Chronic environmental inorganic arsenic exposure causes social behavioral changes in juvenile zebrafish (Danio rerio).

Arsenic (As) is a metalloid commonly found worldwide. Environmental As exposure may cause potential health hazards and behavioral changes in humans and animals. However, the effects of environmental As concentrations on social behavior, especially during the juvenile stage, are unclear. In this study, we observed behavioral changes in juvenile zebrafish after 28 days of exposure to inorganic As (NaAsO2 100 and 500 ppb) in water, especially anxiety and social deficits. Additionally, the level of oxidative stress in the zebrafish brain after As treatment increased, the content of dopamine (DA) decreased, and the transcription level of genes involved in DA metabolism with the activity of monoamine oxidase (MAO) increased. Oxidative stress is a recognized mechanism of nerve damage induced by As exposure. The zebrafish were exposed to N-acetylcysteine (NAC) to reduce As exposure-induced oxidative stress. The results showed improvements in social behavior, DA content, MAO activity, and gene transcription in zebrafish. In conclusion, environmental As exposure can induce behavioral abnormalities, such as anxiety and social deficits in zebrafish, which may be caused by As-induced oxidative stress altering gene transcription levels, causing an increase in MAO activity and a decrease in DA.

Light exposure at night, sleep duration, melatonin, and breast cancer: a dose-response analysis of observational studies.

Evidence from observational studies on light at night (LAN) exposure, sleep duration, endogenous melatonin levels, and risk for breast cancer in women is conflicting. This led us to conduct a dose-response analysis of published observational data. Pertinent studies were identified by searching Medline, Web of Science, and EMBASE through April 2013. The dose-response relationship between sleep duration, urinary 6-sulphatoxymelatonin levels, and breast cancer was assessed using the restricted cubic spline model and by multivariate random-effects metaregression. A separate meta-analysis was also carried out to calculate the relative risks (RRs) with 95% confidence intervals (CIs) for breast cancer for the comparable categories or highest levels of exposure versus the lowest levels. Twelve case-control and four cohort studies were included in the analysis. High artificial LAN exposure is associated with an increased risk for breast cancer (RR=1.17, 95% CI: 1.11-1.23), but not ambient LAN exposure (RR=0.91, 95% CI: 0.78-1.07). The summary RR for breast cancer is 1.00 (95% CI: 0.995-1.01) for an increment of 1 h of sleep per night. No significant dose-response relationship between sleep duration and breast cancer was found either for the linearity test (Ptrend=0.725) or for the nonlinearity (Ptrend=0.091) test. An increasein of 15 ng/mg creatinine in urinary 6-sulphatoxymelatonin is associated with a 14% reduced risk for breast cancer (RR=0.86, 95% CI: 0.78-0.95), with a linear dose-response trend (Ptrend=0.003). There was no evidence of substantial heterogeneity or publication bias in the analysis. Our study adds to the evidence of LAN breast cancer theory. Further research in this area is warranted.

An evidence-based appraisal of global association between air pollution and risk of stroke.

BACKGROUND: The aim of this study was to evaluate the transient effects of air pollutants on stroke morbidity and mortality using the meta-analytic approach. METHODS: Three databases were searched for case-crossover and time series studies assessing associations between daily increases in particles with diameter<2.5 µm (PM2.5) and diameter<10 µm (PM10), sulfur dioxide (SO2), carbon monoxide (CO), nitrogen dioxide (NO2), ozone, and risks of stroke hospitalizations and mortality. Risk estimates were combined using random-effects model. RESULTS: A total of 34 studies were included in the meta-analysis. Stroke hospitalizations or mortality increased 1.20% (95%CI: 0.22-2.18) per 10 µg/m3 increase in PM2.5, 0.58% (95%CI: 0.31-0.86) per 10 µg/m3 increase in PM10, 1.53% (95%CI: 0.66-2.41) per 10 parts per billion (ppb) increase in SO2, 2.96% (95%CI: 0.70-5.27) per 1 ppm increase in CO, and 2.24% (95%CI: 1.16-3.33) per 10ppb increase in NO2. These positive associations were the strongest on the same day of exposure, and appeared to be more apparent for ischemic stroke (for all 4 gaseous pollutants) and among Asian countries (for all 6 pollutants). In addition, an elevated risk (2.45% per 10 ppb; 95%CI: 0.35-4.60) of ischemic stroke associated with ozone was found, but not for hemorrhagic stroke. CONCLUSION: Our study indicates that air pollution may transiently increase the risk of stroke hospitalizations and stroke mortality. Although with a weak association, these findings if validated may be of both clinical and public health importance given the great global burden of stroke and air pollution.

Tea consumption and risk of type 2 diabetes: a dose-response meta-analysis of cohort studies.

Tea consumption has inconsistently been shown to be associated with the risk of type 2 diabetes (T2D). The aim of the present study was to conduct a dose-response meta-analysis of cohort studies assessing the association between consumption of tea and risk of developing T2D. Pertinent studies were identified by searching PubMed, Web of Science and EMBASE through 31 March 2013. A total of sixteen cohorts from fifteen articles that reported 37,445 cases of diabetes among 545,517 participants were included. A significant linearly inverse association between tea consumption and T2D risk was found (P for linear trend = 0.02). An increase of 2 cups/d in tea consumption was found to be associated with a 4.6 (95% CI 0.9, 8.1) % reduced risk of T2D. On the basis of the dose-response meta-analysis, the predicted relative risks of diabetes for 0, 1, 2, 3, 4, 5 and 6 cups of tea consumed per d were 1.00 (referent), 0.97 (95% CI 0.94, 1.01), 0.95(95% CI 0.92, 0.98), 0.93 (95% CI 0.88, 0.98), 0.90 (95% CI 0.85, 0.96), 0.88 (95 % CI 0.83, 0.93) and 0.85 (95% CI 0.80, 0.91), respectively. There was a statistically significant heterogeneity within the selected studies (Q= 45.32, P< 0.001, I 2= 60.3 %). No evidence of substantial small-study bias was found (P= 0·46). Our findings suggest that tea consumption could be linearly inversely associated with T2D risk. Future well-designed observational studies that account for different characteristics of tea such as tea types, preparation methods and tea strength are needed to fully characterise such an association.

[TALE nuclease engineering and targeted genome modification].

Artificial designer nucleases targeting specific DNA sequences open up a new field for reverse genetics study. The rapid development of engineered endonucleases (EENs) enables targeted genome modification theoretically in any species. The construction of transcription activator-like effector nucleases (TALENs) is simpler with higher specificity and less toxicity than zinc-finger nucleases (ZFNs). Here, we summarized the recent progresses and prospects of TALEN technology, with an emphasis on its structure, function, and construction strategies, as well as a collection of species and genes that have been successfully modified by TALENs, especially the application in zebrafish.

[Progress in zinc finger nuclease engineering for targeted genome modification].

Zinc finger nuclease (ZFN) is an artificially engineered hybrid protein that contains a zinc finger protein (ZFP) domain and a Fok I endonuclease cleavage domain. It has recently emerged as a powerful molecular tool for targeted genome modifications. ZFNs recognize and bind to specific DNA sequences to generate a double-strand break (DSB) by its nuclease activity. Based on this finding, various genetic methods, including gene targeting (gene disruption), gene addition, gene correction etc., are being designed to manipulate the genomes of different species at specific loci. One particular advantage of this new technique is its broad applications, which can be employed to generate desirable inheritable mutations both at the organismal level and at the cellular level. Here, we review the recent progress and prospects of ZFN technology. This article focused on the mechanism of how it works, currently available target assessment, ZFP library construction and screening methods, target modification strategies, as well as a collection of specie and genes that have been successfully modified by ZFN. This review will provide a useful reference for researchers who are interested in applying this new technique in their studies.