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Separation of dyes and antibiotics is particularly important in wastewater treatment. In this work, the hydrophilic modified polyvinylidene fluoride (PVDF) membranes were prepared by deposition of halloysite nanotubes (HNTs), tannic acid (TA) and ferric chloride (FeCl3). The surface morphology of the modified membranes was studied using scanning electron microscopy (SEM) and atomic force microscopy (AFM). In addition, the Fourier transform infrared (FTIR) and X-ray photoelectron spectroscopy (XPS) were used to evaluate the chemical compositions of the membrane. The measurements of water contact angle (CA) and pure water flux (Jw) show that the PVDF membrane has excellent permeability and hydrophilicity. The PVDF modified membrane has good separation performance for dyes, and the rejection ratios of methyl orange, methylene blue and rhodamine B were 98.2%, 94.6% and 96.9%, respectively. In addition, the rejection ratios of modified membrane for tetracyclines and bisphenol A were significantly improved. Most important of all, the TA-Fe(III)/HNTs/PVDF membrane has excellent antifouling performance after cycles tests. These results indicate that the TA-Fe(III)/HNTs/PVDF modified membranes have a great application prospect in dye and antibiotic wastewater treatment.

Purpose: To investigate the role of dexmedetomidine in gastric ischemia/reperfusion injury using gastric mucosal epithelial cell (GES-1) model. Methods: GES-1 were subjected to oxygen-glucose deprivation conditions, followed by increasing dexmedetomidine concentrations (0.5, 1.0, or 1.5 μM) for 4 h of reoxygenation. Cell viability and apoptosis were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide and flow cytometry, respectively. Oxidative stress and inflammation were analyzed by enzyme-linked immunosorbent assay (ELISA). Results: Oxygen-glucose deprivation conditions induced cytotoxicity in GES-1 by decreasing cell viability and increasing apoptosis. Dexmedetomidine treatment significantly increased the cell viability of hypoxia/reoxygenation-induced GES-1 (p < 0.01) but reduced apoptosis. Dexmedetomidine also attenuated the hypoxia/reoxygenation-induced increase in malondialdehyde and myeloperoxidase, but the decrease in superoxide dismutase and glutathione in GES-1. Moreover, upregulated tumor necrosis factor-α, interleukin (IL)-1β, and IL-18 in hypoxia/reoxygenation-induced GES-1 was downregulated by dexmedetomidine treatment. Dexmedetomidine also enhanced IL-10 levels and inhibited proinflammatory factor production (p < 0.01). High-mobility group box 1 (HMGB1) protein in GES-1 was upregulated by hypoxia/reoxygenation but decreased by dexmedetomidine. HMGB1 over-expression attenuated the dexmedetomidine-induced increase in cell viability and the decrease in apoptosis, oxidative stress, and inflammation in hypoxia/reoxygenation-induced GES-1 (p < 0.01). Conclusion: Dexmedetomidine protects GES-1 against ischemia/reperfusion-induced apoptosis, inflammation, and oxidative stress by inhibiting HMGB1, thus providing a potential strategy for treating gastric ischemia/reperfusion injury. Keywords: Dexmedetomidine; gastric mucosal epithelial cells; Ischemia/reperfusion; Apoptosis; Inflammation; Oxidative stress; High-mobility group box 1 (HMGB1)

This network meta-analysis was conducted to compare the predictive value of eight SNPs on the efficacy of antidepressants in major depressive disorder (MDD), including 5-HTTLPR, 5HTR2A (rs6311, rs6314, rs7997012 and rs6313), 5HTR2A (rs6295), BDNF (rs6265) and 5HTTSTin2. Databases were searched for related studies published up to December 2019. A total of 16 studies were included in this study. The predictive value were evaluated by the use of the odd ratios (OR) and drawing surface under the cumulative ranking curves (SUCRA). The pairwise meta-analysis indicated that in terms of overall response ratio, the SNPs were not associated with the efficacy of antidepressants in MDD. The result of this network meta-analysis suggested that there was no significant difference in predictive value of eight SNPs on the efficacy of antidepressants in MDD. More research is needed to explore the relationship between SNPs and antidepressant response.

Recently, favorable outcomes of primary anterior cruciate ligament (ACL) repair have been reported in patients with proximal tears and good tissue quality. If the tear involves the midsubstance of the ACL fibers or Sherman type II or III injury, independent primary repair will cause a higher failure rate at long-term follow-up. For these cases, we conduct primary repair and apply an internal brace and single-bundle reconstruction as hybrid augmentation. This hybrid repair technique encourages natural healing of the primary ligament by the internal brace and single-bundle graft as a provisional scaffold during the healing phase, as well as early mobilization. We describe our ACL hybrid repair technique, using a video and illustrations.

The newly discovered Juyuan tungsten deposit is hosted in Triassic granite in the Beishan Orogen, NW China. The tungsten mineralization occurred as quartz veins, and the main ore minerals included wolframite and scheelite. The age, origin, and tectonic setting of the Juyuan tungsten deposit, however, remain poorly understood. According to the mineralogical assemblages and crosscutting relationships, three hydrothermal stages can be identified, i.e., the early stage of quartz veins with scheelite and wolframite, the intermediate stage of quartz veinlets with sulfides, and the late stage of carbonate-quartz veinlets with tungsten being mainly introduced in the early stage. Quartz formed in the two earlier stages contained four compositional types of fluid inclusions, i.e., pure CO2, CO2-H2O, daughter mineral-bearing, and NaCl-H2O, but the late-stage quartz only contained the NaCl-H2O inclusions. The inclusions in quartz formed in the early, intermediate, and late stages had total homogenization temperatures of 230–344 °C, 241−295 °C, and 184−234 °C, respectively, with salinities no higher than 7.2 wt.% NaCl equiv (equivalent). Trapping pressures estimated from the CO2-H2O inclusions were 33−256 MPa and 36−214 MPa in the early and intermediate stages, corresponding to mineralization depths of 3–8 km. Fluid boiling and mixing caused rapid precipitation of wolframite, scheelite, and sulfides. Through boiling and inflow of meteoric water, the ore-forming fluid system evolved from CO2-rich to CO2-poor in composition and from magmatic to meteoric, as indicated by decreasing δ18Owater values from early to late stages. The sulfur and lead isotope compositions in the intermediate-stage suggest that the Triassic granite was a significant source of ore metals. The biotite 40Ar/39Ar age from the W-bearing quartz shows that the Juyuan tungsten system was formed at 240.0 ± 1.0 Ma, coeval with the emplacement of granitic rocks at the deposit. Integrating the data obtained from the studies including regional geology, ore geology, biotite Ar-Ar geochronology, fluid inclusion, and C-H-O-S-Pb isotope geochemistry, we conclude that the Juyuan tungsten deposit was a quartz-vein type system that originated from the emplacement of the granites, which was induced by collision between the Tarim and Kazakhstan–Ili plates. A comparison of the characteristics of tungsten mineralization in East Tianshan and Beishan suggests that the Triassic tungsten metallogenic belt in East Tianshan extends to the Beishan orogenic belt and that the west of the orogenic belt also has potential for the discovery of further quartz-vein-type tungsten deposits.

Polyvinylidene fluoride (PVDF) membranes were surface-modified via a simple coating method for improvement of the hydrophilicity performance. In this work, TP/PEI/PVDF modified membrane was successfully prepared by using tea polyphenol as a multifunctional coating. The physicochemical properties of membranes were characterized by Fourier transform infrared spectroscopy, X-ray energy-dispersive spectrometry, X-ray photoelectron spectroscopy scanning electron microscopy and atomic force microscopy. The water contact angle, pure water flux and methylene blue rejection ratio of membranes were investigated in detail. Compared with the pristine membrane, the water contact angle of the modified membrane decreased to 48.8°, and the rejection ratios were increased to 95.2% when the modified membrane was used to separate methylene blue. In addition, the modified membrane showed excellent antifouling performance in the experiment, and the flux recovery ratio still reached 84.6% after three fouling/washing cycles. In the oxidation experiment, the modified membranes were immersed in KMnO4 solution for 6 h, and the results show that the water contact angle, pure water flux and methylene blue rejection of the modified membranes only have changed slightly. Therefore, this study could have a great potential for widening the application of membranes in the treatment of dye wastewater containing oxidants.

A novel Bi2MoO6/reduced graphene oxide/BiOBr (Bi2MoO6/RGO/BiOBr) composite was successfully synthesized via a facile solvothermal synthesis and precipitation method. The Bi2MoO6/RGO/BiOBr composite was characterized by X-ray diffraction, X-ray photoelectron spectroscopy, scanning electron microscopy, transmission electron microscopy, UV–vis diffuse reflectance spectroscopy (UV–vis DRS) and photoelectrochemical measurements. The photocatalytic properties were explored for removal of methylene blue (MB) and norfloxacin (NFX) under visible-light irradiation. The Bi2MoO6/RGO/BiOBr composite exhibits the highest degradation rate compared with Bi2MoO6, BiOBr and Bi2MoO6/BiOBr composite, and that removal ratios of MB and NFX were 96.93% and 78.12%, respectively. A Z-scheme catalytic mechanism suitable for the system was proposed based on the results of UV–vis DRS, free radical trapping experiments and M–S carve analysis, in which RGO as an electronic medium can accelerate electron transfer. It is noteworthy that the close contact interface structure promotes the separation of electrons and holes and improves the photocatalytic performance.

Objective The aim of this review is to identify and summarize factors that are associated with public attitudes towards people with various disabilities systematically. Methods An electronic search of three databases was performed (Medline, EMBASE and Cochrane) covering the period from 1950 to present. A comprehensive search strategy was developed and the lists of citations were screened for potential eligible studies. Only quantitative studies using valid measurements were included, and the methodological quality of included studies was appraised based on three criteria (sample, measurement, analysis) by two independent reviewers. Results The initial electronic search yielded 995 articles after duplicates removed, and 27 studies met the eligibility criteria were included in the study. Three categories of the factors were found to be associated with the public attitudes, which are related to the attitude provider, disabled people, and society respectively. Specifically, the more people know about disabilities, the more likely they were to have positive attitude; and the frequency and quality of the contact with the disabled are also proved to be influential to the attitudes. Meanwhile, the type of disability is also closely correlated to the public’s attitude towards the disabilities. Conclusion People’s knowledge of the disability and their contact with individuals with disabilities are the main influential factors in public attitudes towards persons with disabilities.

BACKGROUND Diabetic wound (DW) treatment is a serious challenge for clinicians, and the underlying mechanisms of DWs remain elusive. We sought to identify the critical genes in the development of DWs and provide potential targets for DW therapies. MATERIAL AND METHODS Datasets of GSE38396 from the Gene Expression Omnibus (GEO) database were reviewed. Pathway analysis was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology term analyses were carried out, and Cytoscape software (Cytoscape 3.7.2) was used to construct the protein interaction network. Serum samples from patients with diabetes and control participants were collected, and the expression of estrogen receptor 1 (ESR1) was measured by quantitative reverse-transcription polymerase chain reaction. In addition, the function of ESR1 in human skin fibroblasts was investigated in vitro. RESULTS Eight samples were analyzed using the Morpheus online tool, which identified 637 upregulated and 448 downregulated differentially expressed genes. The top 5 KEGG pathways of upregulated differentially expressed genes were associated with sphingolipid metabolism, estrogen signaling, ECM-receptor interaction, MAPK signaling, and PI3K-Akt signaling. The hub genes for DWs were JUN, ESR1, CD44, SMARCA4, MMP2, BMP4, GSK3B, WDR5, PTK2, and PTGS2. JUN, MMP2, and ESR1 were the upregulated hub genes, and ESR1 was found to be consistently enriched in DW patients. Inhibition of ESR1 had a stimulative role in human skin fibroblasts. CONCLUSIONS ESR1 was identified as a crucial gene in the development of DWs, which suggests potential therapeutic targets for DW healing.

The study of income distribution, education input and education return rate has always been a hot topic in the theoretical circle. Most of the existing researches have drawn a conclusion that there is a significant positive correlation between the years of education and the income level. There is a two-way causal relationship between income distribution and education. In addition, the distribution of education and the rate of return on education will also have an impact on education. This paper aims to focus on the impact of gender differences in income distribution on education based on previous research, while focusing on the distribution of education and the rate of return on education in different genders. Based on the specific quantitative indicators of the differences, some theoretical support and policy recommendations on education and education reform are given.

Uterine fibroid embolization has been proven effective in treating symptomatic uterine fibroids for appropriately selected patients as an alternative option to surgical approaches. The most common adult uterine position is anteverted followed by a retroverted uterus which can be found in roughly 15%-20% of normal adult females. The positioning of the uterus can change from anteversion to retroversion due to the filling of bladder or during pregnancy; however, changing from retroverted to anteverted position without prior pregnancy or endometriosis is rather uncommon. Here, we describe a case of uterine orientation change from retroversion to anteversion presenting 6 months after uterine fibroid embolization. Keywords: Anteverted uterus, Retroverted uterus, Anteversion, UFE, Flipped uterus, Tipped uterus

Background Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in angiogenesis and maintenance of endothelial integrity. Whether circulating BDNF levels are associated with von Willebrand factor (vWF) levels, which are indicators of endothelial dysfunction is not known. This study investigated the association between plasma BNDF and vWF levels and whether these biomarkers could predict cardiovascular events at a 12-month follow-up in patients with stable coronary artery disease (CAD). Methods We recruited 234 patients with suspected angina pectoris. Subjects were divided into CAD (n = 143) and control (n = 91) groups based on coronary angiography. Plasma BDNF and vWF levels were measured using ELISA. Patients were followed-up for one year, and information on adverse cardiac events was collected. Results CAD patients exhibited significantly lower plasma BDNF and higher vWF levels than those of control patients. High vWF levels were associated with low BDNF levels even after adjustment for age, gender, low-density lipoprotein (LDL) levels, and the presence of diabetes mellitus. A receiver operating characteristic curve was used to determine whether low BDNF and high vWF levels could predict adverse cardiovascular events. The area under the curve for vWF and the inverse of BDNF were 0.774 and 0.804, respectively. Conclusions These findings suggest that endothelial dysfunction is an important determinant of the impaired circulating BDNF levels, and they further reflected cardiovascular prognosis in stable CAD patients.

Diabetes and vascular calcification are intrinsically linked. We previously reported that advanced glycation end products (AGEs) accelerate calcium deposition in vascular smooth muscle cells (VSMCs) via excessive oxidative stress. However, the underlying mechanism remains poorly understood. Pyruvate dehydrogenase kinase 4 (PDK4) is an important mitochondrial matrix enzyme in cellular energy metabolism. Since hyperactivation of PDK4 has been reported in calcified vessels and in patients with diabetes mellitus, inhibition of PDK4 expression may be a strategy for the prevention of diabetic vascular calcification. In this study, we used a rat VSMC model to investigate the role of PDK4 in diabetic vascular calcification and further explore the underlying mechanisms. We observed that Nε-carboxymethyl-lysine (CML), which is a major immunogen of AGEs, accelerated calcium deposition in VSMCs through PDK4 activation. An elevated level of reactive oxygen species (ROS) acted as a signal transduction intermediate to increase PDK4 expression. Either inhibition of PDK4 expression or RAGE (receptor for AGEs) blockade attenuated CML-induced VSMC calcification, as shown by decreased alkaline phosphatase (ALP) activity and runt-related transcription factor 2 (RUNX2) expression. Glucose consumption and lactate production were increased during CML-induced VSMC calcification. Importantly, CML accelerates glycolysis in VSMCs via a PDK4-dependent pathway. In conclusion, this study demonstrates a novel mechanism by which CML promotes VSMC calcification via PDK4 activation and alters glucose metabolism in VSMCs.

Clustering is an important technique in data mining. The innovative algorithm proposed in this paper obtains clusters by first identifying boundary points as opposed to existing methods that calculate core cluster points before expanding to the boundary points. To achieve this, an affine space-based boundary detection algorithm was employed to divide data points into cluster boundary and internal points. A connection matrix was then formed by establishing neighbor relationships between internal and boundary points to perform clustering. Our clustering algorithm with an affine space-based boundary detection algorithm accurately detected clusters in datasets with different densities, shapes, and sizes. The algorithm excelled at dealing with high-dimensional datasets.

Background MicroRNAs (miRNAs) have emerged as the critical modulators of the tumorigenesis and tumor progression. Methods The levels of miR-663 in ovarian cancer cell lines and clinical tissues were detected using qRT-PCR assays. The Transwell invasion and wound healing assay were conducted to assess the roles of miR-663 in the migration and invasion of ovarian cancer cell in vitro. Rescue assays were carried out to confirm the contribution of tumor suppressor candidate 2 (TUSC2) in the aggressiveness of cancer cell which was regulated by miR-663. Results The levels of miR-663 were up-regulated in ovarian cancer tissues in comparison with the corresponding normal tissues. Up-regulation of miR-663 increased the proliferation, colony formation, migration and invasion of ovarian cancer SKOV3 cell. Additional, over-expression of miR-663 increased the tumor growth of SKOV3 in xenograft model. Bioinformatics analysis and luciferase reporter assay identified that miR-663 decreased the level of TUSC2 via binding to the 3′-UTR of TUSC2 gene. Finally, the expression of TUSC2 was inversely associated with the level of miR-663 in ovarian carcinoma tissue and over-expression of TUSC2 inhibited the migration and invasion abilities of SKOV3 that was promoted by miR-663. Conclusion Altogether, these results indicate that miR-663 acts as a potential tumor-promoting miRNA through targeting TUSC2 in ovarian cancer. Electronic supplementary material The online version of this article (10.1186/s40659-019-0219-6) contains supplementary material, which is available to authorized users.

Constructing efficient and green photocatalysts to remove organic pollutants is of great significance to environmental purification. We used the facile one-pot hydrothermal method to couple lamellar SnS2 with RGO and BiOBr to synthesize a novel Z-scheme SnS2/RGO/BiOBr ternary photocatalyst. Compared with the single component, the obtained ternary composite material has enhanced photodegradation activity.It can be concluded that the 0.2SnS2/RGO/BiOBr composite exhibits the best performance, 99.15% methylene blue removed after 15 min irradiation,reaching a 38.9% improvement compared to the pure BiOBr. Besides, the degradation rate of norfloxacin reached 81.6%. The excellent photocatalytic properties were studied by photoluminescence spectroscopy, and a Z-scheme charge transfer mechanism appropriate for SnS2/RGO/BiOBr composite was proposed according to the results of UV–vis diffuse reflectance spectroscopy and free radical capture experiments, in which RGO acted as an electron transfer medium to accelerate the transfer of photogenerated electrons between SnS2 and BiOBr, thereby effectively limiting the recombination of photogenerated carriers.

Germline polymorphisms are linked with differential survival outcomes in cancers but are not well studied in nasopharyngeal carcinoma (NPC). Here, a two‐phase association study is conducted to discover germline polymorphisms that are associated with the prognosis of NPC. The discovery phase includes two consecutive hospital cohorts of patients with NPC from Southern China. Exome‐wide genotypes at 246 173 single nucleotide polymorphisms (SNPs) are determined, followed by survival analysis for each SNP under Cox proportional hazard regression model. Candidate SNP is replicated in another two independent cohorts from Southern China and Singapore. Meta‐analysis of all samples (n = 5553) confirms that the presence of rs1131636‐T, located in the 3′‐UTR of RPA1, confers an inferior overall survival (HR = 1.33, 95% CI = 1.20–1.47, P = 6.31 × 10−8). Bioinformatics and biological assays show that rs1131636 has regulatory effects on upstream RPA1. Functional studies further demonstrate that RPA1 promotes the growth, invasion, migration, and radioresistance of NPC cells. Additionally, miR‐1253 is identified as a suppressor for RPA1 expression, likely through regulation of its binding affinity to rs1131636 locus. Collectively, these findings provide a promising biomarker aiding in stratifying patients with poor survival, as well as a potential drug target for NPC., This study reveals a functional germline polymorphism at RPA1 to be associated with survival outcome of patients with nasopharyngeal carcinoma (NPC). The study also shows that RPA1 is able to regulate tumor progression and radioresistance in NPC cells. Together, the study proposes the genetic variation of RPA1 as a promising germline biomarker for precise treatment planning and prognosis of NPC.

Cardiovascular disease (CVD) is a leading cause of mortality and morbidity among patients with diabetes. Endothelial dysfunction is an early physiological event in CVD. Metformin, a common oral antihyperglycemic agent, has been demonstrated to directly affect endothelial cell function. Brain-derived neurotrophic factor (BDNF), originally discovered in the brain as a neurotrophin, has also been reported to play a protective role in the cardiovascular system. In our study, we demonstrated that high glucose (HG) reduced cell proliferation and induced cell apoptosis via changes in BDNF expression and that metformin reversed the effects of HG injury by upregulating BDNF expression. Furthermore, we found that cyclic AMP response element binding (CREB) phosphorylation was reduced in HG-treated human umbilical vein endothelial cells (HUVECs), and this effect was reversed by the metformin treatment. However, the metformin effect on BDNF levels in HG-incubated HUVECs was blocked by a CREB inhibitor, which indicated that BDNF expression is regulated by metformin through CREB activation. In addition, we found that adenosine monophosphate-activated protein kinase (AMPK) activation is involved in CREB/BDNF regulation in HG-incubated HUVECs treated with metformin and that an AMPK inhibitor impaired the protective effects of metformin on HG-treated HUVECs. In conclusion, this study demonstrated that metformin affects cell proliferation and apoptosis via the AMPK/CREB/BDNF pathway in HG-incubated HUVECs.

Arterial media calcification is associated with diabetes mellitus. Previous studies have shown that advanced glycation end products (AGEs) are responsible for vascular smooth muscle cell (VSMC) calcification, but the underlying mechanisms remain unclear. Hypoxia-inducible factor-1α (HIF-1α), one of the major factors during hypoxia, and pyruvate dehydrogenase kinase 4 (PDK4), an important mitochondrial matrix enzyme in cellular metabolism shift, have been reported in VSMC calcification. The potential link among HIF-1α, PDK4, and AGEs-induced vascular calcification was investigated in this study. We observed that AGEs elevated HIF-1α and PDK4 expression levels in a dose-dependent manner and that maximal stimulation was attained at 24 h. Two important HIF-1α-regulated genes, vascular endothelial growth factor A (VEGFA) and glucose transporter 1 (GLUT-1), were significantly increased after AGEs exposure. Stabilization or nuclear translocation of HIF-1α increased PDK4 expression. PDK4 inhibition attenuated AGEs-induced VSMC calcification, which was evaluated by measuring the calcium content, alkaline phosphatase (ALP) activity and runt-related transcription factor 2 (RUNX2) expression levels and by Alizarin red S staining. In addition, the glucose consumption, lactate production, key enzymes of glucose metabolism and oxygen consumption rate (OCR) were decreased during AGEs-induced VSMC calcification. In conclusion, this study suggests that AGEs accelerate vascular calcification partly through the HIF-1α/PDK4 pathway and suppress glucose metabolism.

Background: The osteogenic differentiation of vascular smooth muscle cell (VSMCs) is important for the development of vascular calcification (VC), particularly in diabetes. Exosomes derived from Mesenchymal Stromal Cells (MSCs) are effective against cardiovascular diseases, yet their role in VC remains unclear. Advanced glycation end products (AGEs) inhibit bone marrow stromal cell osteogenesis by targeting osteogenesis-associated genes. Thus, we investigated the role of exosomes derived from MSCs pretreated with AGEs-BSA in VC and its potential mechanisms. Methods: Primary VSMCs and MSCs were isolated from the aorta and bone marrow of Sprague-Dawley rats, respectively. VSMCs were cultured with AGEs-BSA to induce osteogenic differentiation. Exosomes were harvested from MSCs by ultracentrifugation. MSCs and VSMCs were cocultured in Transwells, and exosomes were added to VSMC culture medium to assess their effects on osteogenic differentiation. Double luciferase reporter assay was applied to confirm that miR-146a directly targets the 3' UTR of the thioredoxin-interacting protein (TXNIP) gene. Results: Pretreatment of VSMCs with AGEs-BSA increased the expression of thioredoxin-interacting protein (TXNIP) by inhibiting that of miR-146a, resulting in enhanced ROS production and VSMC calcification. By contrast, the expression of miR-146a in MSCs was increased by AGEs-BSA treatment. Thus, miR-146a was transferred from AGEs-BSA-pretreated or miR-146a-transfected MSCs to VSMCs via exosomes. After coculture with miR-146a-containing exosomes, the AGEs-BSA-mediated increase in VSMC calcification was diminished, accompanied by decreased TXNIP expression and ROS production. Furthermore, TXNIP overexpression counteracted the anti-calcification effects of MSC-derived miR-146a-containing exosomes. In addition, TXNIP was identified as a target gene of miR-146a, and the results of double luciferase reporter assay confirmed that TXNIP was the direct target gene of miR-146a. Conclusions: Exosomes secreted by MSCs pretreated with AGEs-BSA contained a high level of miR-146a, which was transferred to VSMCs and inhibited AGEs-BSA-induced calcification in a TXNIP-dependent manner. Thus, miR-146a-containing exosomes may be a potential therapeutic target for VC.

Exercise induces a number of benefits, including angiogenesis in post‑myocardial infarction (MI); however, the underlying mechanisms have not been fully clarified. Neurotrophic brain‑derived neurotrophic factor (BDNF) serves a protective role in certain adult cardiac diseases through its specific receptor, BDNF/NT‑3 growth factors receptor (TrkB). The present study explored the mechanisms by which exercise improves cardiac function, with a focus on the involvement of the BDNF/TrkB axis. MI rats were assigned to Sham, sedentary, exercise, exercise with K252a (a TrkB inhibitor), and exercise with NG‑nitro‑L‑arginine methyl ester (L‑NAME) groups. The exercise group was subjected to 8 weeks of treadmill running. The results demonstrated that the rats in the exercise group exhibited increased myocardial angiogenesis and improved cardiac function, which was attenuated by K252a. Exercise induced activation of the BDNF/TrkB axis in the ischaemic myocardium and increased serum BDNF levels were abated by exposure to L‑NAME. Improvements in angiogenesis and left ventricular function exhibited a positive association, with changes in serum BDNF. In the in vitro experiments, human umbilical vein endothelial cells were exposed to shear stress (SS) of 12 dyn/cm2 to mimic the effects of exercise training on vascular tissue. An increased tube‑forming capacity, and a nitric oxide (NO)‑dependent prolonged activation of the BDNF/TrkB‑full‑length axis over 12 h, but not the TrkB‑truncated axis, was observed. The SS‑related angiogenic response was attenuated by TrkB inhibition. Overall, these results demonstrate that exercise confers certain aspects of its cardioprotective effects through the activation of the BDNF/TrkB axis in an NO‑dependent manner, a process in which fluid‑induced SS may serve a crucial role.

Background: Gustilo Anderson III B/C open tibial fractures are more difficult to manage than I, II, and III A fractures. These open tibial fractures are often associated with wound infection, soft tissue necrosis, bone nonunion, osteomyelitis or amputation. Staged treatment for this severe trauma is very necessary. Materials and Methods: 25 cases of Gustilo Anderson IIIB/C open tibial fractures with serious soft-tissue defects treated between January 2010 and January 2015 were included in this study. The treatment was administered in three stages. The first stage included emergency debridement, external fixation, repair of damaged main blood vessels and nerves, covering of the wound, and infection control. The second stage involved skin flap or skin graft placement to repair wounds. The third stage involved replacement of the external fixator with an internal fixator and the placement of bone grafts. Results: All the skin flaps or skin grafts survived, and a small necrotic area in the distal flap was observed in only two cases (which resolved spontaneously after the dressing was changed). Bone union occurred at the predicted time in 23 cases, while it was delayed in 2 cases. The rate of excellent and good was 88%. Conclusion: Staged treatment was safe and effective for Gustilo Anderson IIIB/C tibial fractures. The timing for the placement of internal and external fixators and choosing the appropriate skin flap repair technique are important.

Background Single nucleotide polymorphisms (SNPs) located in the vascular endothelial growth factor (VEGF) gene may be correlated with the susceptibility to coronary artery disease (CAD) – although results have been controversial. The aim of this meta–analysis is to clarify the effects of VEGF –2578A/C (rs699947), −1154G/A (rs1570360), +405C/G (rs2010963), and + 936C/T (rs3025039) polymorphisms on CAD risk. Methods Pooled odds ratio (OR) and corresponding 95% confidence intervals (CIs) were calculated to estimate the strength of the association between VEGF gene polymorphisms and CAD risk. Fixed- or random-effects model was used depending on the heterogeneity between studies. Results In total, 13 eligible articles containing 29 studies were analysed. The pooled analysis indicated that the VEGF gene polymorphisms of rs699947, rs2010963, and rs3025039 were associated with an increased risk of CAD, whereas no significant associations were observed with the rs1570360 polymorphism. A subgroup analysis stratified by ethnicity revealed that the rs699947 and rs3025039 polymorphisms were associated with CAD risk in Asian populations. In addition, stratification by control source indicated an increased risk of CAD susceptibility with the rs699947 polymorphism for population–based studies of reduced heterogeneity. Conclusions In summary, we concluded that the VEGF gene polymorphisms rs699947, rs2010963, and rs3025039 are correlated with an elevated CAD risk. Electronic supplementary material The online version of this article (10.1186/s12881-018-0628-3) contains supplementary material, which is available to authorized users.

Variation in the use of inferior vena cava filters (IVCFs) across hospitals has been observed, suggesting differences in quality of care. Hospitalization metrics associated with venous thromboembolism (VTE) patients have not been compared based on IVCF utilization rates using a national sample. We conducted a descriptive retrospective study using the Nationwide Readmissions Database (NRD) to delineate the variability of hospitalization metrics across the hospital quartiles of IVCF utilization for VTE patients. The NRD included all-payer administrative inpatient records drawn from 22 states. Adult (≥ 18 years) patients with VTE hospitalizations with or without IVCF were identified from January 1, 2013 through December 31, 2014 and hospitals were divided into quartiles based on the IVCF utilization rate as a proportion of VTE patients. Primary outcome measures were observed rates of in-hospital mortality, 30-day all-cause readmissions and VTE-related readmissions, cost, and length of stay. Patient case-mix characteristics and hospital-level factors by hospital quartiles of IVCF utilization rates, were compared. Overall, 12.29% of VTE patients had IVCF placement, with IVCF utilization ranging from 0% to 46.84%. The highest quartile had fewer pulmonary embolism patients relative to deep vein thrombosis patients, and older patient ages were present in higher quartiles. The highest quartile of hospitals placing IVCFs were more often private, for-profit, and non-teaching. Patient and hospital characteristics and hospitalization metrics varied by IVCF utilization rates, but hospitalization outcomes for non-IVCF patients varied most between quartiles. Future work investigating the implications of IVCF utilization rates as a measure of quality of care for VTE patients is needed.

Lipoprotein lipase (LPL) is widely linked to lipid and lipoprotein metabolism, but its effects on coronary artery disease (CAD) are not clearly elucidated. The aim of the present study was to clarify the association between LPL gene polymorphisms and CAD susceptibility. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated to estimate the strength of the relationship between LPL gene polymorphisms and CAD risk. Comprehensive electronic databases, including PubMed, EMBASE, Web of Science, and the Cochrane Library, were systematically searched. A total of 45 records containing 80 eligible studies were analyzed. The results indicated an increased risk between the LPL D9N polymorphism and susceptibility to CAD in the dominant genetic model (AA + GA vs. GG: OR = 1.46, 95% CI = 1.14–1.87), whereas the LPL HindIII polymorphism showed a protective effect against CAD under all tested models (GG + GT vs. TT: OR = 0.85, 95% CI = 0.75–0.97; GG vs. TT + TG: OR = 0.62, 95% CI = 0.47–0.83; G vs. T: OR = 0.81, 95% CI = 0.71–0.92). No significant association was identified for the LPL N291S and PvuII polymorphisms. Stratification analysis by ethnicity suggested a significant correlation between the LPL S447X polymorphism and CAD susceptibility in Caucasians under the dominant and allele genetic models. In summary, our meta-analysis indicated that the LPL D9N polymorphism was associated with an increased risk of CAD, whereas the S447X and HindIII polymorphisms showed protective effects. There was no association observed between the N291S and PvuII polymorphisms and CAD risk.

Background Retrieval of inferior vena cava filters (IVCFs) is important to decrease the long-term risk of complications associated with indwelling devices. Our hospital experienced low retrieval rates and implemented a low-cost intervention and evaluation for quality improvement. The working hypothesis was that a simple, mailed letter intervention could increase retrieval rates by increasing patient and primary care provider knowledge of the need for retrieval. Methods For all prospective patients who received a retrievable IVCF during the intervention period from January 1, 2014 to February 29, 2016, patients and their primary care providers were mailed letters encouraging contact with the clinic for evaluation of eligibility for retrieval. The main outcome was retrieval of the IVCF if clinically indicated with a secondary outcome of time-to-retrieval. A pre-intervention control group from October 1, 2011 to December 31, 2013 was used to evaluate the impact of the intervention. Competing risks, time-to-event analysis was used to compare the pre- and post-intervention period retrieval rates correcting for patients who died during follow-up. Results Between the pre- and post-intervention periods, crude retrieval rates increased from 4.4% to 8.1% with a 12-fold change at comparable time points. The time-to-retrieval in the pre-intervention period was a mean (SD) of 503 (207) days with a median (IQR) of 505 (301–742). In the post-intervention period, time-to-retrieval was a mean (SD) of 119 (83) days and with median (IQR) of 128 (38–164) days. Conclusions This low-cost intervention significantly increased retrieval rates in a single clinic. However, retrieval rates remain low and can be further improved. Ongoing interventions, including improved patient follow-up and physician education, are being implemented to further improve retrieval and use of inferior vena cava filters. Implanting clinics should implement quality improvement initiatives to improve patient care and follow-up with IVCFs to ensure retrievals occur once clinically relevant in order to minimize long-term complications.

MnO 2 nanostructures can be directly and conformably deposited on the highly conductive Ketjen Black (KB) substrate by an in situ redox reaction between KMnO 4 and C. By controlling the MnO 2 contents in KB-MnO 2 composites, the use of extra conductive enhancers can be avoided. When the MnO 2 content is 37 wt% (KB–MnO 2 -37), its specific capacity ( C g ) is up to 252 F g −1 at 5 mV s −1 and the capacity retention is 50% as the scan rate increases 60 times to 300 mV s −1 . Moreover, asymmetric supercapacitors based on KB-MnO 2 -37 can reversibly charge/discharge at a cell voltage of 2.0 V in 1 M Na 2 SO 4 electrolyte solution. A sulfonated pitch porous carbon//KB-MnO 2 -37 asymmetric supercapacitor delivers an energy density of 31.1 Wh kg −1 and a power density of 150 W kg −1 . KB-MnO 2 composites have a great potential in large-scale energy storage applications.

NOP14, which is functionally conserved among eukaryotes, has been implicated in cancer development. Here, we show that NOP14 is poorly expressed in breast cancer cells and invasive breast cancer tissues. In vivo and in vitro studies indicated that NOP14 suppressed the tumorigenesis and metastasis of breast cancer cells. Further investigations revealed that NOP14 enhanced ERα expression and inhibited the Wnt/β-catenin pathway by up-regulating NRIP1 expression. Survival analysis indicated that low NOP14 expression was significantly associated with poor overall survival (P = 0.0006) and disease-free survival (P = 0.0007), suggesting that NOP14 is a potential prognostic factor in breast cancer. Taken together, our findings reveal that NOP14 may suppress breast cancer progression and provide new insights into the development of targeted therapeutic agents for breast cancer.

Lipoprotein lipase (LPL) is widely linked to lipid and lipoprotein metabolism, but its effects on coronary artery disease (CAD) are not clearly elucidated. The aim of the present study was to clarify the association between LPL gene polymorphisms and CAD susceptibility. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated to estimate the strength of the relationship between LPL gene polymorphisms and CAD risk. Comprehensive electronic databases, including PubMed, EMBASE, Web of Science, and the Cochrane Library, were systematically searched. A total of 45 records containing 80 eligible studies were analyzed. The results indicated an increased risk between the LPL D9N polymorphism and susceptibility to CAD in the dominant genetic model (AA + GA vs. GG: OR = 1.46, 95% CI = 1.14–1.87), whereas the LPL HindIII polymorphism showed a protective effect against CAD under all tested models (GG + GT vs. TT: OR = 0.85, 95% CI = 0.75–0.97; GG vs. TT + TG: OR = 0.62, 95% CI = 0.47–0.83; G vs. T: OR = 0.81, 95% CI = 0.71–0.92). No significant association was identified for the LPL N291S and PvuII polymorphisms. Stratification analysis by ethnicity suggested a significant correlation between the LPL S447X polymorphism and CAD susceptibility in Caucasians under the dominant and allele genetic models. In summary, our meta-analysis indicated that the LPL D9N polymorphism was associated with an increased risk of CAD, whereas the S447X and HindIII polymorphisms showed protective effects. There was no association observed between the N291S and PvuII polymorphisms and CAD risk.

Table S1. MOOSE checklist for meta-analysis. Table S2. Methodological quality of the included studies according to the Newcastle-Ottawa Scale. Figure S1. Forest plot for the association between the VEGF rs699947 polymorphism and CAD risk in dominant genetic models. Figure S2. Forest plot for the association between the VEGF rs699947 polymorphism and CAD risk in recessive genetic models. Figure S3. Forest plot for the association between the VEGF rs699947 polymorphism and CAD risk in heterozygous genetic models. Figure S4. Forest plot for the association between the VEGF rs699947 polymorphism and CAD risk in homozygous genetic models. Figure S5. Forest plot for the association between the VEGF rs699947 polymorphism and CAD risk in allele genetic models. Figure S6. Forest plot for the association between the VEGF rs2010963 polymorphism and CAD risk in dominant genetic models. Figure S7. Forest plot for the association between the VEGF rs2010963 polymorphism and CAD risk in recessive genetic models. Figure S8. Forest plot for the association between the VEGF rs2010963 polymorphism and CAD risk in heterozygous genetic models. Figure S9. Forest plot for the association between the VEGF rs2010963 polymorphism and CAD risk in homozygous genetic models. Figure S10. Forest plot for the association between the VEGF rs2010963 polymorphism and CAD risk in allele genetic models. Figure S11. Forest plot for the association between the VEGF rs3025039 polymorphism and CAD risk in dominant genetic models. Figure S12. Forest plot for the association between the VEGF rs3025039 polymorphism and CAD risk in recessive genetic models. Figure S13. Forest plot for the association between the VEGF rs3025039 polymorphism and CAD risk in heterozygous genetic models. Figure S14. Forest plot for the association between the VEGF rs3025039 polymorphism and CAD risk in homozygous genetic models. Figure S15. Forest plot for the association between the VEGF rs3025039 polymorphism and CAD risk in allele genetic models. (DOC 3267 kb)

Objective: To systematically evaluate the precise role of the excision repair cross-complementing group 1 (ERCC1) polymorphism Asn118Asn (C19007T, rs11615) in curative effects and prognosis of patients with advanced colorectal cancer (CRC) receiving oxaliplatin-based chemotherapy. Methods: Qualified studies were retrieved from databases including PubMed, EMBASE, Wanfang and CNKI until January 31st, 2015. Literature published in English and Chinese were selected for metaanalysis on relationship between ERCC1 polymorphism Asn118Asn and therapeutic effects and prognosis of advanced CRC patients receiving oxaliplatin-based chemotherapy. Data extracted from these articles included study ID, title, author, publication year, ethnicity, country, numbers of cases and controls, progression-free survival (PFS) and overall survival (OS). Pooled odds ratios (ORs) and their 95% confidence intervals (CIs) were used to estimate objective response with hazard ratios (HRs) using Stata software (version 11.0). Results: A total of 13 articles were included in the study. Overall, meta-analysis showed no significant correlation between the ERCC1 C118T polymorphism and objective response (OR=0.78; 95% CI for 0.29-2.07), PFS (HR=1.70, 95% CI=0.92-3.14) or OS (HR=1.69, 95% CI=0.91-3.14) in advanced CRC patients with oxaliplatin-based chemotherapy. Stratified analysis among Asian and Caucasian populations showed that the ERCC1 C118T polymorphism was not significantly correlated with objective response (OR=2.03 vs. 0.40; 95% CI=0.62-6.68 vs. 0.12-1.30), but was significantly correlated with PFS and OS. Moreover, Asian patients carrying T/T or T/C genotypes of ERCC1 C118T had significant shorter PFS (HR=2.41, 95% CI=1.86-3.11) and OS (HR=2.36, 95% CI=1.76-3.16). Conclusion: In patients with advanced CRC undergoing oxaliplatin-based chemotherapy, there is no correlation between ERCC1 Asn118Asn (C/T) gene polymorphism and therapeutic effects. Asian patients with T allele has shorter PFS and OS.

Objective: To investigate the correlation between the promoter methylation of TGF-β1 and chemoresistance in epithelial ovarian cancer, and to explore the therapeutic strategy. Methods: 68 samples of ovarian cancer and 38 normal ovarian tissues were carried out for analysis of the correlation between the promoter methylation of TGF-β1 and chemoresistance in epithelial ovarian cancer. qRT-PCR and Western blotting assay were performed to detect the expression of TGF-β1 and 5- aza-dc. Demethylation reagent was used to detect the effect of methylation on proliferation of cells with resistance to Paclitaxel (PTX). Results: By comparing the methylation rate between the sensitive cells and resistant cells, we found statistical difference in SKOV3/TR and SKOV cell lines (94.3% versus 42.9%, χ2=64.43, p