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Objective: To compare the difference in the clinical therapeutic effect on dysmenorrhea in the patients with adenomyosis between acupuncture and ibuprofen sustained release capsules. Methods: A total of 40 patients were randomized into an acupuncture group and an ibuprofen group, 20 cases in each one. The treatment was given consecutively for 3 menstrual cycles and the follow-up lasted for 2 menstrual cycles. The score of visual analogue scale (VAS) at the most painful time during menstruation, menstrual flow, the score of COX menstrual symptom scale (CMSS) and the score of endometriosis health profile-5 (EHP-5), as well as the patients’ satisfaction and acceptance were compared between the two groups. Results: Three menstrual cycles after treatment, the VAS score at the most painful time, menstrual flow, CMSS score and EHP-5 score were all lower than those before treatment in either group, with statistical significance (all P 0.05), the menstrual flow was lower (P > 0.05), CMSS score was higher (P 0.05). The score of the patients’ satisfaction and acceptance in the acupuncture group were all higher than the ibuprofen group (both P Conclusion: Acupuncture is effective for analgesia and symptom-relief and the long-term effect is superior to the oral administration of ibuprofen.

Poly(ethylene oxide) (PEO) and its derivatives based gel polymer electrolytes (GPEs) are severely limited in advanced and safe lithium-ion batteries (LIBs) owing to the intrinsically high flammability of liquid electrolytes and PEO. Directly adding flame retardants to the GPEs can suppress their flammability and thus improve the safety of LIBs, but results in deteriorative electrochemical performance. Herein, a novel GPE with chemically bonded flame retardant (i.e. diethyl vinylphosphonate) in cross-linked polyethylene glycol diacrylate matrix, featuring both high-safety and high-performance, is designed. This as-prepared GPE storing the commercial 1 mol L−1 LiPF6 electrolyte resists high temperature of 200 °C and cannot be ignited as well as possesses a high ionic conductivity (0.60 mS cm−1) and good compatibility with lithium. Notably, the LiFePO4/Li battery with this GPE delivers a satisfactory capacity of 142.2 mA h g−1 and a superior cycling performance with a capacity retention of 96.3% and a coulombic efficiency of close to 100% for 350 cycles at 0.2 C under ambient temperature. Furthermore, the battery can achieve steady charge–discharge for 100 cycles with a coulombic efficiency of 99.5% at 1 C under 80 °C and run normally even at a high temperature of 150 °C or under the exposure to butane flame. Differential scanning calorimetry manifests significantly improved battery safety compared to commercial battery systems. This work provides a new pathway for developing next-generation advanced LIBs with enhanced performance and high safety.

In this study, a boron doped diamond (BDD) electrode (RSM2), fabricated at a boron/carbon (B/C) ratio = 0.75%, a carbon/hydrogen (C/H) ratio = 1.00%, and a reaction chamber pressure (P) = 5.00 torr, exhibited the best performance in terms of electrochemical degradation of guaifenesin [guaiacol glyceryl ether (GGE)] and total organic carbon (TOC) removal among 11 BDD electrodes prepared according to the response surface methodology (RSM). Associated with the B/C, C/H, and P parameters, BDD's diamond crystallite structure, graphite-sp2 C, and grain size influenced the performance of the fabricated BDD electrodes. At 0.125 A cm−2 and 25 °C, the pseudo-first order reaction rate constants of the GGE and TOC removals were 0.33 and 0.031 min−1, respectively, and such removals were better in 0.5 M Na2SO4 than in real hospital wastewater. Both direct and indirect oxidation of GGE occurred during electrolysis. Solution pH affected the indirect oxidation of GGE by •OH, SO4•−, or persulfate electrochemically generated during electrolysis. Several intermediates, including guaiacol, quinones, (aromatic and aliphatic) acids, and hexane-2,5-dione were detected and used to picture the GGE degradation pathways.

The general problem under consideration is the determination of the best (i.e., smallest) constant C p , q , r such that ‖ X Y − Y X ‖ p ≤ C p , q , r ‖ X ‖ q ‖ Y ‖ r for all n × n matrices X and Y , where ‖ ⋅ ‖ p is the Schatten p-norm. Among the open situations, the problem is solved when (i) 2 p ∞ , q = r = 1 ; (ii) 2 p ∞ , q = 1 , 1 r 2 , and X, Y are 2 × 2 real matrices. The result for (i) is obtained via the study of the region (recently obtained in [5] ) of singular values of the commutator X Y − Y X , where X and Y are normalized rank one matrices. As a result of independent interest, for 2 × 2 real matrices, the region of singular values of the commutator X Y − Y X , where X is rank one and normalized, and ‖ Y ‖ r = 1 , is determined. The result for (ii) is a consequence of the case when r lies between 1 and 2.

Published evidences have shown that autophagy plays an important role in silica-induced lung inflammation and collagen deposition. Our previous study found that the level of growth arrest-specific protein 6 (Gas6) in bronchoalveolar lavage fluid was increased after silica exposure. However, it is unclear whether Gas6 is involved in the regulation of silica-induced autophagy dysfunction. In this study, we observed an autophagosomes accumulation in wild-type C57BL/6 (WT) mice lung after silica intratracheal instillation and then investigated whether genetic loss of Gas6 (Gas6−/−) could ameliorate it. Our data showed that Gas6−/− mice exhibited a limited autophagosomes accumulation from days 7–84 after silica exposure, revealed by reduced induction and increased degradation of autophagosomes in mice lung tissue. Interestingly, silica particles could elevate the expression of Mer receptor, which was significantly decreased in Gas6−/− mice (P

A novel and green method to prepare porous membrane is reported by simply blending methylcellulose (MC) and lithium polymethacrylic acid (LiPMA) in water. Thanks to the coordination between oxygen atom in MC and Li+ in LiPMA and subsequent micro-phase separation between them, a porous membrane can be obtained after water evaporated. A series of membranes with different pore size and morphology are prepared by controlling the mass ratio of MC/LiPMA. All the membranes exhibit good thermal and electrochemical stability. With the increasing proportion of LiPMA, the obtained membrane has higher electrolyte uptake, resulting in higher ionic conductivity of corresponding gel polymer electrolyte (GPE). When the mass ratio is 5:20, the membrane has the highest the lithium ion transference (0.57), and the GPE reveals the higher ionic conductivity of 0.65 mS cm−1 at room temperature. What's more, the aforementioned GPE exhibits excellent discharge capacity and good cycling performance. Without use of any organic solvents and tedious preparation process, this novel method is environmentally friendly and low-cost, and the obtained GPE exhibits excellent performance, which has a greatly commercial potential.

Spot continual induction hardening (SCIH) is one kind of selective surface treatments, which has been proven to be appropriate for improving the tribological property and the fatigue behavior of specific areas of treated components. In our work, an electromagnetic-thermal-mechanical-metallurgical coupled numerical model was developed based on a novel co-simulation of ANSYS and ABAQUS/standard via making use of these two commercial finite element softwares' respective advantages to describe the SCIH process. The simulated results agreed well with experimental data in temperature development and the distributions of hardness, phase and residual stresses. The relationship between the inductor velocity and surface characteristics was discussed and the optimization of induction coil velocity was carried out based on the validated numerical model.

Acrolein is a significant high priority hazardous air pollutant with pulmonary toxicity and the leading cause of most noncancer adverse respiratory effects among air toxics that draws great attention. Whether and how acrolein exposure impacts pulmonary function remain inconclusive.To assess the association of acrolein exposure with pulmonary function and the underlying roles of oxidative DNA damage, inflammation, and pulmonary epithelium integrity.Among 3,279 Chinese adults from the Wuhan-Zhuhai cohort, associations of urinary acrolein metabolites (N-Acetyl-S-(2-carboxyethyl)-L-cysteine, CEMA; N-Acetyl-S-(3-hydroxypropyl)-L-cysteine, 3HPMA) as credible biomarkers of acrolein exposure with pulmonary function were analyzed by linear mixed models. Joint effects of biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine), inflammation (C-reactive protein, CRP), and pulmonary epithelium integrity (Club cell secretory protein, CC16) with acrolein metabolites on pulmonary function and the mediating roles of these biomarkers were assessed. Besides, a subgroup (N = 138) was randomly recruited from the cohort to assess the stabilities of acrolein metabolites and their longitudinal associations with pulmonary function change in three years.Significant inverse dose-response relationships between acrolein metabolites and pulmonary function were found. Each 10-fold increment in CEMA, 3HPMA, or ΣUACLM (CEMA + 3HPMA) was cross-sectionally related to a 68.56-, 40.98-, or 46.02-ml reduction in FVC and a 61.54-, 43.10-, or 50.14-ml reduction in FEVAcrolein exposure of general adults was cross-sectionally and longitudinally related to pulmonary function decline, which was aggravated and/or partly mediated by oxidative DNA damage, inflammation, and pulmonary epithelium injury.

Background: Hearing loss has become an increasingly prevalent disability and has greatly increased the global burden of diseases. However, evidences on the associations between hearing loss and total and cause-specific mortality are limited. Thus, we aimed to investigate the associations of hearing loss with total and cause-specific mortality among US adults. Methods: 11,732 individuals derived from the National Health and Nutrition Examination Survey (NHANES) 1999-2012 were included in this study. Data of death was extracted from the NHANES Public-Use Linked Mortality File through December 31, 2015. Cox proportional hazards models were used to explore the associations between hearing loss and total or cause-specific mortality. A meta-analysis was conducted to summarize the epidemiological evidences on the association of hearing loss with total mortality. Findings: A total of 1,253 deaths occurred with a median follow-up of 12.15 years. Significant positive dose-response relationship between hearing loss in speech frequency and total mortality was observed, and the HRs and 95% CIs were 1.16 (0.91, 1.47), 1.54 (1.19, 2.00) and 1.85 (1.36, 2.50), respectively for mild, moderate and severe speech-frequency hearing loss (SFHL) with a Ptrend of 0.0003. In addition, moderate (HR: 1.90, 95%CI: 1.20-3.00) and greater (3.50, 1.38-8.86) SFHL significantly elevated risk of heart diseases mortality. With regard to the frequency, hearing thresholds of >25 dB at 500, 1000, or 2000 Hz were significantly associated with elevated mortality from all causes (1.40, 1.17-1.68; 1.44, 1.20-1.73; and 1.33, 1.10-1.62, respectively) and heart diseases (1.89, 1.08-3.34; 1.95, 1.21-3.16; and 1.89, 1.16-3.09, respectively). The meta-analysis further revealed the positive association between hearing loss and total mortality (pooled HR: 1.33, 95%CI: 1.11-1.60). Interpretation: Hearing loss is associated with increased risks of total mortality and heart diseases mortality, especially for hearing loss at speech frequency. Funding Statement: National Natural Science Foundation of China (81903291). Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The NHANES protocol was approved by the NCHS Ethics Review Board and written informed consent was obtained from all participants.

We aim to analyze the effects of polycyclic aromatic hydrocarbons (PAHs) exposure and genetic predisposition on blood lipid through a longitudinal epidemiological study.We enrolled 4,356 observations who participated at baseline (n = 2,435) and 6-year follow-up (n = 1,921) from Wuhan-Zhuhai cohort. Ten urinary PAHs metabolites and blood lipid (i.e., total cholesterol [TC], triglycerides [TG], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) were measured at both baseline and follow-up. The polygenic risk scores (PRS) of blood lipid were constructed by the corresponding genome-wide association studies. Linear mixed models were fit to identify associations between urinary PAHs metabolites, blood lipid, and lipid-PRSs in the repeated-measure analysis. Besides, longitudinal relationships of blood lipid with urinary PAHs metabolites and respective lipid-PRSs were examined by using linear regression models.Compared with subjects who had persistently low urinary total hydroxyphenanthrene (ΣOHPh), those with persistently high levels had an average increase of 0.137 mmol/l for TC and 0.129 mmol/l for LDL-C over 6 years. Each 1-unit increase of TC-, TG-, LDL-C-, and HDL-C-specific PRS were associated with an average increase of 0.438 mmol/l for TC, 0.264 mmol/l for TG, 0.198 mmol/l for LDL-C, and 0.043 mmol/l for HDL-C over 6 years, respectively. Compared with subjects who had low genetic risk and persistently low ΣOHPh, subjects with high LDL-specific PRS and persistently high ΣOHPh had an average increase of 0.652 mmol/l for LDL-C.Our results suggest that high-level ΣOHPh exposure is associated with an average increase of LDL-C over 6 years, and those relationships can be aggravated by a higher LDL-C-genetic risk. No significant relationships were observed between other PAHs metabolites (including hydroxynaphthalene, hydroxyfluorene, and hydroxypyrene) and blood lipid changes over 6 years. Our findings emphasize the importance of preventing PAHs exposure, particularly among those with a higher genetic predisposition of hyperlipidemia.

Acrylamide (ACR) exposure and consequent health hazards are alarming public health issues that attract worldwide concern. The World Health Organization urges more researches into health hazards from ACR exposure. However, whether and how ACR exposure increases cardiovascular risk remain unclear, and we sought to address these issues in this prospective cohort study conducted on 3024 general adults with 3-year follow-up (N = 871 at follow-up). Individual urinary ACR metabolites (N-Acetyl-S-(2-carbamoylethyl)-L-cysteine [AAMA] and N-Acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine [GAMA]) as credible biomarkers of ACR exposure were detected to assess their cross-sectional and longitudinal relationships with 10-year cardiovascular disease (CVD) risk, a well measure of overall cardiovascular risk. Besides, biomarkers of oxidative stress (urinary 8-hydroxy-deoxyguanosine [8-OHdG] and 8-iso-prostaglandin-F2α [8-iso-PGF2α]) and inflammation (circulating mean platelet volume [MPV] and plasma C-reactive protein [CRP]) as well as plasma transforming growth factor-β1 (TGF-β1) were measured to assess their mediating/mechanistic roles in the relationships of ACR metabolites with 10-year CVD risk. We found AAMA, GAMA, and ΣUAAM (AAMA + GAMA) were cross-sectionally and longitudinally related to increased 10-year CVD risk with odds ratios (95% confidence intervals [CIs]) of 1.32 (1.04, 1.70), 1.81 (1.36, 2.40), and 1.40 (1.07, 1.82), respectively, and risk ratios (95% CIs) of 1.99 (1.10, 3.60), 2.48 (1.27, 4.86), and 2.13 (1.15, 3.94), respectively. Furthermore, 8-OHdG, 8-iso-PGF2α, MPV, CRP, and TGF-β1 were found to significantly mediate 8.06-48.92% of the ACR metabolites-associated 10-year CVD risk increment. In summary, daily ACR exposure of general adults was cross-sectionally and longitudinally associated with increased cardiovascular risk, which was partly mediated by oxidative stress, inflammation, and TGF-β1, suggesting for the first time that ACR exposure may well increase cardiovascular risk of general adult population partly by mechanisms of inducing oxidative stress, inflammation, and TGF-β1. Our findings have important public health implications that provide potent epidemiological evidence and vital mechanistic insight into cardiovascular risk increment from ACR exposure.

Wnt5a is a key mediator of non-canonical Wnt signaling, and an early indicator of epithelial injury and lung dysfunction. Polycyclic aromatic hydrocarbons (PAHs) could induce acute pulmonary pathogenesis, of which the underlying mechanism remains unclear. To elucidate the potential role of Wnt5a-mediated non-canonical Wnt-YAP/TAZ signaling in the lung injury induced by short-term exposure of benzo(a)pyrene (BaP, a representative PAHs), intratracheally instilled mouse model was used and further interfered with its Wnt5a level by small molecule antagonists and agonists. Our data revealed that BaP exposure induced the lung inflammatory response and reduced the expression of Clara cell secretory protein (CC16) in a dose-dependent manner. More importantly, the activation of Wnt5a and downstream YAP/TAZ were accompanied with the enhanced release of epithelial-derived thymic stromal lymphopoietin and interleukin-33, which acted as pro-inflammatory cytokines. Functionally, inhibition of Wnt5a attenuated the BaP-induced inflammation and recuperated CC16 expression, as well as suppressed the epithelial cytokines release. Whereas promoting Wnt5a expression affected the toxic effects of BaP oppositely. Our findings together suggest that Wnt5a is a potential endogenous regulator in lung inflammation and airway epithelial injury, and Wnt5a-YAP/TAZ signaling contributes to lung dysfunction in acute exposure to BaP.

We aim to investigate the long-term adverse effects of polycyclic aromatic hydrocarbons (PAHs) exposure on heart rate variability (HRV) reduction, and to assess the potential role of transforming growth factor-β1 (TGF-β1) in such relationship. We enrolled 2985 adult residents with 4100 observations who participated at baseline and 6-years follow-up from Wuhan-Zhuhai cohort. Ten detectable urinary PAHs metabolites and two HRV indices were repeatedly measured at baseline and follow-up; and plasma TGF-β1 levels were also determined for all subjects. We observed that both total urinary low molecular weight PAHs (ΣLWM OH-PAH) and total urinary high molecular weight PAHs (ΣHWM OH-PAH) were negatively associated with HRV reductions (P 0.05). Subjects with persistent high levels of ΣHWM OH-PAH had a significant reduction in HRV over 6 years, and the incensement of TGF-β1 could aggravate above adverse effects in a dose-response manner. All kinds of PAHs were positively associated with plasma TGF-β1 elevation, which in turn, were negatively related to HRV indices. Increased TGF-β1 significant mediated 1.34-3.62% of PAHs-associated HRV reduction. Our findings demonstrated that long-term high levels of PAHs exposure could cause HRV reductions, and TGF-β1 may play an essential role in such association.

Whether propylene oxide (PO) exposure is associated with hyperglycemia were rarely explored. We aimed to determine the relationship between PO exposure and glucose metabolism, and potential role of oxidative stress. Among 3294 Chinese urban adults, urinary PO metabolite (N-Acetyl-S-(2-hydroxypropyl)-L-cysteine, 2HPMA), biomarkers of oxidative DNA damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) and lipid peroxidation (8-isoprostane, 8-iso-PGF2α) in urine were determined. The associations of 2HPMA with 8-OHdG, 8-iso-PGF2α, fasting plasma glucose (FPG), and risk of diabetes were explored. The roles of 8-OHdG and 8-iso-PGF2α on association of 2HPMA with FPG and risk of diabetes were detected. After adjusted for potential confounders, each 1-unit increase in log-transformed concentration of 2HPMA was associated with a 0.15-mmol/L increase in FPG level, and the adjusted OR (95% CI) of diabetes by the associations of log-transformed urinary 2HPMA concentrations was 1.47 (95% CI: 1.03–2.11). Combination effects of 2HPMA with 8-OHdG or 8-iso-PGF2α on risk of diabetes were detected, and elevated 8-iso-PGF2α significantly mediated 34.5% of the urinary 2HPMA-associated FPG elevation. PO exposure was positively associated with FPG levels and risk of diabetes. PO exposure combined with DNA oxidative damage or lipid peroxidation may increase the risk of diabetes, and lipid peroxidation may partially mediate the PO exposure-induced FPG elevation.

The paper concerns generalizations of the Bottcher–Wenzel inequality to contracted products of tensors. We show that the best constant in the inequality is as expected in some cases and present an example where the best constant is larger than expected.