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Yi-Sheng He,1,2,* Gui-Hong Wang,3,* Qian Wu,1,2,* Zheng-Dong Wu,1,2 Yue Chen,1,2 Jin-Hui Tao,4 Xin-Yu Fang,1,2 Zhiwei Xu,5 Hai-Feng Pan1,2 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, People’s Republic of China; 2Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, Anhui, People’s Republic of China; 3Department of Rheumatology, Anqing Hospital Affiliated to Anhui Medical University, Anqing, Anhui, People’s Republic of China; 4Department of Rheumatology and Immunology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, People’s Republic of China; 5School of Public Health, Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia*These authors contributed equally to this workCorrespondence: Zhiwei Xu; Hai-Feng Pan Email xzw1011@gmail.com; panhaifeng1982@sina.comObjective: Gout is a chronic disease caused by the deposition of sodium urate (MSU) crystals. Available data on the association between environmental hazards and gout are scarce. The present study was present to investigate the relationship between short-term exposure to air pollution and hospitalizations for acute gout from 2016 to 2020 in Anqing City, China.Methods: Daily records of hospital admissions for acute gout in Anqing from 1 January 2016 to 31 December 2020 were retrieved from the tertiary first-class hospitals in Anqing. Air pollutants and meteorological data were obtained from the China Environmental Monitoring Station and China Meteorological Data Service Center respectively. We used a time-series analysis to explore the association between air pollution (NO2, O3, and CO) and hospitalizations for acute gout, and conducted stratified analyses by gender, age and season.Results: We observed an association between NO2 and hospitalizations for gout (lag 0, relative risk (RR):1.022, 95% confidence interval (CI):1.004– 1.041). For every 1 mg/m3 increase in CO concentration, hospitalizations for gout increased by 3.9% (lag 11 days, RR=1.039, 95% CI: 1.004– 1.076). Intriguingly, there was a negative association between O3 and hospitalizations for gout (lag0, RR=0.986, 95% CI: 0.976– 0.996). Stratified analyses showed that exposure to high levels of NO2 was considered to be more vulnerable to gout in cold season.Conclusion: Our study showed that short-term exposure to NO2 and CO has a significant effect on hospitalizations for acute gout.Keywords: gout, air pollutants, carbon monoxide, nitrogen dioxide, ozone

Previous studies have found that non-optimal temperature influences the development of gout, but the results have been inconsistent. The present study aimed to explore the effects of high temperature and high temperature variation on hospitalizations for gout in Anqing, China. We collected daily data on air pollutants, meteorological factors, and hospitalizations for gout between 1January 2016 and 31 December 2020 in Anqing City, China. We used Poisson generalized linear regression model and a distributed lag non-linear model (DLNM) to explore the relationship of high temperature, diurnal temperature range (DTR), and temperature change between neighboring days (TCN) with hospitalizations for gout. Stratified analysis by gender (male, female) and age (

Chronic kidney disease (CKD), a global disease burden related to high rates of incidence and mortality, manifests as progressive and irretrievable nephron loss and decreased kidney regeneration capacity. Emerging studies have suggested that exposure to air pollution is closely relevant to increased risk of CKD, CKD progression and end-stage kidney disease (ESKD). Inhaled airborne particles may cause vascular injury, intraglomerular hypertension, or glomerulosclerosis through non-hemodynamic and hemodynamic factors with multiple complex interactions. The mechanisms linking air pollutants exposure to CKD include elevated blood pressure, worsening oxidative stress and inflammatory response, DNA damage and abnormal metabolic changes to aggravate kidney damage. In the present review, we will discuss the epidemiologic observations linking air pollutants exposure to the incidence and progression of CKD. Then, we elaborate the potential roles of several air pollutants including particulate matter and gaseous co-pollutants, environmental tobacco smoke, and gaseous heavy metals in its pathogenesis. Finally, this review outlines the latent effect of air pollution in ESKD patients undergoing dialysis or renal transplant, kidney cancer and other kidney diseases. The information obtained may be beneficial for further elucidating the pathogenesis of CKD and making proper preventive strategies for this disease.

Cooking is one of the main sources of indoor air pollution in China. Given emerging evidence of a link between air pollutants and neurodevelopmental delays, we examined whether maternal experiences with cooking during gestation might increase their child's hyperactivity at 3 years of age. The participants involved 45 518 mothers of children who were newly enrolled at kindergarten in the Longhua District of Shenzhen from 2015 to 2017. The results show that maternal exposure to cooking fumes during pregnancy was related to an increased risk of their offspring having hyperactivity behaviors at the age of 3 years. Compared with pregnant mothers who never cooked, pregnant mothers who cooked sometimes, often, or always had children who showed a significantly higher hyperactivity risk. Households using cooking fuels such as coal, gas during the mothers’ pregnancy, exhibited more hyperactivity behaviors in the young child when compared to those using electricity for cooking. In addition, poor ventilation during cooking, while mothers were pregnant, was found to be a significant risk factor for clinical levels of the offspring's hyperactive behaviors. Furthermore, the positive association with maternal cooking during pregnancy and their offsprings’ hyperactivity was relatively consistent across strata defined by social class, education, and other covariates.

Previous studies investigating the association between 5,10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and colon cancer risk have generated conflicting results. The aim of our meta-analysis was to clarify the precise association. A systematic literature search was conducted to identify all relevant studies. Pooled odds ratio (ORs) with 95% confidence interval (CI) were used to estimate the strength of the association. In this meta-analysis, a total of 13 articles, involving 5,386 cases and 8,017 controls met the inclusion criteria. Overall, a significant association was found between colon cancer risk and the MTHFR C667 polymorphism (TT vs CC+CT: OR=0.79; 95%CI=0.65-0.96; p=0.017). Stratification by ethnicity revealed that MTHFRC667 was associated with colon cancer risk in the non-Asian group (TT vs CC+CT:OR=0.77, 95%CI=0.68-0.89, p=0.000; TT vs CC: OR=0.84, 95%CI=0.73-0.97, p=0.016). Stratification by source of control indicated that MTHFR C667 also correlated with colon cancer risk in the population-based subgroup (TT vs CC: OR=0.85, 95%CI=0.74-0.97, p=0.017; TT vs CC+CT: OR=0.78, 95%CI=0.68-0.89, p=0.000) and hospital-based subgroup (TT vs CC+CT: OR=0.65, 95%CI=0.49-0.86, p=0.003). However, risk was significantly increased for MTHFR A1298C polymorphisms and colon cancer risk in hospital-based studies (C vs A: OR=1.52, 95%CI=1.26-1.83, p=0.000; CC+AC vs AA: OR=1.93, 95%CI=1.47-2.49, p=0.000) but reduced in population-based studies (CC vs AA: OR=0.83, 95%CI=0.70-0.99, p=0.042). In conclusion, the results of our meta-analysis suggest that the MTHFR C667 polymorphism is associated with reduced colon cancer risk, especially for non-Asian populations.

Background Prenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of ADHD or ADHD-like behaviors. But we still lack a comprehensive assessment of household air pollutants exposure on the development of ADHD-like behaviors during childhood. Object We aimed to assess whether prenatal household inhalants exposure is associated with preschoolers’ ADHD-like behaviors in a nonclinical population. Methods This study used the baseline data of the Longhua Child Cohort Study. During 2015–2017, we recruited 42,983 mothers and their kindergarten-aged children who enrolled at kindergarten in the Longhua district of Shenzhen, to obtain the demographic data and relevant exposure information through self-administrated questionnaire survey. The source of prenatal household inhalants exposure include cooking fumes, environmental tobacco smoke, mosqutio coils, home renovated and indoor burning incense. Logistic and censored least absolute deviations (CLAD) models were used to reveal the association between prenatal exposure to household air pollutants and hyperactive behaviors in child. Results We found that exposure to five types of household inhalants during pregnancy were independently associated with an increased risk of child hyperactive behaviors. Moreover, we observed a significant interaction between exposure to environmental tobacco smoke and cooking fumes during gestation on child hyperactive behaviors in CLAD models. We also found a significant joint effect between burning mosquito coils and incense during gestation for child hyperactive behaviors risk both in CLAD and Logistic models. Furthermore, a household inhalants exposure index was used to demonstrate a dose-response relationship between the cumulative effect of exposure to the five household air pollutants and child hyperactivity. Conclusions Our results suggest that prenatal exposure to different household inhalants might increase the risk of children's hyperactive behaviors at around 3 years of age with the presence of interaction effects between some inhalants.

Systemic lupus erythematosus (SLE) is complex autoimmune disease which involves various facets of the immune system. Signaling transducers and activators of transcription 1 (STAT1) belongs to the family of STAT transcription factors that mediate various biological responses. Recently, studies in both experimental animal models of lupus and patients with SLE have revealed expression and activation of STAT1 is closely associated with the pathogenesis of SLE. Moreover, increased production of interferons (IFNs) and aberrant activation of IFNs signaling, which is mechanistically linked to increased level of STAT1, are crucial for the development of SLE. Therefore, we will focus on the association of STAT1 and SLE based on recent understandings to render more information about the mechanisms of STAT1 might perform in. Hopefully, the information obtained will lead to a better understanding of the development and pathogenesis of systemic autoimmune diseases, as well as its clinical implications and therapeutic potential.

Brachial plexus injury (BPI) often involves the complete or partial avulsion of one or more of the cervical nerve roots, which leads to permanent paralysis of the innervated muscles. Reimplantation surgery has been attempted as a clinical treatment for brachial plexus root avulsion but has failed to achieve complete functional recovery. Lithium is a mood stabilizer drug that is used to treat bipolar disorder; however, its effects on spinal cord or peripheral nerve injuries have also been reported. The purpose of this study was to investigate whether lithium can improve functional motor recovery after ventral root avulsion and reimplantation in a rat model of BPI. The results showed that systemic treatment with a clinical dose of lithium promoted motor neuron outgrowth and increased the efficiency of motor unit regeneration through enhanced remyelination. An analysis of myelin-associated genes showed that the effects of lithium started during the early phase of remyelination and persisted through the late stage of the process. Efficient remyelination of the regenerated axons in the lithium-treated rats led to an earlier functional recovery. Therefore, we demonstrated that lithium might be a potential clinical treatment for BPI in combination with reimplantation surgery.

Rheumatoid arthritis (RA) is a chronic, destructive inflammatory autoimmune disease. Cytokine-mediated immunity has been found to play an important role in the pathogenesis of autoimmune diseases including RA. Recently, much attention has been paid on the role of IL-15, which is a member of the 4 α-helix bundle cytokine family. IL-15 was detected in serum and synovial fluid from RA patients and arthritis mice models. Moreover, administration of IL-15 leads to the development of severe inflammatory arthritis, suggesting that IL-15 may be therapeutically relevant in RA. Therefore, targeting IL-15 may be significantly important and valuable. In this article, we discuss the biological features and effects of IL-15 and summarize recent advances on the pathological roles of IL-15 in RA and treatment for RA.

E2F1 is a transcriptional activator, which binds to DNA, and regulates the expression of genes involved in the cell cycle progression. Many elegant studies have revealed that E2F1 plays a crucial role in regulating the apoptosis process of DC and T cells. In addition, the pathogenesis of SLE involves marked immune dysfunction, and in particular, the function of immunosuppressive elements of the immune system is impaired, including regulatory T cell function and DC. Thus, therapeutic agents targeting E2F1 might result in important innovative therapies for SLE.