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Prolonged inhalation of environmental crystalline silica (CS) can cause silicosis, characterized by persistent pulmonary inflammation and irreversible fibrosis, but the mechanism has not been elucidated. To uncover the role and underlying mechanism of glycolytic reprogramming in CS-induced pulmonary inflammation, the mouse silicosis models and glycolysis inhibition models were established in vivo. And the CS-induced macrophage activation models were utilized to further explore the underlying mechanism in vitro. The results showed that CS induced lung inflammation accompanied by glycolytic reprogramming and pyroptosis. The application of glycolysis inhibitor (2-DG) suppressed CS-induced pyroptosis and alleviated lung inflammation. In vitro, 2-DG effectively impeded CS-induced macrophage pyroptosis and inflammatory response. Mechanistically, 2-DG suppressed pyroptosis by inhibiting NLRP3 inflammasome activation both in vivo and in vitro. Furtherly, metabolite lactate facilitated NLRP3-dependent pyroptosis synergistically with CS particles, while blocking the source of lactate largely alleviated NLRP3 inflammasome activation and subsequent pyroptosis triggered by CS. More profoundly, the increment of lactate induced by CS might drive NLRP3-dependent pyroptosis by increasing histone lactylation levels. In conclusion, our findings demonstrated inhibiting glycolytic reprogramming could alleviate CS-induced inflammatory response through suppressing NLRP3 -dependent pyroptosis. Increased glycolytic metabolite lactate and protein lactylation modifications might represent significant mechanisms during CS-induced NLRP3 activation and macrophage pyroptosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

This paper presents a study on the integration of domain-specific knowledge in prompt engineering to enhance the performance of large language models (LLMs) in scientific domains. The proposed domain-knowledge embedded prompt engineering method outperforms traditional prompt engineering strategies on various metrics, including capability, accuracy, F1 score, and hallucination drop. The effectiveness of the method is demonstrated through case studies on complex materials including the MacMillan catalyst, paclitaxel, and lithium cobalt oxide. The results suggest that domain-knowledge prompts can guide LLMs to generate more accurate and relevant responses, highlighting the potential of LLMs as powerful tools for scientific discovery and innovation when equipped with domain-specific prompts. The study also discusses limitations and future directions for domain-specific prompt engineering development., Competing Interests: No potential conflict of interest was reported by the authors., (© 2024 The Authors.)

Environmental exposure to crystalline silica (CS) particles is common and occurs during natural, industrial, and agricultural activities. Prolonged inhalation of CS particles can cause silicosis, a serious and incurable pulmonary fibrosis disease. However, the underlying mechanisms remain veiled. Herein, we aim to elucidate the novel mechanisms of interleukin-11 (IL-11) driving fibroblast metabolic reprogramming during the development of silicosis. We observed that CS exposure induced lung fibrosis in mice and activated fibroblasts, accompanied by increased IL-11 expression and metabolic reprogramming switched from mitochondrial respiration to glycolysis. Besides, we innovatively uncovered that elevated IL-11 promoted the glycolysis process, thereby facilitating the fibroblast-myofibroblast transition (FMT). Mechanistically, CS-stimulated IL-11 activated the extracellular signal-regulated kinase (ERK) pathway and the latter increased the expression of hypoxia inducible factor-1α (HIF-1α) via promoting the translation and delaying the degradation of the protein. HIF-1α further facilitated glycolysis, driving the FMT process and ultimately the formation of silicosis. Moreover, either silence or neutralization of IL-11 inhibited glycolysis augmentation and attenuated CS-induced lung myofibroblast generation and fibrosis. Overall, our findings elucidate the role of IL-11 in promoting fibroblast metabolic reprogramming through the ERK-HIF-1α axis during CS-induced lung fibrosis, providing novel insights into the molecular mechanisms and potential therapeutic targets of silicosis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

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., (© 2023. The Author(s).)

Silica particles are commonly encountered in natural and industrial activities. Long-term environmental exposure to silica can result in silicosis, which is characterized by chronic inflammation and abnormal tissue repair in lung. To uncover the role of m 6 A modification in silica-induced pulmonary inflammation, we conducted this study using established mouse and macrophage models. In this study, the aerodynamic diameter of silica particles was approximately 1-2 µm. We demonstrated that silica exposure in mice caused pulmonary inflammation and increased global m 6 A modification levels, the downregulation of alkB homolog 5 (ALKBH5) might contribute to this alteration. Besides, we found that F4/80, a macrophage-specific biomarker, was co-expressed with ALKBH5 through dual immunofluorescent staining. In vitro studies using MeRIP assays suggested that Slamf7 was a target gene regulated by m 6 A modification, and specific inhibition of ALKBH5 increased Slamf7 expression. Mechanistically, ALKBH5 promoted m 6 A modification of Slamf7, which decreased Slamf7 mRNA stability in an m 6 A-dependent manner, ultimately regulating Slamf7 expression. In addition, silica exposure activated PI3K/AKT and induced macrophage autophagy. Inhibition of Slamf7 promoted autophagy, reduced the secretion of pro-inflammatory cytokines, and improved silica-induced pulmonary inflammation. In summary, ALKBH5 can regulate silica-induced pulmonary inflammation by modulating Slamf7 m 6 A modification and affecting the function of macrophage autophagy., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Tin dioxide (SnO 2 ) is being investigated as a promising anode material for both lithium-ion batteries (LIBs) and sodium-ion batteries (SIBs). Effectively dispersing small sized SnO 2 crystals in well-designed carbonaceous matrices using eco-friendly materials and simplified methods is an urgent task. Herein, gallic acid (GA) molecules, abundant in plant kingdom, are firstly selected to react with few-layered graphene oxide (GO) in mild hydrothermal condition, and the GA modulated reduced graphene oxide (GA@RGO) supporting skeleton can be obtained. Then Sn-GA metal-organic framework (MOF) domains can be directly engineered on the surface of the GA@RGO sheets with controlled size and improved dispersion. Finally, the well-designed Sn-GA@RGO precursor is converted to the SnO 2 /C/RGO nanocomposite with significantly optimized microstructure. The SnO 2 /C/RGO sample delivers an excellent specific capacity of 823.6 mAh·g -1 after 700 cycles at 1000 mA·g -1 in half-cells and 741.3 mAh·g -1 after 50 cycles at 200 mA·g -1 in full-cells for LIBs, a specific capacity of 370.3 mAh·g -1 after 600 cycles at 200 mA·g -1 in half-cells for SIBs. The sample preparation strategy is rationally established by comprehensively understanding the interactions between GO sheets, Sn 2+ ions and GA molecules, and the engineered SnO 2 /C/RGO nanocomposite has good prospects in wider fields., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

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 H 2 O 2 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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

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., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer XX declared a shared affiliation with the authors at the time of review., (Copyright © 2023 Zhang, Liu, Yang, Liu and Yin.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

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., (© 2022. The Author(s).)

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-1β 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-1β 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-1β 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-1β 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-1β in alveolar macrophages., (© 2022 Wiley Periodicals LLC.)

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-1β, IL-1β, 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., Competing Interests: The authors report no conflicts of interest in this work., (© 2022 Ma et al.)

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-1β, 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., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Yin, Fang, Wang, Xia, Tian, Ma, Zhang, Li, Li, Yao and Zhang.)

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., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

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.

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Extensive application of nanomaterials has dramatically increased the risk of silica nanoparticle (SiNP, SiO 2 ) 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.

Exposure to PM 2.5 has been linked to respiratory disorders, yet knowledge of the molecular mechanism is limited. Here, PM 2.5 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 ± 69 μg/m 3 , PM 2.5 was rich in heavy metals and organic pollutants. After exposure to PM 2.5 , 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, PM 2.5 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., (Copyright © 2020 Elsevier B.V. All rights reserved.)

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.

In this work, a facile strategy for the construction of single crystalline Ni 3 S 2 nanowires coated with N-doped carbon shell (NC) forming Ni 3 S 2 @NC core/shell arrays by one-step chemical vapor deposition process is reported. In addition to the good electronic conductivity from the NC shell, the nanowire structure also ensures the accommodation of large volume expansion during cycling, leading to pre-eminent high-rate capacities (470 mAh g -1 at 0.05 A g -1 and 385 mAh g -1 at 2 A g -1 ) and outstanding cycling stability with a capacity retention of 91% after 100 cycles at 1 A g -1 . Furthermore, ex situ transmission electron microscopy combined with X-ray diffraction and Raman spectra are used to investigate the reaction mechanism of Ni 3 S 2 @NC during the charge/discharge process. The product after delithiation consists of Ni 3 S 2 and sulfur, suggesting that the capacity of the electrode comes from the conversion reaction of both Ni 3 S 2 and sulfur with Li 2 S., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Omnibearing acceleration of charge/ion transfer in Li 4 Ti 5 O 12 (LTO) electrodes is of great significance to achieve advanced high-rate anodes in lithium-ion batteries. Here, a synergistic combination of hydrogenated LTO nanoparticles (H-LTO) and N-doped carbon fibers (NCFs) prepared by an electrodeposition-atomic layer deposition method is reported. Binder-free conductive NCFs skeletons are used as strong support for H-LTO, in which Ti 3+ is self-doped along with oxygen vacancies in LTO lattice to realize enhanced intrinsic conductivity. Positive advantages including large surface area, boosted conductivity, and structural stability are obtained in the designed H-LTO@NCF electrode, which is demonstrated with preeminent high-rate capability (128 mAh g -1 at 50 C) and long cycling life up to 10 000 cycles. The full battery assembled by H-LTO@NCFs anode and LiFePO 4 cathode also exhibits outstanding electrochemical performance revealing an encouraging application prospect. This work further demonstrates the effectiveness of self-doping of metal ions on reinforcing the high-rate charge/discharge capability of batteries., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Autophagy is essential for cellular metabolism and plays pivotal roles in carcinogenesis, while excessive autophagy induces toxicity and cell death. Our previous studies have suggested that let-7a-5p/BCL-xL might regulate autophagy in lung cancer, but the regulatory mechanism is unclear. The central goal of the study was to figure out the role of let-7a-5p/BCL-xL in the initiation of autophagy and its effect on the migration, invasion, and proliferation of A549 cells as well as its therapeutic potential in lung cancer. Based on the genome-wide expression profiles of lung cancer, BCL-xL and let-7a-5p were found to be dysregulated and negatively correlated in lung adenocarcinoma, which was associated with the survival of lung cancer. The crosstalk between BCL-xL and let-7a-5p was then investigated using dual-luciferase reporter assay, and it was found to suppress the migration and invasion of A549 cells. Further, we found that the crosstalk between BCL-xL and let-7a-5p could lead to toxic autophagy and cell death through activating the PI3K-signaling pathway, which was independent of apoptosis or pyroptosis. These findings indicate that let-7a-5p is a sensitive initiator for toxic autophagy in A549 lung cancer cells and is an appealing target for lung cancer therapy., (© 2019 The Author(s).)