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Growing evidence indicates that nickle and its compounds have adverse effects on the cardiovascular system. In this study, the cytotoxic insults caused by nickel sulfate (NiSO

Indoor air pollution (IAP) is one of the leading risk factors for various adverse health outcomes including premature deaths globally. Even though research related to IAP has been carried out, bibliometric studies with particular emphasis on this topic have been lacking. Here, we investigated IAP research from 1990 to 2019 retrieved from the Web of Science database through a comprehensive and systematic scientometric analysis using the CiteSpace 5.7.R2, a powerful tool for visualizing structural, temporal patterns and trends of a scientific field. There was an exponential increase in publications, however, with a stark difference between developed and developing countries. The journals publishing IAP related research had multiple disciplines; 'Indoor Air' journal that focuses solely on IAP issues ranked fifth among top-cited journals. The terms like 'global burden', 'comparative risk assessment,' 'household air pollution (HAP)', 'ventilation', 'respiratory health', 'emission factor', 'impact,' 'energy', 'household', 'India' were the current topical subject where author Kirk R. Smith was identified with a significant contribution. Research related to rural, fossil-fuel toxicity, IAP, and exposure-assessment had the highest citation burst signifying the particular attention of scientific communities to these subjects. Overall, this study examined the evolution of IAP research, identified the gaps and provided future research directions.

The aim of this study is to identify the role of Tet1-mediated DNA demethylation in the neurotoxicity caused by unconjugated bilirubin (UCB) in vitro. Primary neuronal cells after cultured for 72 h were exposed to UCB (0-100 μmol/L) for 24 h. Following exposure to UCB cytotoxicity was determined with the methyl tetrazolium (MTT) assay, reactive oxygen species (ROS) and caspase-3 activity in neuron cells were measured with the corresponding assay kits. The expression of Tet1 and Klotho was determined with RT-PCR at mRNA level and western blot at protein level. Our results showed that UCB can cause time-dependent and dose-dependent reduction of cell viability of neuronal cells, induce oxidative stress through increasing the production of ROS and increase caspase-3 activity. Quantitative real-time PCR and western blot analysis showed that UCB can inhibit Tet1 and Klotho expression in cultured neuronal cells at both the mRNA and protein level, respectively. These results are first to suggest UCB may, in part, exert its neurotoxicity through alteration of the neuronal antioxidant status and inhibition of Klotho and Tet1 gene expression. The elevation of DNA methylation in global genome through inhibition of Tet1 gene expression may, in part, play an important role in the neurotoxicity caused by UCB in vitro.

Background Hypertension is the leading risk factor for cardiovascular disease (CVD), however, the studies on lifestyle and genetic risks in Chinese pilgrims to Hajj was limited. The aim of this study is to examine the prevalence and associated lifestyle and genetic risks for hypertension among Hui Hajj pilgrims in China. Methods We performed a cross-sectional analysis of data in 1,465 participants aged 30–70 years who participated in a medical examination for Hui Hajj pilgrims from Gansu province, China in 2017. Multiple logistic regression was used to evaluate the association of potential risk factors with hypertension. Deoxyribonucleic acid (DNA) polymorphism was examined at sites in the renin-angiotensin-aldosterone system (RAAS). Results The prevalence of hypertension was 47% among this population. Lifestyle factors such as fried food preference (like vs. dislike: odds ratio [OR]: =1.53, 95% confidence interval [CI]: 1.13–2.09) and barbecued food preference (like vs. dislike: OR = 1.45, 95% CI: 1.06–1.97) were associated with elevated risk of hypertension among Hui pilgrims. Comparing with Angiotensin converting enzyme (ACE) rs4425 AA genotype, TT genotype was associated with hypertension risk (OR = 2.16, 95% CI: 1.17–4.00). Similar results were also observed for ACE rs4437 CC genotype (OR = 1.95, 95% CI: 1.07–3.55), Angiotensin II receptor (ATR) rs129876 AA genotype (OR = 4.10, 95% CI: 2.30–7.32) and Aldosterone synthase (CYP11B2) rs1912 TT genotype (OR = 2.82, 95% CI: 1.57–5.06) genotypes. Conclusions Unhealthy lifestyle and genetic factors were associated with the prevalence of hypertension in Chinese Hui pilgrims and their interactions were also observed. Electronic supplementary material The online version of this article (10.1186/s12889-019-7357-1) contains supplementary material, which is available to authorized users.

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There is an urgent need to identify the potential risk factors for activating latent Mycobacterium tuberculosis infection. In this study, we evaluated the immune function of Rv1737c, which is a latency-associated antigen of dormancy survival regulator (DosR) of M. tuberculosis in a mouse model. Our data showed that mice pretreated with recombinant Rv1737c (rRv1737c) exhibited higher levels of antigen-specific antibodies (IgG, IgM and IgA) than sham-treated mice. Following Bacilli Calmette-Guerin (BCG) challenge, rRv1737c adjuvanted with cholera toxin subunit B (CTB) induced diffuse lung inflammation and fibrosis compared to the control mice. The inflammatory pathogenesis due to rRv1737c pre-exposure was associated with a switch in the macrophage phenotype from M1 to activated M2 and was characterized by IL-10 production. Intracellular cytokine analysis further showed that the rRv1737c-pretreated mice exhibited an increased frequency of Th2 cells in the lungs, lymph nodes and spleen after BCG challenge. Furthermore, IFN-γ expression increased in the lungs after rRv1737c pretreatment compared to that in the sham mice. Accordingly, lung cells from rRv1737c-immunized mice stimulated with killed BCG produced higher levels of multiple cytokines, such as IFN-γ, IL-10 and IL-6. The results confirmed that the pathological features of rRv1737c promoted inflammation. Overall, our findings provide direct evidence of the pro-inflammatory function of rRv1737c in a murine model of BCG infection, indicating that Rv1737c is a pathogenic antigen of M. tuberculosis and may be key to the recurrence of latent infection.

Latent Mycobacterium tuberculosis (Mtb) infection (LTBI) is the main clinical manifestation after Mtb exposure. During the latent phase, Mtb retards the attempts of eradication by the host immune system. The dormancy survival regulator (DosR) is held as essential for Mtb persistence. Rv1737c is predominantly expressed by the Mtb in latent infection. However, the role of Rv1737c in the immune evasion is still largely unknown. In this study, we have characterized the Rv1737c functions in the recruitment and activation of macrophages, which play a cardinal role in the innate and adaptive immunity. For the first time, we have revealed that Rv1737c induced the tolerogenic phenotype of macrophages by upregulating the expression of indoleamine 2,3-dioxygenase 1 (IDO1). Rv1737c-activated macrophages upregulated interleukin (IL)-4, IL-10, and Foxp3 T cells proliferation in vitro. Furthermore, the interaction of Rv1737c with macrophages was found to depend on the Toll-like receptor 2 (TLR2) pathway. It augmented nuclear factor κB (NF-κB) phosphorylation and co-stimulatory molecule expression. Thus, this study provides a crucial insight into a strategy adopted by Mtb to survive in the host by inducing tolerogenic macrophage expansion.

In order to explore the effect of genetic polymorphism of CYP450 2El among the Tibetan population in Qinghai and its relationship to drinking behavior.By the self-reported questionnaires of 325 Tibetan male who contain 193 drinkers and 132 non-drinkers, we analyzed the relationship between drinking behavior and the genetic polymorphism of CYP450 2El by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. So does the 266 Han nationalism.Single variable analysis showed the drinking prevalence was related to occupation, educational status, economic income, marital status and smoking (P0.05). There were no statistical significant differences of genotypes and alleles between male Tibetan and Han population (P0.05). The three genotypes (cl/cl, cl/c2, c2/c2) and the two alleles (cl, c2) of CYP450 2El had statistical significant differences (P0.05) between drinkers and non-drinkers in Tibetan population, and the drinkers had higher frequencies of cl/c2 genotype and c2 allele than that of the opposite group. Compared with safe drinkers, the frequency of c2 allele in the group of dangerous was higher. The related degree of drinking behavior and amount with c2 allele were 0.17 and 0.20. The multivariate statistical analysis showed that CYP450 2E1, incomes and smoking were independent.CYP450 2E1 is the mostly influence factor to drinking behavior in male Tibetan population.

To investigate the genetic polymorphism of ADH3 and ALDH2 among Tibetan population in Qinghai and its relationship with drinking behavior.Polymerase chain reaction-restriction fragment length polymorphism ( PCR-RFLP ) technique was used to detect the genotype of ADH3 and ALDH2. Drinking behavior was obtained by questionnaire.The frequency of ADH3*2 and ALDH2*2 alleles in Tibetan population was 7.79% and 22.21% respectively, the frequency of ALDH2*2 and ADH3*1 alleles in non-drinkers was higher than that in drinkers, and the frequency of ALDH2*2 and ADH3*1 alleles in risk drinkers was lower than that in safe drinkers.ADH3 and ALDH2 are associated with drinking behavior in male Tibetan population.

The main purpose of this study was to identify policy maker opinions and attitudes towards children's environmental health (CEH), potential barriers to child-specific protective legislation and implementation in northwest China, and evaluate knowledge and attitudes about CEH before and after an educational conference. We conducted seventy-two interviews with regional officials, researchers and non-governmental organization representatives from five provinces, and surveyed participants (forty-seven) before and after an educational conference in northwest China about CEH. Interviews identified general consensus among participants of the adverse effects of air pollution on children, yet few participants knew of policies to protect them. Barriers identified included limited funding and enforcement, weak regional governments and absence of child-specific policy-making. After the conference, substantially greater self-efficacy was identified for lead, mercury, air pollution and polychlorinated biphenyls (+0.57-0.72 on a 1-5 Likert scale, p = 0.002-0.013), and the scientific knowledge for the role of environment in children's health (+0.58, p = 0.015), and health care provider control (+0.52, p = 0.025) were rated more strongly. We conclude that policy makers in Northwest China appreciate that children are uniquely vulnerable, though additional regulations are needed to account for that vulnerability. Further research should examine effectiveness of the intervention on a larger scale and scope, and evaluate the usefulness of such interventions in translating research into improved care/reduced exposure to environmental hazards.

Previous work has shown that taurine protected neurons against unconjugated bilirubin (UCB)-induced neurotoxicity by preventing cell apoptosis and maintaining intracellular Ca²⁺ homeostasis in primary neuron culture. This study investigates the neurotoxicity of hyperbilirubinemia and neuroprotection of taurine in a clinically relevant murine model in vivo. A hyperbilirubinemia baby mice model was established by intraperitoneal injection with UCB. After 24 h, the neural apoptotic level, transcriptional activity of caspase-3, and iCa²⁺ concentration were detected. It was found that UCB injection significantly increased both intracellular free Ca²⁺ concentrations and the activities of proapoptosis protease caspase-3, which is related to the elevation of neural apoptosis level. When baby mice were pretreated with 7.5 or 15 mg/kg body weight (bw) taurine for 4 h and then exposed to UCB, apoptotic death was significantly attenuated through down-regulation of activity of caspase-3 and i[Ca²⁺] in the brain. From these observations, it was concluded that taurine limits bilirubin-induced neural damage by inhibiting iCa²⁺ overload as well as decreasing activation of proapoptotic proteases caspase-3. This study might contribute to the development of taurine as a broad-spectrum agent for preventing and/or treating neural damage in neonatal jaundice.

Kernicterus is a bilirubin-induced encephalopathy in newborn. Its spectrum ranges from subtle extrapyramidal to acute encephalopathy and chronic posticteric sequelae. Current treatment of this serious problem is far from optimal. Taurine has been documented to have protective effects on neuronal cells against ischemia in vivo and in vitro. This study used primary neuronal culture to investigate the toxicological effects of unconjugated bilirubin (UCB) and the protection of taurine against UCB-mediated neuron damage. Dose-dependent reduction of cell viability was found. Changes in neurite outgrowth preceded the reduction of cell viability. The bilirubin-mediated neurotoxicity is mainly due to increased rate of cell apoptosis and higher levels of intracellular free calcium ion level. Taurine dramatically improved cell viability in cultured neurons exposed to 12.5microM UCB. Taurine pretreatment reduced UCB-mediated apoptotic cell death in primary cultured neurons in a concentration-dependent manner, which was associated with reversal of the increased intracellular free calcium ion levels caused by UCB. This study suggests the potential of taurine as a broad-spectrum agent for preventing and/or treating neuronal damage in neonatal jaundice.

Background Industrialization in the northwest provinces of the People’s Republic of China is accelerating rapid increases in early life environmental exposures, yet no publications have assessed health care provider capacity to manage common hazards. Methods To assess provider attitudes and beliefs regarding the environment in children’s health, determine self-efficacy in managing concerns, and identify common approaches to managing patients with significant exposures or environmentally-mediated conditions, a two-page survey was administered to pediatricians, child care specialists, and nurses in five provinces (Gansu, Shaanxi, Xinjiang, Qinghai, and Ningxia). Descriptive and multivariable analyses assessed predictors of strong self-efficacy, beliefs or attitudes. Results 960 surveys were completed with 20 affected patients. Only 12.0% reported specific training in environmental history taking, and 12.0% reported owning a text on children’s environmental health. Geographic disparities were most prominent in multivariable analyses, with stronger beliefs in environmental causation yet lower self-efficacy in managing exposures in the northwestern-most province. Conclusions Health care providers in Northwest China have strong beliefs regarding the role of environment in children’s health, and frequently identify affected children. Few are trained in environmental history taking or rate self-efficacy highly in managing common hazards. Enhancing provider capacity has promise for improving children’s health in the region.