Search

Considering the high harmfulness of NO2 to the environment and human healthy, it is pressing to develop NO2 sensors with high sensitivity and selectivity. In this work, we successfully fabricated a novel hierarchical SnO2–Sn3O4 n–n heterostructure through the solvothermal method and subsequent annealing. X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), field-emission scanning electron microscopy (FESEM), and high-resolution transmission electron microscopy (HRTEM) characterization of the material confirmed the hierarchical microsphere structure and the formation of SnO2–Sn3O4 n–n heterojunction. The gas sensing experiment demonstrated that the sample annealed at 600 °C exhibited excellent NO2 sensing performances at 150 °C. Its sensitivities to 5 and 10 ppm NO2 were as high as 48 and 43.6 ppm−1 respectively, and its limit of detection was lower than 20 ppb. Additionally, it possessed excellent selectivity to NO2 as well as good repeatability and stability. With further exploration of the sensing mechanism of hierarchical SnO2–Sn3O4 n–n heterostructure, we proposed that the unique microstructure with a large specific surface area and the formation of n–n-type heterojunctions contribute to the excellent NO2 sensing performance.

MicroRNAs (miRNA) regulate fundamental biological processes, including neuronal plasticity, stress response, and survival. Here, we describe a neuroprotective function of miR-132, the miRNA most significantly downregulated in neurons in Alzheimer’s disease. We demonstrate that miR-132 protects primary mouse and human wild-type neurons and more vulnerable Tau-mutant neurons against amyloid β-peptide (Aβ) and glutamate excitotoxicity. It lowers the levels of total, phosphorylated, acetylated, and cleaved forms of Tau implicated in tauopathies, promotes neurite elongation and branching, and reduces neuronal death. Similarly, miR-132 attenuates PHF-Tau pathology and neurodegeneration, and enhances long-term potentiation in the P301S Tau transgenic mice. The neuroprotective effects are mediated by direct regulation of the Tau modifiers acetyltransferase EP300, kinase GSK3β, RNA-binding protein Rbfox1, and proteases Calpain 2 and Caspases 3/7. These data suggest miR-132 as a master regulator of neuronal health and indicate that miR-132 supplementation could be of therapeutic benefit for the treatment of Tau-associated neurodegenerative disorders. Electronic supplementary material The online version of this article (10.1007/s00401-018-1880-5) contains supplementary material, which is available to authorized users.

Table S1. Demographic and pathological data on brain samples. Figure S1. Characterization of AD brain extracts used for LTP experiments. (a) Half milliliter aliquots of mock immunodepleted (AD) and AW7 immunodepleted (ID-AD) extracts were analyzed by IP/WB. AW7 was used for IP and a combination of 2G3 and 21F12 was used for WB. To enable comparison 2 and 5 ng of Aβ1–42 peptide was also electrophoresed on the gel. IP/WB analysis allows the capture of Aβ structures under native conditions and their detection following denaturing SDS-PAGE. (b) The same samples were also analyzed by an MSD-based Aβx-42 immunoassay. Since GuHCl effectively disaggregates high molecular weight Aβ species, samples were analyzed with and without incubation in denaturant. Analysis of samples in the absence of GuHCl allows the measurement of native Aβ monomer, whereas, analysis of samples treated with GuHCl allows detection of disassembled aggregates. The AD extracts contained much larger amounts of aggregates than monomer, and both monomer and aggregates were effectively removed by AW7 immunodepletion. The experiments shown are typical of at least 3 separate experiments. Figure S2. Bath application of anti-Aβ antibodies had no significant effect on hippocampal LTP. Each data in this graph was average of at least 6 recordings. (DOCX 466 kb)

According to the institution-based view of corporate governance, firm-governance efficiency is influenced by the institutional environment in which the firm operates. In this study, we examine how firms under a family-governance system adapted to institutional reforms over time. The results of the analysis indicate that institutional reforms reduce firm dependence on family governance and eliminate the negative effects on performance exerted by a controlling family’s pyramidal ownership structure. We also find that institutional reforms foster external corporate governance by domestic institutional investors. In conclusion, our study shows that institutional reforms alter the essence of family firm governance.

The incidence of non-small cell lung cancer (NSCLC) has significantly increased in China, while the prognosis of affected patients is poor. The pathogenesis of NSCLC is thought to be regulated by microRNAs (miRs). The present study used a miR array in order to determine the expression of miR-361-5p, which was significantly lower in NSCLC tissues compared with that in adjacent tissues, indicating a crucial role of miR-361-5p during the progression of NSCLC. Furthermore, the effects of transfection-induced upregulation of miR-361-5p on the NSCLC cell line H23 were assessed. Overexpression of miR-361-5p inhibited the proliferation and colony formation ability of H23 cells. In addition, apoptosis of H23 cells was induced by upregulation of miR-361-5p. Furthermore, signal transducer and activator of transcription 6 (STAT6) was confirmed as a direct target of miR-361-5p by a dual-luciferase reporter assay. Moreover, inhibition of STAT6 by small interfering RNA or miR-361-5p also decreased the expression of B-cell lymphoma extra large (Bcl-xL). In vivo, miR-361-5p significantly reduced tumor growth in a nude mouse xenograft model, and suppressed STAT6 and Bcl-xL expression. In conclusion, the present study indicated that miR-361-5p may represent a novel molecular tool for therapeutic and diagnostic strategies in NSCLC.

The complement system is part of the innate immune response responsible for removing pathogens and cellular debris, in addition to helping to refine CNS neuronal connections via microglia-mediated pruning of inappropriate synapses during brain development. However, less is known about the role of complement during normal aging. Here, we studied the role of the central complement component, C3, in synaptic health and aging. We examined behavior as well as electrophysiological, synaptic, and neuronal changes in the brains ofC3-deficient male mice (C3KO) compared with age-, strain-, and gender-matched C57BL/6J (wild-type, WT) control mice at postnatal day 30, 4 months, and 16 months of age. We found the following: (1) region-specific and age-dependent synapse loss in aged WT mice that was not observed inC3KO mice; (2) age-dependent neuron loss in hippocampal CA3 (but not in CA1) that followed synapse loss in aged WT mice, neither of which were observed in agedC3KO mice; and (3) significantly enhanced LTP and cognition and less anxiety in agedC3KO mice compared with aged WT mice. Importantly, CA3 synaptic puncta were similar between WT andC3KO mice at P30. Together, our results suggest a novel and prominent role for complement protein C3 in mediating aged-related and region-specific changes in synaptic function and plasticity in the aging brain.SIGNIFICANCE STATEMENTThe complement cascade, part of the innate immune response to remove pathogens, also plays a role in synaptic refinement during brain development by the removal of weak synapses. We investigated whether complement C3, a central component, affects synapse loss during aging. Wild-type (WT) andC3knock-out (C3KO) mice were examined at different ages. The mice were similar at 1 month of age. However, with aging, WT mice lost synapses in specific brain regions, especially in hippocampus, an area important for memory, whereasC3KO mice were protected. AgedC3KO mice also performed better on learning and memory tests than aged WT mice. Our results suggest that complement C3, or its downstream signaling, is detrimental to synapses during aging.

A porous carbon electrode incorporating considerations both heteroatom doping and pore structure design with: combination of melamine and PEO–PPO–PEO (polyethylene oxide–polypropylene oxide–polyethylene oxide) micelles for the nitrogen-doping and optimization the micron-duct formation; integration of CO2-etching into the carbonization process for the formation of abundant micropores. The structure of these nitrogen-doped carbon xerogels (NCXs) are indeed comprised of a multi-scaled pores having nano-porous carbon in a network of micron-size percolated hollow-channels. The resulted material has an ultrahigh surface area of 4279 m2 g−1 when used as electrode for supercapacitor, which deliver a high specific capacitance of 271 F g−1 with excellent cycle stability and good rate capability.

Lung cancer is the leading cause of cancer-related mortality worldwide. The majority of lung cancers are sporadic, and familial cases are extremely rare. Previous studies have mainly focused on sporadic lung cancer and identified a large quantity of driver genes. However, familial lung cancers are rarer and studied less. The present study recruited a Chinese family in which multiple members had developed lung squamous carcinoma. To find the causative mutations, whole exome sequencing was conducted using a peripheral blood sample of one lung squamous carcinoma patient, and certain variants were validated in more samples. Whole exome sequencing analysis obtained ~2.0 Gb of data (an average of 60x depth for each targeted base), and further validation experiments identified two functional variants in two cancer-related genes (c.1218delA:p.E406fs in PDE4DIP and C1342A:p.L448I in CLTCL1). This study therefore provides useful sources for the further study of hereditary lung cancer.

Three-dimensional (3D) hierarchical NiCo2O4 nanoneedle arrays have been prepared on nickel foam via a facile hydrothermal method followed by annealing in air. Impressively, when investigated as binder-free supercapacitor electrodes, such unique NiCo2O4 nanoneedle arrays on Ni foam exhibit a superior specific capacitance of 2193 F g−1 and 1490 F g−1 at current densities of 1 and 10 A g−1 calculated based on the active mass of NiCo2O4, respectively. Furthermore, the areal capacitance is 3.71 F cm−2 at 1 mA cm−2 and 1.39 F cm−2 at 40 mA cm−2. The remarkable electrochemical performance is due to the hierarchical nanoneedle array structure with bottom crosslinked nanosheets, which has a large surface area, thus providing more sites to facilitate electrochemical reactions, rapid ion/electron transport, and enhanced strain accommodation. Our results demonstrate that the hierarchical NiCo2O4 nanoneedle arrays are a promising material as a binder-free electrode for high performance supercapacitors.

In this work, α-MoO 3 nanoparticles are grown on the surface of nitrogen doped carbon nanotubes (N-CNTs) via a facile electrodeposition method. The morphology of as-prepared nanocomposite shows that the interconnected α-MoO 3 nanoparticles are homogeneously distributed on the surface of N-CNTs. When investigated as a cathode material for lithium ion batteries, the nanocomposite reveals a high reversible discharge capacity of 250 mA h g −1 at a current density of 30 mA g −1 , simultaneously with good cycling performance and excellent rate capability compared with pristine MoO 3 powder. Kinetics of this process is investigated by electrochemical impedance spectroscopy to understand the difference in electrochemical performance and the interface properties between the α-MoO 3 /N-CNTs nanocomposite and pristine MoO 3 powder electrode. The correlation between the unique structural features of α-MoO 3 /N-CNTs nanocomposite and its excellent electrochemical performance is also discussed. The excellent performance makes the as-prepared α-MoO 3 /N-CNTs nanocomposite a promising cathode material for high-performance lithium ion batteries.

Background Accurate assessment of kidney function is clinically important, but estimates of glomerular filtration rate (GFR) by regression are imprecise. Methods We hypothesized that ensemble learning could improve precision. A total of 1419 participants were enrolled, with 1002 in the development dataset and 417 in the external validation dataset. GFR was independently estimated from age, sex and serum creatinine using an artificial neural network (ANN), support vector machine (SVM), regression, and ensemble learning. GFR was measured by 99mTc-DTPA renal dynamic imaging calibrated with dual plasma sample 99mTc-DTPA GFR. Results Mean measured GFRs were 70.0 ml/min/1.73 m2 in the developmental and 53.4 ml/min/1.73 m2 in the external validation cohorts. In the external validation cohort, precision was better in the ensemble model of the ANN, SVM and regression equation (IQR = 13.5 ml/min/1.73 m2) than in the new regression model (IQR = 14.0 ml/min/1.73 m2, P 0.05 for all comparisons of the new regression equation and the other new models. Conclusions An ensemble learning model including three variables, the average ANN, SVM, and regression equation values, was more precise than the new regression model. A more complex ensemble learning strategy may further improve GFR estimates. Electronic supplementary material The online version of this article (10.1186/s12967-017-1337-y) contains supplementary material, which is available to authorized users.

Recent studies have strongly shown that cell-to-cell transmission of neuropathogenic proteins is a common mechanism for the development of neurodegenerative diseases. However, the underlying cause is complex and little is known. Although distinct processes are involved in the pathogenesis of various diseases, they all share the common feature of iron accumulation, an attribute that is particularly prominent in synucleinopathies. However, whether iron is a cofactor in facilitating the spread of α-synuclein remains unclear. Here, we constructed a cell-to-cell transmission model of α-synuclein using SN4741 cell line based on adenovirus vectors. Cells were treated with FeCl2, and α-synuclein aggregation and transmission were then evaluated. In addition, the possible mechanisms were investigated through gene knockdown or over-expression. Our results demonstrated that iron promoted α-synuclein aggregation and transmission by inhibiting autophagosome-lysosome fusion. Furthermore, iron decreased the expression of nuclear transcription factor EB (TFEB), a master transcriptional regulator of autophagosome-lysosome fusion, and inhibited its nuclear translocation through activating AKT/mTORC1 signaling. After silencing TFEB, ratios of α-synuclein aggregation and transmission were not significantly altered by the presence of iron; on the other hand, when TFEB was over-expressed, the transmission of α-synuclein induced by iron was obviously reversed; suggesting the mechanism by which iron promotes α-synuclein transmission may be mediated by TFEB. Taken together, our data reveal a previously unknown relationship between iron and α-synuclein, and identify TFEB as not only a potential target for preventing α-synuclein transmission, but also a critical factor for iron-induced α-synuclein aggregation and transmission. Indeed, this newly discovered role of iron and TFEB in synucleinopathies may provide novel targets for developing therapeutic strategies to prevent α-synuclein transmission in Parkinson's disease.

Background and aims Full blockade of renin-angiotensin-aldosterone system (RAAS) is believed to decrease morbidity and mortality of patients with chronic kidney disease. In non-dialysis patients, combined RAAS blockade with two different RAAS blockers causes more adverse events without improving survival, but its role in maintenance dialysis patients is still unclear. We conducted a systematic review and mediation analysis to investigate the efficacy and safety of combined RAAS blockade in dialysis patients. Methods Comprehensive search was conducted in PubMed, EMBASE, Web of Science and Cochrane Library database to June 2017 to identify relevant studies. Studies comparing combined with single RAAS blockade and reporting all-cause death, cardiovascular death, hypotension or hyperkalemia in dialysis patients were included. Effect sizes were calculated with randomized effects model and summarized as odd ratios (OR). Results A total of 9 studies with 13,050 dialysis patients were included. Compared with single blockade, combined blockade significantly reduced all-cause mortality (OR 0.71, 95% confidence interval 0.54–0.93, p = 0.01), while cardiovascular mortality remained unchanged (0.85, 0.45–1.59, p = 0.61). Combined blockade tended to increase odd of hypotension but not odd of hyperkalemia (1.54, 1.00–2.38, p = 0.05; 0.89, 0.76–1.05, p = 0.17). Further mediation analysis indicated that hypotension might exert a suppression effect on the survival benefit of angiotensin-converting enzyme inhibitor plus angiotensin receptor blocker treatment on cardiovascular mortality. Conclusions Combined RAAS blockade might be a promising treatment in dialysis patients to further reduce mortality if blood pressure was well controlled.

Objective: To evaluate the diagnostic value of endoscopic ultrasonography (EUS) in preoperative staging of esophageal carcinoma (EC).Material and methods: A total of 86 surgical patients with EC who were confirmed by endoscopy and biopsy underwent preoperative TN staging with EUS examination. The EUS findings were compared with surgical pathologic results.Results: The accuracy of EUS in T and N staging of EC was 82.6% and 84.9%, respectively. While determining whether EC invades the muscularis propria or outer membrane, EUS had the favorable sensitivity, specificity, positive predictive value and negative predictive value. The short-axis diameter of lymph nodes of 5mm had high sensitivity and negative predictive value to determine malignance with low specificity and positive predictive value. The short-axis diameter of 10mm presented the satisfactory sensitivity, specificity, positive predictive value and negative predictive value.Conclusion: EUS can accurately determine the TN staging of EC and p...

Compelling genetic evidence links the amyloid precursor protein (APP) to Alzheimer’s disease (AD), and several theories have been advanced to explain the involvement of APP in AD. A leading hypothesis proposes that a small amphipathic fragment of APP, the amyloid β-protein (Aβ), self-associates to form soluble aggregates which impair synaptic and network activity. Here, we report on the plasticity-disrupting effects of Aβ isolated from AD brain and the requirement of APP for these effects. We show that Aβ-containing AD brain extracts block hippocampal long-term potentiation (LTP), augment glutamate release probability and disrupt the excitation/inhibition balance. Notably, these effects are associated with Aβ localizing to synapses, and genetic ablation of APP prevents both Aβ binding and Aβ-mediated synaptic dysfunctions. These findings indicate a role for APP in AD pathogenesis beyond the generation of Aβ and suggest modulation of APP expression as a therapy for AD.AcknowledgmentsWe thank Dr. Tiernan T. O’Malley for useful discussions and technical advice. This work was supported by grants to DMW from the National Institutes of Health (AG046275), Bright Focus, and the United States-Israel Binational Science Foundation (2013244, DMW and IS); grants to TSJ from Alzheimer’s Research UK and the Scottish Government (ARUK-SPG2013-1), Wellcome Trust-University of Edinburgh Institutional Strategic Support funds, and the H2020 European Research Council (ALZSYN); and to the Massachusetts Alzheimer’s Disease Research Center (AG05134).

BACKGROUND Parkinson's disease (PD) is the second most common neurodegenerative disorder worldwide. Epigenetic modifications, specifically DNA methylation, have been implicated in the development of this disease. Genetic variants of DNA methyltransferase 3b (DNMT3b), one of the most important DNA methyltransferases, were shown to be associated with PD in a Brazilian population. However, it is unclear whether genetic variants of DNMT3b increase the risk of PD in the Chinese Han people. The present study aimed to investigate the association of the DNMT3b variants rs2424913, rs998382 and rs2424932 with PD in a Chinese Han population. METHODS We studied 487 Chinese Han patients with sporadic PD and 485 healthy age-, sex- and ethnicity-matched controls. DNA was extracted from peripheral blood leukocytes and the individual genotypes were determined using the SNaPshot method. RESULTS We found that the rs2424932 and rs998382 variants were significantly associated with an increased risk of PD compared to the controls [rs2424932: odds ratio (OR) = 1.632, 95% confidence interval (CI) = 1.108-2.406, p = 0.013; rs998382: OR = 1.612, 95% CI = 1.103-2.382, p = 0.014]. Subgroup analysis suggested that female patients carrying the rs2424932 or rs998382 variants were more likely to develop PD than female controls (rs2424932: OR = 3.863, 95% CI = 2.004-7.445, p < 0.001; rs998382: OR = 3.679, 95% CI = 1.943-6.964, p < 0.001). Haplotype analysis indicated that the three variants comprised one block and that the Trs2424913 -Crs998382 -A rs2424932 haplotype was correlated with an increased risk of PD (p = 0.0046), especially for Chinese Han females (p < 0.0001). CONCLUSIONS The results of the present study strongly suggest that DNMT3b variants are associated with PD in the Chinese Han people, especially females.

MicroRNAs (miRNAs) play critical roles in the development and progression of various cancers, including non-small-cell lung cancer (NSCLC). Studies have suggested that miR-330-5p is involved in the progression of several cancers. However, the role of miR-330-5p in NSCLC remains unclear. We investigated the effect on and mechanism of miR-330-5p in the progression of NSCLC. We found that miR-330-5p was significantly downregulated in NSCLC tissues and cell lines as detected by real-time quantitative polymerase chain reaction (RT-qPCR). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), bromodeoxyuridine (BrdU), colony formation and cell cycle assays showed that overexpression of miR-330-5p markedly inhibited cell growth. Annexin V-FITC/PI and caspase-3 activity assays showed that overexpression of miR-330-5p significantly promoted cell apoptosis of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed NIN/RPN12 binding protein 1 (NOB1) as a target gene of miR-330-5p. RT-qPCR and Western blot analysis showed that overexpression of miR-330-5p inhibited the expression of NOB1 as well as cyclin D1 and cyclin-dependent kinase 4 in NSCLC cells. Moreover, overexpression of NOB1 markedly reversed the miR‑330-5p-mediated inhibitory effect on NSCLC cell growth. Correlation analysis showed that miR‑330-5p expression was inversely correlated with NOB1 mRNA expression in NSCLC tissues. Taken together, our results indicate that miR-330-5p inhibits NSCLC cell growth through downregulation of NOB1 expression. Our study suggests that miR-330-5p may serve as a potential therapeutic target for the treatment of NSCLC.

Evening dosing regimen drug therapy on blood pressure (BP) control is used widely, but its clinical benefits and preservation or re-establishment of the normal 24-h BP dipping pattern in chronic kidney disease (CKD) patients is not known.To investigate the effect of an evening dosing regimen of antihypertensive drugs on BP patterns of CKD patients with hypertension.A systematic review was conducted by searching PUBMED, EMBASE, ASN-ONLINE, the Cochrane Library and the reference lists of relevant articles of published papers. All trials designed to evaluate the effects of evening versus morning dosing regimen drug therapy for CKD patients with hypertension were included. Meta-analysis was performed using random or fixed effects models.Five randomised controlled trials and one comparative study, including 3732 patients, met the inclusion criteria. Compared with morning dosing regimen drug therapy, evening administration of antihypertensive medication was associated with a significant reduction of 40% in non-dipper BP patterns (risk ratio (RR), 95% CI, (0.43, 0.84)). We noted a significant decrease in nocturnal systolic blood pressure (SBP) (MD -3.17 mmHg, 95% CI (-5.41, -0.94)), a significant reduction in nocturnal diastolic blood pressure (DBP) (MD -1.37 mmHg, 95% CI (-2.05, -0.69)) and a significant increase in awake SBP (MD 1.15 mmHg, 95% CI (0.10, 2.19)) in patients assigned to the evening dosing regimen drug therapy group. Patients showed no significant differences for all-cause mortality and cardiovascular mortality.This review shows that evening dosing regimen drug therapy could reverse non-dipper BP patterns in hypertensive CKD patients.

The increase in religion-related conflicts around the world emphasizes the urgent need for a better understanding of the role of religion and religious freedom on socio-economic development, both theoretically and empirically. While studies on the role of religion on economic development have existed as early as Weber (1905), there is a dearth of studies on the effect of religious freedom on economic growth, and the existing studies overlook possible negative impacts on economies by unrestricted religious freedom. Drawing on institutional theory, we propose that different types of religious restrictions can exert either positive or negative effects on economic growth. We test our propositions using a comprehensive dataset on religious freedom covering 198 countries for seven years from 2007 to 2013.

Additional file 1: Figure S1. Trial profile.

The performance of lithium sulfur (Li/S) battery was greatly improved by the employment of nitrogen doped carbon nanotubes (N-CNTs) based cathode. By manipulating its structure thereby creating more defects, N-CNTs presents better dispersion of sulfur particles on N-CNTs and higher electrical conductivity compared with their non-doped counterpart, which explain the reason why N-CNTs/S composite shows improved performance. The specific discharge capacity was maintained at 625 mAh g−1 and 513 mAh g−1 after 100 cycles at 0.2 C and 0.5 C, respectively, which was about 2 times as that of CNTs. This method is proved to be a promising way to develop cathode materials for lithium sulfur batteries.

Although studies have been done on nitrogen doped carbon materials as lithium–oxygen (Li–O2) battery cathodes, few of them focus on the binder-free electrode structure, although they have been proved to bring improved performance. To fill this gap this work not only studies the nitrogen doped binder-free carbon cathode but also determines the performance of these cathodes with different levels of nitrogen doping. To make binder-free electrodes, these CNTs and N-CNTs were synthesized on nickel foam by a floating catalyst chemical vapor deposition method. The study found that the electrochemical performance of binder-free N-CNT cathodes in Li–O2 batteries improves as the level of nitrogen doping increases. To further study the reason why the electrodes with higher nitrogen amounts deliver better electrochemical properties, the morphology of discharge products on the different nanotubes are detected by scanning electron microscopy (SEM). The scan shows that the distribution of discharge products on the surface of CNTs become more and more uniform as the level of nitrogen doping increases and the discharge capacity and cycle performance are subsequently improved. Therefore, these binder-free N-CNT electrodes could be further explored as high capacity cathode materials for Li–O2 battery applications.

This study introduces an economical and environmentally friendly way of synthesizing LiFePO4/C to be used as cathode material in lithium ion batteries via two processes: (1) the synthesis of LiFePO4/C cathode material using a low cost divalent precursor ferrous phosphate, Fe3 (PO4)2·8H2O, as iron source in a polyol process and (2) the modification of the morphology of this precursor by varying the reaction time in a coprecipitation process. The study examines the effects of different structures and morphologies of the precursor on the structure and electrochemical performance of the as-synthesized LiFePO4/C. The LiFePO4/C shows an excellent rate capability and cycle performance, with initial discharge capacities of 153, 128, and 106 mA h g(-1) at 1 C, 5 C, and 10 C. The capacity retention is respectively 98.7%, 98.2%, and 98.7%, after 10 cycles at the corresponding rates. The capacity retention remains at 97% even after 300 cycles at the rate of 10 C. The outstanding electrochemical performance can be attributed to the improved rate of Li(+) diffusion and the excellent crystallinity of synthesized LiFePO4/C powders through the modified precursor. Therefore, this is an economical and environmentally friendly way of synthesizing LiFePO4/C to be used as cathode material in lithium ion batteries.

Evidence for a central role of amyloid β-protein (Aβ) in the genesis of Alzheimer’s disease (AD) has led to advanced human trials of Aβ-lowering agents. The “amyloid hypothesis” of AD postulates deleterious effects of small, soluble forms of Aβ on synaptic form and function. Because selectively targeting synaptotoxic forms of soluble Aβ could be therapeutically advantageous, it is important to understand the full range of soluble Aβ derivatives. We previously described a Chinese hamster ovary (CHO) cell line (7PA2 cells) that stably expresses mutant human amyloid precursor protein (APP). Here, we extend this work by purifying an sodium dodecyl sulfate (SDS)-stable, ∼8 kDa Aβ species from the 7PA2 medium. Mass spectrometry confirmed its identity as a noncovalently bonded Aβ40 homodimer that impaired hippocampal long-term potentiation (LTP) in vivo. We further report the detection of Aβ-containing fragments of APP in the 7PA2 medium that extend N-terminal from Asp1 of Aβ. These N-terminally extended Aβ-containing monomeric fragments are distinct from soluble Aβ oligomers formed from Aβ1-40/42 monomers and are bioactive synaptotoxins secreted by 7PA2 cells. Importantly, decreasing β-secretase processing of APP elevated these alternative synaptotoxic APP fragments. We conclude that certain synaptotoxic Aβ-containing species can arise from APP processing events N-terminal to the classical β-secretase cleavage site.

Purpose– How should a multinational corporation (MNC) from a mature democracy deal with the human rights issues in a country with a poor human rights standard? The paper aims to discuss these issues.Design/methodology/approach– The authors develop a mathematical model to depict MNC's behavior in response to human rights violations in the host country.Findings– The authors show that, first, in a country with a high level of human rights abuses, a firm will have to lower its human rights standards to survive; but, second, a collective effort by all firms is essential to improve the human rights conditions in the host environment; and third, a firm's human rights practices may have a multiplicative effect that can significantly affect the momentum of human rights development in a host country.Originality/value– This study is one of the first attempts to provide a theoretical framework on the issue of MNCs and human rights in host countries.

Purpose – The success and reliability of business transactions and research in emerging markets depend on the quality of financial information. Due to the institutional and historical backgrounds, financial information provided by firms in emerging markets has often been questioned for their accuracy. This study aims to examine the reliability of financial information through various descriptive and statistical analyses in major emerging markets, including Brazil, Russia, India, and China (the BRICs). Design/methodology/approach – The authors use firm-level data from the BRIC countries and apply statistical models to identify patterns of profit misreporting by firms in these countries. Findings – The results show significant and systemic signs of misreporting of financial information in these countries, particularly in China and Russia, which are further examined to understand the possible reasons behind their more severe misreporting. Originality/value – The study then concludes with practical and specific recommendations for investors, managers, and policy makers on how to detect and avoid potential risks due to inaccurate financial information and improve the overall quality of decision making.

Novel multi-scaled porous nitrogen-doped carbon is synthesized by enriching the simple resorcinol–formaldehyde xerogel method with: (a) addition of melamine for nitrogen-doping and micron-duct formation; (b) incorporation of PEO–PPO–PEO micelles for the optimization of the duct percolation; and (c) integration of CO2-etching into the carbonization process for the formation of abundant 2 nm pores. Our experimental results confirm that these nitrogen-doped carbon xerogels (NCXs) indeed comprise a multi-scaled porous structure having nano-porous carbon in a network of micron-size percolated hollow-channels. NCXs prepared by CO2-etching at 950 °C for 8 hours have a high surface area of 2912 m2 g−1. In addition, the lithium ion batteries fabricated using these NCXs show a high specific capacity of 645 mA h g−1, with excellent cycle stability and good rate capability.

Enhancing the electrolyte wetting of separators by surface modification is very critical to prepare high-performance lithium-ion batteries. Herein, we present a new approach named hyperthermal hydrogen induced cross-linking (HHIC) technology to increase the electrolyte-affinity of polypropylene (PP) separators by covalently cross-linking a thin layer of poly(ethylene oxide) (PEO) on surface-inert PP separators. With the HHIC treatment, the polar functionalities of PEO (e.g. –OH, C–O–C) can be preserved through selective cleavage of C–H bonds and subsequent cross-linking of resulting carbon radicals generated on PEO and PP chains. As proved by solvent rinsing tests, contact angle measurements and Fourier transform infrared spectroscopy, a PEO coating was found firmly fixed on the separator surface, which results in significantly improved wetting with the electrolyte. Electrochemical measurements on subsequent lithium-ion batteries with the modified separator by HHIC treatment exhibit a lower internal resistance but higher capacity retention when compared to the pristine separator. HHIC treatment is concluded to be a highly efficient and environmental-friendly approach for separator surface modification without need for other chemical additives (e.g. chemical cross-linkers, initiators, and catalysts) and can preserve the desired macroscopic material properties of separators such as pore structures and mechanical strength.

AMPA receptors (AMPARs) mediate fast excitatory synaptic transmission and are crucial for synaptic plasticity, learning and memory. However, the molecular control of AMPAR stability and its neurophysiological significance remain unclear. Here we report that AMPARs are subject to lysine acetylation at their C-termini. Acetylation reduces AMPAR internalization and degradation, leading to increased cell-surface localization and prolonged receptor half-life. Through competition for the same lysine residues, acetylation intensity is inversely related to the levels of AMPAR ubiquitination. We find that sirtuin 2 (SIRT2) acts as an AMPAR deacetylase regulating AMPAR trafficking and proteostasis. SIRT2 knockout mice (Sirt2−/−) show marked up-regulation in AMPAR acetylation and protein accumulation. Both Sirt2−/− mice and mice expressing acetylation mimetic GluA1 show aberrant synaptic plasticity, accompanied with impaired learning and memory. These findings establish SIRT2-regulated lysine acetylation as a form of AMPAR post-translational modification that regulates its turnover, as well as synaptic plasticity and cognitive function.

The dynamic mechanism of breakdown in polypropylene (PP) were represented based on the discharge-avalanche theory. PP is a typical semi-crystalline thermoplastic polymer with low loss and high thermal stability, which had broad application prospects in recyclable and environment-friendly insulation. Dielectric strength was one of the important properties for polymer insulation, hence research of breakdown mechanism was of great significance for insulation reliability increase and advanced materials development. In this paper, the dielectric strength of PP was enhanced by nano-silica filling, and mechanism of enhancement was discussed based on the change of activation energy measured by thermally stimulated depolarization currents (TSDC).

Using 205 Taiwanese firms spanning five years, this research examines how corporate governance factors specific to emerging economies determine the extent of diversification and moderate its performance. The analyses reveal that controlling family ownership is significantly associated with a greater extent of diversification, which impairs firm value. Conversely, domestic bank ownership significantly decreases diversification, which in turn increases diversification performance. These findings present the evidence of controlling family entrenchment through diversification and the significant role domestic banks play in the principal–principal corporate governance framework.

This study seeks to understand the governance of post–initial public offering (IPO) family firms and its impact on performance. Using an analysis of a balanced panel data set of 205 publicly listed firms in Taiwan spanning 10 years (2,050 firm-years), we found that extensive family control has a negative impact on the post-IPO performance and that nonfamily block shareholders may divest their stockholdings in these firms to protect their investments. To sustain equity support from their block shareholders, post-IPO family firms should combine the use of family control with professional management in their corporate governance structure.

Transforming growth factor β1 (TGF-β1) is a pleiotropic cytokine expressed throughout the CNS. Previous studies demonstrated that TGF-β1 contributes to maintain neuronal survival, but mechanistically this effect is not well understood. We generated a CNS-specific TGF-β1-deficient mouse model to investigate the functional consequences of TGF-β1-deficiency in the adult mouse brain. We found that depletion of TGF-β1 in the CNS resulted in a loss of the astrocyte glutamate transporter (GluT) proteins GLT-1 (EAAT2) and GLAST (EAAT1) and decreased glutamate uptake in the mouse hippocampus. Treatment with TGF-β1 induced the expression of GLAST and GLT-1 in cultured astrocytes and enhanced astroglial glutamate uptake. Similar to GLT-1-deficient mice, CNS-TGF-β1-deficient mice had reduced brain weight and neuronal loss in the CA1 hippocampal region. CNS-TGF-β1-deficient mice showed GluN2B-dependent aberrant synaptic plasticity in the CA1 area of the hippocampus similar to the glutamate transport inhibitor DL-TBOA and these mice were highly sensitive to excitotoxic injury. In addition, hippocampal neurons from TGF-β1-deficient mice had elevated GluN2B-mediated calcium signals in response to extrasynaptic glutamate receptor stimulation, whereas cells treated with TGF-β1 exhibited reduced GluN2B-mediated calcium signals. In summary, our study demonstrates a previously unrecognized function of TGF-β1 in the CNS to control extracellular glutamate homeostasis and GluN2B-mediated calcium responses in the mouse hippocampus.

A nature-inspired approach to encapsulate enzymes in spindle-like copper hydroxysulfate nanocrystals was developed by a biomimetic mineralization process. Several types of enzymes including glucose oxidase (GOx), horseradish peroxidase (HRP), Candida antarctica lipase B (CALB) and cytochrome c (Cyt c) were successfully encapsulated in copper hydroxysulfate nanocrystals quickly (within 1 hour) with maintained or even greatly enhanced catalytic efficiencies (kcat/KM of Cyt c showed a 143-fold increase) and high stabilities, demonstrating the feasibility of utilizing copper hydroxysulfate nanocrystals as a novel type of nanocarrier for enzyme immobilization. In addition, by this approach, for the first time, we showed that an immobilized enzyme can be endowed with self-antibacterial activity by an inorganic component. This self-antibacterial performance together with the improved catalytic efficiencies and stabilities can greatly benefit the enzymatic catalysis in aqueous media and promote the future development of novel biosensors.

INTRODUCTION Dyslipidemia is often detected in patients with chronic kidney disease (CKD). Previous studies of the relationship between lipid profiles and kidney function have yielded variable results. We aimed to investigate the correlation between serum lipid levels and kidney function evaluated by measured glomerular filtration rate (mGFR) in Chinese patients with CKD. METHODS A cross-sectional study was conducted on 2036 Chinese CKD patients who had mGFR. Linear regression analysis was performed to evaluate the correlation between different serum lipid levels and mGFR, while logistic regression analysis was used to investigate the association between CKD stages and the risk of different types of dyslipidemia. RESULTS The mean age was 55 years and the mean mGFR was 63 mL/min/1.73m2. After adjusting for some confounders (age, gender, body mass index, a history of diabetes, fasting glucose, a history of hypertension, systolic blood pressure, diastolic blood pressure, smoking status, hemoglobin, serum potassium, serum albumin, and serum uric acid), serum triglyceride level showed a negative correlation with mGFR (β = -0.006, P = 0.006) in linear regression analysis, and CKD stages were positively related to the risk of hypertriglyceridemia (odds ratios were 1.329, 1.868, 2.514 and P were 0.046, < 0.001, < 0.001 for CKD stage 2, 3, 4/5, respectively) in logistic regression anlysis. CONCLUSIONS Serum triglyceride level is independently association with mGFR. Patients with reduced kidney function are more likely to have higher serum triglyceride levels. Further longitudinal, multicenter and well-conducted studies are needed to provide more evidence.

The early initiation of renal replacement therapy has been recommended for patients with acute renal failure by some studies, but its effects on mortality and renal recovery are unknown. We conducted an updated meta-analysis to provide quantitative evaluations of the association between the early initiation of renal replacement therapy and mortality for patients with acute kidney injury. After applying inclusion/exclusion criteria, 51 studies, including 10 randomized controlled trials, with a total of 8179 patients were analyzed. Analysis of the included trials showed that patients receiving early renal replacement therapy had a 25% reduction in all-cause mortality compared to those receiving late renal replacement therapy (risk ratio [RR] 0.75, 95% CI [0.69, 0.82]). We also noted a 30% increase in renal recovery (RR 1.30, 95% CI [1.07, 1.56]), a reduction in hospitalization of 5.84 days (mean difference [MD], 95% CI [-10.27, -1.41]) and a reduction in the duration of mechanical ventilation of 2.33 days (MD, 95% CI [-3.40, -1.26]) in patients assigned to early renal replacement therapy. The early initiation of renal replacement therapy was associated with a decreased risk of all-cause mortality compared with the late initiation of RRT in patients with acute kidney injury. These findings should be interpreted with caution given the heterogeneity between studies. Further studies are needed to identify the causes of mortality and to assess whether mortality differs by dialysis dose.