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We study the efficiency of the vector greedy algorithms for simultaneous sparse approximation in a Banach space. We employ a unified way of analyzing the approximation properties of the Vector Weak Chebyshev Greedy Algorithm, the Vector Weak Greedy Algorithm with Free Relaxation and the Vector Rescaled Weak Relaxed Greedy Algorithm. We obtain the necessary and sufficient conditions for the convergence and the optimal convergence rate on the basic sparse class for these algorithms. It shows that these vector greedy algorithms are simple but highly efficient in dealing with multi-target element. [ABSTRACT FROM AUTHOR]

Lithium cobalt oxide (LiCoO2) and graphite-based Li-ion batteries have been widely applied for consumer electronics because of the long cycle life and easy preparation. However, the limited capacity for traditional materials hampers the practical application for high energy-density battery. Conventional electrolyte system could not satisfy the need for high-capacity materials. Here, methylene methanedisulfonate (MMDS) was chosen as electrolyte additive for enhancing the available capacity for LiCoO2 and graphite-based battery. The effect of MMDS on the LiCoO2 cathode and graphite anode was investigated via multi electrochemical methods. It was found that the capacity for cells with MMDS electrolyte additive increases (from 142.6 mAh g−1 for pristine to 193.4 mAh g−1 on LiCoO2/Li battery, from 275.5 mAh g−1 for pristine to 407.0 mAh g−1 on graphite/Li battery). The experimental results indicate that improved capacity by MMDS electrolyte additive can be attributable to the stabilized interface on both cathode and anode sides, leading to superior interfacial Li+ kinetics and mitigated bulk structural degradation, which was further confirmed by the ex-situ electrochemical and structural characterization. [ABSTRACT FROM AUTHOR]

In the pursuit of high-energy density lithium-ion battery, Li-rich Mn-based oxide cathode has gained great attention with unexpectedly high capacity, low cost and excellent thermal stability. However, the cause for the sluggish kinetics remains a mystery, hindering the application of Li-rich cathode material. Here, we reveal the interfacial instability is the driving force for the sluggish kinetics, which severely blocks the interfacial Li-ion transport and triggers fast battery failure. Through rice-husk carbon (RHC) and spinel phase modification on Li-rich Mn-based oxide Li1.2Ni0.16Mn0.56Co0.08O2 (LNMC), the poor lithium ion diffusion and interfacial degradation can be effectively prevented, delivering a high specific capacity of around 300 mAh/g and excellent rate performance. These findings provide a universal method to prepare high electrochemical performance Li-rich oxide materials. Through synergetic modification, the Li-rich Mn-based cathode delivers a high available capacity of 300 mAh/g via accelerated Li+ intercalation kinetics [ABSTRACT FROM AUTHOR]

In line with rapid economic development and accelerated urbanization, the increasing discharge of wastewater and agricultural fertilizer usage has led to a gradual rise in ammonia nitrogen levels in rivers. High concentrations of ammonia nitrogen pose a significant challenge, causing eutrophication and adversely affecting the aquatic ecosystems and sustainable utilization of water resources. Traditional ammonia nitrogen detection methods suffer from limitations such as cumbersome sample handling and analysis, low sensitivity, and lack of real-time and dynamic feedback. In contrast, automated monitoring and ammonia nitrogen prediction technologies offer more efficient methods and accurate solutions. However, existing approaches still have some shortcomings, including sample processing complexity, interference issues, and the absence of real-time and dynamic information feedback. Consequently, deep learning techniques have emerged as promising methods to address these challenges. In this paper, we propose the application of a neural network model based on Long Short-Term Memory (LSTM) to analyze and model ammonia nitrogen monitoring data, enabling high-precision prediction of ammonia nitrogen indicators. Moreover, through correlation analysis between water quality parameters and ammonia nitrogen indicators, we identify a set of key feature indicators to enhance prediction efficiency and reduce costs. Experimental validation demonstrates the potential of our proposed approach to improve the accuracy, timeliness, and precision of ammonia nitrogen monitoring and prediction, which could provide support for environmental management and water resource governance. [ABSTRACT FROM AUTHOR]

In the context of escalating global environmental concerns, the importance of preserving water resources and upholding ecological equilibrium has become increasingly apparent. As a result, the monitoring and prediction of water quality have emerged as vital tasks in achieving these objectives. However, ensuring the accuracy and dependability of water quality prediction has proven to be a challenging endeavor. To address this issue, this study proposes a comprehensive weight-based approach that combines entropy weighting with the Pearson correlation coefficient to select crucial features in water quality prediction. This approach effectively considers both feature correlation and information content, avoiding excessive reliance on a single criterion for feature selection. Through the utilization of this comprehensive approach, a comprehensive evaluation of the contribution and importance of the features was achieved, thereby minimizing subjective bias and uncertainty. By striking a balance among various factors, features with stronger correlation and greater information content can be selected, leading to improved accuracy and robustness in the feature-selection process. Furthermore, this study explored several machine learning models for water quality prediction, including Support Vector Machines (SVMs), Multilayer Perceptron (MLP), Random Forest (RF), XGBoost, and Long Short-Term Memory (LSTM). SVM exhibited commendable performance in predicting Dissolved Oxygen (DO), showcasing excellent generalization capabilities and high prediction accuracy. MLP demonstrated its strength in nonlinear modeling and performed well in predicting multiple water quality parameters. Conversely, the RF and XGBoost models exhibited relatively inferior performance in water quality prediction. In contrast, the LSTM model, a recurrent neural network specialized in processing time series data, demonstrated exceptional abilities in water quality prediction. It effectively captured the dynamic patterns present in time series data, offering stable and accurate predictions for various water quality parameters. [ABSTRACT FROM AUTHOR]

Laryngeal cancer is a common type of head and neck malignancy. microRNA is implicated in the development and progression of various tumours. The present study aimed to explore the potential roles and mechanisms of miR‐646 in laryngeal carcinoma cells. We detected the expression of miR‐646 and observed that miR‐646 was reduced in laryngeal cell lines. Subsequently, the proliferation, migration and invasion of TU212 and TU686 cells were evaluated using CCK‐8 assays, cell proliferation ELISA BrdU and transwell assays after transfection with miR‐646 mimic. Overexpression of miR‐646 attenuated the proliferative and invasive abilities of TU212 and TU686 cells. Dual luciferase reporter assay confirmed that glutathione peroxidase 1 (GPX1) is a direct target of miR‐646. Interestingly, restoration of GPX1 promoted cell proliferation and migration, and reversed the biological activities of miR‐646 in cell proliferation and migration. It is worth noting that miR‐646 overexpression blocked the activation of PI3K/AKT pathway, and this was partly abrogated by GPX1. 740Y‐P, a PI3K agonist abolished the effects of miR‐646 on cell proliferation and invasion. Taken together, miR‐646 prohibited the proliferation and invasion of laryngeal carcinoma cells through the PI3K/AKT pathway via targeting GPX1. [ABSTRACT FROM AUTHOR]

Thoracic radiotherapy is a mainstay of the treatment for lung, esophageal, and breast cancers. Radiation-induced pulmonary injury (RIPI) is a common side effect of thoracic radiotherapy, which may limit the radiotherapy dose and compromise the treatment results. However, the current strategies for RIPI are not satisfactory and may induce other side effects. Chinese medicines (CMs) have been used for more than a thousand years to treat a wide range of diseases, including lung disorders. In this review, we screened the literature from 2007 to 2017 in different online databases, including China National Knowledge Infrastructure (CNKI), Chongqing VIP, Wanfang, and PubMed; summarized the effectiveness of CMs in preventing and treating RIPI; explored the most frequently used drugs; and aimed to provide insights into potential CMs for RIPI. Altogether, CMs attenuated the risk of RIPI with an occurrence rate of 11.37% vs. 27.78% (P < 0.001) compared with the control groups. We also found that CMs (alone and combined with Western medical treatment) for treating RIPI exerted a higher efficacy rate than that of the control groups (78.33% vs. 28.09%, P < 0.001). In the screened literature, 38 CMs were used for the prevention and treatment of RIPI. The top five most frequently used CMs were Astragali Radix (with a frequency of 8.47%), Ophiopogonis Radix (with a frequency of 6.78%), Glycyrrhizae Radix et Rhizome (with a frequency of 5.08%), Paeoniae Radix Rubra (with a frequency of 5.08%), and Prunellae Spica (with a frequency of 5.08%). However, further high-quality investigations in CM source, pharmacological effects and underlying mechanisms, toxicological aspects, and ethical issues are warranted. Taken together, CMs might have a potential role in RIPI prevention and treatment and still have a long way to investigate. [ABSTRACT FROM AUTHOR]

• PEDV E protein inhibits the poly(I:C)-induced IFN-β and ISGs production. • PEDV E protein suppresses the expression of RIG-I signaling-associated molecules. • PEDV E interacts IRF3 and further interferes its nuclear translocation. • PEDV E protein acts as an IFN-β antagonist through blockage of the RIG-I/ IRF3 signaling. Porcine epidemic diarrhea virus (PEDV) encodes many multifunctional proteins that inhibit host innate immune response during virus infection. As one of important structural proteins, PEDV E protein has been found to block the production of type I interferon (IFN) in virus life cycle, but little is known about this process that E protein subverts host innate immune. Thus, in this present study, we initiated the construction of eukaryotic expression vectors to express PEDV E protein. Subsequently, cellular localization analysis was performed and the results showed that the majority of PEDV E protein distributed at cytoplasm and localized in endoplasmic reticulum (ER). Over-expression of PEDV E protein significantly inhibited poly(I:C)-induced IFN-β and IFN-stimulated genes (ISGs) productions. We also found that PEDV E protein remarkably suppressed the protein expression of RIG-I signaling-associated molecules, but all their corresponding mRNA levels remained unaffected and unchanged. Furthermore, PEDV E protein obviously interfered with the translocation of IRF3 from cytoplasm to nucleus through direct interaction with IRF3, which is crucial for the IFN-β production induced by poly(I:C). Taken together, our results suggested that PEDV E protein acts as an IFN-β antagonist through suppression of the RIG-I-mediated signaling. This study will pave the way for the further investigation into the molecular mechanisms by which PEDV E protein evades host innate immune response. [ABSTRACT FROM AUTHOR]

• Chinese1 genotype Wh6 strain (TgCtwh6) infection not only leads to phosphorylation of tau via activating GSK3 β but also promotes hippocampal neuron apoptosis. • The signaling of p -GSK3 β - p -tau might be involved in the hippocampal neuron injury infected by an avirulent cyst-forming TgCtwh6. • These results are helpful for better understanding of mental disorders caused by T. gondii infection. • Prevention TgCtWh6 from infection may be an effective method to reduce the occurrence and delay the development of neurodegenerative diseases. Toxoplasma gondii (T. gondii) is a neurophilic and intracellular parasite that can affect plenty of vertebrate animals, including humans. Recent researches indicate that T. gondii infection is associated with neurodegenerative diseases such as Alzheimer's disease(AD). In addition, tau hyper-phosphorylation is a crucial event leading to the formation of nerve fiber tangles in AD. Despite the efforts to understand the interactions between T. gondii and AD, there are no clear results available so far. Here, we infected mice with the T. gondii of the Chinese 1 genotype Wh6 strain (TgCtwh6) for 60 days. Then we observed the formation of tissue cysts in the brain, the damage of neuron and the increased expression of phosphorylated tau (p -tau) in the hippocampal tissue of the mice. Similarly, we also found that p -tau, glycogen synthase kinase 3 beta (GSK3 β), and phosphorylated GSK3 β (p -GSK3 β) were upregulated in vitro in TgCtwh6 challenged hippocampal neuron cell strain, HT22 cells. We noted a down-regulated expression of GSK3 β , p -GSK3 β , and p -tau in HT22 cells, which were pretreated with LiCl, an inhibitor of GSK3 β. These data suggested that p -GSK3 β may mediate tau phosphorylation after TgCtwh6 infection. Furthermore, TgCtwh6 infection also caused the increased expression of Bax and Caspase3, the decreased expression of Bcl-XL in HT22 cells, which had both early and late apoptosis. In all, our results indicated that TgCtwh6 infection not only led to phosphorylation of tau via activating GSK3 β but also promoted hippocampal neuron apoptosis. Our research may partially reveal the mechanism with which TgCtwh6 induce neurofibrillary pathology. [ABSTRACT FROM AUTHOR]

• PEDV ORF3 is a transmembrane protein that localizes at endoplasmic reticulum to induce ER stress response. • PEDV ORF3 protein has no effect on apoptosis, but induces autophagy dependent on ER stress response. • This work provides some new findings for the biological function of the PEDV ORF3 protein. Porcine epidemic diarrhea virus (PEDV), the causative agent of PED, is an enveloped, positive-stranded RNA virus in the genus Alphacoronavirus , family Coronaviridae , order Nidovirales. PEDV non-structural accessory protein ORF3 is an ion channel related to viral infectivity and pathogenicity. Our previous study showed that PEDV ORF3 has expression characteristic of aggregation in cytoplasm, but its biological function remains elusive. Thus in this study, we initiated the construction of various vectors to express ORF3, and found ORF3 localized in the cytoplasm in the aggregation manner. Subsequently, confocal microscopy analysis showed that the aggregated ORF3 localized in endoplasmic reticulum (ER) to trigger ER stress response via up-regulation of GRP78 protein expression and activation of PERK-eIF2α signaling pathway. In addition, our results showed that PEDV ORF3 could induce the autophagy through inducing conversion of LC3-I to LC3-II, but couldn't influence the apoptosis. In contrast, conversion of LC3-I/LC3-II could be significantly inhibited by 4-PBA, an ER stress inhibitor, indicating that ORF3-induced autophagy is dependent on ER stress response. This work not only provides some new findings for the biological function of the PEDV ORF3 protein, but also help us for the further understanding the molecular interaction between PEDV ORF3 protein and cells. [ABSTRACT FROM AUTHOR]

• Lipid rafts are required for activation of PI3K/Akt signaling both at early and late stages of CA16 infection. • Lipid raft-associated PI3K/Akt plays critical roles in mediating SREBP1 maturation during late stage of CA16 infection. • This finding of lipid raft-associated PI3K/Akt/SREBP1 will deepen our understanding mechanism of CA16 infection. Coxsackievirus A16 (CA16) is one of predominant Enterovirus that possesses high pathogenicity. Lipid rafts, as cholesterol - and sphingolipid - enriched membrane nanodomains, are involved into many aspects of the virus life cycle. Our previous study found that lipid rafts integrity was essential for CA16 replication, but how lipid rafts regulate CA16 replication through activating downstream signaling remains largely unknown. Thus, in this study, we revealed that lipid rafts were required for activation of PI3K/Akt signaling at early stage of CA16 infection. Treatment with wortmannin significantly reduced the expression of virus protein, indicating PI3K/Akt signaling was beneficial for early stage of virus infection. In addition, lipid rafts integrity was also indispensable for PI3K/Akt activation during the late stage of CA16 infection, which played critical functions in mediating sterol regulatory element-binding proteins 1 (SREBP1) maturation. Whereas, over-expression of SREBP1 exhibited inhibition on virus replication, suggesting that PI3K/Akt signaling and SREBP1 might positively and negatively influence virus replication in two different stages of infection, respectively. Taken together, our study demonstrates an important role of the lipid raft-associated PI3K/Akt/SREBP1 signaling in modulating CA16 replication, which will deepen our understanding mechanism of CA16 infection. [ABSTRACT FROM AUTHOR]

• PEDV ORF3 inhibits the productions of pro-inflammatory cytokines IL-6 and IL-8. • PEDV ORF3 inhibits NF-κB activation through blockage of p65 activation. • Our study links PEDV ORF3 to inhibition of pro-inflammatory cytokines. Porcine epidemic diarrhea virus (PEDV) is an enveloped, single-stranded positive-sense RNA virus that belongs to a porcine entero-pathogenic alphacoronavirus , causing lethal watery diarrhea in piglets. Despite existing study reports the sole accessory protein ORF3 identified as NF-κB antagonist, the contribution of PEDV ORF3 to production of the pro-inflammatory cytokines mediated by NF-κB signaling remains largely unknown. Thus in this present study, we showed that PEDV ORF3 protein significantly inhibited the productions of pro-inflammatory cytokines interleukin-6 (IL-6) and IL-8. The phosphorylation of IκBα was inhibited by ORF3 protein, but no degradation of IκBα was induced in ORF3-expressing cells. Furthermore, PEDV ORF3 inhibited NF-κB activation through preventing nuclear factor p65 phosphorylation and down-regulating p65 expression level, as well as interfering nuclear translocation of p65, eventually resulting into the inhibition of IL-6 and IL-8 production. Our study definitely links PEDV ORF3 to inhibition of pro-inflammatory cytokines production, which will provide new insight into the molecular mechanisms of NF-κB activity inhibited by PEDV proteins to facilitate virus evasion of host innate immune. [ABSTRACT FROM AUTHOR]

Background: Type 1 Diabetes Mellitus (T1DM) is one of the most common endocrine disorders of childhood and adolescence, showing a rapidly increasing prevalence worldwide. A study indicated that the composition of the oropharyngeal and gut microbiota changed in T1DM. However, no studies have yet associated the changes between the microbiomes of the oropharyngeal and intestinal sites, nor between the flora and clinical indicators. In this study, we examined the composition and characteristics of oropharyngeal and intestinal flora in patients with T1DM in compared to healthy children. We identified correlations between oropharyngeal and intestinal flora and evaluated their association with clinical laboratory tests in patients with T1DM., Methods: The oropharyngeal and fecal samples from 13 T1DM and 20 healthy children were analyzed by high-throughput sequencing of the V3-V4 region of 16S rRNA. The associations between microbes and microorganisms in oropharyngeal and fecal ecological niches, as well as the correlation between these and clinical indicators were further analyzed., Results: It was revealed that T1DM children had distinct microbiological characteristics, and the dominant oropharyngeal microbiota genus included Streptococcus, Prevotella, Leptotrichia, and Neisseria; that of intestinal microbiota included Blautia, Fusicatenibacter, Bacteroides, and Eubacterium&#95;hallii&#95;group. Furthermore, oropharyngeal Staphylococcus was significantly positively correlated with intestinal norank&#95;f&#95;&#95;Ruminococcaceae and Ruminococcus&#95;torques&#95;group in TIDM children. Moreover, in these children, differential genes in oropharyngeal and intestinal samples were enriched in metabolic pathways such as amino acid generation, fatty acid metabolism, and nucleotide sugar biosynthesis. Additionally, correlation analysis between the oropharyngeal/intestinal microbiome with laboratory tests showed significant correlations between several bacterial taxa in the oropharynx and intestines and glycated hemoglobin and C-peptide., Conclusion: Unique microbial characteristics were found in the oropharynx and intestine in children with T1DM compared to healthy children. Positive correlations were found between changes in the relative abundance of oropharyngeal and gut microbiota in children with T1DM. Associations between the oropharyngeal/intestinal microbiota and laboratory investigations in children with T1DM suggest that the composition of the oropharyngeal and intestinal flora in children with T1DM may have some impact on glycemic control., 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., (© 2024 Wang, Gong, Wang, Wang, Yang and Wang.)

Background: Peptidyl-prolyl isomerase H (PPIH) is a member of the cyclophilin protein family, which functions as a molecular chaperone and is involved in the splicing of pre-mRNA. According to reports, the malignant progression of HCC related to hepatitis B virus (HBV) is tightly associated with RNA-binding proteins. Nevertheless, there is no research on PPIH expression or its function in the occurrence and progression of HCC., Results: We are the first to reveal that the mRNA and protein levels of Ppih are substantially overexpressed in HCC, as the outcomes show. A significant correlation existed between enriched expression of Ppih within HCC and more advanced, poorly differentiated, and TP53-mutated tumors., Conclusion: These findings, which suggest that Ppih may serve as a predictive biomarker for people with HCC, serve as a starting point for further investigation into the function of Ppih in the progression of carcinogenesis., Methods: Accordingly, we utilized clinical samples and bioinformatics analysis to assess Ppih's mRNA, protein expression, and gene regulatory system in HCC. Additionally, Wilcoxon signed-rank testing and logistic regression were utilized to inspect the association between clinicopathological factors and Ppih . Clinical pathological traits linked to overall survival (OS) among HCC patients were examined via TCGA data via Cox regression and the Kaplan-Meier approach. Additionally, via TCGA data collection, gene set enrichment assessment was also conducted.

Type 1 diabetes is an insulin-dependent type of diabetes that is most common among children. Due to absolute deficiency of insulin in patients, diabetic ketoacidosis (DKA) can easily ensue. Insulin pump can simulate the physiological secretion of islet, but increases the risk of pain and infection in children due to its traumatic effect. This study aimed to analyze the application effect of nano-insulin pump in children with DKA. Children with DKA admitted to our hospital from May 2018 to May 2020 were included in this study and, according to the random number table method, they were divided into two groups, with each group containing 36 cases. The first group received traditional insulin pump infusion (IP), while the second group received nano-insulin pump infusion (NIP). It was found that the reduction of FBG and PBG in NIP group was greater than that in IP group. The recovery time of urine ketone, blood ketone, glucose, venous pH, and other clinical indicators in the NIP group were all lower than those in the IP group ( P < 0.05). The length of hospital stay, insulin dosage, incidence of hypoglycemia, and infusion site infection rate in the NIP group were all lower than those in the IP group (P <0.05). The findings indicate that the application of nano-insulin pump in children with DKA had a significant effect and could quickly and obviously correct the levels of blood glucose and ketone body in children.

Background: Interferon-α (IFN-α) plays a pivotal role in host antitumor immunity, and the evasion of IFN-α signaling pathway can lead to IFN-α resistance during the treatment of cancer. Although the interplay between IFN-α and tumor cells has been extensively investigated in differentiated tumor cells, much less attention has been directed to tumor-repopulating cells (TRCs)., Methods: Three-dimentional soft fibrin matrix was used to select and grow highly malignant and tumorigenic melanoma TRCs. The regulation of integrin β3 (ITGB3)-c-SRC-STAT signaling pathway in melanoma TRCs was investigated both in vitro and in vivo. The relevant mRNA and protein expression levels were analyzed by qRT-PCR and western blot analysis. Immunoprecipitation and chromatin immunoprecipitation (ChIP) followed by qPCR (ChIP-qPCR) assays were performed to detect protein-protein and protein-DNA interactions. The clinical impacts of retinoic acid inducible gene-I (RIG-I) were assessed in melanoma datasets obtained from The Cancer Genome Atlas and Gene Expression Omnibus profiles., Results: IFN-α-induced apoptosis was decreased in melanoma TRCs. Compared with conventional flask-cultured cells, IFN-α-mediated STAT1 activation was diminished in melanoma TRCs. Decreased expression of RIG-I in melanoma TRCs led to diminished activation of STAT1 via enhancing the interaction between Src homology region 2 domain-containing phosphatase-1 and STAT1. In addition, low expression levels of RIG-I correlated with poor prognosis in patients with melanoma. STAT3 was highly phosphorylated in TRCs and knockdown of STAT3 reversed the downregulation of RIG-I in TRCs. Knockdown of STAT3 resulted in STAT1 activation and increased expression of the pro-apoptosis genes in IFN-α-treated TRCs. Combined treatment of STAT3 inhibitor and IFN-α increased the apoptosis rate of TRCs. Disruption of ITGB3/c-SRC/STAT3 signaling pathway significantly elevated the efficiency of IFN-α-induced apoptosis of TRCs., Conclusions: In melanoma TRCs, ITGB3-c-SRC-STAT3 pathway caused RIG-I repression and then affect STAT1 activation to cause resistance to IFN-α-induced apoptosis. RIG-I is a prognostic marker in patients with melanoma. Combination of STAT3 inhibitor and IFN-α could enhance the efficacy of melanoma treatment. Our findings may provide a new concept of combinatorial treatment for future immunotherapy., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: Interleukin-10 (IL-10) polymorphisms have been reported to be associated with systemic lupus erythematosus (SLE), however, the results are controversial. Therefore, we conducted a meta-analysis with trial sequential analysis to evaluate a more accurate estimation of the associations., Methods: Eligible studies were retrieved by searching PubMed, Embase, Google Scholar, VIP, Wan Fang and China National Knowledge Infrastructure databases. Hardy-Weinberg equilibrium (HWE) was evaluated. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Heterogeneity was evaluated by Q statistic and I2 statistic. Sensitivity analysis and subgroup analysis (stratified by HWE, region, event sample size, source of controls, genotyping method) were conducted and the potential for publication bias was assessed. Trial sequential analysis was introduced to assess the information size and the positive results., Results: Twenty case-control studies were included. Overall results from IL10-1082A/G polymorphism showed increased risk of systemic lupus erythematosus, but no significant associations were observed in both IL10-819C/T and IL10-592C/A polymorphism. Increased risk of SLE was also observed in IL10A/G polymorphism in Asian population, hospital-based and PCR-RFLP (polymerase chain reaction restriction fragment length polymorphism) subgroups. In addition, decreased risk of SLE was widely detected in IL10-819C/T and IL10-592C/A polymorphisms in subgroup analysis., Conclusions: Our study suggests that the IL10-1082A/G polymorphism is a risk factor in systemic lupus erythematosus. A decreased risk of SLE in the IL10-819C/T and IL10-592C/A polymorphisms in subgroups was also observed, but further rigorously studies are needed to confirm these results.

The purpose of this study is to summarize the currently available evidence regarding the concerned issue by performing a comprehensive meta-analysis. Relevant publications reporting the association of metformin use with survival of lung cancer patients with diabetes were electronically searched to identify eligible studies. The meta-analysis was performed with hazard ratios (HRs) and 95% confidence intervals (95% CIs) as effect measures for disease-free survival(DFS) and overall survival(OS) estimates. A total of 17 individual studies from 10 publications were included in the meta-analysis. Overall, the results revealed a significant association of metformin use with a better survival of lung cancer patients with diabetes(for DFS: HR = 0.65, 95%CI = 0.52-0.83; for OS: HR = 0.78, 95%CI = 0.64-0.93). The subgroup analyses showed similar association in Asian region(for DFS:HR = 0.69, 95%CI = 0.59-0.80; for OS: HR = 0.55, 95%CI = 0.46-0.67) but not in Western region. Such association was also presented in small cell lung cancer (for DFS: HR = 0.54, 95%CI = 0.38-0.77; for OS: HR = 0.52, 95%CI = 0.39-0.69) and in non-small cell lung cancer(for DFS: HR = 0.70, 95%CI = 0.51-0.96; for OS: HR = 0.75, 95%CI = 0.58- 0.97). Analyses stratified by treatment strategy showed a reduction in the risk of cancer-related mortality in patients receiving chemotherapy(for DFS: HR = 0.71, 95%CI = 0.64-0.83; for OS: HR = 0.58, 95%CI = 0.47-0.71) but not in patients receiving chemoradiotherapy. The meta-analysis demonstrated that metformin use was significantly associated with a favorable survival outcome of lung cancer patients with diabetes., Competing Interests: The authors declare no conflict of interest.