger receptor class A and increased the expression of ATP-binding cassette transporter A1 (ABCA1) and ABCG1 in lipid-laden macrophages via activation of the extracellular signal-regulated kinase (ERK)/nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. Tan treatment induced the phosphorylation and nuclear translocation of Nrf2 and subsequently increased the expression of HO-1, and these effects were abolished by the specific ERK inhibitors, PD98059 and U0126. Moreover, HO-1 small interfering RNA or zinc protoporphyrin (a HO-1 inhibitor) abrogated Tan-mediated suppression of lipid accumulation in macrophages. Our current findings demonstrate that a novel HO-1-dependent mechanism is involved in the regulation of cholesterol balance by Tan.

The multimorbidity association of metabolic syndrome and depression on type 2 diabetes: a general population cohort study in Southwest China.

Background: Metabolic syndrome(MetS) and depression are independently associated with type 2 diabetes (T2DM) risk. However, little is known about the combined effect of MetS and depression on the risk of T2DM. The present study aims to prospectively explore the impact of MetS and depression on T2DM susceptibility among the Chinese general population. Methods: 6489 general population without T2DM adults in Southwest China were recruited from 2010 to 2012. Depression and MetS were prospectively assessed using a 9-item Patient Health Questionnaire(PHQ-9) and Guideline for the prevention and treatment of type 2 diabetes mellitus in China (2020 edition) (CDS2020) during 2016-2020, respectively. Modified Poisson regression models were conducted to estimate relative risk(RR) and 95% confidence intervals (95%CI) for independent and combined associations of MetS and depression with an incidence of T2DM. Results: During a median follow-up of 6.6 years, 678 cases of T2DM were documented. Individuals with MetS were 1.33 times more likely to develop T2DM than those without MetS. The corresponding RR(95%CI) for depression with no depression was 1.45(1.22-1.72). Notably, compared with no MetS or depression, the multivariate-adjusted RR for a combined effect of MetS and depression on the risk of T2DM was 2.11(1.39-3.22). Moreover, an increased risk of T2DM was more apparent in those ≥ 60 years, males, and overweight. Conclusions: Individuals with multimorbidity of MetS and depression are at a higher risk of T2DM compared with those with no MetS or depression.

Autophagy aggravates multi-walled carbon nanotube-induced ferroptosis by suppressing PGC-1 dependent-mitochondrial biogenesis in lung epithelial cells.

Multi-walled carbon nanotube (MWCNT) induced respiratory toxicity has become a growing concern, with ferroptosis emerging as a novel mechanism implicated in various respiratory diseases. However, whether ferroptosis is involved in MWCNT-elicited lung injury and the underlying molecular mechanisms warrant further exploration. In this study, we found that MWCNT-induced ferroptosis is autophagy-dependent, contributing to its cellular toxicity. Inhibiting of autophagy by pharmacological inhibitors 3-MA or ATG5 gene knockdown significantly attenuated MWCNT-induced ferroptosis, concomitant with rescued mitochondrial biogenesis. Rapamycin, the autophagy agonist, exacerbated the mitochondrial damage and MWCNT-induced ferroptosis. Moreover, lentivirus-mediated overexpression of PGC-1α inhibited ferroptosis, while inhibition of PGC-1α aggravated ferroptosis. In summary, our study unveils ferroptosis as a novel mechanism underlying MWCNT-induced respiratory toxicity, with autophagy promoting MWCNT-induced ferroptosis by hindering PGC-1α-dependent mitochondrial biogenesis.

Association between depression and risk of type 2 diabetes and its sociodemographic factors modifications: A prospective cohort study in southwest China.

BACKGROUND: Depression may be associated with the risk of developing type 2 diabetes. The goal of this study was to explore the association of severe of depression with the risk of type 2 diabetes in adults in Guizhou, China. METHODS: A 10-year prospective cohort study of 7158 nondiabetes adults aged 18 years or older was conducted in Guizhou, southwest China from 2010 to 2020. The Patient Health Questionnaire-9 (PHQ-9) was used to measure the prevalence of depression. Cox proportional hazard models were used to estimated hazard ratios (HRs) and 95% confidence intervals (95% CIs) of depression and incident type 2 diabetes. A quantile regression (QR) analytical approach were applied to evaluate the associations of PHQ-9 score with plasma glucose values. RESULTS: A total of 739 type 2 diabetes cases were identified during a median follow-up of 6.59 years. The HR (95% CI) per 1-SD increase for baseline PHQ-9 score was 1.051 (1.021, 1.082) after multivariable adjustment. Compared with participants without depression, those with mild or more advanced depression had a higher risk of incident type 2 diabetes (HR:1.440 [95% CI, 1.095, 1.894]). Associations between depression with type 2 diabetes were suggested to be even stronger among women or participants aged ≥45 years (p < .05). There are significant positive associations of PHQ-9 score with 2-h oral glucose tolerance test blood glucose levels. CONCLUSION: Depression significantly increased the risk of incident type 2 diabetes, especially in women, participants aged ≥45 years, Han ethnicity, and urban residents. These findings highlighted the importance and urgency of depression health care.

Alternative splicing of PSMD13 mediated by genetic variants is significantly associated with endometrial cancer risk.

OBJECTIVE: Accumulating evidence has shown that aberrant alternative splicing events are closely associated with the onset and development of cancer. However, whether genetic variants-associated alternative splicing is linked to risk of endometrial cancer remains largely uncertain. METHODS: We identified single nucleotide polymorphisms (SNPs) locates in the splicing number trait locus (sQTL) of endometrial cancer using the CancerSplicing QTL database. In parallel with bioinformatics analysis, we conducted a case-control study comprising 2,000 cases and 2,013 controls to assess the association between identified SNP which possesses mRNA splicing function and endometrial cancer susceptibility. Furthermore, we used the Kaplan-Meier Plotter, The Human Protein Atlas, SPNR, and Spliceman2 databases for sQTL and differential gene expression analyses to identify the genetic variant which most potentially influence the risk of endometrial cancer through alternative splicing to reveal the potential mechanism by which candidate SNPs regulate the risk of endometrial cancer. RESULTS: The results indicated that SNP rs7128029 A

Single and joint associations of exposure to polycyclic aromatic hydrocarbons with blood coagulation function during pregnancy: A cross-sectional study.

Association linking polycyclic aromatic hydrocarbons (PAHs) to blood coagulation function during pregnancy remains absent. Hence, we conducted a cross-sectional study including 679 late pregnant women (27.2 ± 5.1 years old) drawn from Zunyi birth cohort, Southwest China. During late pregnancy, ten urinary PAHs metabolites and four clinical blood coagulation parameters were measured, including activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), and fibrinogen (FIB). Multiple linear regression, Restricted cubic spline (RCS) regression, Bayesian kernel machine regression (BKMR), and quantile g-computation (Q-g) regression were used to investigate their single, nonlinear, and mixed associations. Each 2.7-fold increment in 2-hydroxyfluorene (2-OHFlu), 9-hydroxyfluorene (9-OHFlu), 1-hydroxyphenanthrene (1-OHPhe), 2-hydroxyphenanthrene (2-OHPhe), and 3-hydroxyphenanthrene (3-OHPhe) were associated with 0.287 s, 0.190 s, 0.487 s, and 0.396 s shorter APTT, respectively; each 2.7-fold increment in 2-OHPhe was associated with a 0.047 s longer PT; each 2.7-fold increment in 9-hydroxyphenanthrene (9-OHPhe) and 1-hydroxypyrene (1-OHPyr) were associated with 0.087 s and 0.031 s shorter TT, respectively; and each 2.7-fold increment in 1-hydroxynaphthalene (1-OHNap) was associated with 0.032 g/L higher FIB level. The nonlinear association of 2-OHPhe with APTT and 1-OHNap with FIB were also observed. Furthermore, the shortened APTT and TT associated with PAHs mixture were indicated by BKMR and Q-g model. BKMR also revealed a nonlinear association of 2-OHPhe with PT and an interaction effect of 2-OHPhe and 3-OHPhe on APTT. Our results indicate that urinary PAHs was associated with shortened coagulation time and increased FIB. Therefore, more attention should be paid for late pregnant women to prevent PAHs-associated risk of thrombosis. Future perspective studies to confirm our findings and explore the underlying biological mechanism are warranted.

Single and Joint Associations of Polycyclic Aromatic Hydrocarbon Exposure with Liver Function during Early Pregnancy.

The individual and combined associations of polycyclic aromatic hydrocarbons (PAHs) metabolites on liver function during pregnancy are still lacking. We aimed to explore the connection between urinary PAH metabolites and liver function in early pregnant women in southwest China based on the Zunyi birth cohort. Ten urinary PAH metabolites and five liver function parameters during early pregnancy were measured. The associations of single PAHs with parameters of liver function were assessed using multiple linear regression. A Bayesian kernel machine regression (BKMR) model was used to evaluate the joint associations of the PAH mixture with outcomes. We found that each 1% increment of urinary 2-hydroxyphenanthrene (2-OH-PHE) was associated with 3.36% (95% CI: 0.40%, 6.40%) higher alanine aminotransferase (ALT) and 2.22% (95% CI: 0.80%, 3.67%) higher aspartate aminotransferase (AST). Each 1% increment in 1-hydroxy-phenanthrene (1-OH-PHE) was significantly associated with 7.04% (95% CI: 1.61%, 12.75%) increased total bile acid (TBA). Additionally, there was a significant positive linear trend between 2-OH-PHE and AST and 1-OH-PHE and TBA. BKMR also showed a significant positive association of PAH mixture with AST. Our results indicate that PAH metabolites were associated with increased parameters of liver function among early pregnant women. Early pregnant women should pay more attention to the adverse relationships between PAHs and liver function parameters to prevent environment-related adverse perinatal outcomes.

Long-term release kinetic characteristics of microplastic from commonly used masks into water under simulated natural environments.

Masks-related microplastic pollution poses a new threat to the environment and human health that has gained increasing concern. However, the long-term release kinetics of microplastic from masks in aquatic environments have yet to studied, which hampers its risk assessment. Four types of masks, namely cotton mask, fashion mask, N95 mask, and disposable surgical mask were exposed to systematically simulated natural water environments to determine the time-dependent microplastic release characteristics at 3, 6, 9, and 12 months, respectively. In addition, the structure changes of employed masks were examined by scanning electron microscopy. Moreover, Fourier transform infrared spectroscopy was applied to analyze the chemical composition and groups of released microplastic fibers. Our results showed that the simulated natural water environment could degrade four types of masks and continuously produce microplastic fibers/fragments in a time-dependent manner. The dominant size of released particles/fibers was below 20 µm across four types of face masks. The physical structure of all four masks was damaged to varying degrees concomitant with photo-oxidation reaction. Collectively, we characterized the long-term release kinetics of microplastic from four types of commonly used masks under a well-mimic real word water environment. Our findings suggest that urgent action must be taken to properly manage disposable masks and ultimately limit the health threats associated with discarded masks.

Regular consumption of pickled vegetables and fermented bean curd reduces the risk of diabetes: a prospective cohort study.

Objective: The global incidence of diabetes is rising, in part due to the widespread adoption of poor dietary habits. Fermented vegetables have numerous health benefits and are generally affordable. Here, we examined whether regular consumption of pickled vegetables or fermented bean curd reduces the risk of diabetes. Methods: A total of 9,280 adults (≥18 years of age) were recruited via multi-stage sampling from 48 townships in China between 2010 and 2012 for this 10-year prospective study. In addition to demographic information, monthly consumption levels of pickled vegetables and fermented bean curd were recorded. Participants were then monitored for diabetes onset. After the final follow-up, logistic regression analyses with multiple covariant corrections were conducted to estimate the changes in diabetes risk associated with consumption of pickled vegetables and fermented bean curd compared to non-consumption. Results: A total of 6,640 subjects without diabetes at the start of the study were followed up for a median period of 6.49 years, among whom 714 were diagnosed with diabetes during the study. According to a regression model with multivariable adjustment, diabetes risk was significantly reduced by consumption of 0-0.5 kg/month of pickled vegetables (OR = 0.77, 95% CI: 0.63, 0.94) and further reduced by consumption of >0.5 kg/month of pickled vegetables (OR = 0.37, 95% CI: 0.23, 0.60) compared to no consumption (both P-trend < 0.001). Consumption of fermented bean curd also reduced diabetes risk (OR = 0.68, 95% CI: 0.55, 0.84). Conclusion: Regular consumption of pickled vegetables and/or fermented bean curd can reduce the long-term risk of diabetes.

Association of remnant cholesterol with CVD incidence: a general population cohort study in Southwest China.

Background: Emerging evidence has indicated that remnant cholesterol (RC) could predict cardiovascular disease (CVD) incidence. Nevertheless, the relationship between RC and CVD risk, especially within the general Chinese population, remains scarce. Objective: The present research aimed to assess whether RC concentrations and CVD outcomes in general Chinese adults are related. Methods: The Cox proportional hazard model was established to explore the relationship between RC and the outcomes of CVD and CVD subgroups. A restricted cubic spline (RCS) was utilized to investigate the dose-response connection between RC and the risk of CVD outcomes, and the ROC curve was used to calculate the corresponding cutoff values. Moreover, stratified analysis was conducted to investigate the potential effect modification in the association between RC and CVD outcomes. Results: Significant positive associations were found between elevated categorical RC and increased risk of CVD (HR Q4, 1.80; 95% CI 1.15-2.79; P-value = 0.008), atherosclerotic cardiovascular disease (HR Q4, 2.00; 95% CI 1.22-3.27; P-value = 0.007), stroke (HR Q4, 1.66; 95% CI 1.02-2.69; P-value = 0.040), and ischemic stroke (HR Q4, 1.87, 95% CI 1.08-3.25; P-value = 0.034), respectively. Our study suggested that the incidence of CVD outcomes increased when RC levels were above 0.75 mmol/L. Importantly, the CVD risks related to RC were more likely to be those found in subjects aged above 60 years, women, subjects with BMI <24 kg/m2, and subjects with hypertension and unhealthy diet patterns. Conclusions: Aberrant high level of RC is associated with elevated CVD risk, independent of low-density lipoprotein cholesterol (LDL-C). Our data reveal urgent primary prevention for subjects with high RC levels to a low incidence of CVD, especially for the elderly, women, and those with hypertension and unhealthy diet patterns.