Associations among neighborhood walkability, metal exposure, and sex steroid hormone levels: Results from Hangzhou Birth Cohort Study â ¡.

BACKGROUND: Neighborhood walkability may influence maternal-fetal exposure to environmental hazards and maternal-fetal health (e.g., fetal growth restriction, reproductive toxicity). However, few studies have explored the association between neighborhood walkability and hormones in pregnant women. METHODS: We included 533 pregnant women from the Hangzhou Birth Cohort Study II (HBCS-II) with testosterone (TTE) and estradiol (E2) measured for analysis. Neighborhood walkability was evaluated by calculating a walkability index based on geo-coded addresses. Placental metals were measured using inductively coupled plasma mass spectrometry (ICP-MS). TTE and E2 levels in umbilical cord blood were measured using chemiluminescence microparticle immunoassay (CMIA). Linear regression model was used to estimate the relationship between the walkability index, placental metals, and sex steroid hormones. Effect modification was also assessed to estimate the effect of placental metals on the associations of neighborhood walkability with TTE and E2. RESULTS: Neighborhood walkability was significantly linked to increased E2 levels (P trend=0.023). Compared with participants at the first quintile (Q1) of walkability index, those at the third quintiles (Q3) had lower chromium (Cr) levels (ß = -0.212, 95% CI = -0.421 to -0.003). Arsenic (As), cobalt (Co), manganese (Mn), molybdenum (Mo), nickel (Ni), lead (Pb), antimony (Sb), selenium (Se), tin (Sn), and vanadium (V) were linked to decreased TTE levels, and cadmium (Cd) was linked to increased TTE levels. No metal was significantly associated with E2 levels in trend analysis. In the analysis of effect modification, the associations of neighborhood walkability with TTE and E2 were significantly modified by Mn (P = 0.005) and Cu (P = 0.049) respectively. CONCLUSION: Neighborhood walkability could be a favorable factor for E2 production during pregnancy, which may be inhibited by maternal exposure to heavy metals.

[Simulation model of tumor-treating fields].

Tumor-treating fields (TTFields) is a novel treatment modality for malignant solid tumors, often employing electric field simulations to analyze the distribution of electric fields on the tumor under different parameters of TTFields. Due to the present difficulties and high costs associated with reproducing or implementing the simulation model construction techniques, this study used readily available open-source software tools to construct a highly accurate, easily implementable finite element simulation model for TTFields. The accuracy of the model is at a level of 1 mm 3. Using this simulation model, the study carried out analyses of different factors, such as tissue electrical parameters and electrode configurations. The results show that factors influncing the distribution of the internal electric field of the tumor include changes in scalp and skull conductivity (with a maximum variation of 21.0% in the treatment field of the tumor), changes in tumor conductivity (with a maximum variation of 157.8% in the treatment field of the tumor), and different electrode positions and combinations (with a maximum variation of 74.2% in the treatment field of the tumor). In summary, the results of this study validate the feasibility and effectiveness of the proposed modeling method, which can provide an important reference for future simulation analyses of TTFields and clinical applications.

Saturated fatty acids synergizes cadmium to induce macrophages M1 polarization and hepatic inflammation.

Exposure to the toxic metal cadmium (Cd) is a well-established risk factor for hepatic inflammation, but it remains unclear how metabolic components, such as different fatty acids (FAs), interact with Cd to influence this process. Understanding these interactions is essential for identifying potential preventative and therapeutic targets for this disorder. To address this question, we conducted in vitro and in vivo studies to investigate the combinatorial effect of Cd and saturated FAs on hepatic inflammation. Specifically, we assessed the cytotoxicity of Cd on macrophages and their polarization and inflammatory activation upon co-exposure to Cd and saturated FAs. Our results showed that while saturated FAs had minimal impact on the cytotoxicity of Cd on macrophages, they significantly collaborated with Cd in predisposing macrophages towards a pro-inflammatory M1 polarization, thereby promoting inflammatory activation. This joint effect of Cd and saturated FAs resulted in persistent inflammation and hepatic steatohepatitis in vivo. In summary, our study identified macrophage polarization as a novel mechanism by which co-exposure to Cd and saturated lipids induces hepatic inflammation. Our findings suggest that intervening in macrophage polarization may be a potential approach for mitigating the adverse hepatic effects of Cd.

Disruption of mitochondrial redox homeostasis as a mechanism of antimony-induced reactive oxygen species and cytotoxicity.

Occupational and environmental Sb exposure has been associated with increased risk of respiratory diseases and lung cancer, but the toxicities and molecular mechanisms of Sb have been less investigated. In the present study, we first analyzed the Sb toxicity profile of lung adenocarcinoma A549 cells, and found that Sb dose-dependently decreased the cell viability and arrested cell cycle at G2/M but did not induce apoptosis. We next investigated the role of reactive oxygen species (ROS) involved in Sb-induced cytotoxicity. The results showed that Sb did not significantly induce cytosolic ROS production by NADPH oxidase (NOX) and the NOX inhibitors did not ameliorate the Sb-induced cell viability loss in A549 cells. However, the level of mitochondrial ROS (mtROS) was significantly increased in Sb-exposed cells and the mitochondria-targeted antioxidant significantly improved cell viability. These results suggested that mitochondria but not NOX is the major source of ROS production and mtROS plays a critical role in Sb-induced cytotoxicity. Furthermore, we found that Sb induced mitochondria dysfunction including the significant decrease of ATP level and mitochondrial membrane potential. Finally, Sb exposure decreased the activity of complex I and complex III, the level of -SH and GSH in mitochondria, and the activity of mitochondrial GR, GPx and TrxR, but increased the mitochondrial SOD activity, suggesting the disruption of mitochondrial redox homeostasis. Taken together, these findings suggested that Sb impaired mitochondrial redox homeostasis, resulting in formation of mtROS, thereby inhibited mitochondrial function and led to cytotoxicity.

Arsenic exposure during juvenile and puberty significantly affected reproductive system development of female SD rats.

Infertility affects about 10-15% couples over the world, among which a large number of cases the underlying causes are still unclear. Recent studies suggest that environmental factors may play an important role in these idiopathic infertilities. Arsenic is a heavy metal found in drinking water over the world. Its effect on the development of female reproductive system at the environmental-relevant levels is still largely unknown. To test the hypothesis that arsenic exposure during juvenile and puberty may affect sex maturation and female reproductive system development, SD rats of 3 weeks of age were exposed to arsenic with environmental-relevant levels (0, 0.02, 0.2, or 2 mg/L, n = 16/group) through drinking water for about 44 days until the rats reached adulthood (65 days of age). Arsenic exposure significantly reduced the weights of both ovary and uterus without affecting the body weight. Also, arsenic exposure disturbed estrus cycles and reduced the numbers of primordial follicles and corpora lutea while increased atretic follicles. In addition, arsenic reduced serum levels of estradiol, progesterone and testosterone but increased LH and FSH levels in dose-dependent manners. QPCR and Western blot experiments indicated arsenic selectively down-regulated ovarian steroidogenic-related proteins FSHR, STAR, CYP17A1, HSD3B1 and CYP19A1 and signaling molecules PKA-ERK-JNK-cJUN, without affecting AKT and CREB. As about reproductive capacity, arsenic-exposed dams had smaller pups, reduced litter size and lower number of male pups without a change in female pups. In conclusion, juvenile and pubertal arsenic exposures at environmental-relevant levels significantly reduced reproductive functions and capacity by adult. Since the lowest effective dose is very close to the government safety standards, the relevancy of arsenic over exposure to reproductive defects in human deserves further study.

Total arsenic, dimethylarsinic acid, lead, cadmium, total mercury, methylmercury and hypertension among Asian populations in the United States: NHANES 2011-2018.

BACKGROUND: Non-Hispanic Asians (NHA) in USA have been reported with higher arsenic (As), lead (Pb), cadmium (Cd), mercury (Hg) and their specific species levels, comparing with non-NHA. This study aimed to investigate the associations of these metal/metalloid levels with blood pressure levels and prevalence of hypertension among general NHA using the 2011-2018 National Health and Nutrition and Examination Survey (NHANES) data. METHODS: The study included participants aged 20 years and older with determinations of As, Dimethylarsinic acid (DMA), Pb, Cd, Hg and methyl-Hg (MeHg) in blood (n = 10, 177) and urine (n = 5, 175). These metals/metalloid levels were measured by inductively coupled plasma mass spectrometry. Systolic (SBP) and diastolic blood pressure (DBP) levels were examined through a standardized protocol. Censored normal regression model and logistic regression model were employed to explore the associations of As, DMA, Pb, Cd, Hg and MeHg levels with blood pressure levels and prevalence of hypertension respectively, and potential confounders were adjusted in these regression models. Quantile-based g-computation approach was used to analysis joint effect of metals mixture on blood pressure level and hypertension. RESULTS: For NHA, urinary As and Hg levels were associated with increased DBP level; Higher blood Hg and MeHg levels were related to increased blood pressure levels and hypertension; However, negative association was observed between urinary Cd and SBP level; Blood metals mixture (including blood Pb, Cd and Hg) was associated with increased DBP level, but not for hypertension. For non-NHA, urinary As and DMA levels were associated with increased SBP level, but not DBP level and prevalence of hypertension; Urinary Pb level was associated with decreased DBP level; Nevertheless, positive associations were observed between blood Pb levels and SBP and prevalence of hypertension; Blood Hg level was associated with decreased DBP level and prevalence of hypertension; Furthermore, blood MeHg level was associated with decreased DBP level; Positive association was observed between blood metals mixture and increased SBP level among non-NHA. CONCLUSIONS: Highly exposed to Hg level among NHA was associated with increased blood pressure levels and prevalence of hypertension. Urinary As level was associated with increased DBP level among NHA. Furthermore, blood metals mixture was related to increased DBP level among NHA. Further prospective studies with larger sample size should be performed to warrant the results.

Development of prediction models for successful external cephalic version and delivery outcome.

OBJECTIVE: To develop prediction models for the chance of successful external cephalic version (ECV) and delivery outcome. STUDY DESIGN: This is a single-center retrospective study including 350 pregnant women with a singleton non-cephalic pregnancy at or after 36 weeks of gestational age. We selected 22 factors for ECV prediction and 21 for delivery outcome after successful ECV prediction as candidate predictors. Multivariable logistic regression with a stepwise backward selection procedure was used to construct a prediction model for the chance of successful ECV and the other for the delivery outcome. The discrimination and calibration of the models were assessed and internal validation was done with bootstrapping. RESULTS: ECV was successfully performed in 232 cases (66.3%) among 343 women. Eight predictive factors were identified to be associated with a successful ECV: Gestational week at ECV < 39 weeks, multiparous, BMI before pregnancy < 22 kg/m3, palpable fetal head, breech engagement, larger AFI, larger BPD and posterior placenta. This model showed good calibration and good discrimination (c-statistic = 0.82, 95% CI 0.76-0.88). Six predictive factors were identified to be associated with vaginal delivery after successful ECV: age < 35, multiparous, BMI before pregnancy < 22 kg/m3, anterior placenta, lateral placenta and none-front fetal spine position. This model showed fair discrimination (c-statistic = 0.79, 95% CI 0.72-0.85). However, its calibration was not so satisfactory especially when the predicted probability was low. CONCLUSION: We validated a prediction model for ECV and delivery outcome, showing that the model's overall performance is good. This can be used in clinical practice after external validation.

Second-trimester and third-trimester maternal lipid profiles significantly correlated to LGA and macrosomia.

BACKGROUND: According to the theory of fetal-derived adult diseases, abnormal fetal development might affect the occurrence of diseases in adulthood, and appropriate fetal growth status intrauterine might have a beneficial effect on it. To adapt properly for fetal development, there are numerous changes in the maternal physiology during pregnancy, including blood lipid metabolism. The aim of this study is to evaluate the association between lipid profiles in the second and third trimesters of normal pregnancy and fetal birth weight. MATERIALS AND METHODS: The study population was derived from 5695 pregnant women, who maintained routine prenatal care at the women's hospital of Zhejiang University, School of medicine January 1, 2014, and December 31, 2014. The pregnant women in this study all carried uncomplicated singleton pregnancies to at least 37 weeks. RESULTS: The mean (standard deviation) birth weight was 3361.00 (385.94) g; 413 (7.3%) of the infants were large for gestational age, and 330 (5.8%) were macrosomia. On multiple linear regression analysis, positive determinants of birth weight were gravidity, parity, gestational age at delivery, male infant, maternal height, and weight before pregnancy, weight gain during pregnancy, fasting blood glucose (FBG) level, second-trimester cholesterol (TC) and third-trimester triglyceride (TG), gestational albumin (ALB), and third-trimester high-density lipoprotein (HDL-C) levels were each negatively associated with birth weight. On logistic regression analysis, the significant metabolic lipid predictors of delivering a large-for-gestational-age infant were second- and third-trimester TG (aOR = 1.178, 95% CI 1.032-1.344, p = 0.015; aOR = 1.106, 95% CI 1.043-1.173, p = 0.001, respectively) and second- and third-trimester HDL-C level (aOR = 0.655, 95% CI 0.491-0.874, p = 0.004; aOR = 0.505, 95% CI 0.391-0.651, p < 0.001, respectively). Third-trimester TG and HDL-C were stable predictors of large-for-gestational-age infants in stratification analysis. High TG and low HDL-C level during third trimester could be considered as indicators of a high risk of large for gestational age (LGA) and macrosomia, regardless of infant gender. CONCLUSION: These results suggest that future lifestyle programs in women of reproductive age with a focus on lowering TG levels (i.e., diet, weight reduction, and physical activity) may help to reduce the incidence of LGA and macrosomia.

Nuclear localization of ING3 is required to suppress melanoma cell migration, invasion and angiogenesis.

Inhibitor of growth family member 3 (ING3), a tumor suppressor, plays crucial roles in cell cycle regulation, apoptosis and transcription. Previous studies suggest important roles of nuclear ING3, however, the nuclear localization sequence (NLS) of ING3 is not defined and its biological functions remain to be elucidated. In this study, various ING3 mutants were generated to identify its NLS. The NLS of ING3 was determined as KKFK between 164 and 167 amino acids. More intriguingly, replacement of Lysine 164 residue of ING3 with alanine (K164A) resulted in retention of ING3 in the cytoplasm. Overexpression of ING3 led to inhibition of melanoma cell migration, invasion, and angiogenesis respectively, however, this inhibition was abrogated in cells with overexpression of ING3-K164A mutant. In conclusion, this study identified the NLS of ING3 and demonstrated the significance of ING3 nuclear localization for tumor suppressive functions of ING3, and future studies await to elucidate the role of ING3 (K164) post-modificaton in its nuclear transportation and cancer development.

The Relative Permittivity Changes of EGF by 50 Hz MF Exposure Neither Affect the Interaction of EGF With EGFR Nor Its Biological Effects.

The biophysical mechanism of magnetic fields (MFs) acting on living systems is not clear. Previous research showed that, similar to epidermal growth factor (EGF), MF exposure induced EGF receptor (EGFR) clustering and activated EGFR signaling. In this study, we investigated whether MF exposure induced the changes in physical characteristics of EGF and downstream effects of EGF and EGFR interaction. The phase-interrogation surface plasmon resonance (SPR) sensing analyses showed that 50 Hz MF exposure at 4.0 mT for 1 h induced reversible relative permittivity changes of EGF solution. However, compared with sham-exposed EGF solution, the MF-exposed EGF solution did not affect the binding of EGF to EGFR, nor the cell viability and EGFR clustering in human amniotic epithelial cells (FL cells). Our data suggest that cellular EGFR clustering response to MF exposure might not be a result of changes in relative permittivity of EGF in cell culture solution. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.

The decreased permittivity of zebrafish embryos culture medium by magnetic fields did not affect early development of zebrafish embryos.

Epidemiological studies have shown associations between exposure to environmental extremely low frequency magnetic fields (ELF-MF) and health effects, but the mechanisms of ELF-MF induced biological effects remain unclear. We hypothesized that ELF-MF may regulate functions of tissues or cells via its effects on surrounding environment, e.g., culture medium. To test this hypothesis, we investigated the effects of 50 Hz MF on the relative permittivity of zebrafish embryos culture medium as well as of MF-exposed medium on zebrafish embryos development. The responses of medium to 50 Hz MF exposure were evaluated by a phase-sensitive surface plasmon resonance (SPR) system. The results demonstrated that MF treatment decreased relative permittivity of zebrafish embryos medium in a dose and time-dependent way. Interestingly, the decreased permittivity induced by MF exposure gradually recovered and approached to the base level when the exposure was removed off. However, MF-exposed medium did not trigger adverse consequences of embryos during zebrafish embryonic development, including mortality, malformation, hatching and heart rate when the MF pre-exposed medium was subjected to one cell-stage embryos. Moreover, the MF-exposed medium did not induce apoptosis of zebrafish embryos at 48 and 72 h post fertilization. Our data demonstrated that the relative permittivity of zebrafish embryos medium was decreased by MF exposure, whereas this decrease failed to result in abnormal development of zebrafish embryos.

Ataxia telangiectasia mutated deficiency does not result in genetic susceptibility to 50 Hz magnetic fields exposure in mouse embryonic fibroblasts.

Extremely low frequency magnetic field (ELF-MF) has been classified as a possible carcinogen to humans by the International Agency for Research on Cancer [2002]. However, debate on the genotoxic effects of ELF-MF has continued due to lack of sufficient experimental evidence. Ataxia telangiectasia mutated (ATM) plays a central role in DNA damage repair; its deficiency can result in cellular sensitivity to DNA-damaging agents. To evaluate the genotoxicity of ELF-MF, we investigated the effects of 50 Hz MF on DNA damage in ATM-proficient (Atm+/+ ) mouse embryonic fibroblasts (MEFs) and ATM-deficient (Atm-/- ) MEFs, a radiosensitive cell line. Results showed no significant difference in average number of γH2AX foci per cell (9.37 ± 0.44 vs. 9.08 ± 0.28, P = 0.58) or percentage of γH2AX foci positive cells (49.22 ± 1.86% vs. 49.74 ± 1.44%, P = 0.83) between sham and exposure groups when Atm+/+ MEFs were exposed to 50 Hz MF at 2.0 mT for 15 min. Extending exposure duration to 1 or 24 h did not significantly change γH2AX foci formation in Atm+/+ MEFs. Similarly, the exposure did not significantly affect γH2AX foci formation in Atm-/- MEFs. Furthermore, 50 Hz MF exposure also did not significantly influence DNA fragmentation, cell viability, or cell cycle progression in either cell types. In conclusion, exposure to 50 Hz MF did not induce significant DNA damage in either Atm+/+ or Atm-/- MEFs under the reported experimental conditions. Bioelectromagnetics. 39:476-484, 2018. © 2018 Wiley Periodicals, Inc.

Factors affecting the live-birth rate in women with diminished ovarian reserve undergoing IVF-ET.

PURPOSE: The occurrence of diminished ovarian reserve (DOR) in women was growing in recent years. Although in vitro fertilization and embryo transfer (IVF-ET) became an effective treatment for DOR, the live-birth (LB) rate remains unsatisfactory. This study aimed to investigate the impact factors of LB rate in women with DOR undergoing assisted reproduction. METHODS: This was a single-center retrospective cohort study. A total of 2277 IVF-ET or ICSI cycles from 1957 DOR women were analysed. Impact factors of LB rate were explored via Student's t test, Pearson's Chi-square test, and multivariate logistic regression models. RESULTS: There were statistically significant differences in maternal age (P < 0.001), duration of infertility (P < 0.001), female body mass index (P = 0.039), first IVF cycle (P = 0.004), poor ovarian response (P < 0.001), paternal age (P < 0.001), total gonadotropin dose (P = 0.010), endometrial thickness (P = 0.021), number of follicles ≥ 14 mm (P = 0.007), number of oocytes retrieved (P < 0.001), number of frozen embryos (P = 0.014), and the stage (P < 0.001) and number (P < 0.001) of embryos transferred between the non-live-birth (NLB) and LB groups. However, only factors of maternal age, the stage and number of embryos transferred remained different after adjusting for potential confounders. CONCLUSIONS: Maternal age, the stage and number of embryos transferred were independent impact factors affecting the live-birth rate in women with DOR seeking for assisted conception.

RF-EMF exposure at 1800 MHz did not elicit DNA damage or abnormal cellular behaviors in different neurogenic cells.

Despite many years of studies, the debate on genotoxic effects of radiofrequency electromagnetic fields (RF-EMF) continues. To systematically evaluate genotoxicity of RF-EMF, this study examined effects of RF-EMF on DNA damage and cellular behavior in different neurogenic cells. Neurogenic A172, U251, and SH-SY5Y cells were intermittently (5 min on/10 min off) exposed to 1800 MHz RF-EMF at an average specific absorption rate (SAR) of 4.0 W/kg for 1, 6, or 24 h. DNA damage was evaluated by quantification of γH2AX foci, an early marker of DNA double-strand breaks. Cell cycle progression, cell proliferation, and cell viability were examined by flow cytometry, hemocytometer, and cell counting kit-8 assay, respectively. Results showed that exposure to RF-EMF at an SAR of 4.0 W/kg neither significantly induced γH2AX foci formation in A172, U251, or SH-SY5Y cells, nor resulted in abnormal cell cycle progression, cell proliferation, or cell viability. Furthermore, prolonged incubation of these cells for up to 48 h after exposure did not significantly affect cellular behavior. Our data suggest that 1800 MHz RF-EMF exposure at 4.0 W/kg is unlikely to elicit DNA damage or abnormal cellular behaviors in neurogenic cells. Bioelectromagnetics. 38:175-185, 2017. © 2016 Wiley Periodicals, Inc.

Childhood pesticide poisoning in Zhejiang, China: a retrospective analysis from 2006 to 2015.

BACKGROUND: Pesticide poisoning in children has been a serious public health issue around the world, especially in the developing countries where agriculture is still one of the largest economic sectors. The purpose of this study was to analyze epidemiological characteristics of acute pesticide poisoning in children from Zhejiang province, China. METHODS: The pesticide poisoning cases for children were retrieved from Occupational Disease Surveillance and Reporting System, Zhejiang Provincial Center for Disease Control and Prevention, China. The incident cases, deaths, and fatality rate of child pesticide poisoning from 2006 through 2015 were calculated. RESULTS: During the study period, totally 2952 children were poisoned by pesticides, with 66 deaths, resulting in a fatality rate of 2.24%. Among them, there were 1607 male cases with 28 deaths, and 1345 female cases with 38 deaths. Most of the cases occurred in preschool children (1349) and adolescent age group (1269). Organophosphate and carbamate insecticides were the cause of most poisonings (1130), leading to 34 deaths. The highest fatality rate (3.13%) was due to poisoning by herbicides and fungicides, causing 14 deaths out of 448 cases. Poisoning occurred mostly in rural areas (78%). And most pesticide poisoning occurred in the summer (896) and fall (811), while fewest poisoning cases in the winter (483) but with the highest fatality rate (3.52%). CONCLUSIONS: This study shows that pesticide poisoning of children is a major health problem in Zhejiang, suggesting preventive strategies should be conducted to control childhood pesticide poisoning.

Anti-muscarinic adjunct therapy accelerates functional human oligodendrocyte repair.

Therapeutic repair of myelin disorders may be limited by the relatively slow rate of human oligodendrocyte differentiation. To identify appropriate pharmacological targets with which to accelerate differentiation of human oligodendrocyte progenitors (hOPCs) directly, we used CD140a/O4-based FACS of human forebrain and microarray to hOPC-specific receptors. Among these, we identified CHRM3, a M3R muscarinic acetylcholine receptor, as being restricted to oligodendrocyte-biased CD140a(+)O4(+) cells. Muscarinic agonist treatment of hOPCs resulted in a specific and dose-dependent blockade of oligodendrocyte commitment. Conversely, when hOPCs were cocultured with human neurons, M3R antagonist treatment stimulated oligodendrocytic differentiation. Systemic treatment with solifenacin, an FDA-approved muscarinic receptor antagonist, increased oligodendrocyte differentiation of transplanted hOPCs in hypomyelinated shiverer/rag2 brain. Importantly, solifenacin treatment of engrafted animals reduced auditory brainstem response interpeak latency, indicative of increased conduction velocity and thereby enhanced functional repair. Therefore, solifenacin and other selective muscarinic antagonists represent new adjunct approaches to accelerate repair by engrafted human progenitors.

Effects of electromagnetic fields exposure on plasma hormonal and inflammatory pathway biomarkers in male workers of a power plant.

PURPOSE: The potential health risks of electromagnetic fields (EMFs) have currently raised considerable public concerns. The aim of this study was to evaluate the effects of EMF exposure on levels of plasma hormonal and inflammatory pathway biomarkers in male workers of an electric power plant. METHODS: Seventy-seven male workers with high occupational EMF exposure and 77 male controls with low exposure, matched by age, were selected from a cross-sectional study. Moreover, high EMF exposure group was with walkie-talkies usage and exposed to power frequency EMF at the work places for a longer duration than control group. A questionnaire was applied to obtain relevant information, including sociodemographic characteristics, lifestyle factors, and EMF exposures. Plasma levels of testosterone, estradiol, melatonin, NF-κB, heat-shock protein (HSP) 70, HSP27, and TET1 were determined by an enzyme-linked immunosorbent assay. RESULTS: EMF exposure group had statistically significantly lower levels of testosterone (ß = -0.3 nmol/L, P = 0.015), testosterone/estradiol (T/E2) ratio (ß = -15.6, P = 0.037), and NF-κB (ß = -20.8 ng/L, P = 0.045) than control group. Moreover, joint effects between occupational EMF exposure and employment duration, mobile phone fees, years of mobile phone usage, and electric fees on levels of testosterone and T/E2 ratio were observed. Nevertheless, no statistically significant associations of EMF exposures with plasma estradiol, melatonin, HSP70, HSP27, and TET1 were found. CONCLUSIONS: The findings showed that chronic exposure to EMF could decrease male plasma testosterone and T/E2 ratio, and it might possibly affect reproductive functions in males. No significant associations of EMF exposure with inflammatory pathway biomarkers were found.

MicroRNA-409-3p suppresses colorectal cancer invasion and metastasis partly by targeting GAB1 expression.

Colorectal cancer (CRC) is one of the most common cancers worldwide and its metastasis accounts for the majority of deaths. However, the molecular mechanisms underlying CRC progression are not well characterized. In this study, we identified miR-409-3p as a tumor suppressor of CRC. MiR-409-3p expression was significantly downregulated in CRC tissue compared to adjacent non-tumor tissue, and reduced miR-409-3p expression was correlated with CRC metastasis. In vitro and in vivo studies revealed that miR-409-3p negatively regulated CRC metastatic capacities, including suppressing cancer cell migration, invasion and metastasis. To explore the mechanism of action of miR-409-3p, we adopted a pathway and pathophysiological event-based target screening and validation approach, and found nine known metastasis-related genes as potential targets. The 3'-UTR binding assays between the candidates and miR-409-3p suggested that only GAB1, NR4A2 and LMO4 were directly regulated by the miRNA. However, endogenous expression analysis revealed that only GAB1 was modulated by miR-409-3p in CRC cells at both the mRNA and protein levels. Furthermore, we provided evidence to conclude that GAB1 was partially responsible for miR-409-3p-mediated metastasis. Taken together, our data demonstrate that miR-409-3p is a metastatic suppressor, and post-transcriptional inhibition of the oncoprotein GAB1 is one of the mechanisms of action of this miRNA. Our finding suggests miR-409-3p might be a novel target for CRC metastasis treatment.

Study of miniemulsion formulation containing 1-octyl-3-methylimidazolium hexafluorophosphate for its application in low-emitting coating products.

Room temperature ionic liquids (RTILs) are non-volatile organic salts, and few of them with low melting point may replace the conventional coalescing agents in waterborne coatings, thus preventing volatile organic compounds (VOCs) emission, caused by coalescing agents. The formation of waterborne coating containing RTILs can be achieved by the encapsulation of RTILs inside latexes via miniemulsion polymerization. Achieving a stable miniemulsion is a crucial step for further polymerization. In this study, 1-octyl-3-methylimidazolium hexafluorophosphate (C8mimPF6) was chosen, and various factors which might affect droplet size and its stability, including surfactant type, surfactant concentration, and C8mimPF6 concentration, were investigated. It was found that the presence of a small amount of C8mimPF6 coupled with the surfactant would offer marked effects on the droplet size reduction and droplet stability. Such effect may reach its maximum from 1 to 5 wt% C8mimPF6. Above the critical concentration, adding more C8mimPF6 to the oil phase may cause a larger initial droplet size as well as weaken the droplet stability. Such observations were consistent with the zeta potential measurements for miniemulsions prepared under similar conditions.

Is there association between Glutathione S Transferases polymorphisms and cataract risk: a meta-analysis?

BACKGROUND: Glutathione S transferase (GST) polymorphisms have been considered as risk factors for age-related cataracts, but the results remain controversial. In this study, we have performed a meta-analysis to evaluate the association between polymorphisms of GSTM1 and GSTT1 and cataract risk. METHODS: Published literature from PubMed and other databases were retrieved. The case-control studies regarding the association between GSTM1 or GSTT1 polymorphism and cataract risk were included. Pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated using random- or fixed-effects model. RESULTS: Fifteen studies on GSTM1 (3,065 patients and 2,105 controls), and nine studies on GSTT1 (2,374 patients and 1,544 controls) were included. By pooling all the studies, GSTM1 null polymorphism was not associated with cataract risk, and this negative association maintained in subgroup analyses. However, GSTT1 null polymorphism was significantly associated with increased risk of posterior subcapsular (OR, 1.42; 95 % CI, 1.04-1.94) but not other subtypes of cataract. Stratified analyses demonstrated an association of GSTT1 null genotype with increased risk of cataract in Asian (OR, 1.44; 95 % CI, 1.14-1.83) but not Caucasian populations. In addition, seven pooled studies showed no association of cataract risk with the combined GSTM1 and GSTT1 null genotypes. CONCLUSIONS: This meta-analysis suggests that GSTT1 null polymorphism is associated with increased risk of posterior subcapsular cataract. Given the limited sample size, the association between GSTT1 null polymorphism and cataract risk in Asian awaits further investigation.