Microplastics are plastic fibers, particles, or films with a particle size of less than 5 mm. They are widely found in water, soil, and atmospheric environments. Because of their small particle size, large surface area, strong adsorptive capacity and other characteristics, they can adsorb heavy metals, persistent organic pollutants, environmental endocrine disruptors and other substances. When humans are exposed to microplastics, the particles can not only have toxic effects on the contact sites, but also penetrate tissue barriers and acess other organs, potentially causing systemic toxic effects. Existing epidemiological and toxicological studies have shown that microplastics can cause damage to the digestive, respiratory, nervous and reproductive systems. However, their bio-distribution, metabolic characteristics and toxic mechanisms have not been fully clarified. This study provides a systematic review of the absorption, distribution, metabolism and excretion characteristics of microplastics in living organisms. By integrating factors such as particle size and chemical composition, this study also investigates the toxic effects of microplastics on multiple organ systems (e.g., digestive and nervous systems) and key organs (e.g., intestine and liver), as well as the underlying molecular mechanisms. The aim is to provide a scientific basis for a comprehensive assessment of the health risks of microplastics and to offer theoretical support for the development of relevant prevention and control strategies.

The adverse effects of fine particulate matter (PM 2.5) on human health have become a major global public health concern. Pregnant women and fetuses, as susceptible populations, are more vulnerable to the threat of PM 2.5 pollution. Increasing studies indicate that PM 2.5 exposure is an important risk factor of fetal growth restriction (FGR), and oxidative stress, inflammatory response, endocrine disorders, epigenetic modifications, autophagic abnormalities, and gut microbiota dysbiosis may be the biological mechanisms underlying PM 2.5-induced FGR. This study offers insights for the development of targeted preventive and therapeutic methods for FGR caused by PM 2.5.

The adverse effects of fine particulate matter (PM 2.5) on human health have become a major global public health concern. Pregnant women and fetuses, as susceptible populations, are more vulnerable to the threat of PM 2.5 pollution. Increasing studies indicate that PM 2.5 exposure is an important risk factor of fetal growth restriction (FGR), and oxidative stress, inflammatory response, endocrine disorders, epigenetic modifications, autophagic abnormalities, and gut microbiota dysbiosis may be the biological mechanisms underlying PM 2.5-induced FGR. This study offers insights for the development of targeted preventive and therapeutic methods for FGR caused by PM 2.5.

Objective:To analyze the differentially expressed genes and related functional pathways of mouse sciatic nerves of Schwann cells(SCs)in early in vitro Wallerian degeneration(WD).Methods:The sciatic nerves of adult male C57BL/6J mice were Wallerian degeneration in vitro,and total RNA was extracted and transcriptome sequencing was performed at 3 h and 6 h after degeneration,respectively.The differentially expressed genes(DEGs),gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment were analyzed by bioinformatics.Results:Compared with the Control group,3961 and 5538 DEGs were screened in the WD 3 h group(WD3h)and the 6 h group(WD6h)of in vitro,respectively.The most significantly up-regulated genes mainly included molecules related to inflammation and immunity and neurotrophic factors.GO analysis showed that DEGs in both groups were enriched in positive transcriptional regulation and metabolic processes.KEGG pathway enrichment analysis revealed that DEGs were mainly concentrated in TNF signaling pathway,MAPK signaling pathway and ribosome production.Conclusion:At the early stage of WD,SCs up-regulates the genes related to inflammation and immunity to promote the progression of WD and secrete neurotrophic factors to support the survival of neurons,accompanied by the activation of TNF signaling path-way and MAPK signaling pathway.

Objective:To analyze the differentially expressed genes and related functional pathways of mouse sciatic nerves of Schwann cells(SCs)in early in vitro Wallerian degeneration(WD).Methods:The sciatic nerves of adult male C57BL/6J mice were Wallerian degeneration in vitro,and total RNA was extracted and transcriptome sequencing was performed at 3 h and 6 h after degeneration,respectively.The differentially expressed genes(DEGs),gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment were analyzed by bioinformatics.Results:Compared with the Control group,3961 and 5538 DEGs were screened in the WD 3 h group(WD3h)and the 6 h group(WD6h)of in vitro,respectively.The most significantly up-regulated genes mainly included molecules related to inflammation and immunity and neurotrophic factors.GO analysis showed that DEGs in both groups were enriched in positive transcriptional regulation and metabolic processes.KEGG pathway enrichment analysis revealed that DEGs were mainly concentrated in TNF signaling pathway,MAPK signaling pathway and ribosome production.Conclusion:At the early stage of WD,SCs up-regulates the genes related to inflammation and immunity to promote the progression of WD and secrete neurotrophic factors to support the survival of neurons,accompanied by the activation of TNF signaling path-way and MAPK signaling pathway.

Fine particulate matter (PM_2.5) is a critical environmental factor that currently affects human health. It primarily enters the body through inhalation and can induce adverse health effects in multiple systems, including respiratory, cardiovascular, nervous, and digestive systems. The homeostasis of gut microbiota is crucial for human health, and gut microbiota may exert multiple effects through the regulation of immune function, metabolic balance, and neural signal transmission. Recently, more and more studies have indicated that exposure to PM_2.5 may alter the composition and richness of gut microbiota and play a crucial role in the development and progression of various diseases through multiple pathways. Given the close interaction between PM_2.5 exposure and gut microbiota, we comprehensively reviewed the effects of ambient PM_2.5 exposure on gut microbiota and the potential underlying mechanisms based on existing epidemiological and toxicological studies. Additionally, the role of gut microbiota in the adverse health effects induced by PM_2.5 exposure, particularly in the context of gut-lung, gut-brain and gut-liver axis were also explored here.

Air pollution is a global issue that threatens human health. In recent years, more and more studies have found that air pollution is closely related to the occurrence of depression. As a serious neuropsychiatric disorder whose incidence is rising rapidly year by year, depression has become an invisible killer of public health. At present, studies on the correlation between air pollution and depression are still very limited, and the underlying molecular mechanisms by which air pollution affects depression are not clear. Based on existing epidemiological and toxicological studies, this paper provided a review of the relationship between air pollution and depression and the possible biological mechanisms, with a focus on the relationship between air pollution and depression indicators and the possible factors affecting depression such as types of air pollutants, exposure time, age and health status of study subjects. In addition, the potential roles of neuroinflammation, oxidative stress, neurogenesis, and apoptosis in the process of air pollution-induced depression were also discussed in order to provide a scientific basis for the prevention and treatment of air pollution-induced depression.

Near-surface ozone is a profoundly reactive and highly oxidizing gas and one of the critical respiratory toxicants. Numerous epidemiological investigations have indicated that asthmatic individuals are the vulnerable group of ozone exposure， and there is a strong correlation between ozone exposure and asthma morbidity and mortality rates. The potential mechanisms include oxidative stress， inflammatory response， autonomic nerve impairment， and immune dysfunction. The present study summarized and discussed the effect of ozone exposure on asthma and its underlying biological mechanisms in order to galvanize public cognizance concerning the perils of ozone pollution and serve as a reference for future research on ozone exposure and asthma.

Temporomandibular joint (TMJ) diseases are common clinical conditions. The number of patients with TMJ diseases is large, and the etiology, epidemiology, disease spectrum, and treatment of the disease remain controversial and unknown. To understand and master the current situation of the occurrence, development and prevention of TMJ diseases, as well as to identify the patterns in etiology, incidence, drug sensitivity, and prognosis is crucial for alleviating patients′suffering.This will facilitate in-depth medical research, effective disease prevention measures, and the formulation of corresponding health policies. Cohort construction and research has an irreplaceable role in precise disease prevention and significant improvement in diagnosis and treatment levels. Large-scale cohort studies are needed to explore the relationship between potential risk factors and outcomes of TMJ diseases, and to observe disease prognoses through long-term follw-ups. The consensus aims to establish a standard conceptual frame work for a cohort study on patients with TMJ disease while providing ideas for cohort data standards to this condition. TMJ disease cohort data consists of both common data standards applicable to all specific disease cohorts as well as disease-specific data standards. Common data were available for each specific disease cohort. By integrating different cohort research resources, standard problems or study variables can be unified. Long-term follow-up can be performed using consistent definitions and criteria across different projects for better core data collection. It is hoped that this consensus will be facilitate the development cohort studies of TMJ diseases.

OBJECTIVE To investigate the effects of erianin （ERI） on the apoptosis of ovarian granulosa cells in rats with polycystic ovary syndrome （PCOS） and its mechanism. METHODS PCOS rat model was constructed by subcutaneous injection of dehydroepiandrosterone， and the successfully constructed rats were randomly divided into PCOS group， ERI low-dose， medium- dose and high-dose groups （10， 20， 40 mg/kg） and ERI high dose + verteporfin group （40 mg/kg ERI + 10 mg/kg verteporfin）， with 10 rats in each group. Another 10 normal rats were selected as the normal group. Rats in each administration group were given corresponding dose of ERI and/or intraperitoneal injection of vitiporfin， and rats in the PCOS group and normal group were orally administered an equal volume of 1% dimethyl sulfoxide， once a day， for 6 consecutive weeks. After administration， the body weight， fasting blood glucose （FPG）， serum levels of estradiol （E2）， testosterone （T）， follicle stimulating hormone （FSH） and luteinizing hormone （LH） were detected in each group； morphological changes in ovarian tissue were observed， and the apoptosis of ovarian tissue cells was analyzed. Apoptosis-associated proteins [B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， Caspase-3] and Hippo-YAP signaling pathway associated proteins [large tumor suppressor kinase 1 （LATS1）， phosphorylated LATS1 （p-LATS1） and Yes associated protein （YAP）， phosphorylated YAP （p-YAP）， transcriptional co-activator with PDZ binding motif （TAZ）] were detected in ovarian tissue. RESULTS Compared with PCOS group， the ovarian polycystic characteristics of the ERI low-dose， medium-dose，and high-dose groups were reduced， the number of atretic follicles was reduced， and the granulosa cell layer was thickened； the body mass， FPG， T， LH， LH/FSH， the number of cystic follicles， cell apoptosis index， protein expressions of Bax， Caspase-3， p-LATS1 and p-YAP were greatly decreased （P＜0.05）； the number of corpus luteum， protein expressions of E2， Bcl-2， LATS1， YAP and TAZ were greatly increased （P＜0.05）. Compared with ERI high-dose group， the above indexes in ERI high-dose + vitiporfin group were inhibited （P＜0.05）. CONCLUSIONS ERI can promote the proliferation of ovarian granulosa cells and improve the level of sex hormones in PCOS rats， and its mechanism of action may be related to the inhibition of the Hippo-YAP signaling pathway.