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Objective: Alterations in the gut microbiota and host responses have been implicated in the progression of end-stage renal disease, increased cardiovascular risk, uremic toxicity, and inflammation. The purpose of this study was to evaluate the clinical efficacy of probiotics on malnutrition and health-related quality of life in patients undergoing peritoneal dialysis (PD)., Design and Methods: A total of 116 patients undergoing PD were randomly divided into an intervention group (n = 58) and a control group (n = 58). The intervention group received a daily dose of probiotics (1 × 10 9  CFU/day, i.e., 2 capsules, tid) for 2 months, while the control group did not receive probiotics during the same period. Biochemical indicators, physical measurements, and scores on the SF-36 were measured before and 2 months after the intervention., Results: A total of 98 patients completed the study (50 in the intervention group and 48 in the control group). Among patients receiving probiotics, the levels of high-sensitivity C-reactive protein and interleukin-6 decreased after 2 months of treatment, while the serum albumin levels, upper arm circumference, and triceps skinfold thickness increased significantly. The probiotic group had higher scores on the physical functioning and social functioning domains than the control group after 2 months., Conclusions: Probiotics could significantly decrease the serum levels of high-sensitivity C-reactive protein and interleukin-6 and increase the serum albumin levels, upper arm circumference, and triceps skinfold thickness in patients undergoing PD. As a result, malnutrition and health-related quality of life partially improved after probiotic supplementation in patients undergoing PD., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

α-Terpineol, terpinen-4-ol, and δ-terpineol, isomers of terpineol, are among the compounds that give Cinnamomum longepaniculatum leaf oil its distinguished pleasant smell. The objective of this study was to evaluate the antimicrobial activity of these three isomeric terpineols. The determination of antibacterial activity was based on the minimum inhibition concentration (MIC) and minimum bactericide concentration (MBC). Changes in time-kill curve, alkaline phosphatase (AKP), UV-absorbing material, membrane potential, and scanning electron microscopy (SEM) were measured to elucidate the possible antimicrobial mechanism. α-Terpineol, terpinen-4-ol, and δ-terpineol demonstrated good inhibitory effects against several gram-negative bacteria, particularly Shigella flexneri. MIC and MBC of α-terpineol and terpinen-4-ol were similar (0.766 mg/mL and 1.531 mg/mL, respectively) for S. flexneri, while the MIC and MBC values of δ-terpineol were 0.780 mg/mL and 3.125 mg/mL, respectively. Time-kill curves showed that the antibacterial activities of the tested compounds were in a concentration-dependent manner. Release of nucleic acids and proteins along with a decrease in membrane potential proved that α-terpineol, terpinen-4-ol, and δ-terpineol could increase the membrane permeability of Shigella flexneri. Additionally, the release of AKP suggested that the cell wall was destroyed. SEM analysis further confirmed that S. flexneri cell membranes were damaged by α-terpineol, terpinen-4-ol, and δ-terpineol. Our research suggests that these three isomeric terpineols have the potential of being used as natural antibacterial agents by destroying the cell membrane and wall, resulting in cell death. However, the specific antibacterial activity differences need further investigation.

Secretory phospholipase A2 group IB (sPLA2-IB) and M-type phospholipase A2 receptor (PLA2R) are closely associated with proteinuria in idiopathic membranous nephropathy (IMN). Podocytes constitute an important component of glomerular filtration, and high basal autophagy is indispensable for podocyte function. The current study aimed to analyze the relationship between sPLA2-IB and podocyte autophagy in IMN and determine whether sPLA2-IB mediates abnormal autophagy regulation in podocytes. The serum sPLA2-IB level and podocyte autophagy were detected, and clinical data were collected from IMN patients with different proteinuria levels. Then, the effects of sPLA2-IB on autophagy signaling pathways were evaluated in cultured human podocytes treated with sPLA2-IB, rapamycin, p38 inhibition, and PLA2R-siRNA in vitro. We found that IMN patients with nephrotic-range proteinuria have a significantly higher level of sPLA2-IB and fewer autophagosomes than those with non-nephrotic-range proteinuria. In vitro sPLA2-IB-induced insufficient autophagy in podocytes and promoted podocyte injury via activation of the mTOR/ULK1 ser757 signaling pathway. Moreover, inhibition of p38 MAPK evidently abrogated sPLA2-IB-induced autophagy and the activation of mTOR/ULK1 ser757 . Additionally, PLA2R silencing demonstrated that sPLA2-IB-induced abnormal autophagy was also PLA2R-dependent. In conclusion, the results revealed that sPLA2-IB downregulated autophagy and contributed to podocyte injury via PLA2R though activation of the p38MAPK/mTOR/ULK1 ser757 signaling pathway., (© 2020 Federation of American Societies for Experimental Biology.)

Myelodysplastic syndromes (MDSs) are a group of heterogeneous hematopoietic stem/progenitor cells clonal diseases, characteristic features with myeloid dysplasia, leading to abnormality of neutrophils. Recent studied have showed that neutrophils act not only as professional killers, but also as regulators of innate and adaptive immune in infection and inflammatory condition. The CD54 high CD181 low neutrophils are a kind of reverse-transmigrated neutrophils characterized proinflammatory phenotype. We investigated the frequency and functional properties of circulating CD54 high CD181 low neutrophils in patients with untreated MDS. Frequency of CD54 high CD181 low neutrophils was significantly increased in MDS patients and related to the severity of the disease. Furthermore, CD54 high CD181 low neutrophils suppressed CD8+ T cells functions in vitro . CD54 high CD181 low neutrophils lead to upregulation of PD1 on CD8+ T cells. Higher CD54 high CD181 low neutrophils were related to poor prognosis and more infections. The frequency of CD54 high CD181 low neutrophils decreased in high risk MDS patients who had response after treatment with decitabine. Overall, we identified CD54 high CD181 low neutrophils expanded in MDS. The exact mechanisms of increased CD54 high CD181 low neutrophils and its effect on immune function remain to be elucidated., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Yang, Li, Liu, Xie, Zhang, Niu, Shao, Xing and Wang.)

Safer and more-effective drugs are urgently needed to counter infections with the highly pathogenic SARS-CoV-2, cause of the COVID-19 pandemic. Identification of efficient inhibitors to treat and prevent SARS-CoV-2 infection is a predominant focus. Encouragingly, using X-ray crystal structures of therapeutically relevant drug targets (PL pro , M pro , RdRp, and S glycoprotein) offers a valuable direction for anti-SARS-CoV-2 drug discovery and lead optimization through direct visualization of interactions. Computational analyses based primarily on MMPBSA calculations have also been proposed for assessing the binding stability of biomolecular structures involving the ligand and receptor. In this study, we focused on state-of-the-art X-ray co-crystal structures of the abovementioned targets complexed with newly identified small-molecule inhibitors (natural products, FDA-approved drugs, candidate drugs, and their analogues) with the assistance of computational analyses to support the precision design and screening of anti-SARS-CoV-2 drugs., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Author(s).)

Si anodes suffer from poor cycling efficiency because of the pulverization induced by volume expansion, lithium trapping in Li-Si alloys, and unfavorable interfacial side reactions with the electrolyte; the comprehensive consideration of the Si anode design is required for their practical deployment. In this article, we develop a cabbage-inspired graphite scaffold to accommodate the volume expansion of silicon particles in interplanar spacing. With further interfacial modification and prelithiation processing, the Si@G/C anode with an areal capacity of 4.4 mA h cm -2 delivers highly reversible cycling at 0.5 C (Coulombic efficiency of 99.9%) and a mitigated volume expansion of 23%. Furthermore, we scale up the synthetic strategy by producing 10 kg of the Si@G/C composite in the pilot line and pair this anode with a LiNi 0.8 Co 0.1 Mn 0.1 O 2 cathode in a 1 A h pouch-type cell. The full-cell prototype realizes a robust cyclability over 500 cycles (88% capacity retention) and an energy density of 301.3 W h kg -1 at 0.5 C. Considering the scalable fabrication protocol, holistic electrode formulation design, and harmony integration of key metrics evaluated both in half-cell and full-cell tests, the reversible cycling of the prelithiated silicon species in the graphite scaffold of the composite could enable feasible use of the composite anode in high-energy density lithium batteries.

The purpose of the present study was to explore the effects of emodin on renal injury in a BXSB mouse model of lupus and its mechanisms. BXSB mice were fed different concentrations of emodin (0, 5, 10 and 20 mg/kg.d), and the levels of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α) and fibronectin (FN) levels in the glomeruli and serum levels of the anti-dsDNA antibody were determined. Mesangial cells (MCs) were cultured in vitro, and IgG-type anti-dsDNA antibody and/or emodin were added to the MC culture supernatant. In addition, TNF-α small interfering RNA (siRNA) was transfected into MCs to explore the mechanism of action of emodin. The results showed that the mice fed emodin presented decreases in the urinary protein content and glomerular TNF-α, ICAM-1 and FN levels (P<0.05). Moreover, the urine protein, TNF-α, ICAM-1 and FN levels were decreased in a dose-dependent manner (P<0.05). In vitro, the anti-dsDNA antibody group exhibited increased levels of ICAM-1 and TNF-α (P<0.05), and the anti-dsDNA antibody group showed myofibroblast-like structural changes. The aforementioned indexes were decreased in the emodin group (P<0.05), and the extent of transdifferentiation was significantly reduced. Moreover, the level of ICAM-1 decreased with the down-regulation of TNF-α (P<0.05). Emodin reduced the urine protein levels and serum levels of the anti-dsDNA antibody in a mouse model of lupus nephritis (LN). The underlying mechanism may be related to decreased levels of TNF-α, ICAM-1 and FN and the inhibition of dsDNA antibody-induced MC damage., (© 2020 The Author(s).)

During mitosis chromosomes reorganise into highly compact, rod-shaped forms, thought to consist of consecutive chromatin loops around a central protein scaffold. Condensin complexes are involved in chromatin compaction, but the contribution of other chromatin proteins, DNA sequence and histone modifications is less understood. A large region of fission yeast DNA inserted into a mouse chromosome was previously observed to adopt a mitotic organisation distinct from that of surrounding mouse DNA. Here, we show that a similar distinct structure is common to a large subset of insertion events in both mouse and human cells and is coincident with the presence of high levels of heterochromatic H3 lysine nine trimethylation (H3K9me3). Hi-C and microscopy indicate that the heterochromatinised fission yeast DNA is organised into smaller chromatin loops than flanking euchromatic mouse chromatin. We conclude that heterochromatin alters chromatin loop size, thus contributing to the distinct appearance of heterochromatin on mitotic chromosomes., Competing Interests: MF, PT, AP, HO, LY, SW, RA No competing interests declared, JD Reviewing editor, eLife, (© 2020, Fitz-James et al.)

Background: Ferroptosis is a form of iron-dependent non-apoptotic cell death, with characteristics of loss of the activity of the lipid repair enzyme, glutathione (GSH) peroxidase 4 (GPX4), and accumulation of lethal reactive lipid oxygen species. The mechanism of ferroptosis in myelodysplastic syndrome (MDS) is unclear., Methods: Cell viability assay, reactive oxygen species (ROS) assay, GSH assay, and GPX activity assay were performed to study the regulation of ferroptosis in MDS cells obtained from MDS patients, the iron overload model mice, and cell lines., Results: The growth-inhibitory effect of decitabine could be partially reversed by ferrostatin-1 and iron-chelating agent [desferrioxamine (DFO)] in MDS cell lines. Erastin could increase the cytotoxicity of decitabine on MDS cells. The level of GSH and the activity of GPX4 decreased, whereas the ROS level increased in MDS cells upon treatment with decitabine, which could be reversed by ferrostatin-1. The concentration of hemoglobin in peripheral blood of iron overload mice was negatively correlated with intracellular Fe 2+ level and ferritin concentration. Iron overload (IO) led to decreased viability of bone marrow mononuclear cells (BMMNCs), which was negatively correlated with intracellular Fe 2+ level. Ferrostatin-1 partially reversed the decline of cell viability in IO groups. The level of GSH and the activity of GPX4 decreased, whereas the ROS level increased in BMMNCs of IO mice. DFO could increase the level of GSH. Ferrostatin-1 and DFO could increase the GPX4 activity of BMMNCs in IO mice. Ferrostatin-1 could significantly reverse the growth-inhibitory effect of decitabine in MDS patients. Decitabine could significantly increase the ROS level in MDS groups, which could be inhibited by ferrostatin-1 or promoted by erastin. Ferrostatin-1 could significantly reverse the inhibitory effect of decitabine on GSH levels in MDS patients. Erastin combined with decitabine could further reduce the GSH level. Erastin could further decrease the activity of GPX4 compared with the decitabine group., Conclusion: Ferroptosis may account for the main mechanisms of how decitabine induced death of MDS cells. Decitabine-induced ROS raise leads to ferroptosis in MDS cells by decreasing GSH level and GPX4 activity., (Copyright © 2020 Lv, Niu, Yue, Liu, Yang, Liu, Jiang, Dong, Shao, Xing and Wang.)

Overexpression of PTBP3, a factor involved in alternative splicing, may inhibit the differentiation of leukemia cells. However, its role in gastric cancer differentiation and the specific pathways involved are unclear. In this study, we found that PTBP3 was upregulated in the poorly differentiated gastric cancer tissues. Patients with high levels of PTBP3 expression had significantly shorter survival than those with low PTBP3 expression. In gastric cancer cells, the regulatory effect of PTBP3 on alternative splicing of the Id1 gene was investigated. Following sodium butyrate-induced differentiation of MKN45 cells, the expression of Id1a decreased, but the expression of Id1b increased. RNA interference and overexpression experiments showed that PTBP3 upregulated Id1a expression and downregulated Id1b expression. RNA immunoprecipitation (RIP) assays indicated PTBP3 could interact with Id1. UV cross-linking assays indicated that PTBP3 interacted with the CU rich region of the Id1 gene. Two-hybrid experiments and a gel mobility shift assays found that Id1b had a more potent affinity for Hes1 than Id1a. Chromatin immunoprecipitation (ChIP) assays verified the association of Hes1 and the promoter of PTBP3 gene. Luciferase assays revealed that Hes1 bound the N-box sequence in the PTBP3 promoter. After silencing or overexpression of Hes1, PTBP3 protein expression remained unchanged. Thus, the loss of feedback regulation among PTBP3, Id1, and Hes1 in gastric cancer cells may be one of the causes of inhibited differentiation and malignant proliferation of these cells., (Copyright © 2020 Chen, Chen, Mu, Yang, Gu, Zhao, Liang and Liu.)

Wearable piezoresistive sensors have attracted wide attention for application in human activities monitoring, smart robots, medical detection, etc. However, most of the sensing signals collected from the piezoresistive sensor are triggered by coupling forces, such as the combination of tension and pressure. Thus, the piezoresistive sensor would be incapable of accurately monitoring and evaluating specific human motion due to the mutual interference from tension and pressure, as the tension is difficult to be decoupled or eliminated from the coupling forces. Herein a prestretchable conductive yarn (PCY) sensor with pressure sensitivity but tension insensitivity was introduced to remove the disturbance from tension. The PCY-based piezoresistive sensor is tension insensitive (gauge factor of 0.11) but pressure sensitive (sensitivity of 187.33 MPa -1 ). The fabric-based pressure sensor assembled with cross-arranged PCY weft and warp revealed magnified pressure sensitivity compared with the single PCY yarn sensor, as well as tension insensitivity to strain and tensile angle. Moreover, it possessed benign cyclicity during 5000 cycles of pressing/releasing. Therefore, the fabric piezoresistive sensor based on weaved conductive yarns is suitable for highly accurate and large area pressure detection, such as monitoring massage intensity of acupuncture points.

The novel and highly pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has become a continued focus of global attention due to the serious threat it poses to public health. There are no specific drugs available to combat SARS-CoV-2 infection. Natural products (carolacton, homoharringtonine, emetine, and cepharanthine) and natural product-inspired small molecules (ivermectin, GS-5734, EIDD-2801, and ebselen) are potential anti-SARS-CoV-2 agents that have attracted significant attention due to their broad-spectrum antiviral activities. Here, we review the research on potential landmark anti-SARS-CoV-2 agents, systematically discussing the importance of natural products and natural-product-inspired small molecules in the research and development of safe and effective antiviral agents., (Copyright © 2020 Wang and Yang.)

Background: Armyworm (Mythimna separata) is a destructive herbivore for maize. Balsas teosinte (Zea mays ssp. parviglumis), the direct wild ancestor of cultivated maize, has shown great potential to defend against herbivory. Here, based on armyworm bioassay, we compared responses of teosinte and B73 maize inbred during armyworm attack in their transcriptome profiles to elucidate the gene expression changes involved in teosinte responses to armyworm attack. The goal of this study was to identify novel resistance alleles that could serve as valuable resources for modern maize breeding., Results: Our bioassay revealed that armyworm larvae grew less on teosinte than on maize. A follow-up transcriptomic comparison showed more down-regulated genes in maize B73 and similar numbers of up-regulated genes in both genotypes under armyworm attack. The up-regulated genes in teosinte were markedly enriched in MAPK cascade-mediated signaling pathway and phytohormone pathway. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that phytohormones jasmonic acid, ethylene, salicylic acid and abscisic acid (ABA) were actively involved in armyworm resistance of teosinte plants, and so were transcription factors such as MYBs, WRKYs and TIFYs. Interestingly, teosinte also showed high regulation in three ABA receptor PYLs. Based on differential expression analysis, we identified 30 candidate defense-related genes in teosinte, which belong to 11 gene families and the majority of the genes were up-regulated, while some of them were nonresponsive in maize., Conclusion: This study demonstrates that teosinte showed more vigorous defense response than maize toward armyworm attack and might be a beneficial genetic resource to improve pest resistance in cultivated maize. © 2019 Society of Chemical Industry., (© 2019 Society of Chemical Industry.)

Recombinant inbred lines (RILs) are an important resource for mapping genes controlling complex traits in many species. While RIL populations have been developed for maize, a maize RIL population with multiple teosinte inbred lines as parents has been lacking. Here, we report a teosinte nested association mapping (TeoNAM) population, derived from crossing five teosinte inbreds to the maize inbred line W22. The resulting 1257 BC 1 S 4 RILs were genotyped with 51,544 SNPs, providing a high-density genetic map with a length of 1540 cM. On average, each RIL is 15% homozygous teosinte and 8% heterozygous. We performed joint linkage mapping (JLM) and a genome-wide association study (GWAS) for 22 domestication and agronomic traits. A total of 255 QTL from JLM were identified, with many of these mapping near known genes or novel candidate genes. TeoNAM is a useful resource for QTL mapping for the discovery of novel allelic variation from teosinte. TeoNAM provides the first report that PROSTRATE GROWTH1 , a rice domestication gene, is also a QTL associated with tillering in teosinte and maize. We detected multiple QTL for flowering time and other traits for which the teosinte allele contributes to a more maize-like phenotype. Such QTL could be valuable in maize improvement., (Copyright © 2019 by the Genetics Society of America.)

In the course of generating populations of maize with teosinte chromosomal introgressions, an unusual sickly plant phenotype was noted in individuals from crosses with two teosinte accessions collected near Valle de Bravo, Mexico. The plants of these Bravo teosinte accessions appear phenotypically normal themselves and the F 1 plants appear similar to typical maize × teosinte F 1 s. However, upon backcrossing to maize, the BC 1 and subsequent generations display a number of detrimental characteristics including shorter stature, reduced seed set, and abnormal floral structures. This phenomenon is observed in all BC individuals and there is no chromosomal segment linked to the sickly plant phenotype in advanced backcross generations. Once the sickly phenotype appears in a lineage, normal plants are never again recovered by continued backcrossing to the normal maize parent. Whole-genome shotgun sequencing reveals a small number of genomic sequences, some with homology to transposable elements, that have increased in copy number in the backcross populations. Transcriptome analysis of seedlings, which do not have striking phenotypic abnormalities, identified segments of 18 maize genes that exhibit increased expression in sickly plants. A de novo assembly of transcripts present in plants exhibiting the sickly phenotype identified a set of 59 upregulated novel transcripts. These transcripts include some examples with sequence similarity to transposable elements and other sequences present in the recurrent maize parent (W22) genome as well as novel sequences not present in the W22 genome. Genome-wide profiles of gene expression, DNA methylation, and small RNAs are similar between sickly plants and normal controls, although a few upregulated transcripts and transposable elements are associated with altered small RNA or methylation profiles. This study documents hybrid incompatibility and genome instability triggered by the backcrossing of Bravo teosinte with maize. We name this phenomenon "hybrid decay" and present ideas on the mechanism that may underlie it., (Copyright © 2019 by the Genetics Society of America.)

CyclinB1 is a regulatory protein involved in mitosis. Multiple lines of evidence indicate that cyclinB1 depletion constrains proliferation and induces apoptosis in human tumor cells. The cells become susceptible to suffer a critical situation when cyclinB1 is downregulated. Autophagy is a major intracellular degradation system that recycles nutrients, removes damaged organelles, and promotes cell survival under stressful conditions, whereas the role of autophagy in cyclinB1-deprived neoplastic cell as well as the underlying molecular mechanism remains obscure. Here we pioneeringly elaborated that specific knockdown of cyclinB1 triggered autophagy via AMPK-ULK1-dependent signal pathway through the elevation of ROS, rather than ATP in the cell lines of CNE-1 and CNE-2. Moreover, ROS scavengers demonstrated that the observed effect of cyclinB1 silencing on AMPK phosphorylation was ROS dependent. Additionally, double knockdown of AMPK and cyclinB1 evidently abrogated cyclinB1 silencing-induced autophagy. Summarily, this study first revealed that downregulation of cyclinB1 induced autophagy via AMPK-ULK1-dependent signal pathway, which represents a key step toward unveiling the mechanism how cell cycle checkpoint proteins regulate autophagy.

Stability remains as a challenge of perovskite solar cells although encouraging progress has been made toward their maximum achievable power conversion efficiency in recent years. Light-soaking issue, where the device performance improves upon continuous light illumination and reduces upon storage in dark, is widely observed and marked as the early-stage instability during device operation. In this work, we have employed conjugated polymer PCDTBT as the dopant-free hole-transport layer to fabricate devices without hysteresis but with reversible light-soaking instability. The introduction of n-type molecules, either organic molecule PDI2 or fullerene derivative PC 61 BM, as the interfacial layer between TiO 2 and perovskite layers can effectively reduce or eliminate this instability owing to the efficient charge transport and defect passivation at the electron-transport layer interface, accompanied with an efficiency of 15.7 and 17.7%, respectively. We conclude that the light-soaking instability of these perovskite solar cells is mainly originated from the charge accumulation at the TiO 2 /perovskite interface and can be eliminated once the interfacial charge can be suppressed by interfacial modifications to improve charge transport at the interface.

Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal stem cell disorders characterized by cytopenia and dysplasia. Anemia is the most common symptom in patients with MDS. Mitophagy and mitochondrial dysfunction might be involved in the development of MDS. In this study, we investigated the change of mitophagy in erythroid precursors in MDS patients. We found that NIX-mediated mitophagy was impaired in bone marrow nucleated red blood cells (NRBC) of MDS patients, associated with an increased amount of damaged mitochondria and increased ROS level which might lead to apoptosis and ineffective erythropoiesis. The results showed that the amount of mitochondria in GlycoA + NRBC positively correlated with the count of ring sideroblasts in bone marrow samples. Meanwhile, the level of autophagy-associated marker LC3B in GlycoA + NRBC had a positive correlation with hemoglobin (Hb) levels, and the amount of mitochondria in GlycoA + NRBC had a negative correlation with Hb levels in high-risk MDS patients. Our results indicated that mitophagy might involve the pathogenesis of anemia associated with MDS. Autophagy might be a novel target in treatments of MDS patients.

An all-small-molecule ternary solar cell is achieved with a power conversion efficiency of 10.48% by incorporating phenyl-C 71 -butyric-acid-methyl ester (PC 71 BM) into a nonfullerene binary system. The addition of PC 71 BM is found to modulate the film morphology by improving the domain purity and decreasing the domain size. This modulation facilitates charge generation and suppresses charge recombination, as manifested by the significantly enhanced short-circuit current density and fill factor. The results correlate the domain characteristics with the device performance and offer new insight from the perspective of morphology modulation for constructing efficient ternary devices., (© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Myelodysplastic syndromes (MDS) are a group of clonal hematopoietic diseases which have a high risk of progressing to acute myeloid leukemia. MDS patients have immunologic deficiency, including T and B cells dysfunction. Follicular T helper cells (Tfh, CD4 + CXCR5 + ) are an important subset of helper T cells which help to the formation of germinal centers and B cells differentiation. In this study, we investigated the proportion and function of Tfh using NUP98-HOXD13 transgenic (NHD13) mice model with MDS phenotype. The proportion of Tfh from bone marrow and spleen of NHD13 mice decreased compared with wild type (WT) mice tested by flow cytometry. In NHD13 mice spleens, there were decreased CXCR5 + cells and increased PD-1 + cells using immunohistochemistry. The active markers (ICOS, CD40L and OX40) expressed on Tfh of NHD13 mice were decreased. In contrast, PD-1 expression on Tfh of NHD13 mice was higher than that of WT mice. After coculture with Tfh from NHD13 mice, IgG and IgM production of B cells were decreased. In conclusion, the proportion and function of Tfh in the MDS mice model were altered. The dysfunction and reduction of Tfh may inhibit B cells differentiation and antibody production. Abnormal Tfh might contribute to the immune tolerance promoting the progression of MDS., Competing Interests: CONFLICTS OF INTEREST The author declares no conflicts of interest.

Metal oxide charge transport layers have been widely employed to prepare inverted polymer solar cells with high efficiency and long lifetime. However, the intrinsic defects in the metal oxide layers, especially those prepared from low-temperature routes, overshadow the high efficiency that can be achieved and also introduce "light-soaking" issues to these devices. In this work, we have employed polyethyleneimine (PEI) and poly(9,9-bis(6'-(N,N-diethylamino)propyl)-fluorene-alt-9,9-bis-(3-ethyl(oxetane-3-ethyloxy)-hexyl)-fluorene] (PFN-OX) to modify our low-temperature-processed TiO 2 electron transport layer (ETL) and demonstrated that the light-soaking issue can be effectively eliminated by PEI modifications because of the formation of abundant dipole moments, whereas PFN-OX was ineffective as a result of deficient dipole moments at the interface. Excitingly, PEI modifications enable versatile device architectures to obtain light-soaking-free, inverted PTB7-Th:PC 71 BM solar cells with efficiencies of over 10%, by adding PEI either in the bulk or as an adjacent layer below or above the TiO 2 ETL.

Compositional modification and surface treatments of a TiO 2 film prepared by a low-temperature route are carried out by a new promising method. Inverted polymer solar cells incorporating the post-treated TiO 2 :TOPD electron-transport layer achieve the highest efficiency of 10.5%, and more importantly, eliminate the light-soaking problem that is commonly observed in metal-oxide-based inverted polymer solar cells., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

MiR-139-5p down-regulation has frequently been implicated in colorectal carcinoma. However, there is little known about its biological function between inflammation and cancer in vivo. Here, a transgenic murine model of colorectal carcinoma was used to investigate pathogenetic role of miR-139-5p in colitis and colitis-associated tumorigenesis. We showed that miR-139-5p knockout mice were higher sensitive to DSS-induced colitis and enhanced formation of intestinal neoplasia was observed when mice were exposed to AOM/DSS treatment. MiR-139-5p knockout mice exhibited an increased expression of genes involved in Wnt pathway. Such genes are closely associated with cell proliferation and differentiation, promoting the β-catenin nuclear accumulation. Furthermore, biochemical studies in HCT-116 cells revealed that the over-expression of miR-139-5p inhibited the crosstalk between PI3K/AKT and Wnt pathway mediated by IGF-1R. Collectively, these findings indicate that miR-139-5p plays a crucial role in the development and progression of colitis-associated tumorigenesis and suggest that miR-139-5p may serve as a potential therapeutic target for the treatment of colitis-associated cancer in the future.

Objective: Xanthomonas campestris pv. campestris (Xcc) is the cause agent of black rot of crucifers. Xcc uses type III secretion system (T3SS) to deliver T3SS effectors (T3SEs) directly into host cells, where they play important roles in pathogenesis. Many identified T3SEs genes contain plant-inducible promoter(PIP) box and -10 box in their promoter regions. However, the relation among PIP-box, -10 box and -10 region, -35 region of the classic promoter is unclear, and the conservative characteristic of -10 box sequence is hardly reported. The aim of this study was to analyze the putative promoter region of T3SE gene avrAC(Xcc8004)., Methods: Through 5' RACE, the transcriptional start site of avrAC(Xcc8004) was identified. Fusion PCR was introduced to generate the site-mutagenesis of -10 box for constructing the GUS fusion report strains., Results: The 5' RACE results indicate that the transcription start site was A. After analysis, we found that -35 region was located 8 bp downstream of PIP-box, and -10 box was exactly overlapped with -10 region. The whole motif of PIP-box, -35 region, and -10 box was then counted as: TTCAC-N15-TTCGC-N8-TTGATG-N18-TACGTT. The GUS assay results demonstrate that the site-mutagenesis of -10 box caused a higher expression of avrAC(Xcc8004). The GUS activities in the mutant strains delta hrpX and delta hrpG were significantly lower than that in the wild type Xcc strains., Conclusion: PIP-box is tandem with -35 region, -10 box is just the same as -10 region, -10 box is important for the transcription of avrAC(Xcc8004), and HrpG and HrpX activate the expression of avrAC(X8004), despite of -10 box site-mutagenesis.

Memory cross-reactive CD8+ T-cell responses may induce protection or immunopathology upon secondary viral challenge. To elucidate the potential role of T cells in sequential flavivirus infection, we characterized cross-reactive CD4+ and CD8+ T-cell responses between attenuated and pathogenic Japanese encephalitis virus (JEV) and pathogenic West Nile virus (WNV). A previously reported WNV NS4b CD8+ T-cell epitope and its JEV variant elicited CD8+ T-cell responses in both JEV- and WNV-infected mice. The peptide variant homologous to the immunizing virus induced greater cytokine secretion and activated higher frequencies of epitope-specific CD8+ T cells. However, there was a virus-dependent, peptide variant-independent pattern of cytokine secretion; the IFNgamma+-to-IFNgamma+TNFalpha+ CD8+ T-cell ratio was greater in JEV- than in WNV-infected mice. Despite similarities in viral burden for pathogenic WNV and JEV viruses, CD8+ T cells from pathogenic JEV-immunized mice exhibited functional and phenotypic profiles similar to those seen for the attenuated JEV strain. Patterns of killer cell lectin-like receptor G1 (KLRG1) and CD127 expression differed by virus type, with a rapid expansion and contraction of short-lived effector cells in JEV infection and persistence of high levels of short-lived effector cells in WNV infection. Such cross-reactive T-cell responses to primary infection may affect the outcomes of sequential flavivirus infections.

Objectives: To assess the relation between exposure to carbonless copy paper (CCP), paper dust, and fumes from photocopiers and printers (FPP), and the occurrence of sick building syndrome (SBS)-related symptoms, chronic respiratory symptoms and respiratory infections., Methods: A population-based cross-sectional study with a random sample of 1016 adults, 21-63 years old, living in Pirkanmaa District in South Finland was conducted. This study focused on 342 office workers classified as professionals, clerks or administrative personnel according to their current occupation by the International Standard Classification of Occupations-88. They answered a questionnaire about personal information, health, smoking, occupation, and exposures in the work environment and at home., Results: In logistic regression analyses adjusting for age, sex and a set of other confounders, all three exposures were related to a significantly increased risk of general symptoms (headache and fatigue). Exposure to paper dust and to FPP was associated with upper respiratory and skin symptoms, breathlessness, tonsillitis and middle ear infections. Exposure to CCP increased the risk of eye symptoms, chronic bronchitis and breathlessness. It was also associated with increased occurrence of sinus and middle ear infections and diarrhoea. A dose-response relations was observed between the number of exposures and occurrence of headache. The risk of tonsillitis and sinus infections also increased with increasing number of exposures. All chronic respiratory symptoms, apart from cough, were increased in the highest exposure category (including all three exposures)., Conclusions: This study provides new evidence that exposure to paper dust and to FPP is related to the risk of SBS symptoms, breathlessness and upper respiratory infections. It strengthens the evidence that exposure to CCP increases the risk of eye symptoms, general symptoms, chronic respiratory symptoms and some respiratory infections. Reduction of these exposures could improve the health of office workers.