Family Income and Child Depression: The Chain Mediating Effect of Parental Involvement, Children's Self-Esteem, and Group Differences.

Family income is an important factor that affects depression in children and can indirectly be associated with children's development through family and individual factors. However, few studies have examined the mechanism of multiple risk factors. Therefore, this study focused on the relationship between family income and child depression, as well as the chain mediating the roles of parental involvement and children's self-esteem both in single-parent families and intact families. A total of 1355 primary school students completed questionnaires that assessed family income, parental involvement, children's self-esteem, and depression. The results showed that family income influenced child depression through both the mediating roles of parental involvement and children's self-esteem and the chain mediating role of parental involvement and children's self-esteem. Meanwhile, family income only influenced child depression through chain mediation in single-parent families. The group differences in the mechanism of depression provide a reference for empirical research on depression intervention in children from different family structures.

Magnesium alleviates extracellular histone-induced apoptosis and defective bacterial phagocytosis in macrophages by regulating intracellular calcium signal.

Extracellular histones have been determined as important mediators of sepsis, which induce excessive inflammatory responses in macrophages and impair innate immunity. Magnesium (Mg2+), one of the essential nutrients of the human body, contributes to the proper regulation of immune function. However, no reports indicate whether extracellular histones affect survival and bacterial phagocytosis in macrophages and whether Mg2+ is protective against histone-induced macrophage damage. Our clinical data revealed a negative correlation between circulating histone and monocyte levels in septic patients, and in vitro experiments confirmed that histones induced mitochondria-associated apoptosis and defective bacterial phagocytosis in macrophages. Interestingly, our clinical data also indicated an association between lower serum Mg2+ levels and reduced monocyte levels in septic patients. Moreover, in vitro experiments demonstrated that Mg2+ attenuated histone-induced apoptosis and defective bacterial phagocytosis in macrophages through the PLC/IP3R/STIM-mediated calcium signaling pathway. Importantly, further animal experiments proved that Mg2+ significantly improved survival and attenuated histone-mediated lung injury and macrophage damage in histone-stimulated mice. Additionally, in a cecal ligation and puncture (CLP) + histone-induced injury mouse model, Mg2+ inhibited histone-mediated apoptosis and defective phagocytosis in macrophages and further reduced bacterial load. Overall, these results suggest that Mg2+ supplementation may be a promising treatment for extracellular histone-mediated macrophage damage in sepsis.

Lineage Tracing Identifies Dynamic Contribution of Endothelial Cells to Cardiac Valve Mesenchyme During Development.

Heart valve disease is an important cause of morbidity and mortality among cardiac patients worldwide. However, the pathogenesis of heart valve disease is not clear, and a growing body of evidence hints at the importance of the genetic basis and developmental origins of heart valve disease. Therefore, understanding the developmental mechanisms that underlie the formation of heart valves has important implications for the diagnosis, prevention, and treatment of congenital heart disease. Endothelial to mesenchymal transition is a key step in initiating cardiac valve development. The dynamic changes in the relative localization and proportion of different cell sources in the heart valve mesenchymal population are still not fully understood. Here, we used the Cdh5-CreER;R26R-tdTomato mouse line to trace endocardial cushion-derived endothelial cells to explore the dynamic contribution of these cells to each layer of the valve during valve development. This is beneficial for elaborating on the role of endocardial cells in the process of valve remodeling from a precise angle.

The influence of stressful life events on procrastination among college students: multiple mediating roles of stress beliefs and core self-evaluations.

Introduction: Few studies have documented the relationship between stressful life events and procrastination, which is a prevalent and troubling problem among college students. In this regard, the current study examined the association between stressful life events and procrastination through potential mediating effects of stress beliefs and core self-evaluations. Methods: A cross-sectional design was carried out and data were collected from a total of 794 Chinese college students with measures of stressful life events, core self-evaluations, stress beliefs, and procrastination. Results: Stressful life events was positively associated with procrastination in college students. Stress beliefs and core self-evaluations played multiple mediating roles in this relationship. Discussion: The study provided a novel perspective of finding the possible causes of procrastination in college students and highlighted the roles of stress beliefs and core self-evaluations.

Radiotherapy plus cetuximab or cisplatin in head and neck squamous cell carcinoma: an updated systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: The present meta-analysis was updated with randomized controlled trials (RCTs) to revaluate the efficacy and safety of cetuximab vs. cisplatin combined with radiotherapy in patients of head and neck squamous cell carcinoma (HNSCC). METHODS: A meta-analysis containing RCTs that compared the efficacy or toxicity of cetuximab and cisplatin in HNSCC patients was conducted. RESULTS: Seven RCTs were included in the final analysis. The patients treated by cetuximab plus radiotherapy showed an inferior overall survival (OS) and locoregional control (LRC) compared to cisplatin plus radiotherapy. The tendency of progression-free survival (PFS) was in agreement with OS and LRC. Subgroup analysis showed that cetuximab had poorer OS relative to cisplatin in the absence of induction chemotherapy. The profile of severe adverse events (SAEs) varied between the two groups, no significant difference in total SAEs was shown for the two arms. DISCUSSION: Cetuximab combined with radiotherapy shows significantly reduced therapeutic efficacy compared to cisplatin plus radiotherapy in HNSCC patients.

Emerging concepts regarding pro- and anti tumor properties of B cells in tumor immunity.

Controversial views regarding the roles of B cells in tumor immunity have existed for several decades. However, more recent studies have focused on its positive properties in antitumor immunity. Many studies have demonstrated a close association of the higher density of intratumoral B cells with favorable outcomes in cancer patients. B cells can interact with T cells as well as follicular dendritic cells within tertiary lymphoid structures, where they undergo a series of biological events, including clonal expansion, somatic hypermutation, class switching, and tumor-specific antibody production, which may trigger antitumor humoral responses. After activation, B cells can function as effector cells via direct tumor-killing, antigen-presenting activity, and production of tumor-specific antibodies. At the other extreme, B cells can obtain inhibitory functions by relevant stimuli, converting to regulatory B cells, which serve as an immunosuppressive arm to tumor immunity. Here we summarize our current understanding of the bipolar properties of B cells within the tumor immune microenvironment and propose potential B cell-based immunotherapeutic strategies, which may help promote cancer immunotherapy.

Application of zebrafish in the study of the gut microbiome.

Zebrafish (Danio rerio) have attracted much attention over the past decade as a reliable model for gut microbiome research. Owing to their low cost, strong genetic and development coherence, efficient preparation of germ-free (GF) larvae, availability in high-throughput chemical screening, and fitness for intravital imaging in vivo, zebrafish have been extensively used to investigate microbiome-host interactions and evaluate the toxicity of environmental pollutants. In this review, the advantages and disadvantages of zebrafish for studying the role of the gut microbiome compared with warm-blooded animal models are first summarized. Then, the roles of zebrafish gut microbiome on host development, metabolic pathways, gut-brain axis, and immune disorders and responses are addressed. Furthermore, their applications for the toxicological assessment of aquatic environmental pollutants and exploration of the molecular mechanism of pathogen infections are reviewed. We highlight the great potential of the zebrafish model for developing probiotics for xenobiotic detoxification, resistance against bacterial infection, and disease prevention and cure. Overall, the zebrafish model promises a brighter future for gut microbiome research.

The -172 A-to-G variation in ADAM17 gene promoter region affects EGR1/ADAM17 pathway and confers susceptibility to septic mortality with sepsis-3.0 criteria.

BACKGROUND: A disintegrin and metalloproteinase 17 (ADAM17) is a proteolytic cleaving protein with a crucial function in the inflammatory responses, especially sepsis. But the clear role of ADAM17 in sepsis and the underlying mechanism remained unknown. In this study, we aim to determine the clinical association of ADAM17 -172A > G (rs12692386) promoter polymorphism with sepsis and to further explore the effect and mechanism of the early growth response 1 (EGR1)/ADAM17 pathway in inflammatory process during sepsis. METHODS: A total of 477 sepsis patients and 750 controls were enrolled in this study to determine the association of ADAM17 -172A > G polymorphism with sepsis. The transcription factor binding to the promoter region of ADAM17 gene was predicted by bioinformatics analysis and verified by Chromatin Immunoprecipitation (ChIP) and luciferase assays. Quantitative real-time PCR and Western blot were performed to detect EGR1 and ADAM17 expression. Cytokine production was detected by enzyme-linked immunosorbent assay. The effect of EGR1/ADAM17 pathway on sepsis-induced inflammatory responses was evaluated in EGR1-silenced cells and endotoxemia mouse model. RESULTS: The frequencies of non-survivors among the sepsis patients with the -172AG/GG genotypes and G allele were distinctly higher than those among patients with the AA genotype (53.9% vs. 39.7%, OR = 1.779, 95% CI = 1.119-2.829, P = 0.0142) and A allele (30.9% vs. 22.2%, OR = 1.570, 95% CI = 1.095-2.251, P = 0.0136). The Kaplan-Meier survival analysis indicated that the 28-day survival in septic patients with -172AG/GG genotypes of this functional ADAM17 promoter polymorphism was much worse than in the AA genotype carriers (log-rank = 5.358, P = 0.021). The results of in vitro lipopolysaccharide-stimulated and luciferase assays indicated that the -172 A-to-G variation could functionally upregulate promoter activity and transcription of ADAM17 gene via enhancing the binding affinity of its promoter region with the EGR1. The ChIP assay identified the direct interaction. Further studies demonstrated that inhibition of EGR1 significantly decreased ADAM17 expression and the pro-inflammatory cytokine secretion in vitro, and improved the survival and inflammatory response of sepsis mouse model. CONCLUSIONS: These results provided evidence that the ADAM17 -172A > G polymorphism functionally promoted ADAM17 expression and enhanced sepsis-induced inflammatory responses via the EGR1/ADAM17 pathway, which ultimately conferred susceptibility to sepsis mortality and poor prognosis.

Distribution of arsenic species and pathological characteristics of tissues of the mice fed with arsenic-supplemented food simulating rice.

The exposure and harm of arsenic have attracted wide attention. Rice is an arsenic-rich crop. The purpose of this study was to learn the distribution of arsenic species and the pathological changes in tissues of mice exposed to arsenic-supplemented food simulating rice. Test groups of mice were orally exposed with prepared arsenic feeds supplemented with four arsenic species (arsenite iAsIII, arsenate iAsV, monomethylarsonate MMA, and dimethylarsinate DMA) at three doses (total As concentration: 0.91, 9.1 and 30 µg/g), which simulated the arsenic species ratio in rice. After 112 days, the concentrations of the arsenic species in the spleen, thymus, heart, skin and hair were detected, and histopathology of the spleen, heart and skin was observed. Each arsenic species was detected and their total concentration increased in a dose-dependent manner with a few exceptions. One interesting phenomenon is that ratio of the organic arsenic to inorganic arsenic also increased in a dose-dependent manner. For the other, the order of tissues from high to low arsenic concentration was the same in the medium- and high-dose groups. The histopathological sections of the spleen, heart and skin showed dose-dependent debilitating alterations in tissue architecture. Hyperplasia, hyaline degeneration and sclerosis of fibrous connective tissue occurred in the spleen. Myocardial cell atrophy and interstitial edema occurred in the heart. Hyperpigmentation, hyperkeratosis and atypia of basal cells occurred in the skin. In summary, the long-term intake of high arsenic rice has a health risk. Further studies are needed to assess it.

Long noncoding RNAs: A potential target in sepsis-induced cellular disorder.

Sepsis, an inflammation-related clinical syndrome, is characterized by disrupted immune homeostasis accompanied by infection and multiple organ dysfunction as determined by the Sequential Organ Failure Assessment (SOFA). Substantial evidence has recently suggested that lncRNAs orchestrate various biological processes in diseases, and lncRNAs play special roles in the diagnosis and management of sepsis. To date, very few reviews have provided clear and comprehensive clues to demonstrate the roles of lncRNAs in the pathogenesis of sepsis. Based on previously published studies, in this review, we summarize the different functions of lncRNAs in sepsis-induced cellular disorders and sepsis-induced organ failure to show the potential roles of lncRNAs in the diagnosis and management of sepsis. We further depict the function of some lncRNAs known to be pivotal regulators in the pathogenesis of sepsis to discuss the underlying molecular events. Additionally, we list and discuss several hotspots in research on lncRNAs, which may be conducive to future lncRNA-targeted therapeutic approaches for sepsis treatment.

A gain-of-function NLRP3 3'-UTR polymorphism causes miR-146a-mediated suppression of NLRP3 expression and confers protection against sepsis progression.

Nucleotide-binding domain and leucine-rich repeat (LRR)-containing family protein 3 (NLRP3) regulated the maturation of inflammation-related cytokines by forming NLRP3 inflammasome, which plays pivotal roles in sepsis pathogenesis. In this study, we evaluated the genetic association of NLRP3 polymorphisms with sepsis (640 patients and 769 controls) and characterized the impact of NLRP3 polymorphisms on NLRP3 expression and inflammatory responses. No significant differences were observed in genotype/allelic frequencies of NLRP3 29940G>C between sepsis cases and controls. The G allele was significantly overrepresented in patients with septic shock than those in sepsis subgroup, and the GC/GG genetypes were related to the 28-day mortality of sepsis. Lipopolysaccharide challenge to peripheral blood mononuclear cells showed a significant suppression of NLRP3 mRNA expression and release of IL-1ß and TNF-α in CC compared with the GC/GG genotype category. Functional experiments with luciferase reporter vectors containing the NLRP3 3'-UTR with the 29940 G-to-C variation in HUVECs and THP-1 cells showed a potential suppressive effect of miR-146a on NLRP3 transcription in the presence of the C allele. Taken together, these results demonstrated that the 29940 G-to-C mutation within the NLRP3 3'-UTR was a gain-of-function alteration that caused the suppression of NLRP3 expression and downstream inflammatory cytokine production via binding with miR-146a, which ultimately protected patients against susceptibility to sepsis progression and poor clinical outcome.

Parent-child conflict among primary and middle school students during the COVID-19 epidemic and its countermeasures / 中国学校卫生

Objective@#To investigate parent-child conflict among primary and secondary school students and their parents, and to promote family harmony and mental health of children and adolescents during the COVID-19 pandemic.@*Methods@#An anonymous online survey was completed by 12 711 parents of primary and middle school students during mid-March, 2020. Emotional translation, coping style, parent-child conflict were collected and analyzed by grade.@*Results@#The incidence of parent-child conflict was emotional opposition (62.3%), verbal conflict (52.6%) and physical conflict (20.5%), respectively. About 38.1% of parents and 23.6% of students experienced negative emotions, such as anxiety and anger, and the students used coping styles that were more uniform than those of their parents. About 77.9% of families reported that they experienced different levels of parent-child conflict, which was mainly caused by child learning difficulties(45.6%), daily arrangements(22.1%), and the use of electronic devices(10.2%); compared with the previous year, about 31.4% of families reported an increase in the frequency of parent-child conflicts in the last month.@*Conclusion@#Parent-child conflict is highly prevalent in the families of primary and middle school students, and such conflicts were affected by stress-related factors, which included COVID-19. It s necessary to improve the provision of relevant mental health education and psychological assistance.

4-Hydroxyisoleucine relieves inflammation through iRhom2-dependent pathway in co-cultured macrophages and adipocytes with LPS stimulation.

BACKGROUND: 4-Hydroxyisoleucine (4-HIL) is an active ingredient extracted from Trigonella foenum-graecum L., a Chinese traditional herbal medicine, which exerts the efficacy of anti-obesity and anti-diabetes. We previously reported that 4-HIL potentiates anti-inflammatory and anti-insulin resistance effects through down-regulation of TNF-α and TNF-α converting enzyme (TACE) in 3 T3-L1 adipocytes and HepG2 cells. In the present study, we further investigate the effects and mechanisms of 4-HIL on obesity-induced inflammation in RAW264.7 macrophages and 3 T3-L1 adipocytes co-culture system. METHODS: RAW264.7 macrophages and 3 T3-L1 adipocytes were co-cultured to mimic the microenvironment of adipose tissue. siRNA-iRhom2 transfection was performed to knockdown iRhom2 expression in RAW264.2 macrophages. The mRNA and protein expression of iRhom2 and TACE were measured by real-time quantitative PCR (RT-qPCR) and western blotting. The production of tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1), IL-6 and IL-10 were evaluated by ELISA. The ratio of M2/M1 was detected by flow cytometry. RESULTS: 4-HIL significantly repressed the mRNA and protein levels of iRhom2 and TACE in RAW264.7 macrophages after LPS stimulated. Meanwhile, the levels of pro-inflammatory cytokines, including TNF-α, MCP-1, and IL-6, were substantially suppressed by 4-HIL in the co-culture system. Moreover, the level of anti-inflammatory cytokine IL-10 was increased significantly by 4-HIL in the co-culture system after LPS stimulation. Additionally, the ratio of M2/M1 was also increased by 4-HIL in the co-culture system after LPS stimulation. Finally, these effects of 4-HIL were largely enhanced by siRNA-iRhom2 transfection. CONCLUSION: Taken together, our results indicated that obesity-induced inflammation was potently relieved by 4-HIL, most likely through the iRhom2-dependent pathway.

Presence of the apolipoprotein E-ε4 allele is associated with an increased risk of sepsis progression.

Growing evidence indicated that single nucleotide polymorphisms (SNPs) in the apolipoprotein E (APOE) gene are related to increase the risk of many inflammatory-related diseases. However, few genetic studies have associated the APOE gene polymorphism with sepsis. This study was to investigate the clinical relevance of the APOE gene polymorphism in the onset and progression of sepsis. A multicenter case-control association study with a large sample size (601 septic patients and 699 healthy individuals) was conducted. Clinical data showed that the APOEε4 allele was overrepresented among all patients with septic shock (p = 0.031) compared with sepsis subtype, suggesting that APOEε4 allele may associated with increased susceptibility to the progression of sepsis. Moreover, the APOE mRNA levels decreased after lipopolysaccharide (LPS) stimulation in cells in culture. Then 21 healthy individuals to extract PBMC for genotype grouping (APOE4+ group 8; APOE4- group 13) was selected to evaluate the effect on APOE level, and results showed that the expression level of APOE in APOE4+ group and APOE4- group did not differ in mRNA levels after an LPS challenge, but the protein levels in APOE4+ group decreased slower than that in APOE4- group, and this process was accompanied by the upregulation of proinflammatory cytokines. These results provide evidence that the APOEε4 allele might be associated with the development of sepsis and a potential risk factor that can be used in the prognosis of sepsis.

Fenugreek attenuates obesity-induced inflammation and improves insulin resistance through downregulation of iRhom2/TACE.

AIMS: We previously reported that fenugreek-derived 4-hydroxyisoleucine ameliorates insulin resistance via regulation of TNF-α converting enzyme (TACE) expression. In the present study, we further investigate the effects and mechanisms of fenugreek on obesity-induced inflammation and insulin signaling in the high-fat diet (HFD)-challenged obese mice. MAIN METHODS: After 12 weeks of HFD intervention, mice were treated with the low or high dosages of fenugreek. Serum levels of glucose, insulin, lipid profile, inflammation cytokines, and adipokines were detected. Macrophage infiltration and adipose tissue morphology were observed. Western blot was conducted to investigate the expressions of inactive rhomboid 2 (iRhom2) and TACE as well as other signaling pathways in subcutaneous adipose tissue. KEY FINDINGS: We showed that fenugreek significantly suppressed body weight gain and fat accumulation in HFD-challenged obese mice. Meanwhile, fasting glucose, insulin, and HOMA-IR in fenugreek-treated mice were remarkably decreased, which were properly explained by fenugreek-induced activation of the insulin receptor signaling pathway. Moreover, the anti-inflammatory properties of fenugreek were shown by the decrease of systemic and local expressions of pro-inflammatory cytokines as well as reduced macrophage infiltration into adipose tissue. Additionally, fenugreek markedly deactivated NF-κB and JNK pathways. Finally, we demonstrated that fenugreek strikingly repressed the transcriptions and expressions of iRhom2 and TACE. SIGNIFICANCE: Fenugreek shows an encouraging and promising property in ameliorating insulin resistance and suppressing inflammation in obesity, which might be realized by fenugreek-mediated inhibition of iRhom2/TACE axis-facilitated TNF-α release from adipocytes.

Target control based on edge dynamics in complex networks.

In the past decade, the study of the dynamics of complex networks has been a focus of research. In particular, the controllability of complex networks based on the nodal dynamics has received strong attention. As a result, significant theories have been formulated in network control. Target control theory is one of the most important results among these theories. This theory addresses how to select as few input nodes as possible to control the chosen target nodes in a nodal linear dynamic system. However, the research on how to control the target edges in switchboard dynamics, which is a dynamical process defined on the edges, has been lacking. This shortcoming has motivated us to give an effective control scheme for the target edges. Here, we propose the k-travel algorithm to approximately calculate the minimum number of driven edges and driver nodes for a directed tree-like network. For general cases, we put forward a greedy algorithm TEC to approximately calculate the minimum number of driven edges and driver nodes. Analytic calculations show that networks with large assortativity coefficient as well as small average shortest path are efficient in random target edge control, and networks with small clustering coefficient are efficient in local target edge control.

miR-23b Negatively Regulates Sepsis-Induced Inflammatory Responses by Targeting ADAM10 in Human THP-1 Monocytes.

BACKGROUND: Previous studies have demonstrated pivotal roles of disintegrin and metalloproteinase 10 (ADAM10) in the pathogenesis of sepsis. MicroRNA- (miR-) 23b has emerged as an anti-inflammatory factor that prevents multiple autoimmune diseases. However, the underlying mechanisms of miR-23b in the regulation of ADAM10 and sepsis remain uncharacterized. METHODS: The expression levels of ADAM10 and miR-23b were detected by quantitative RT-PCR and western blot analysis. Cytokine production and THP-1 cell apoptosis were measured by enzyme-linked immunosorbent and annexin V apoptosis assays. Bioinformatics analyses and qRT-PCR, western blot, and luciferase reporter assays were performed to identify ADAM10 as the target gene of miR-23b. RESULTS: miR-23b expression was downregulated in the peripheral blood mononuclear cells of sepsis patients and LPS-induced THP-1 cells and was negatively correlated with the expression of ADAM10 and inflammatory cytokines. miR-23b regulated ADAM10 expression by directly binding to the 3'-UTR of ADAM10 mRNA. The overexpression of miR-23b alleviated the LPS-stimulated production of inflammatory cytokines (TNF-α, IL-1ß, and IL-6) and apoptosis by targeting ADAM10 in THP-1 cells. The inhibitor or knockdown of ADAM10 elicited effects similar to those of miR-23b on THP-1 cells upon LPS stimulation. CONCLUSIONS: The present study demonstrated that miR-23b negatively regulated LPS-induced inflammatory responses by targeting ADAM10. The molecular regulatory mechanism of miR-23b in ADAM10 expression and sepsis-induced inflammatory consequences may provide potential therapeutic targets for sepsis.

A Functional Polymorphism-Mediated Disruption of EGR1/ADAM10 Pathway Confers the Risk of Sepsis Progression.

Increasing evidence has indicated that single nucleotide polymorphisms (SNPs) are related to the susceptibility of sepsis and might provide potential evidence for the mechanisms of sepsis. Our recent preliminary study showed that the ADAM10 genetic polymorphism was clinically associated with the development of sepsis, and little is known about the underlying mechanism. The aim of this study was to confirm the association between the ADAM10 promoter rs653765 G→A polymorphism and the progression of sepsis and to discover the underlying mechanism. Clinical data showed that the rs653765 G→A polymorphism was positively correlated with the development of sepsis, as evidenced by a multiple-center case-control association study with a large sample size, and showed that EGR1 and ADAM10 levels were associated well with the different subtypes of sepsis patients. In vitro results demonstrated that the rs653765 G→A variants could functionally modulate ADAM10 promoter activity by altering the binding of the EGR1 transcription factor (TF) to the ADAM10 promoter, affecting the transcription and translation of the ADAM10 gene. Electrophoretic mobility shift assay (EMSA) followed by chromatin immunoprecipitation (ChIP) assay indicated the direct interaction. Functional studies further identified that the EGR1/ADAM10 pathway is important for the inflammatory response. EGR1 intervention in vivo decreased host proinflammatory cytokine secretion and rescued the survival and tissue injury of the mouse endotoxemia model.IMPORTANCE Sepsis is characterized as life-threatening organ dysfunction, with unacceptably high mortality. Evidence has indicated that functional SNPs within inflammatory genes are associated with susceptibility, progression, and prognosis of sepsis. These mechanisms on which these susceptible sites depended often suggest the key pathogenesis and potential targets in sepsis. In the present study, we confirmed that a functional variant acts as an important genetic factor that confers the progression of sepsis in a large sample size and in multiple centers and revealed that the variants modulate the EGR1/ADAM10 pathway and influence the severity of sepsis. We believe that we provide an important insight into this new pathway involving the regulation of inflammatory process of sepsis based on the clinical genetic evidence, which will enhance the understanding of nosogenesis of sepsis and provide the potential target for inflammation-related diseases.

Efficacy and Safety of Compound Kushen Injection on Patients with Advanced Colon Cancer: A Meta-Analysis of Randomized Controlled Trials.

OBJECTIVE: The efficacy and safety of Compound Kushen Injection (CKI) on advanced colon cancer remain controversial. We undertook a systematic meta-analysis of randomized controlled clinical studies on this issue. METHODS: A comprehensive literature search was conducted by searching the following electronic databases: PubMed, Cochrane, Chinese Biological Medical disc, Chinese National Knowledge Infrastructure, and Wan-Fang Database in China by the end of January 31, 2017, without language restriction. Meta-analysis was performed by using the random effects model to estimate the summary odd ratio (OR) with 95% confidence interval (CI) according to the study design. Stata 12.0 software was used for data analysis. The heterogeneity, sensitivity, and publication bias were assessed, respectively. RESULTS: A total of 14 trials met the inclusion criteria in present meta-analysis. The results suggested that CKI combined with chemotherapeutic drugs was favorable for the treatment of advanced colon cancer and could improve the patients' life quality. Funnel plot analysis and Egger's test suggested that there was not significant publication bias, and the sensitivity analysis indicated stable results. CONCLUSION: The current evidence suggested that CKI is favorable to improve the efficacy of chemotherapeutic drugs in patients with advanced colon cancer.