Long-term night shift work, genetic predisposition, and risk of incident asthma: a prospective cohort study.

BACKGROUND: Evidence about a potential link between current and lifetime night shift work and risk of incident asthma is insufficient. AIM: To investigate the association of current and lifetime night shift work with risk of incident asthma, and the modified effect of genetic susceptibility on this association. DESIGN AND METHODS: We included 253,773 individuals with complete night shift work information in the UK biobank. We calculated the standard polygenetic risk score (PRS) for asthma. The Cox proportional hazard models were conducted to estimate hazard ratios (HRs) and 95% CIs. RESULTS: After multivariable adjustments, we found that current night shift work was associated with an increased risk of incident asthma in a dose-response fashion (P for trend<0.001). Compared with day workers, those working usual/permanent night shifts had a 17% (95% CI: 1.04-1.33) higher risk of asthma incidence. In addition, we observed significant dose-dependent relationships of longer lifetime duration or frequency of night shift work with elevated risk of asthma incidence (all P for trend<0.05). Compared with never night shift workers, those with a duration (≥5 years) or frequency (≥8 nights/month) of night shift work exhibited a 20% (95% CI: 1.03-1.39) or 22% (95% CI: 1.03-1.44) higher risk of incident asthma, respectively. Moreover, the elevated risk of incident asthma related to current and lifetime night shift work exposure was strengthened by high PRS, although no significant shift work-PRS interactions were detected. CONCLUSION: Both current and lifetime night shift work may increase the risk of incident asthma, regardless of genetic predisposition to asthma.

Associations of polychlorinated biphenyls exposure, lifestyle, and genetic susceptibility with dyslipidemias: Evidence from a general Chinese population.

Polychlorinated biphenyls (PCBs) are endocrine-disrupting chemicals that have been associated with various adverse health conditions. Herein we explored the associations of PCBs with dyslipidemia and further assessed the modification effect of genetic susceptibility and lifestyle factors. Six serum PCBs (PCB-28, 101, 118, 138, 153, 180) were determined in 3845 participants from the Wuhan-Zhuhai cohort. Dyslipidemia, including hyper-total cholesterol (HyperTC), hyper-triglyceride (HyperTG), hyper-low density lipoprotein cholesterol (HyperLDL-C), and hypo-high density lipoprotein cholesterol (HypoHDL-C) were determined, and lipid-specific polygenic risk scores (PRS) and healthy lifestyle score were constructed. We found that all six PCB congeners were positively associated with the prevalence of dyslipidemias, and ΣPCB level was associated with HyperTC, HyperTG, and HyperLDL-C in dose-response manners. Compared with the lowest tertiles of ΣPCB, the odds ratios (95% confidence intervals) in the highest tertiles were 1.490 (1.258, 1.765) for HyperTC, 1.957 (1.623, 2.365) for HyperTG, and 1.569 (1.316, 1.873) for HyperLDL-C, respectively. Compared with those with low ΣPCB, healthy lifestyle, and low genetic risk, participants with high ΣPCB, unfavorable lifestyle, and high genetic risk had the highest odds of HyperTC, HyperTG, and HyperLDL-C. Our study provided evidence that high PCB exposure exacerbated the association of genetic risk and unhealthy lifestyle with dyslipidemia.

Associations between long-term night shift work and incidence of chronic obstructive pulmonary disease: a prospective cohort study of 277,059 UK Biobank participants.

BACKGROUND: Little is known about the effects of night shifts and their interactions with genetic factors on chronic obstructive pulmonary disease (COPD). In this study, we aim to investigate relationships between long-term night shift work exposure and COPD risk, and assess modification effects of genetic predisposition. METHODS: A total of 277,059 subjects who were in paid employment or self-employed were included in the UK Biobank. Information on current and lifetime employment was obtained, and a weighted COPD-specific genetic risk score (GRS) was constructed. We used Cox proportional hazard models to investigate associations between night shift work and COPD risk, and their interaction with COPD-specific GRS. RESULTS: The cohort study included 277,059 participants (133,063 men [48.03%]; mean [SD] age, 52.71 [7.08] years). During a median follow-up of 12.87 years, we documented 6558 incidents of COPD. From day work, irregular night shifts to regular night shifts, there was an increased trend in COPD incidence (P for trend < 0.001). Compared with day workers, the hazard ratio (HR) and 95% confidence interval (CI) of COPD was 1.28 (1.20, 1.37) for subjects with rarely/sometimes night shifts and 1.49 (1.35, 1.66) for those with permanent night shifts. Besides, the longer durations (especially in subjects with night shifts ≥ 10 years) and increasing monthly frequency of night shifts (in workers with > 8 nights/month) were associated with a higher COPD risk. Additionally, there was an additive interaction between night shifts and genetic susceptibility on the COPD risk. Subjects with permanent night shifts and high genetic risk had the highest risk of COPD (HR: 1.90 [95% CI: 1.63, 2.22]), with day workers with low genetic risk as a reference. CONCLUSIONS: Long-term night shift exposure is associated with a higher risk of COPD. Our findings suggest that decreasing the frequency and duration of night shifts may offer a promising approach to mitigating respiratory disease incidence in night shift workers, particularly in light of individual susceptibility.

Research progress on the mechanical compatibility of restorative materials with dental tissue / 口腔疾病防治

@#As the main means of mastication, teeth can withstand countless functional contacts. The mechanical properties of teeth are closely related to their tissue structure. Enamel and dentin have a high hardness and modulus of elasticity, and their graded structure allows them to withstand bite forces without being susceptible to fracture. When tooth tissue is defective, full crown restoration is often needed to restore the normal shape and function of the tooth. Metal materials, ceramic materials, and polyetheretherketone (PEEK) materials are commonly used for crown restoration. Metal materials have certain disadvantages in terms of aesthetics and are relatively rarely used in clinical practice. Ceramic materials with different compositions exhibit differences in performance and aesthetics, but their elastic modulus and hardness are much higher than those of dental tissue, resulting in mismatching mechanical properties. In contrast, the elastic modulus of PEEK is lower than that of tooth tissue and similar to that of bone tissue, but its properties can be improved by fiber reinforcement. Notably, when the mechanical properties of a restoration material and tooth tissue are not fully matched, the interface between them often forms a potential weak link, which ultimately affects the stability and long-term effect of the restoration. This article introduces the mechanical properties and corresponding structural characteristics of enamel and dentin. On this basis, the advantages and limitations of existing restoration materials are analyzed, and the possibility of biomimetic design of full crowns is further explored.

Translation and psychometric properties of the Mandarin Chinese version of the COVID-19 Impact Scale in college students.

The COVID-19 pandemic has caused significant long psychological impacts that require a novel measurement tool to capture the changes in such impacts. To this end, the COVID-19 Impact Scale (CIS) was developed as an instrument to evaluate psychological responses associated with the pandemic, and has shown evidence of a one-factor structure. The CIS was initially created using an Korea University students sample, and has since been translated and validated in Turkish. A total of 504 College students, aged 17-25, took part in the study from two universities in Jinan, located in Shandong Province, Eastern China, via an online survey platform. They were administered the Chinese versions of the following self-report instruments: Mandarin Chinese CIS, Fear of COVID-19 Scale, Depression Anxiety Stress Scale-21 and Satisfaction With Life Scale. Moreover, a sample of 86 participants who provided their contact information and agreed to participate in the second-round survey were asked to reassess using the Mandarin Chinese CIS after a period of 3 weeks following the initial testing. Results showed that Mandarin Chinese CIS had good internal consistency and test-retest reliability. Additionally, the Mandarin Chinese CIS presented good criterion validity and estimates of convergent validity and incremental validity. In confirmatory factor analysis, the one-factor model showed an acceptable fit after incorporating correlations between error terms. Our findings suggest that the Mandarin Chinese CIS is a reliable and valid self-report tool that demonstrates robust psychometric properties and acceptable construct validity when used with a Chinese university students.

Efficient removal of As(III) from groundwaters through self-alkalization in an asymmetric flow-electrode electrochemical separation system.

It remains a great challenge to efficiently remove As(III) from groundwater using traditional technologies due to its stable electroneutral form. This study constructed an asymmetric flow-electrode electrochemical separation (AFES) system, which overcomes the drawback of H+ release from anodic carbon oxidation and achieves continuous self-alkalization function and highly efficient removal of As(III) from groundwater. At the applied voltage of 1.2 V and initial pH 7.5, the system could rapidly decrease the total As (T-As) concentration from 150.0 to 8.9 µg L-1 within 90 min, with an energy consumption of 0.04 kWh m-3. The self-alkalization was triggered by the generation of H2O2 from dissolved oxygen reduction and the adsorption of H+ on the cathode in the feed chamber, which significantly promoted the dissociation and oxidation of As(III), resulting in the removal of T-As predominantly in the form of As(V). The removal performance of T-As was slightly affected by the initial pH and coexisting ions in the feed chamber. The AFES system also exhibited considerable stability after 20 cycles of continuous experiments and superior performance in treating As-containing real groundwater. Moreover, the pH of the alkalized solution can be restored to the initial level by standing or aeration operation. This work offers a novel and efficient pathway for the detoxication of As(III)-contaminated groundwaters.

Mechanical properties, biosafety, and shearing bonding strength of glass fiber-reinforced PEEK composites used as post-core materials.

OBJECTIVE: To investigate the mechanical properties, biosafety, and shearing bonding strength of glass fibers-reinforced polyether-ether-ketone (PEEK-GF) for post-core materials. METHODS: PEEK-GF composites with different glass fiber contents were prepared by extrusion injection and named PEEK-GF30, PEEK-GF40, and PEEK-GF50. Mechanical properties including flexural modulus, flexural strength, Vickers hardness, and compression strength were tested. The cross-sectional morphology was examined using scanning electron microscopy (SEM). Cytotoxicity was studied in vitro with Cell-counting kit-8 (CCK-8). Cell morphology was observed under a microscope. Cell growth on the composites' surfaces was analyzed with DAPI staining. The shearing bonding strength (SBS) of PEEK-GF50 was assessed after applying different pretreatments. Failure modes were evaluated by microscopy. SEM and contact-angle measurements were performed on the surfaces. Statistical analysis was conducted using one-way ANOVA (P < 0.05). RESULTS: The mechanical properties of PEEK-GF composites improved with increased GF content. The PEEK-GF50 group exhibited flexural modulus (17.4 ± 0.5 GPa) close to that of dentin (18.6 GPa) and showed the highest flexural strength (350.0 ± 2.9 MPa), Vickers hardness (47.6 ± 4.5 HV), and compressive strength (264.0 ± 18.0 MPa). The SEM analysis demonstrated that the PEEK matrix combined well with glass fibers. The CCK-8 results confirmed the biosafety of all groups. DAPI staining indicated that cells were growing well on the composites' surface. The sample that was pretreated with sandblasting and plasma showed the highest SBS (16.0 ± 1.7 MPa). SIGNIFICANCE: The PEEK-GF composites demonstrated excellent mechanical properties, biosafety, and SBS, and have great potential to serve as post-core materials.

The emerging role of epigenetic regulation in the progression of silicosis.

Silicosis is one of the most severe occupational diseases worldwide and is characterized by silicon nodules and diffuse pulmonary fibrosis. However, specific treatments for silicosis are still lacking at present. Therefore, elucidating the pathogenesis of silicosis plays a significant guiding role for its treatment and prevention. The occurrence and development of silicosis are accompanied by many regulatory mechanisms, including epigenetic regulation. The main epigenetic regulatory mechanisms of silicosis include DNA methylation, non-coding RNA (ncRNA), and histone modifications. In recent years, the expression and regulation of genes related to silicosis have been explored at epigenetic level to reveal its pathogenesis further, and the identification of aberrant epigenetic markers provides new biomarkers for prediction and diagnosis of silicosis. Here, we summarize the studies on the role of epigenetic changes in the pathogenesis of silicosis to give some clues for finding specific therapeutic targets for silicosis.

Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner.

Introduction: Silica nanoparticles (SiNPs) are one of the most widely used inorganic nanomaterials, and exposure to SiNP has been demonstrated to induce pulmonary inflammation, primarily promoted by the NLRP3-mediated macrophage pyroptosis. However, mechanisms underlying the activation of NLRP3 signaling are complex, and whether cathepsin B (CTSB), an enzyme released by the ruptured lysosome, could trigger NLRP3 assembly is controversial. Methods: To further characterize the role of CTSB in silica-induced pyroptosis, we conducted this study by establishing SiNP exposure models in vitro. The morphological features of SiNPs were exhibited by the SEM and TEM, and the effects of SiNPs' internalization on macrophages were examined by the TEM and immunofluorescent staining. Moreover, Western blot was performed to detect the expression of proteins related to pyroptosis and CTSB after blocking the expression of NLRP3 and CTSB. Results: We found that SiNPs internalization caused the rupture of macrophage membrane and promoted the aging of cells with increased intracellular vacuoles. Also, the expression of NLRP3, ASC, Caspase-1, GSDMD, Pro-IL-1ß, IL-1ß, and CTSB increased under the stimulation of SiNP, which could be suppressed by additional treatment with MCC950, an NLRP3-specific inhibitor. Besides, we found SiNP joint treatment with leupeptin, a CTSB inhibitor, could inhibit the expression of CTSB, but it had no effect on the expression of NLRP3, ASC, and Caspase-1, and the process of macrophage pyroptosis was also not affected. Conclusion: SiNP exposure induces rupture of macrophages and the release of lysosomal CTSB, but CTSB fails to specifically act on the NLRP3 inflammasome to induce pyroptosis which is causally linked to lung inflammation and fibrosis.

NF-κB mediates silica-induced pulmonary inflammation by promoting the release of IL-1ß in macrophages.

Long-term exposure to respirable silica particles causes pulmonary inflammation and fibrosis primarily promoted by cytokines released from alveolar macrophages, yet the underlying mechanism is still unclear. From the perspective of nuclear factor kappa B (NF-κB), we studied the mechanism of IL-1ß biosynthesis and release. Utilizing BAY 11-7082, an NF-κB specific inhibitor, we showed the alteration of macrophage viability and examined the expression of both IL-1ß and NF-κB in vitro. We found that silica nanoparticles (SiNPs) were internalized by macrophages and caused damage to cell integrity. The immunofluorescence assay showed that SiNPs exposure enhanced the expression of IL-1ß and NF-κB, which could be effectively suppressed by BAY 11-7082. Besides, we built silica exposure mouse model by intratracheally instilling 5 mg of SiNPs and checked the effect of silica exposure on pulmonary pathological changes. Consistently, we found an upregulation of IL-1ß and NF-κB after SiNPs exposure, along with the aggravated inflammatory cell infiltration, thickened alveolar wall, and enhanced expression of collagens. In conclusion, SiNPs exposure causes pulmonary inflammation and fibrosis that is regulated by NK-κB through upregulating IL-1ß in alveolar macrophages.

Acute Silica Exposure Triggers Pulmonary Inflammation Through Macrophage Pyroptosis: An Experimental Simulation.

Silica is an essential substrate of various materials, and inhaling silica induces pulmonary diseases potentially associated with macrophage pyroptosis. Utilizing silica of micro- and nano- sizes, we explored the role of macrophage pyroptosis in silica-induced pulmonary inflammation. Under the transmission electron microscopy, we found that the internalization of silica nanoparticle induced membrane rupture and increased the number of intracellular vacuoles, and both sizes of silica could suppress cell viability and proliferation. Also, silica-exposed macrophages generated higher levels of ROS, together with the upregulated expression of NLRP3, ASC, Caspase-1, GSDMD, IL-1ß, and IL-6. However, the expression of these proteins was suppressed after removing ROS or NLRP3. In addition, we found increased expression of TLR4 and NF-κB responsible for silica recognition and pyroptosis priming after silica exposure. For in vivo studies, we established animal model by intratracheally instilling 5 mg of silica into mice with/without NLRP3 inhibition. Four weeks later, we found diffused infiltration of inflammatory cells and enhanced collagen hyperplasia partially reversed by additional treatment with MCC950, so as the expression of pyroptotic molecules and proinflammatory cytokines. In particular, the dual immunofluorescent staining showed co-expression of macrophage-specific biomarker F4/80 and NLRP3 within the cells, and silica of nano-size showed more potent toxicity and pathogenicity than that of the micro-sized particles both in vitro and in vivo. To sum up, macrophage pyroptosis is an upstream event of silica-induced pulmonary inflammation promoted by ROS through the TLR4/NLRP3/NF-κB signaling axis.

Chemical conjugation of FITC to track silica nanoparticles in vivo and in vitro: An emerging method to assess the reproductive toxicity of industrial nanomaterials.

Previous studies have demonstrated that silica nanoparticle (SiNP) exposure induces pulmonary and cardiovascular diseases, yet their transportation and degradation in vivo have not been fully elucidated. From the perspective of reproduction, this study was implemented to examine the uterine accumulation of SiNP and explore its reproductive toxicity and pathogenic mechanisms. First, we coupled FITC onto SiNPs and intratracheally instilled them into pregnant mice on the fifth gestational day, and the toxic effect of SiNP was evaluated in vitro and in vivo. It was found that SiNP penetrated the trophoblast membrane, leading to apoptosis and suppression of cell proliferation, tube formation, and invasion in a dose-dependent manner. Mechanistically, SiNP dysregulated the expression of Scd1, Slc27a1, and Cpt1a, and induced over synthesis and efflux obstruction of fatty acid through the PPARγ signaling pathway. The downregulation of Caspase-3 triggered apoptosis of trophoblast, which was causally associated with intracellular fatty acid accumulation as revealed by the correlation analysis. Besides, SiNP induced uterine inflammation in vivo, which aggravated with the observation prolongation within 24 h. Overall, SiNPs were visualized by coupling with FITC, and the uterine accumulation of SiNP induced fatty acid metabolic disorder, biological dysfunction, and trophoblast apoptosis, which were mediated in part by the PPARγ signaling pathway. These findings would contribute to understanding the environmental impacts of SiNP better, as well as the development of control measures for environmental pollution.

Effect of pyrethroid pesticides on the testis of male rats: A meta-analysis.

This study quantitatively evaluated the effects of pyrethroid pesticides on the testis of male rats. An extensive literature search for relevant studies was conducted on PubMed, Web of Science, Excerpta Medica Database, the Chinese National Knowledge Infrastructure, and Chinese Biomedical Literature Database. Pooled standard mean difference with corresponding 95% confidence interval was calculated via the random-effects model. I 2 was used to evaluate heterogeneity among studies. A total of 19 studies were included for analysis in our study. Results indicated that the sperm count of rats exposed to fenvalerate was lower than that of rats in control groups. The sperm count, sperm motility, and testosterone level of rats exposed to cypermethrin and deltamethrin were lower than those of rats in control groups. Moreover, the sperm morphology of rats exposed to these pyrethroid pesticides was abnormal compared with that of rats in control groups. The present meta-analysis indicates that pyrethroid pesticides decrease rat sperm count, sperm motility, and testosterone level and cause abnormal rat sperm morphology. Therefore, pyrethroid pesticides can damage the testis of male rats.

Uterine metabolic disorder induced by silica nanoparticles: biodistribution and bioactivity revealed by labeling with FITC.

Extensive application of nanomaterials has dramatically increased the risk of silica nanoparticle (SiNP, SiO2) exposure, yet their biological effect on reproduction has not been fully elucidated. By tracking the uterine biodistribution of SiNP in pregnant mice, this study was conducted to evaluate the biological effect of SiNP on reproduction. First, SiNP was conjugated with FITC, and then the FITC-SiNP was administrated to trophoblast (100 µg/mL, 24 h) in vitro and pregnant mice (0.25 mg/mouse, 2-24 h) in vivo. It was found that the FITC-SiNP was internalized by trophoblast and deposited in the uterus. The internalization of SiNP caused trophoblast dysfunction and apoptosis, while SiNP accumulation in the uterus induced diffuse inflammatory infiltration. The genome-wide alteration of gene expression was studied by high throughput sequencing analysis, where 75 genes were found to be dysregulated after SiNP exposure, among which ACOT2, SCD1, and CPT1A were demonstrated to regulate the biosynthesis of unsaturated fatty acids. Moreover, the suppression of unsaturated fatty acids caused mitochondrial overload of long-chain fatty acyl-CoA (LACoA), which further induced both trophoblast apoptosis and endometrial inflammation. In conclusion, the successful conjugation of FITC onto SiNP facilitated the tracking of SiNP in vitro and in vivo, while exposure to FITC-SiNP induced uterine metabolic disorder, which was regulated by the ACOT/CPT1A/SCD1 axis through the biosynthesis of unsaturated fatty acids signaling pathway.

Uterine pyruvate metabolic disorder induced by silica nanoparticles act through the pentose phosphate pathway.

Silica nanoparticles (SiNPs) have drawn considerable attention due to their environmental health effects, while enhanced understanding of metabolic disorders has provided insight into related diseases. To investigate the impacts of SiNPs exposure on reproduction and reveal their pathogenic mechanisms, this study was designed and conducted from a metabolic perspective. First, fluorescein isothiocyanate (FITC)-SiNPs were chemically synthesized and applied to track SiNPs in vitro and in vivo. Next, 30 pregnant mice were intratracheally instilled with 1.25 mg of SiNPs/mouse, then sacrificed 24 h post-treatment. We found that SiNPs penetrated the trophoblast membrane, triggering apoptosis and inhibiting cell proliferation, invasion, and tube formation in a dose-dependent manner. Mechanistically, SiNPs dysregulated phosphofructokinase (Pfkl) and fructose-bisphosphatase 2 (Fbp2) and induced glucose depletion and pyruvate accumulation via the pentose phosphate pathway. Besides, the downregulation of caspase-3 suggested a causal relationship between pyruvate accumulation, pentose phosphate pathway activation, and cell apoptosis. Pfkl and Fbp2 was also dysregulated in vivo, and the uterine inflammation aggravated in a time-dependent manner. In conclusion, SiNPs triggered acute cytotoxicity and uterine inflammation by inducing glucose depletion and pyruvate overload in trophoblasts, which were mediated in part by Pfkl and Fbp2 via the pentose phosphate pathway.

In vitro and in vivo uterine metabolic disorders induced by silica nanoparticle through the AMPK signaling pathway.

Exposure to silica nanoparticles (SiNPs) has been suggested to cause physical disorders, yet the effects of SiNPs on female reproduction have not been illustrated. This study was implemented to explore the reproductive toxicity of SiNPs on female and reveal its underlying mechanisms. Methodologically, the fluorescein isothiocyanate (FITC)-SiNPs were synthesized by coupling with FITC and then used to track the biodistribution of SiNPs in vitro and in vivo. In total, 30 mice were intratracheally injected 0.25 g of FITC-SiNPs, and 6 mice injected with the same volume of saline were used as controls. The results showed that SiNPs penetrated the cellular membrane, triggering apoptosis and inhibiting proliferation, tube formation, and invasion of trophoblast. Mechanistically, SiNPs was demonstrated to dysregulate Fbp2, Cpt1a, Scd1, and Pfkl, and further induced accumulation of pyruvate and fatty acid in mitochondria through the AMPK signaling pathway, which finally activated the Caspase-3-dependent apoptosis. Consistently, the similar alterations of these genes were detected in vivo, and the uterine inflammatory infiltration aggravated with the extension of the observation duration. These results suggested that SiNPs induced trophoblast apoptosis and uterine inflammation, and ultimately caused acute reproductive toxicity on female. The underlying mechanism might be explained by the dysregulation of Fbp2/Cpt1a/Pfkl/Scd1 axis, which promoted the overload of glucose and lipid through the AMPK signaling pathway. These findings were of great significance to guide a comprehensive understanding of the reproductive toxicity of SiNPs as well as the development of environmental standards.

Mechanism of PM2.5-induced human bronchial epithelial cell toxicity in central China.

Exposure to PM2.5 has been linked to respiratory disorders, yet knowledge of the molecular mechanism is limited. Here, PM2.5 was monitored and collected in central China, and its cytotoxicity mechanism on human bronchial epithelial cells (BEAS-2B) was investigated. With the average concentration of 109 ±â€¯69 µg/m3, PM2.5 was rich in heavy metals and organic pollutants. After exposure to PM2.5, the viability of BEAS-2B cells decreased, where 510 dysregulated genes were predicted to induce necroptosis via inhibiting ATP synthesis through the oxidative phosphorylation signaling pathway. Cellular experiments demonstrated that the content of ATP was downregulated, while the expression of RIP3, a necroptosis indicator, was upregulated. Besides, four enzymes in charge of ATP synthesis were downregulated, including ATP5F, NDUF, COX7A, and UQCR, while two genes of RELA and CAPN1 responsible for necroptosis were upregulated. Furthermore, N-acetylcysteine was applied as an enhancer for ATP synthesis, which reversed the downregulation of ATP5F, NDUF, and COX7A, and consequently alleviated the elevation of RELA, CAPN1, and RIP3. In conclusion, PM2.5 exposure downregulates ATP5F, NDUF, COX7A, and UQCR, and that inhibits ATP synthesis via the oxidative phosphorylation signaling pathway, which subsequently upregulates RELA and CAPN1 and ultimately leads to necroptosis of BEAS-2B cells.

Comprehensive characterization of endometrial competing endogenous RNA network in infertile women of childbearing age.

Endometriosis is widely associated with infertility in women of childbearing age, for which there have been no effective treatments. Recent studies suggest that the dysregulation of RNAs contributes to the pathogenesis of endometriosis, so we conduct the case-control genetic analysis to characterize the expression and interaction of different subtypes of RNAs in infertile women with endometriosis. The ectopic and eutopic endometrium of patients undergoing infertility treatment were collected and subjected to high throughput sequencing, and bioinformatics analysis was conducted to construct the competing endogenous RNA (ceRNA) network. As a result, the RNA interactive network was constructed in endometriosis, and a set of mRNAs such as cyclin-dependent kinase 1 (CDK1) and proliferating cell nuclear antigen (PCNA) along with their corresponding miRNAs and lncRNAs were found to promote the growth and death of endometrial stromal cells, which was essential for the pathogenesis of endometriosis. These data suggest that RNA crosstalk is a crucial segment in the development of endometriosis, where CDK1 and PCNA may serve as emerging targets for the treatment of endometriosis-related infertility in women of childbearing age.