Background Coronavirus disease 2019 (COVID-19) patients with pneumonia should receive the guidance of initial risk stratification and early warning as soon as possible. Whether the prehospital Pandemic Respiratory Infection Emergency System Triage (PRIEST) score can accurately predict the short-term prognosis of them remains unknown. Accordingly, we aimed to assess the performance of prehospital PRIEST in predicting the 30-day mortality of patients.Methods This retrospective study evaluated the accuracy of five physiological parameters scores commonly used in prehospital disposal for mortality prediction using receiver operating characteristic curves and decision curve analysis. Cox proportional hazard regression analysis was conducted to evaluate independent predictors associated with the 30-day mortality.Results A total of 231 patients were included in this study, among which 23 cases (10.0%) died within 30 days after admission. Compared with survivor patients, non-survivor patients had greater numbers of comorbidities, signs and symptoms, complications, and physiological parameters scores and required greater prehospital care (p < 0.05). When the PRIEST score was >12, the sensitivity was 91.3%, and the specificity was 77.4%. We found that the area under the curve of the PRIEST score (0.887, p < 0.05) for mortality prediction was greater than that of the quick Sequential Organ Failure Assessment (0.724), CRB-65 (0.780), Rapid Emergency Medicine Score (0.809), and National Early Warning Score 2 (0.838). Moreover, prehospital PRIEST scores were positively correlated with numbers of comorbidities and numbers of prehospital treatment measures. The 30-day survival rate of patients with PRIEST scores ≤12 (98.8%) significantly exceeded that of patients with PRIEST scores >12 (69.1%) (p < 0.001). Prehospital PRIEST scores >12 (HR = 7.409) was one of the independent predictors of the 30-day mortality.Conclusions The PRIEST can accurately, quickly, and conveniently predict the 30-day mortality of COVID-19 patients with pneumonia in the prehospital phase and can guide their initial risk stratification and treatment.

Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) are present in human umbilical connective tissue and can differentiate into various cell types. Our previous studies have proved that hUC-MSCs do not lead to allergies and tumorigenesis. In the present study, the acute and long-term toxicity of hUC-MSCs in mice and rats was evaluated. The acute toxicity of hUC-MSCs was assessed in 8-week-old mice receiving two caudal intravenous (i.v.) injections of hUC-MSCs at the maximum tolerated dose of 1.5 × 107 cells/kg with an interval of 8 h and the observation period sustained for 14 days. For the long-term toxicity evaluation, rats were randomly divided into control, low-dose (3.0 × 105 cells/kg), mid-dose (1.5 × 106 cells/kg), and high-dose (7.5 × 106 cells/kg) groups, which were treated with hUC-MSCs via a caudal i.v. injection every 3 days for 90 days. Weight and food intake evaluation was performed for all rats for 2 weeks after the hUC-MSC administration. The animals were then sacrificed for hematological, blood biochemical, and pathological analyses, as well as organ index determination. We observed no obvious acute toxicity of hUC-MSCs in mice at the maximum tolerated dose. Long-term toxicity tests in rats showed no significant differences between HUC-MSC-treated and control groups in the following parameters: body weight, hematological and blood biochemical parameters, and histopathologic changes in the heart, liver, kidneys, and lungs. This study provides evidence of the safety of i.v. hUC-MSCs infusion for future clinical therapies.

Background: Acute-on-chronic liver failure (ACLF) is always associated with thrombocytopenia or leukocytosis. Therefor the platelet to white blood cell ratio (PWR) in ACLF patients is always reduced. Objectives: Here, we assessed the relationship between PWR and prognosis in ACLF patients. Methods: A retrospective cohort of 415 patients, including 100 patients that were diagnosed of chronic hepatitis B, 104 patients suffered of HBV-related liver cirrhosis and 211 patients suffered of HBV-related ACLF, was investigated. Univariate and multivariate COX models were used to investigate the relationship between PWR and 30-day survival in patients with ACLF. Factors affecting PWR in ACLF patients were also analysed using logistic regression analysis. Results: At baseline, the platelet count in patients with HBV-related ACLF was significantly lower than that in patients with CHB and patients suffered of HBV-related cirrhosis. The PWR value was much higher in the survivors of ACLF than in ACLF patients who died. PWR, age, total bilirubine, prothrombin activity, and aspartate transaminase were independent predictors of the 30-day survival rate of ACLF patients. We also found that ascites and infection were independent factors related to the decrease of PWR in ACLF patients. Conclusions: The PWR value was significant declined in ACLF patients. And it was independent risk factors for the survival rate of those patients.

Acute traumatic coagulopathy (ATC) is an extremely common but silent murderer; this condition presents early after trauma and impacts approximately 30% of severely injured patients who are admitted to emergency departments (EDs). Given that conventional coagulation indicators usually require more than 1 hour after admission to yield results-a limitation that frequently prevents the ability for clinicians to make appropriate interventions during the optimal therapeutic window-it is clearly of vital importance to develop prediction models that can rapidly identify ATC; such models would also facilitate ancillary resource management and clinical decision support. Using the critical care Emergency Rescue Database and further collected data in ED, a total of 1385 patients were analyzed and cases with initial international normalized ratio (INR) values >1.5 upon admission to the ED met the defined diagnostic criteria for ATC; nontraumatic conditions with potentially disordered coagulation systems were excluded. A total of 818 individuals were collected from Emergency Rescue Database as derivation cohorts, then were split 7:3 into training and test data sets. A Pearson correlation matrix was used to initially identify likely key clinical features associated with ATC, and analysis of data distributions was undertaken prior to the selection of suitable modeling tools. Both machine learning (random forest) and traditional logistic regression were deployed for prediction modeling of ATC. After the model was built, another 587 patients were further collected in ED as validation cohorts. The ATC prediction models incorporated red blood cell count, Shock Index, base excess, lactate, diastolic blood pressure, and potential of hydrogen. Of 818 trauma patients filtered from the database, 747 (91.3%) patients did not present ATC (INR ≤ 1.5) and 71 (8.7%) patients had ATC (INR > 1.5) upon admission to the ED. Compared to the logistic regression model, the model based on the random forest algorithm showed better accuracy (94.0%, 95% confidence interval [CI]: 0.922-0.954 to 93.5%, 95% CI: 0.916-0.95), precision (93.3%, 95% CI: 0.914-0.948 to 93.1%, 95% CI: 0.912-0.946), F1 score (93.4%, 95% CI: 0.915-0.949 to 92%, 95% CI: 0.9-0.937), and recall score (94.0%, 95% CI: 0.922-0.954 to 93.5%, 95% CI: 0.916-0.95) but yielded lower area under the receiver operating characteristic curve (AU-ROC) (0.810, 95% CI: 0.673-0.918 to 0.849, 95% CI: 0.732-0.944) for predicting ATC in the trauma patients. The result is similar in the validation cohort. The values for classification accuracy, precision, F1 score, and recall score of random forest model were 0.916, 0.907, 0.901, and 0.917, while the AU-ROC was 0.830. The values for classification accuracy, precision, F1 score, and recall score of logistic regression model were 0.905, 0.887, 0.883, and 0.905, while the AU-ROC was 0.858. We developed and validated a prediction model based on objective and rapidly accessible clinical data that very confidently identify trauma patients at risk for ATC upon their arrival to the ED. Beyond highlighting the value of ED initial laboratory tests and vital signs when used in combination with data analysis and modeling, our study illustrates a practical method that should greatly facilitates both warning and guided target intervention for ATC.

Targeting single mediators has failed to reduce the mortality of sepsis. We developed a telodendrimer (TD) nanotrap (NT) to capture various biomolecules via multivalent, hybrid and synergistic interactions. Here, we report that the immobilization of TD-NTs in size-exclusive hydrogel resins simultaneously adsorbs septic molecules, e.g. lipopolysaccharides (LPS), cytokines and damage- or pathogen-associated molecular patterns (DAMPs/PAMPs) from blood with high efficiency (92–99%). Distinct surface charges displayed on the majority of pro-inflammatory cytokines (negative) and anti-inflammatory cytokines (positive) allow for the selective capture via TD NTs with different charge moieties. The efficacy of NT therapies in murine sepsis is both time-dependent and charge-dependent. The combination of the optimized NT therapy with a moderate antibiotic treatment results in a 100% survival in severe septic mice by controlling both infection and hyperinflammation, whereas survival are only 50–60% with the individual therapies. Cytokine analysis, inflammatory gene activation and tissue histopathology strongly support the survival benefits of treatments.

Blast injury is the main cause of injury in the battlefield, which also occurs frequently in the civil field and modern society. The damage caused by blast is more complicated than other types of trauma. Primary blast injury is a common type of blast injury, which can cause multiple organ damage with complex mechanism. Tissue and vascular endothelium damage and organ hypoperfusion are the consistent manifestations of most organ damage. However, due to the concealed damage caused by the primary blast injury, it is difficult to recognize it in time. The study of coagulation function and acid-base balance change after primary blast injury can bring benefits to its early diagnosis and intervention, thus improving the prognosis and mortality of blast injury. However, at present, the research on primary blast injury mostly focuses on single organ damage. Lack of research on systemic coagulation and acid-base balance changes calls for further research. Such research has a practical significance for the early diagnosis and optimization of tactical care for primary blast injury. This article reviews the injury characteristics, epidemiology, mechanism and the relationship with trauma-induced coagulopathy (TIC) in primary blast injury to provide reference for related researches.

This article aims to test a minimally invasive interventional approach by real-time transcranial contrast-enhanced ultrasound (CEUS) through a small bur hole to achieve an early local hemostatic drug therapy in a novel traumatic intracerebral hematoma (ICH) model of pigs with hemostatic abnormalities. The effects of hemostasis in the hemocoagulase atrox (HA) injection group and saline injection group groups were observed by transcranial CEUS at three time points: 0 s, 10 s, 2nd. We successfully established a novel traumatic ICH model of pigs with hemostatic abnormalities by the methods of interventional ultrasound techniques and observed the effect of hemostasis by using HA in a local injection method with the assistance of minimally invasive interventional ultrasound technique. At 0 s, four pigs (100%) were observed that active bleeding was significantly weakened, and the range of hematoma became smaller in the HA group. At 10 s, four pigs (100%) were observed that active bleeding became much weaker, and the range of hematoma became further smaller in the HA group. At 2nd, zero pigs (0/4, 0%) were observed that active bleeding could be clearly identified and four pigs (100%) with ICH could also be observed in the HA group. We believe this useful technique could minimize the invasiveness and be operated at the bedside, which would bring much more benefits for traumatic ICH patients.

ObjectivesTo determine whether real‐time 3‐dimensional ultrasound (RT3DUS) could provide additional information on early detection and evaluation in the management of solid abdominal organ trauma based on an animal model.MethodsNine bleeding lesions were developed in the livers (n = 3), kidneys (n = 3), and spleens (n = 3) from 9 pigs. An ultrasound contrast agent was administered intravenously (liver, 0.025 mL/kg; kidney, 0.008 mL/kg; and spleen, 0.013 mL/kg) after an unenhanced 2‐dimensional ultrasound (2DUS) examination (B‐mode and color Doppler). After contrast agent injection, bleeding lesions were imaged by 2DUS and sequentially imaged by 3‐dimensional static ultrasound (3DSUS) and RT3DUS to identify active bleeding, observe the relationship between bleeding lesions and peripheral blood vessels, and evaluate the spatial scope of the bleeding lesions in the organs.ResultsFor the identification of active bleeding, there was no statistical difference in contrast‐enhanced 2DUS, 3DSUS, and RT3DUS. For observation of the relationship between bleeding lesions and peripheral blood vessels, RT3DUS performed statistically better than 2DUS (P < .05), as reconstructed RT3DUS could show more information about the relationship. For the evaluation of the spatial scope of the bleeding lesion in the organ, RT3DUS also performed statistically better than 2DUS from the multiplanar observation by postprocessing of the 3‐dimensional real‐time volumes (P < .05).ConclusionsReal‐time 3‐dimensional ultrasound improves early detection and evaluation of solid abdominal organ trauma and provides additional information over the current contrast‐enhanced 2DUS.

OBJECTIVESTrauma predisposes to systemic sterile inflammation (systemic inflammatory response syndrome) as well as infection, but the mechanisms linking injury to infection are poorly understood. Mitochondrial debris contains formyl peptides. These bind formyl peptide receptor-1, trafficking neutrophils to wounds, initiating systemic inflammatory response syndrome, and wound healing. Bacterial formyl peptides, however, also attract neutrophils via formyl peptide receptor-1. Thus, mitochondrial formyl peptides might suppress neutrophils antimicrobial function. Also, formyl peptide receptor-1 blockade used to mitigate systemic inflammatory response syndrome might predispose to sepsis. We examined how mitochondrial formyl peptides impact neutrophils functions contributing to antimicrobial responses and how formyl peptide receptor-1 antagonists affect those functions.DESIGNProspective study of human and murine neutrophils and clinical cohort analysis.SETTINGUniversity research laboratory and level 1 trauma center.PATIENTSTrauma patients, volunteer controls.ANIMAL SUBJECTSC57Bl/6, formyl peptide receptor-1, and formyl peptide receptor-2 knockout mice.INTERVENTIONSHuman and murine neutrophils functions were activated with autologous mitochondrial debris, mitochondrial formyl peptides, or bacterial formyl peptides followed by chemokines or leukotrienes. The experiments were repeated using formyl peptide receptor-1 antagonist cyclosporin H, "designer" human formyl peptide receptor-1 antagonists (POL7178 and POL7200), or anti-formyl peptide receptor-1 antibodies. Mouse injury/lung infection model was used to evaluate effect of formyl peptide receptor-1 inhibition.MEASUREMENTS AND MAIN RESULTSHuman neutrophils cytosolic calcium, chemotaxis, reactive oxygen species production, and phagocytosis were studied before and after exposure to mitochondrial debris, mitochondrial formyl peptides, and bacterial formyl peptides. Mitochondrial formyl peptide and bacterial formyl peptides had similar effects on neutrophils. Responses to chemokines and leukotrienes were suppressed by prior exposure to formyl peptides. POL7200 and POL7178 were specific antagonists of human formyl peptide receptor-1 and more effective than cyclosporin H or anti-formyl peptide receptor-1 antibodies. Formyl peptides inhibited mouse neutrophils responses to chemokines only if formyl peptide receptor-1 was present. Formyl peptide receptor-1 blockade did not inhibit neutrophils bacterial phagocytosis or reactive oxygen species production. Cyclosporin H increased bacterial clearance in lungs after injury.CONCLUSIONSFormyl peptides both activate and desensitize neutrophils. Formyl peptide receptor-1 blockade prevents desensitization, potentially both diminishing systemic inflammatory response syndrome and protecting the host against secondary infection after tissue trauma or primary infection.

This study aimed to identify the potential key genes associated with severe pneumonia using mRNA-seq. Nine peripheral blood samples from patients with severe pneumonia alone (SP group, n=3) and severe pneumonia accompanied with chronic obstructive pulmonary disease (COPD; CSP group, n=3), as well as volunteers without pneumonia (control group, n=3) underwent mRNA-seq. Based on the sequencing data, differentially expressed genes (DEGs) were identified by Limma package. Following the pathway enrichment analysis of DEGs, the genes that were differentially expressed in the SP and CSP groups were selected for pathway enrichment analysis and coexpression analysis. In addition, potential genes related to pneumonia were identified based on the information in the Comparative Toxicogenomics Database. In total, 645 and 528 DEGs were identified in the SP and CSP groups, respectively, compared with the normal controls. Among these DEGs, 88 upregulated genes and 80 downregulated genes were common between the two groups. The functions of the common DEGs were similar to those of the DEGs in the SP group. In the coexpression network, the commonly downregulated genes (including ND1, ND3, ND4L, and ND6) and the commonly upregulated genes (including TSPY6P and CDY10P) exhibited a higher degree. In addition, 131 DEGs (including ND1, ND3, ND6, MIR449A and TAS2R43) were predicted to be potential pneumonia-related genes. In conclusion, the present study demonstrated that the common DEGs may be associated with the progression of severe pneumonia.

BACKGROUND Trauma causes inflammation by releasing mitochondria that act as Danger-Associated Molecular Patterns (DAMPs). Trauma also increases susceptibility to infection. Human mitochondria contain 13 N-formyl peptides (mtFPs). We studied whether mtFPs released into plasma by clinical injury induce neutrophil (PMN) inflammatory responses, whether their potency reflects their similarity to bacterial FPs and how their presence at clinically relevant concentration affects PMN function. METHODS N-terminal sequences of the 13 mtFPs were synthesized. Changes in human PMN cytosolic Ca2+ concentration ([Ca2+](i)) and chemotactic responses to mtFPs were studied. Sequence similarity of mtFPs to the canonical bacterial peptide f-Met-Leu-Phe (fMLF/fMLP) was studied using the BLOcks SUbstitution Matrix 62 (BLOSUM 62) system. The presence of mtFPs in plasma of trauma patients was assayed by Enzyme-linked immunosorbent assay (ELISA). The effects of the most potent mtFP (ND6) on PMN signaling and function were then studied at ambient clinical concentrations by serial exposure of native PMN to ND6, chemokines and leukotrienes. RESULTS Five mtFPs (ND6, ND3, ND4, ND5, and Cox 1) induced [Ca2+](i) flux and chemotaxis in descending order of potency. Evolutionary similarity to fMLF predicted [Ca2+](i) flux and chemotactic potency linearly (R-2 = 0.97, R-2 = 0.95). Chemoattractant potency was also linearly related to [Ca2+](i) flux induction (R-2 = 0.92). Active mtFPs appear to circulate in significant amounts immediately after trauma and persist through the first week. The most active mtFP, ND6, suppresses responses to physiologic alveolar chemoattractants (CXCL-1, leukotriene B-4) as well as to fMLF where CXCL-1 and leukotriene B-4 do not suppress N-formyl peptide receptor (FPR)-1 responses to mtFPs. Prior FPR-1 inhibition rescues PMN from heterologous suppression of CXCR-1 and BLT-1 by mtFPs. CONCLUSION The data suggest mtFPs released by injured tissue may attract PMN to trauma sites while suppressing PMN responses to other chemoattractants. Inhibition of mtFP-FPR1 interactions might increase PMN recruitment to lung bacterial inoculation after trauma. These findings suggest new paradigms for preventing infections after trauma. LEVEL OF EVIDENCE Therapeutic, Level IV.

The nuclear factor I (NFI) family members, especially NFIA and NFIB, play essential roles in cancers. The roles of NFIA and NFIB in esophageal squamous cell carcinoma (ESCC) and esophagogastric junction adenocarcinoma (EJA) remain poorly known. This study aimed to determine the expression of NFIA and NFIB in ESCC and EJA and elucidate their prognostic significance. The expression of NFIA and NFIB was examined in 163 ESCC samples and 26 EJA samples by immunohistochemistry. The results showed that high NFIA expression correlated significantly with poor differentiation, lymph node metastasis, and advanced TNM stage in patients with ESCC. High NFIB expression only correlated with poor differentiation in patients with ESCC. Survival analysis showed that NFIA but not NFIB associated with short overall survival (OS) and disease-free survival (DFS) of patients with ESCC. On the other hand, high NFIB expression correlated with lymph node metastasis, advanced TNM stage, and short OS and DFS in patients with EJA. Finally, multivariate analysis demonstrated that high NFIA expression was an independent prognostic factor for ESCC. Taken together, these results demonstrated that NFIA and NFIB could serve as prognostic indicators for ESCC and EJA, respectively.

OBJECTIVE:To introduce Medical Information Mart for Intensive Care (MIMIC) database and elaborate the approach of critically emergent research with big data based on the feature of MIMIC and updated studies both domestic and overseas, we put forward the feasibility and necessity of introducing medical big data to research in emergency. Then we discuss the role of MIMIC database in emergency clinical study, as well as the principles and key notes of experimental design and implementation under the medical big data circumstance. The implementation of MIMIC database in emergency medical research provides a brand new field for the early diagnosis, risk warning and prognosis of critical illness, however there are also limitations. To meet the era of big data, emergency medical database which is in accordance with our national condition is needed, which will provide new energy to the development of emergency medicine.

Hepatocyte growth factor (HGF) is a potent mitogen for mature hepatocytes, and has been shown to prevent cirrhosis during liver regeneration. Transplantation of mesenchymal stem cells (MSCs) reduces the development of cirrhosis after liver injury. However, the production and secretion of transplanted MSCs in liver were not studied yet. Here we found that the MSCs expressed low levels of HGF protein, but surprisingly high levels of HGF mRNA. Further investigation using bioinformatics analyses and luciferase reporter assay showed that MSCs expressed high levels of microRNA-26a-5p (miR-26a-5p), which targeted 3'-UTR of HGF mRNA to inhibit its protein translation. In vivo, miR-26a-5p-depleted MSCs were transplanted into mice with carbon tetrachloride (CCl4)-induced cirrhosis. We found that suppression of miR-26a-5p in MSCs further ameliorated the severity of liver fibrosis, reduced the portal hypertension and sodium retention, compared to transplantation of control MSCs. Hence, our study suggests that suppression of miR-26a-5p in MSCs may improve their therapeutic effects against cirrhosis through increasing HGF production.

Hair follicle morphogenesis and regeneration depend on intensive but well-orchestrated interactions between epithelial and mesenchymal components. Therefore, an alternative strategy to reproduce the process of epithelial-mesenchymal interaction in vitro could use a 3D system containing appropriate cell populations. The 3D air-liquid culture system for reproducibly generating hair follicles from dissociated epithelial and dermal papilla (DP) cells combined with a collagen-chitosan scaffold is described in this study. Wnt-CM was prepared from the supernatant of Wnt1a-expressing bone marrow mesenchymal stem cells (BM-MSCs) that maintain the hair-inducing gene expression of DP cells. The collagen-chitosan scaffold cells (CCS cells) were constructed using a two-step method by inoculating the Wnt-CM-treated DP cells and epidermal (EP) cells into the CCS. The cells in the air-liquid culture formed dermal condensates and a proliferative cell layer in vitro. The CCS cells were able to induce hair regeneration in nude mice. The results demonstrate that Wnt-CM can maintain the hair induction ability of DP cells in expansion cultures, and this approach can be used for large-scale preparation of CCS cells in vitro to treat hair loss. Copyright © 2015 John Wiley & Sons, Ltd.

Background: This study aimed to uncover the molecular mechanisms underlying mild and severe pneumonia by use of mRNA sequencing (RNA-seq).Material/Methods: RNA was extracted from the peripheral blood of patients with mild pneumonia, severe pneumonia, and healthy controls. Sequencing was performed on the HiSeq4000 platform. After filtering, clean reads were mapped to the human reference genome hg19. Differentially expressed genes (DEGs) were identified between the control group and the mild or severe group. A transcription factor-gene network was constructed for each group. Biological process (BP) terms enriched by DEGs in the network were analyzed and these genes were also mapped to the Connectivity map to search for small-molecule drugs.Results: A total of 199 and 560 DEGs were identified from the mild group and severe group, respectively. A transcription factor-gene network consisting of 215 nodes and another network consisting of 451 nodes were constructed in the mild group and severe group, respectively, and 54 DEGs (e.g., S100A9 and S100A12) were found to be common, with consistent differential expression changes in the 2 groups. Genes in the transcription factor-gene network for the mild group were mainly enriched in 13 BP terms, especially defense and inflammatory response (e.g., S100A8) and spermatogenesis, while the top BP terms enriched by genes in the severe group include response to oxidative stress (CCL5), wound healing, and regulation of cell differentiation (CCL5), and of the cellular protein metabolic process.Conclusions: S100A9 and S100A12 may have a role in the pathogenesis of pneumonia: S100A9 and CXCL1 may contribute solely in mild pneumonia, and CCL5 and CXCL11 may contribute in severe pneumonia.

Background: The purpose of this study was to comprehensively evaluate the role of PCT (procalcitonin) in diagnosis and prognosis of community acquired pneumonia (CAP) by a meta-analysis. Methods: Two researchers independently performed a retrieve on the databases of PubMed, Embase and Cochrane published in English up to July 2015. The search strategy was("community acquired pneumonia" OR CAP) AND procalcitonin. The risk ratio (RR) with 95% CI (confidence interval) was used for the analysis of dichotomous data. Standardized mean differences (SMD) and 95% CI were used to perform the analysis for continuous outcomes. All statistical analyses were performed by using RevMan (Review Manager) 5.3 software and Stata 12.0 statistical software package. Heterogeneity was analyzed with the Cochran Q test and I-2 test. Stata 12.0 was used to perform sensitivity analysis. Results: A total of 15 studies (6401 adult patients diagnosed with CAP) were selected in this meta-analysis. The number of patient mortality in PCT >= 0.5 ng/ml was twice that of PCT<0.5 ng/ml (RR = 0.50 (95% CI: 0.40, 0.62)). The number of patients that pathogen could be detected was 1.31 times that of could not be detected (RR = 1.31 (95% CI: 1.11, 1.55)). PCT levels of death cases were significantly higher than those of survival cases (SMD = -0.31 (95% CI: -0.50, -0.13)). The sensitivity analysis showed that this meta-analysis result was stable. Conclusions: Serum PCT levels are significantly related with detection of CAP pathogen and severity of CAP cases.

Objective To study the effect of IL -6 on the development of zygotes of mice after controlled ovarian hyperstimulation. Methods The present experiment included three parts: a) Addition of IL-6: 80 female ICR mice were divided into 7 groups by random number table including 6 groups of superovulation (10 each) and a group of natural ovulation cycle (n=20). According to addition of IL-6 in different concentration to culture media, the superovulated ICR mice were divided into superovulation control group (0pg/ml IL -6 group), 1pg/ml IL-6 group, 5pg/ml IL-6 group, 10pg/ml IL -6 group, 25pg/ml IL-6 group, and 50pg/ml IL-6 group, with ICR mice in natural ovulation cycle served as control. b) Addition of IL-6 receptor antibody (RA): 90 female ICR mice were divided into 7 groups according to the random number table, including 5 groups of superovulation (10 each) on the basis of addition of different concentrations IL-6 and IL-6 RA to culture media (0pg/ml IL-6+RA groups, 1pg/ml IL-6+RA group, 5pg/ml IL-6+RA group, 10pg/ml IL-6+RA group, 25pg/ml IL-6+RA group), and 2 groups of normal natural cycle (20 each), including control group and the control group+IL -6 RA (100pg/ml) group. Mice in normal control group conceived naturally while those in superovulation group conceived after superovulation. The zygotes were collected and cultured in vitro for 1 day till the formation of 2-cell embryos, then the rate of 2-cell formation was observed under microscope. Experiments of each group were repeated three times. c) Immunofluorescence identification: 10 female ICR mice were divided into control group and superovulation group (5 each) by random number table method. The expressions of IL -6 in zygotes were determined with confocal immunofluorescence method. Results IL-6 addition experiment: the rate of 2-cell formation was significantly lower (P<0.05) in superovulated control group, 1pg/ml IL -6, 25pg/ml IL -6 and 50pg/ml IL-6 groups than in control group (P=0.023, P=0.026, P=0.000 and P=0.000, respectively). IL -6 receptor antibody (RA) addition experiment: compared with normal control group, the rate of 2-cell formation decreased in superovulation group (P=0.017), so did in other IL -6 RA groups (P=0.000). Immunofluorescence identification: the expression of IL-6 in zygote was obviously lower in superovulation group than in control group. Conclusion Controlled superovulation can reduce the expression of IL-6 in zygote, and it may be related to its effect on embryonic development of mice. DOI: 10.11855/j.issn.0577-7402.2016.04.04

Phthalates are extensively used as plasticizers in a variety of daily-life products, resulting in widespread distribution in aquatic environments. However, limited information is available on the endocrine disrupting effects of phthalates in aquatic organisms. The aim of the present study was to examine whether exposure to mono-(2-ethylhexyl) phthalate (MEHP), the hydrolytic metabolite of di-(2-ethylhexyl) phthalate (DEHP) disrupts thyroid endocrine system in fish. In this study, zebrafish (Danio rerio) embryos were exposed to different concentrations of MEHP (1.6, 8, 40, and 200 μg/L) from 2 h post-fertilization (hpf) to 168 hpf. The whole-body content of thyroid hormone and transcription of genes involved in the hypothalamic-pituitary-thyroid (HPT) axis were examined. Treatment with MEHP significantly decreased whole-body T4 contents and increased whole-body T3 contents, indicating thyroid endocrine disruption. The upregulation of genes related to thyroid hormone metabolism (Dio2 and UGT1ab) might be responsible for decreased T4 contents. Elevated gene transcription of Dio1 was also observed in this study, which might assist to degrade increased T3 contents. Exposure to MEHP also significantly induced transcription of genes involved in thyroid development (Nkx2.1 and Pax8) and thyroid hormone synthesis (TSHβ, NIS and TG). However, the genes encoding proteins involved in TH transport (transthyretin, TTR) was transcriptionally significantly down-regulated after exposure to MEHP. Overall, these results demonstrate that acute exposure to MEHP alters whole-body contents of thyroid hormones in zebrafish embryos/larvae and changes the transcription of genes involved in the HPT axis, thus exerting thyroid endocrine toxicity.

The four-herb Chinese medicine ANBP is a pulverized mixture of four herbs including Agrimonia Eupatoria (A), Nelumbo Nucifera Gaertn (N), Boswellia Carteri (B) and Pollen Typhae Angustifoliae (P). The combination of the four herbs was first described in Chinese canonical medicine about 2000 years ago for treatment of various trauma disorders, such as hemostasis, antiinflammatory, analgesia, and wound healing, etc. However, the precise mechanisms of ANBP are still unclear. In our study, using rabbit ear hypertrophic scar models of full-thickness skin defect, we showed that local ANBP treatment not only significantly enhanced wound healing by relieving inflammation, increasing formation of granulation tissue and accelerating re-epithelialization, but also reduced scar formation by decreasing collagen production, protuberant height and volume of scars, and increasing collagen maturity. We demonstrated that these effects of ANBP are associated with transforming growth factor (TGF)-β1-mediated signalling pathways through Smad-dependent pathways. ANBP treatment significantly increased expression of TGF-β1 and Smad2/3 mRNA at the early stage of wound healing, and led to markedly decrease expression of TGF-β1 and Smad2/3 compared with the control group after 14 days post-wounding. Taken together, our results defined a bidirectional regulation role of ANBP for TGF-β1/Smad pathway in promoting wound healing and alleviating scar formation, which may be an effective therapy for human wounds at the earliest stage.