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Abstract Adverse effects and multidrug resistance remain significant obstacles in conventional cancer therapy. Nanomedicines, with their intrinsic properties such as nano-sized dimensions and tunable surface characteristics, have the potential to mitigate the side effects of traditional cancer treatments. While nanomaterials have been widely applied in cancer treatment, challenges such as low targeting efficiency and poor tumor penetration persist. Recent research has shown that anaerobic bacteria exhibit high selectivity for primary tumors and metastatic cancers, offering good safety and superior tumor penetration capabilities. This suggests that combining nanomaterials with bacteria could complement their respective limitations, opening vast potential applications in cancer therapy. The use of bacteria in combination with nanomaterials for anticancer treatments, including chemotherapy, radiotherapy, and photothermal/photodynamic therapy, has contributed to the rapid development of the field of bacterial oncology treatments. This review explores the mechanisms of bacterial tumor targeting and summarizes strategies for synthesizing bacterial-nanomaterial and their application in cancer therapy. The combination of bacterial-nanomaterial hybrids with modern therapeutic approaches represents a promising avenue for future cancer treatment research, with the potential to improve treatment outcomes for cancer patients. Graphical Abstract

MXenes, as a new type of two-dimensional nanomaterial, have great potential for biomedical applications due to their unique structural features and excellent physicochemical properties. In recent years, numerous studies have demonstrated that MXenes materials also possess good antibacterial, anti-inflammatory, and antioxidant activities, which has greatly promoted the development of MXenes in the field of tissue engineering and skin regeneration. A series of emerging studies on the introduction of MXenes into wound dressings has significantly advanced the research progress of novel wound dressings. This review provides a brief overview of the application of MXenes in wound healing, focusing on the properties of MXenes in wound healing and the specific applications of MXenes as wound dressings, as well as some suggestions and opinions on their future development.

The aim of this study was to monitor the spectrum of viral pathogens involved in febrile rash illness (FRI) and their epidemiology. A large-scale study was conducted in multiple provinces of China from 2009 to 2021. A total of 14,168 patients of all age groups were enrolled and tested for seven common viruses causing FRI: measles virus (MV), rubella virus (RuV), enterovirus (EV), varicella zoster virus (VZV), human parvovirus B19 (HPV B19), human herpes virus 6 (HHV6), and dengue virus (DENV). Of 14,168 patients with FRI, 9,443 tested positive for a virus, thus yielding a viral positivity rate of 66.65%. Among the seven viruses detected, EV (61.04%), MV (23.32%), RuV (7.74%), and VZV (5.26%) had high detection rates and exhibited different age-specific positivity rates and seasonal prevalence patterns. Early in the Coronavirus Disease 2019 (COVID-19) pandemic, the number of EV, MV, RuV, and VZV cases significantly declined, and the seasonal patterns also changed in 2020, with delay or disappearance of traditional epidemic peaks. EV, MV, RuV, and VZV were found to be the main causal pathogens of FRI among patients in China, and their epidemic levels and seasonal patterns changed during the COVID-19 pandemic, because of large-scale implementation of non-pharmacological interventions.

Nicotine, an addictive component of cigarettes, causes cognitive defects, particularly when exposure occurs early in life. However, the exact mechanism through which nicotine causes toxicity and alters synaptic plasticity is still not fully understood. The aim of the current study is to examine how non-coding developmental regulatory RNA impacts the hippocampus of mice offspring whose mothers were exposed to nicotine. Female C57BL/6J mice were given nicotine water from one week before pregnancy until end of lactation. Hippocampal tissue from offspring at 20 days post-birth was used for LncRNA and mRNA microarray analysis. Differential expression of LncRNAs and mRNAs associated with neuronal development were screened and validated, and the CeRNA pathway mediating neuronal synaptic plasticity GM13530/miR-7119–3p/mef2c was predicted using LncBase Predicted v.2. Using protein immunoblotting, Golgi staining and behavioral tests, our findings revealed that nicotine exposure in offspring mice increased hippocampal NMDAR receptor, activated receptor-dependent calcium channels, enhanced the formation of NMDAR/nNOS/PSD95 ternary complexes, increased NO synthesis, mediated p38 activation, induced neuronal excitability toxicity. Furthermore, an epigenetic CeRNA regulatory mechanism was identified, which suppresses Mef2c-mediated synaptic plasticity and leads to modifications in the learning and social behavior of the offspring during adolescence. This study uncovers the way in which maternal nicotine exposure results in neurotoxicity in offspring.

Coal worker's pneumoconiosis (CWP) is a common occupational disease that coal miners are highly susceptible due to long-term exposure to coal dust particles (CDP). CWP can induce the accumulation of immune cells surrounding the bronchioles and alveoli in the lungs, resulting in pulmonary fibrosis and compromised immune function. Using single-cell RNA sequencing (scRNA-Seq), our previous studies disclose that CDP exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis, while Vitamin D3 (VitD3) supplementation reduces CDP-induced cytotoxicity; however, the mechanism by which how VitD3 regulates immune status in coal pneumoconiosis remains unclear. In this study, we elucidated the heterogeneity of pulmonary lymphocytes in mice exposed to CDP and demonstrated the therapeutic efficacy of VitD3 using scRNA-Seq dataset. The validation of key lymphocyte markers and their functional molecules was performed using immunofluorescence. The results demonstrated that VitD3 increased the number of naive T cells by modulating CD4 + T cell differentiation and decreased the number of Treg cells in CDP-exposed mice, thereby enhancing the cytotoxic activity of CD8 + effector T cells. These effects markedly alleviated lung fibrosis and symptoms. Taken together, the mechanism by which VitD3 regulates the functions of lymphocytes in CWP provides a new perspective for further research on the prevention and treatment of CWP.

Inhaling silica causes the occupational illness silicosis, which mostly results in the gradual fibrosis of lung tissue. Previous research has demonstrated that hypoxia-inducible factor-1α (HIF-1α) and glycolysis-related genes are up-regulated in silicosis. The role of 2-deoxy-D-glucose (2-DG) as an inhibitor of glycolysis in silicosis mouse models and its molecular mechanisms remain unclear. Therefore, we used 2-DG to observe its effect on pulmonary inflammation and fibrosis in a silicosis mouse model. Furthermore, in vitro cell experiments were conducted to explore the specific mechanisms of HIF-1α. Our study found that 2-DG down-regulated HIF-1α levels in alveolar macrophages induced by silica exposure and reduced the interleukin-1β (IL-1β) level in pulmonary inflammation. Additionally, 2-DG reduced silica-induced pulmonary fibrosis. From these findings, we hypothesize that 2-DG reduced glucose transporter 1 (GLUT1) expression by inhibiting glycolysis, which inhibits the expression of HIF-1α and ultimately reduces transcription of the inflammatory cytokine, IL-1β, thus alleviating lung damage. Therefore, we elucidated the important regulatory role of HIF-1α in an experimental silicosis model and the potential defense mechanisms of 2-DG. These results provide a possible effective strategy for 2-DG in the treatment of silicosis.

Traditional microtubule inhibitors fail to significantly enhance the effect of colorectal cancer; hence, new and efficient strategies are necessary. In this study, a supramolecular nanoreactor (DOC@TA-Fe3+) based on tannic acid (TA), iron ion (Fe3+), and docetaxel (DOC) with microtubule inhibition, reactive oxygen species (ROS) generation, and glutathione peroxidase 4 (GPX4) inhibition, is prepared for ferroptosis/apoptosis treatment. After internalization by CT26 cells, the DOC@TA-Fe3+ nanoreactor escapes from the lysosomes to release payloads. The subsequent Fe3+/Fe2+ conversion mediated by TA reducibility can trigger the Fenton reaction to enhance the ROS concentration. Additionally, Fe3+ can consume glutathione to repress the activity of GPX4 to induce ferroptosis. Meanwhile, the released DOC controls microtubule dynamics to activate the apoptosis pathway. The superior in vivo antitumor efficacy of DOC@TA-Fe3+ nanoreactor in terms of tumor growth inhibition and improved survival is verified in CT26 tumor-bearing mouse model. Therefore, the nanoreactor can act as an effective apoptosis and ferroptosis inducer for application in colorectal cancer therapy.

Abstract The material basis for soil formation is rock weathering debris. Understanding the particle size composition characteristics of rock weathering debris and its impacts is important for improving the soil structure of dry farmland in the central dry zone of Ningxia,China. In this study, the particle sizes of weathered debris collected from grey–green slate after indoor simulations of freeze–thaw and dry–wet cycles tests were examined. The results were as follows: (1) Under 16 treatments, the weathering debris of grey–green slate contained about 10% or less very fine sand and coarse silt, while clay, fine silt, and fine sand were the most abundant sizes (at least 60% of the total). (2) Under each treatment, the average particle size of the grey–green slate weathered debris was 5.52Ф (silt grade). The overall skewness was high, but the symmetry was poor. The particle size frequency distribution curve had many broad peaks or multiple peaks. (3) The fractal dimension was associated with very fine silt but had a strong negative correlation with fine sand and medium-coarse sand. The results indicate that fractal dimension can reflect the grain size characteristics of weathered debris. The mineral element content of the grey–green slate somewhat affected the fractal dimension, and it positively correlated with environmental electrical conductivity (EC) and element-leaching amount; it negatively correlated with particle size, temperature, and pH. According to the findings, the fractal dimension can accurately represent the particle size distribution of weathered debris. The generation of grey–green slate weathering debris should be considered in the formation and development of local soil.

Silicosis is one of the most common forms of pneumoconiosis globally. Workers who engage in mining, construction, ceramics, and many other industries have a high risk of developing silicosis. Chronic and repeated inhalation of free silica (SiO2) dust (

Abstract Background Coal dust particles (CDP), an inevitable by-product of coal mining for the environment, mainly causes coal workers’ pneumoconiosis (CWP). Long-term exposure to coal dust leads to a complex alternation of biological processes during regeneration and repair in the healing lung. However, the cellular and complete molecular changes associated with pulmonary homeostasis caused by respiratory coal dust particles remain unclear. Methods This study mainly investigated the pulmonary toxicity of respirable-sized CDP in mice using unbiased single-cell RNA sequencing. CDP (< 5 μm) collected from the coal mine was analyzed by Scanning Electron Microscope (SEM) and Mass Spectrometer. In addition, western blotting, Elisa, QPCR was used to detect gene expression at mRNA or protein levels. Pathological analysis including HE staining, Masson staining, immunohistochemistry, and immunofluorescence staining were performed to characterize the structure and functional alternation in the pneumoconiosis mouse and verify the reliability of single-cell sequencing results. Results SEM image and Mass Spectrometer analysis showed that coal dust particles generated during coal mine production have been crushed and screened with a diameter of less than 5 µm and contained less than 10% silica. Alveolar structure and pulmonary microenvironment were destroyed, inflammatory and death (apoptosis, autophagy, and necrosis) pathways were activated, leading to pneumoconiosis in post 9 months coal dust stimulation. A distinct abnormally increased alveolar type 2 epithelial cell (AT2) were classified with a highly active state but reduced the antimicrobial-related protein expression of LYZ and Chia1 after CDP exposure. Beclin1, LC3B, LAMP2, TGF-ß, and MLPH were up-regulated induced by CDP, promoting autophagy and pulmonary fibrosis. A new subset of macrophages with M2-type polarization double expressed MLPH + /CD206 + was found in mice having pneumoconiosis but markedly decreased after the Vitamin D treatment. Activated MLPH + /CD206 + M2 macrophages secreted TGF-β1 and are sensitive to Vitamin D treatment. Conclusions This is the first study to reconstruct the pathologic progression and transcriptome pattern of coal pneumoconiosis in mice. Coal dust had obvious toxic effects on lung epithelial cells and macrophages and eventually induced pulmonary fibrosis. CDP-induced M2-type macrophages could be inhibited by VD, which may be related to the alleviation of the pulmonary fibrosis process.

Photodynamic therapy (PDT) as emerging phototherapy has attracted extensive attention in cancer therapy. However, the overexpressed glutathione (GSH) and hypoxic conditions of the tumor microenvironment (TME) sevely limit the therapeutic efficiency of PDT. Herein, we design a multifunctional nanoplatform (CBDM) for cancer therapy consisting of photosensitizer (Ce6), bovine serum albumin (BSA), and polydopamine-manganese dioxide (MnO2) nanocomplex, which is simultaneously modified by nucleolin-targeting AS1411 aptamer. This MnO2-based nanoplatform ameliorates tumor hypoxia and promotes oxygen production via the reaction between MnO2 and endogenous H2O2 and acid H+ in the TME. Besides, this biocompatibility nanoplatform exhibits an augmented PDT effect and high photothermal conversion efficiency under 808 nm laser irradiation. Importantly, the MnO2-based nanoplatform achieves a significant in vivo synergistic therapeutic effect and fights against liver metastasis of breast cancer. As a result, the excellent biocompatibility, especially the superior anticancer efficacy, and suppression of tumor metastasis make the MnO2-based nanoplatform a promising candidate for cancer therapy.

The combination of photothermal therapy with chemotherapy has gradually developed into promising cancer therapy. Here, a synergistic photothermal-chemotherapy nanoplatform based on polydopamine (PDA)-coated gold nanoparticles (AuNPs) were facilely achieved via the in situ polymerization of dopamine (DA) on the surface of AuNPs. This nanoplatform exhibited augmented photothermal conversion efficiency and enhanced colloidal stability in comparison with uncoated PDA shell AuNPs. The i-motif DNA nanostructure was assembled on PDA-coated AuNPs, which could be transformed into a C-quadruplex structure under an acidic environment, showing a characteristic pH response. The PDA shell served as a linker between the AuNPs and the i-motif DNA nanostructure. To enhance the specific cellular uptake, the AS1411 aptamer was introduced to the DNA nanostructure employed as a targeting ligand. In addition, Dox-loaded NPs (DAu@PDA-AS141) showed the pH/photothermal-responsive release of Dox. The photothermal effect of DAu@PDA-AS141 elicited excellent photothermal performance and efficient cancer cell inhibition under 808 nm near-infrared (NIR) irradiation. Overall, these results demonstrate that the DAu@PDA-AS141 nanoplatform shows great potential in synergistic photothermal-chemotherapy.

Silicosis is a diffuse fibrotic lung disease in which excessive inflammatory responses are triggered by silica exposure. Pyroptosis, a pro-inflammatory mode of programmed cell death, is mediated by gasdermin and may play a pivotal role in the development of silicosis. The caspase-1 inhibitor, VX-765, was used in vivo and in vitro to investigate the effects of silica-induced early inflammatory injury and later lung fibrosis. Our findings show that VX-765 reduces inflammatory lung injury by inhibiting silica-induced pyroptosis of alveolar macrophages in a silicosis mouse model. VX-765 limits the infiltration of inflammatory M1 alveolar macrophages, decreasing expression of inflammatory cytokines, including IL-1β, TNF-α, IL-6, CCL2, and CCL3, and down-regulating endogenous DAMPs and inflammatory immune-related cell pattern recognition receptors TLR4 and NLRP3. Furthermore, VX-765 alleviates fibrosis by down-regulating α-smooth muscle actin (α-SMA), collagen, and fibronectin. In this study, we illustrate that Alveolar macrophages pyroptosis occur in the early stages of silicosis, and VX-765 can alleviate the development of silicosis by inhibiting the pyroptosis signaling pathway. These results may provide new insight into the prevention and treatment of early-stage silicosis.

Colorectal cancer (CRC) is the third most common cancer in global incidence and second most common cancer in global mortality rates, accounting for 10% of all cancer cases and 9.4% of all cancer-related deaths. CRC is a heterogeneous disease, mostly comprising sporadic tumors. Approximately 19%–28% of patients have postoperative metastasis. In this study, we report an epigallocatechin gallate (EGCG)-based metal polyphenol network (MPN) with CD44 targeting, glutathione (GSH) sensitivity and pH response for the codelivery of the photosensitizers chlorin e6 (Ce6) and Fe3+. Photodynamic therapy (PDT) has become a potential clinical treatment method because of its noninvasive nature, low toxicity and spatiotemporally controlled treatment capability. Ferroptosis is a nonapoptotic cell death caused by peroxidative modification of phospholipid membranes via iron-dependent mechanisms. We unified ferroptosis and PDT into a nanoreactor (BSA-Ce6@MPN, BCM) to treat CRC. In vitro analysis showed that laser-irradiated BCM increased the cellular reactive oxygen species (ROS) and lipid peroxide (LPO) contents and decreased the expression levels of GSH and glutathione peroxidase 4 (GPX4). BCM-mediated ferroptosis and PDT synergistic therapy were significantly effective in the CT26 tumor-bearing mouse model, demonstrating the efficacy of the combination therapy. These results suggest that the nanoreactor for the synergistic treatment of ferroptosis and PDT holds great promise for clinical translation.

Long-term coal dust exposure triggers complex inflammatory processes in the coal workers’ pneumoconiosis (CWP) lungs. The progress of the inflammation is reported to be affected by disordered cell metabolism. However, the changes in the metabolic reprogramming associated with the pulmonary inflammation induced by the coal dust particles are unknown. Herein, we show that coal dust exposure causes glycogen accumulation and the reprogramming of glucose metabolism in the CWP lung. The glycogen accumulation caused by coal dust is mainly due to macrophages, which reprogram glycogen metabolism and trigger an inflammatory response. In addition, 2-deoxy-D-glucose (2-DG) reduced glycogen content in macrophages, which was accompanied by mitigated inflammation and restrained NF-κB activation. Accordingly, we have pinpointed a novel and crucial metabolic pathway that is an essential regulator of the inflammatory phenotype of coal dust-exposed macrophages. These results shed light on new ways to regulate CWP inflammation.

Background Coal workers’ pneumoconiosis (CWP) is an occupational disease that severely damages the life and health of miners. However, little is known about the molecular and cellular mechanisms changes associated with lung inflammation and fibrosis induced by coal dust. As a non-destructive technique for measuring biological tissue, confocal Raman spectroscopy provides accurate molecular fingerprints of label-free tissues and cells. Here, the progression of lung inflammation and fibrosis in a murine model of CWP was evaluated using confocal Raman spectroscopy. Methods A mouse model of CWP was constructed and biochemical analysis in lungs exposed to coal dust after 1 month (CWP-1M) and 3 months (CWP-3M) vs control tissues (NS) were used by confocal Raman spectroscopy. H&E, immunohistochemical and collagen staining were used to evaluate the histopathology alterations in the lung tissues. Results The CWP murine model was successfully constructed, and the mouse lung tissues showed progression of inflammation and fibrosis, accompanied by changes in NF-κB, p53, Bax, and Ki67. Meanwhile, significant differences in Raman bands were observed among the different groups, particularly changes at 1,248, 1,448, 1,572, and 746 cm−1. These changes were consistent with collagen, Ki67, and Bax levels in the CWP and NS groups. Conclusion Confocal Raman spectroscopy represented a novel approach to the identification of the biochemical changes in CWP lungs and provides potential biomarkers of inflammation and fibrosis.

The identification of reliable indicators in the tumor microenvironment (TME) is critical for tumor prognosis. Tumor associated macrophages (TAMs) are the major component of non-tumor stromal cells in TME and have increasingly been recognized as a predictive biomarker for lung adenocarcinoma (LUAD) prognosis. Here, we report the development of a prognosis model for LUAD using three immune-related genes (IRGs) detected in The Cancer Genome Atlas (TCGA) which potentially regulate TAMs in TME. In 497 LUAD patients, higher immune scores conferred better overall survival (OS). We identified 93 hub IRGs out of 234 for further prognostic significance. Among them, three IRGs (BTK, Cd1c, and S100P) were proved to be closely correlated to the prognosis of patients with LUAD. Moreover, the immune risk score (IRS) based on the gene expression level of the three IRGs was an independent prognostic factor for OS. Higher IRS predicted lower OS, higher mortality and worse tumor stage. With a good predictive ability [area under the ROC curve (AUC) in TCGA = 0.701, AUC in GEO = 0.722], the IRS contributed to a good risk stratification ability of the nomogram. Immunologically, the three IRGs were related to M1 macrophages and NK cell subsets in TME. Interestingly, by characterizing these immune components in situ we found that S100P is a driver for tumor cells to induce TAM migration and M2 polarization in the immunosuppressive tumor niche. We identified the key genes driving TAM migration and transformation and elucidated the immune landscape of LUAD. The data suggest that IRGs from TME have the potential to become indicators for estimating cancer prognosis and guiding individualized treatment.

Abstract Background: As an infectious disease closely related to Mycobacterium tuberculosis, autoimmunity, inflammation, environment and heredity, the relationship between the single nucleotide polymorphism of elongase 2 gene and the susceptibility to tuberculosis is still unknown. Methods: Between January 2016 and November 2018, a hospital-based case-control study was conducted. This epidemiological survey was conducted in both hospitals every three months. rs3798719, rs1570069, and rs2236212 in ELOVL2 gene were detected by Sanger sequencing. Results: Stratified by gender, the genotypes and allele frequencies of rs3798719, rs1570069 and rs2236212 showed significant differences between the two groups (χ2 = 6.987, P = 0.030), Genetic modeling showed that rs3798719 was statistically different in the overdominance model (χ2 = 4.784, OR = 1.414, 95% CI: 1.036-1.929, P < 0.05). The polymorphism of rs2236212 between male TB patients and healthy controls was statistically different in the dominance model. (χ2 = 4.192, OR = 0.507; 95% CI: 0.262-0.981, P < 0.05). Conclusion: The rs3798719 of ELOVL2 gene may be associated with susceptibility to TB in female population and the rs2236212 of ELOVL2 gene may be associated with TB incidence in male patients.

This study sought to evaluate the potential of mulched gravel to release nutrients in the field by conducting trials with three variations of wet-and-dry cycling of the soil beneath gravel mulch and bare soil. The results revealed that quartz, muscovite, clinochlore, and albite were the most abundant minerals in the gravels. Throughout the whole wet-and-dry cycle, the total content of 30 elements measured in the gravel-mulched soil was higher than in the bare soil treatment, and the content of the total element rose with increasing wet–dry cycle humidity. The enrichment ratio (Br) of each element in soil under gravel mulch relative to bare soil was in the sequence Mg > Ca > K > Cr > Na > Mn > V > Zn > Fe > Ti > Si > C > N > B> Co > (Br = 0) > Pb > Cu > Ga > P > Sn > Sr > Al > Be > Li > Mo > Ni > Se > As > S. Under gravel mulch, the elements impacted by the wet–dry cycle are primarily rock-forming, whereas the elements affected under bare soil are primarily trace elements. The wet-and-dry cycles of gravel affected soil nutrients mainly by increasing soil K, Ca, Na, and Mg contents. The differences in soil K and Ca contents significantly affected the growth of jujube trees and the jujube fruit yield. A dry/wet cycle level of 5 L/d per tree under gravel cover conditions can effectively improve soil nutrients and increase the jujube fruit yield without causing environmental problems.

Epigallocatechin Gallate (EGCG) is the main component of green tea which can strongly bind to proteins, small molecular drugs, and DNA. Therefore, EGCG can be used to deliver biomacromolecules and drugs. In this study, a doxorubicin (DOX) delivery system (FPE/DOX NPs) based on the folic acid-functionalized EGCG was developed for the targeting therapy of ovarian cancer. Cellular uptake studies showed that FPE/DOX NPs enhanced DOX uptake by SKOV3 cells compared with PE/DOX NPs that without folic acid modification. In vitro, the toxicity of FPE/DOX NPs to SKOV3 cells was stronger than nanoparticles without folic acid modification. In vivo, the SKOV3 tumor growth inhibition effect of FPE/DOX NPs was substantially more effective than other groups. Together, the results of this study suggested that FPE/DOX NPs may have promising applications in ovarian cancer therapy.

Accumulating evidence reveal that maternal smoking or perinatal nicotine replacement therapy impairs hippocampal neurogenesis, neural development, and cognitive behaviors in the offspring. Microglia is a source of non-neural regulation of neuronal development and postnatal neurogenesis. In this study, we explored the impact of nicotine on the microglia during the development of hippocampus. Developmental nicotine exposure in a mouse model was conducted by supplementing nicotine in the drinking water to mother mice during gestation and lactation period. We found that juvenile offspring with maternal nicotine exposure presented physical and neurobehavioral development delay and an increase in anxiety-like behavior in the open field test on postnatal day (PND) 20. To further detect possible developmental neurotoxic effects of nicotine in offspring and underlying mechanism, whole genome microarray analysis of the expression profile of the hippocampus was performed on postnatal day 20. Significant alterations in the expression of genes related to inflammatory, neurotransmitter, and synapsis were observed in the hippocampus after maternal nicotine exposure, as compared to the vehicle control. Concurrently, an increase in microglial markers and the presence of M2 polarity state in the hippocampus of the nicotine offspring were observed by histological analysis and confocal z-stacking scanning. The M2 microglial polarization state was further confirmed with in vitro primary microglia culture by cytokine array, and double-positive expression of BDNF/Iba1 in microglia by immunohistochemical staining in the juvenile offspring hippocampus was visualized. We also found that nicotine offspring showed an increase of neurite length in the molecular layer and CA1 by Tuj1 staining, as well as an increase in the expression of synapse associated protein, PSD95, but the expression of NeuroD1 in CA1 and CA3 reduced. In summary, maternal nicotine exposure dysregulates immune-related genes expression by skewing the polarity of M2 microglia in the hippocampus, which may cause abnormal cognitive and behavioral performance in the offspring.

Objective To search for evidence of the relationship between occupational silica exposure and heart disease.Design A systematic review and meta-analysis.Background Growing evidence suggests a relationship between occupational silica exposure and heart disease; however, the link between them is less clear.Data sources PubMed, ScienceDirect, Springer and EMBASE were searched for articles published between 1 January 1995 and 20 June 2019. Articles that investigated the effects of occupational silica exposure on the risk of heart disease were considered.Study selection We included cohort studies, including prospective, retrospective and retroprospective studies.Data extraction and synthesis We extracted data using a piloted data collection form and conducted random-effects meta-analysis and exposure-response analysis. The meta-relative risk (meta-RR), a measure of the average ratio of heart disease rates in those with and without silica exposure, was used as an inverse variance-weighted average of relative risks from the individual studies. The Newcastle-Ottawa Quality Assessment Scale for cohort studies was used for study quality assessment.Outcome measure We calculated the risk of heart diseases such as pulmonary heart disease, ischaemic heart disease and others.Results Twenty cohort studies were included. The results suggest a significant increase in the risk of overall heart disease (meta-RR=1.08, 95% CI 1.03 to 1.13). Stronger evidence of association with pulmonary heart disease was found in the risk estimate of both categories of heart disease (meta-RR=1.24, 95% CI 1.08 to 1.43) and in the exposure-response analysis (meta-RR=1.39, 95% CI 1.19 to 1.62). Our subgroup analyses also revealed that the statistical heterogeneity among studies could be attributed mainly to the diversity in reference group, occupation and study quality score.Conclusions Silica-exposed workers are at an increased risk for overall heart disease, especially pulmonary heart disease. Further research is needed to better clarify the relationship between occupational silica exposure and ischaemic heart disease.PROSPERO registration number CRD42019124673.

Background: Dietary patterns analysis may provide insights into the influence of overall diet on overweight/obesity. In the past two decades, the relation between dietary patterns and overweight/obesity has been a research focus and a number of results were reported in the research field. Methods: An electronic literature search was conducted in PubMed and Web of Science, to identify human studies published by Mar 2015 and written in English. The following keywords or phrases were involved: dietary patterns, dietary pattern, factor analysis, principal component analysis, diet, obesity, adiposity, overweight and BMI. All the studies were retrieved and prudent/healthy (n=17) and western/unhealthy (n=18) dietary patterns were identified. Results: When compared with the lowest categories of a prudent/healthy dietary pattern, a reduced overweight/obesity risk was shown in the highest (OR=0.64; 95% CI: 0.52, 0.78; P

Recent researches on long noncoding RNAs (lncRNAs) have expanded our horizon of gene regulation and the cellular complexity. However, the number, characteristics and expression patterns of lncRNAs remain poorly characterized and how these lncRNAs biogenesis are regulated in response to drought stress in cotton are still largely unclear. In the study, using a reproducibility-based RNA-sequencing and bioinformatics strategy to analyze the lncRNAs of 9 samples under three different environment stresses (control, drought stress and re-watering, three replications), we totally identified 10,820 lncRNAs of high-confidence through five strict steps filtration, of which 9,989 were lincRNAs, 153 were inronic lncRNAs, 678 were anti-sense lncRNAs. Coding function analysis showed 6,470 lncRNAs may have the ability to code proteins. Small RNAs precursor analysis revealed that 196 lncRNAs may be the precursors to small RNAs, most of which (35.7%, 70) were miRNAs. Expression patterns analysis showed that most of lncRNAs were expressed at a low level and most inronic lncRNAs (75.95%) had a consistent expression pattern with their adjacent protein-coding genes. Further analysis of transcriptome data uncovered that lncRNAs XLOC_063105 and XLOC_115463 probably function in regulating two adjacent coding genes CotAD_37096 and CotAD_12502, respectively. Investigations of the content of plant hormones and proteomics analysis under drought stress also complemented the prediction. We analyzed the characteristics and the expression patterns of lncRNAs under drought stress and re-watering treatment, and found lncRNAs may be likely to involve in regulating plant hormones pathway in response to drought stress.

Reactive oxygen species (ROS)-mediated immunogenic cell death (ICD) is crucial in radioimmunotherapy by boosting innate antitumor immunity. However, the hypoxic tumor microenvironment (TME) often impedes ROS production, limiting the efficacy of radiotherapy. To tackle this challenge, a combination therapy involving radiotherapy and immune checkpoint blockade (ICB) with anti-programmed death-ligand 1 (PD-L1) has been explored to enhance antitumor effects and reprogram the immunosuppressive TME. Here, we introduce a novel PD-L1 aptamer-functionalized nanoradiosensitizer designed to augment radiotherapy by increasing X-ray deposition specifically at the tumor site. This innovative X-ray-activated nanoradiosensitizer, comprising gold-MnO2 nanoflowers, efficiently enhances ROS generation under single low-dose radiation and repolarizes M2-like macrophages, thereby boosting antitumor immunity. Additionally, the ICB inhibitor BMS-202 synergizes with the PD-L1 aptamer-assisted nanoradiosensitizer to block the PD-L1 receptor, promoting T cell activation. Furthermore, this nanoradiosensitizer exhibits exceptional photothermal conversion efficiency, amplifying the ICD effect. The PD-L1-targeted nanoradiosensitizer effectively inhibits primary tumor growth and eliminates distant tumors, underscoring the potential of this strategy in optimizing both radioimmunotherapy and photothermal therapy. [ABSTRACT FROM AUTHOR]