Flower-like molybdenum disulfide/cobalt ferrite composite for the extraction of benzotriazole UV stabilizers in environmental samples.

Benzotriazole UV stabilizers (BUVSs) are a class of emerging contaminants of concern; the development of rapid and convenient monitoring method for these trace-level pollutants in waters is of crucial significance in environmental science. Here, a novel magnetic flower-like molybdenum disulfide/cobalt ferrite nanocomposite (MoS2/CoFe2O4) was synthesized by hydrothermal reaction. Compared with the conventional Fe3O4-based magnetic composites, the proposed material just required a minimum consumption of Co/Fe towards the equivalent of MoS2 while providing superior magnetization performance. Taking advantages of high adsorption capacity, extraordinary stability, and repeatability in construction, MoS2/CoFe2O4 was applied to the extraction to BUVSs. The enrichment factors of three BUVSs were in the range 164-193 when 20 mL of environmental water sample was loaded on 40 mg of the adsorbent. MoS2/CoFe2O4 could be regenerated and recycled at least 10 cycles of adsorption/desorption with recoveries of 80.1-111%. The method of MoS2/CoFe2O4-based extraction coupled with high-performance liquid chromatography-variable wavelength detector was applied to the monitoring of BUVSs in seawater, lake water, and wastewater, which gave detection limits (S/N = 3) of 0.023-0.030 ng·mL-1 and recoveries of 80.1-110%. The intra-day and inter-day precisions (relative standard deviation, RSDs, n = 3) were in the range 1.6-7.5% and 3.2-11.5%, respectively. The approach is an alternative for efficient and sensitive extraction and determination of trace-level environmental pollutants in waters.

MicroRNA­126 protects SH­SY5Y cells from ischemia/reperfusion injury­induced apoptosis by inhibiting RAB3IP.

MicroRNA (miR)­126 is known to inhibit inflammatory responses in various inflammatory­related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR­126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH­SY5Y was cultured in an oxygen­glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR­126 expression and cell viability. SH­SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH­SY5Y cells were transfected with a miR­126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH­SY5Y cells were co­transfected with RAB3IP overexpression or NC plasmid together with mimic­NC or mimic­miR, and then maintained in an OGD/R environment to evaluate miR­126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR­126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic­miR, cell viability increased compared with the mimic­NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic­miR group compared with the mimic­NC group. RAB3IP expression was reduced following mimic­miR transfection. In rescue experiments, miR­126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR­126. In addition, RAB3IP overexpression attenuated the protective effect of miR­126 on OGD/R­induced apoptosis. These findings suggest that miR­126 protects against cerebral I/R injury by targeting RAB3IP.

Association Between Obesity-Mediated Atrial Fibrillation and Therapy With Sodium Channel Blocker Antiarrhythmic Drugs.

Importance: The association between obesity, an established risk factor for atrial fibrillation (AF), and response to antiarrhythmic drugs (AADs) remains unclear. Objective: To test the hypothesis that obesity differentially mediates response to AADs in patients with symptomatic AF and in mice with diet-induced obesity (DIO) and pacing induced AF. Design, Setting, and Participants: An observational cohort study was conducted including 311 patients enrolled in a clinical-genetic registry. Mice fed a high-fat diet for 10 weeks were also evaluated. The study was conducted from January 1, 2018, to June 2, 2019. Main Outcomes and Measures: Symptomatic response was defined as continuation of the same AAD for at least 3 months. Nonresponse was defined as discontinuation of the AAD within 3 months of initiation because of poor symptomatic control of AF necessitating alternative rhythm control therapy. Outcome measures in DIO mice were pacing-induced AF and suppression of AF after 2 weeks of treatment with flecainide acetate or sotalol hydrochloride. Results: A total of 311 patients (mean [SD] age, 65 [12] years; 120 women [38.6%]) met the entry criteria and were treated with a class I or III AAD for symptomatic AF. Nonresponse to class I AADs in patients with obesity was less than in those without obesity (30% [obese] vs 6% [nonobese]; difference, 0.24; 95% CI, 0.11-0.37; P = .001). Both groups had similar symptomatic response to a potassium channel blocker AAD. On multivariate analysis, obesity, AAD class (class I vs III AAD [obese] odds ratio [OR], 4.54; 95% Wald CI, 1.84-11.20; P = .001), female vs male sex (OR, 2.31; 95% Wald CI, 1.07-4.99; P = .03), and hyperthyroidism (OR, 4.95; 95% Wald CI, 1.23-20.00; P = .02) were significant indicators of the probability of failure to respond to AADs. Pacing induced AF in 100% of DIO mice vs 30% (P < .001) in controls. Furthermore, DIO mice showed a greater reduction in AF burden when treated with sotalol compared with flecainide (85% vs 25%; P < .01). Conclusions and Relevance: Results suggest that obesity differentially mediates response to AADs in patients and in mice with AF, possibly reducing the therapeutic effectiveness of sodium channel blockers. These findings may have implications for the management of AF in patients with obesity.

[Association between joint of heat and noise and metabolic syndrome in steel workers].

OBJECTIVE: To analyze the relationship between joint of heat and noise, and metabolic syndrome in a steel rolling factory workers. METHODS: A total of 590 steel workers were selected as subjects by cluster sampling method from workers of a steel factory. They were investigated by face to face way with the unified questionnaire which contents included personal information, occupational history, personal history, habits and other factors. Furthermore, height, weight, waist circumference and blood pressure were measured. Referring to the 2005 International Diabetes Federation (IDF) issued by the metabolic syndrome (MS) worldwide uniform definition combines waist diagnosis MS. A database was built by Epidata 3.0 software, and data was analyzed by SPSS 17.0. RESULTS: 571 steel workers were from 22 to 60 years, mean age (41.2 -7.9) years old. The prevalence of metabolic syndrome in steel workers was 17.9%. The prevalence of metabolic syndrome of those who exposed to high temperature was 18.8%, higher than that of those who did not expose to high temperature (5.3%), there was a statistically significant difference (P < 0.05). The prevalence of metabolic syndrome of those who exposed to noise was 20.6%, higher than that of those who did not exposed to noise (14.0%) (P < 0.05). After adjusting for the effects of confounding factors, the prevalence of MS those who exposed to high temperatures and noise is 1.118 times as high as that of those who did not exposed to high temperatures and noise. CONCLUSIONS: The combined effects of heat and noise is related to the increasing prevalence of MS of steel workers.