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Formation of lithium vapor cloud occurs above lithium surface as temperature goes up. Experiments devoted to investigating lithium vapor cloud interacting with expanding argon plasma under applied electric field have been carried out in a linear plasma device. Lithium spectrum has been characterized by utilizing optical emission spectroscopy (OES) and many emission lines of lithium atoms have been observed, including Li_670.78 nm (1.9 eV), Li_610.36 nm (3.87 eV), Li_460.30 nm (4.54 eV) and Li_323.26 nm (3.83 eV). Enhanced erosion of lithium surface caused by surface adatoms was found when bias is high, its effective adatoms sublimation energy was calculated to be 1.72 eV at the high temperature through Arrhenius plot in enhanced region. The surface temperature of liquid lithium has been monitored by a thermocouple. Since incident argon ion energy has been elevated due to the applied electric field acceleration, the temperature of lithium surface will have different behaviors with different biases, and it turns out that the temperature has a linear relation with bias, about an increase of 16–17 °C per 5 V bias voltage. By calculating evaporation power, excitation power and ionization power, indicating that at temperatures above 700–800 °C, heat flux dissipated in the lithium vapor can have a huge meaningful decrease.

Background Aortic dissection (AD) represents a clinically uncommon aortic pathology which predicts a dismal prognosis if not promptly treated. In acute Debakey type I AD (ADIAD), aortic lesion extends from aortic root to even distal abdominal aorta among which aortic arch and its three main branches still remain a great surgical challenge for repair and reconstruction. Several decades have witnessed the painstaking efforts of cardiovascular surgeons across the globe for optimizing the surgical procedures, from total or hemi-arch replacement, “elephant trunk” technique to branched stent graft. However, operative mortality and morbidity still remain to be reduced and surgical strategy is to be advanced and simplified, particularly the repair and reconstruction of aortic arch and supra-aortic vessels. Methods In this paper, we reviewed the relevant literature concerning recent advances in surgical intervention of aortic arch and summarized our opinions in the application of branched stent graft in ADIAD. Results The operative strategy for acute Debakey type I aortic dissection still remain to be advanced and simplified, especially the repair and reconstruction of aortic arch and supra-aortic vessels. For selection of branched stent grafts, the anatomic features and pathological changes of diseased arch are the crucial factors for clinical decision making. Conclusions Branched stent graft is potentially an effective alternative for the treatment of type I AD with diseased aortic arch and supra-aortic vessels. The selection of branched stent grafts still remains to be further discussed in large-scale studies in the future.

The structural and optical properties of Er 3+ /Yb 3+ codoped LaF 3 phosphors are investigated using X-ray diffraction (XRD) and upconversion luminescence spectra. The result shows that the hexagonal phase of LaF 3 keep stability at temperature lower than 800 °C in air condition and will be oxidized to be LaOF at higher temperature. Its upconversion emission intensity varies with the doping concentrations of Yb 3+ ions and reaches a maximum at around 7 mol% Yb 3+ . The power-dependent luminescence reveals the possible emission mechanisms and the corresponding upconversion processes. Furthermore, the optical temperature sensing properties of LaF 3 : Er 3+ /Yb 3+ are studied based on the fluorescence intensity ratio (FIR) technique for two thermally coupled levels ( 2 H 11/2 and 4 S 3/2 ) of Er 3+ . The maximum sensitivity is found to be about 0.00157 K −1 at 386 K, revealing this phosphor to be a promising prototype for applications in optical temperature sensing.

Despite progress in antibiotic treatment, mechanical ventilation, fluid resuscitation and blood glucose maintenance, sepsis remains a cause of high mortality in the intensive care unit to date, there are no proven treatment strategies for the routine management of septic patients. The extensive interaction between inflammation and coagulation contributes to the basic pathophysiology of sepsis. Thus, the agents that attenuate the activation of both inflammation and coagulation may improve the outcome in sepsis. Apart from the well-known anticoagulant effects of heparin, it also possesses various immunomodulatory properties and protects glycocalyx from shedding. Hence, heparin seems to be such an agent. Immunothrombosis plays an important role in early host defence against bacterial dissemination, thus the proper timing for anticoagulant therapy should be determined. We review the available experimental and clinical data supporting the use of heparin in sepsis. At this time the use of heparin in the treatment of sepsis is conflicting. Future trials of heparin therapy for sepsis should concentrate on the very severely ill patients, in whom benefit is most likely to be demonstrated.

Introduction In the pathogenesis of sepsis-induced acute lung injury (ALI), the crosstalk between inflammation and coagulation plays a pivotal role. The aim of this study was to investigate the role of Rho kinase (ROCK) inhibitor in alleviating pulmonary inflammation and coagulation in lipopolysaccharide (LPS)-induced acute lung injury (ALI) models. Methods In the in vivo study, mice were randomized to four different groups: Control, Y-27632 (Y), LPS, and LPS + Y-27632 (LPS + Y). ALI was induced by intranasally administering LPS (10 μg in 50 μL PBS). Y-27632 (10 mg/kg body weight,) was injected intraperitoneally at 18 h and 1 h before LPS challenge. Mice were euthanized at 3 h or 8 h post LPS challenge (N = 8 per group). In the in vitro study, human pulmonary microvascular endothelial cells (HPMECs) were incubated with LPS alone (1 μg/mL) or in combination with 10 μM Y-27632 or 50 μM BAY11-7082. Cells were pretreated with the inhibitors 30 min before exposure to LPS. Three hours later, cells were isolated for subsequent analysis. Results The myeloperoxidase (MPO) activity and fibrinogen deposits in the lung tissue significantly decreased and the lung damage in ALI mouse was attenuated. Pretreatment with Y-27632 markedly reduced the LPS-induced expression of interleukins 1β and 6, and the activation of nuclear factor (NF)-κB. Furthermore, ROCK inhibitor treatment antagonized the expression of tissue factor (TF) and plasminogen activator inhibitor (PAI)-1 in lung tissue and HPMECs. Conclusions ROCK inhibition protects against the endotoxin-induced pulmonary inflammation and coagulation via NF-kappaB pathway modulation.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection mostly presents with mild respiratory symptoms, although more severely affected patients may die of refractory acute respiratory distress syndrome (ARDS). The pulmonary function of surviving patients may decrease significantly in the early stages post-weaning due to the massive alveolar damage. Therefore, early pulmonary rehabilitation is important in these patients. We would like to share our experience of early pulmonary rehabilitation program in severe SARS-CoV-2 pneumonia, and hope that can remind ICUs of pulmonary rehabilitation in managing severe SARS-CoV-2 pneumonia.

To investigate the effects of heparin on the secretion of monocyte chemotactic protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVEC) and the adhesion of monocytes to endothelial cells stimulated by lipopolysaccharide (LPS).HUVEC were cultured in vitro, and the cells between generation 4 and 5 were used for the experiments. The cells were divided into phosphate buffer saline (PBS) control group, heparin control group, LPS group, and heparin+LPS group. The LPS group was challenged with LPS 10 mg/L; the PBS control group was added with the same amount of PBS; the heparin group was added with 10 kU/L unfractionated heparin; the heparin+LPS group was treated with 10 kU/L unfractionated heparin 15 minutes before LPS stimulation. The cells were harvested at 6 hours and 12 hours after LPS stimulation in each group, and the MCP-1 mRNA expression was determined by real-time fluorescent quantitative reverse transcription-polymerase chain reaction (qRT-PCR). After incubation with each group, the fluorescent dyelabeled human monocyte cell line THP-1 was cultured with each group for 1 hour in the dark, and the adhesion density of THP-1 and HUVEC was observed under fluorescence microscope.Compared with the PBS control group, the MCP-1 mRNA expression significantly increased at 6 hours and 12 hours after LPS stimulation and peaked at 6 hours, then decreased gradually, but remained significantly higher than the PBS control group at 12 hours [2Heparin preconditioning could inhibit the MCP-1 mRNA expression , thereby reduce the adhesion of THP-1 to HUVEC, thus play a protective role in sepsis.

INTRODUCTION Recently transcatheter aortic valve replacement (TAVR) has emerged as a feasible alternative for traditional surgical aortic valve replacement (SAVR) in patients with intermediate to high risk. There is currently no clear consensus regarding the optimal antiplatelet strategy after TAVR. The primary objective of this updated meta-analyses was to compare the outcomes of dual antiplatelet therapy (DAPT) versus single antiplatelet therapy (SAPT) following TAVR. EVIDENCE ACQUISITION A meta-analysis of eligible studies of patients undergoing TAVR which reported our outcomes of postoperative DAPT in comparison with SAPT, was carried out. The outcomes included the all-cause mortality, stroke, major/life-threatening bleeding, myocardial infarction and a composite endpoint of mortality, stroke, bleeding and myocardial infarction. EVIDENCE SYNTHESIS Three randomized controlled trials (RCTs, N.=421) and 5 observational studies (N.=6683) were included in this updated meta-analysis. All-cause mortality was comparable between the two groups (OR 1.13 [95% CI: 0.70-1.81], P=0.619). Besides, DAPT resulted in an augmented risk of major/life-threatening bleeding (OR 2.45 [95% CI: 1.08-5.59], P=0.032). No statistically significant difference was found between the two groups in the rates of stroke (OR 0.83 [95% CI: 0.62-1.10], P=0.212) and myocardial infarction (OR 1.17 [95% CI: 0.47-2.91], P=0.728). And DAPT led to an increased rate of the composite endpoint (OR 2.39 [95% CI: 1.63-3.50], P

To investigate the changes in coagulation of sepsis rats with protein-malnutrition or energy-malnutrition.108 male Sprague-Dawley (SD) rats were divided into three groups by random number table, with 36 rats in each group. The rats in normal feeding group were given a free diet (27 g/d, containing 18% protein fodder), and the rats in protein-malnutrition group were given a low protein diet (27 g/d, containing 5% protein fodder). The rats in energy-malnutrition group were given a low energy diet (9 g/d, containing 18% protein fodder). After 4 weeks of continuous feeding, 8 rats from each group were sacrificed for malnutrition evaluation. The weights of body, thymus and spleen were measured. The percentages of spleen T lymphocyte subsets and M1 macrophage were determined by flow cytometry. Plasma interleukins (IL-6 and IL-10) levels were determined by enzyme-linked immunosorbent assay (ELISA). The remaining 28 rats in each group were collected for cecal ligation and puncture (CLP) to reproduce the sepsis model, 20 rats of which were used for Kaplan-Meier survival analysis, and the other 8 rats were sacrificed at 8 hours after CLP. The levels of plasma IL-6 and IL-10 were determined by ELISA, and the percentage of spleen M1 macrophages was determined by flow cytometry. The mRNA expressions of tissue factor (TF) and plasminogen activation inhibitor-1 (PAI-1) in liver tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR). Pearson correlation method was used to analyze the correlation between the mRNA expressions of TF and PAI-1 and IL-6 in rats after CLP.(1) After 4 weeks of feeding, the rats in the normal feeding group and protein-malnutrition group gained weight, while those in the energy-malnutrition group lost 25% of their initial body weight. The weights of body, thymus and spleen in the protein-malnutrition group and the energy-malnutrition group were significantly lower than those in the normal feeding group. Compared with the normal feeding group and the protein-malnutrition group, the percentages of spleen CD3Long-term sustained stress (starvation) leads to sustained chronic inflammatory state, and stimulated the release of related inflammatory factors and activation of the coagulation system after infection. And the inflammatory factors in sepsis rats without sustained stress protein malnutrition were significantly reduced.

Background: Paraoxonase-1 (PON1) participates in several vital steps of lipid metabolism, which is associated with calcific aortic valve stenosis (CAVS). Although a few studies have suggested that PON1 in blood could inhibit aortic valve calcification, they did not provide detailed descriptions. In this study, we hypothesized that PON1 is expressed in the aortic valve and that the PON1 level is related to the severity of CAVS. Methods: A total of 118 consecutive patients with CAVS were enrolled in the study; 35 individuals without aortic valve calcification were included in the control group. Aortic valve tissue was obtained from postoperative pathologic specimens. PON1 was detected qualitatively using immunohistochemistry and quantitatively using an enzyme-linked immunosorbent assay. The severity of aortic stenosis was evaluated using echocardiography. Results: We detected PON1 in the aortic valve and noticed that the PON1 level was significantly lower in the case group than in the control group (P

Objective Atherosclerosis (AS) is one of the most common causes of human death and disability. This study is designed to investigate the roles of aldosterone (Aldo) and oxidized low-density lipoprotein (Ox-LDL) in this disease by clinical data and cell model. Materials and Methods In this experimental study, clinical data were collected to investigate the Aldo role for the patients with primary aldosteronism or adrenal tumors. Cell viability assay, fluorescence-activated cell sorting (FACS) assay, apoptosis assay, cell aging analysis, and matrigel tube formation assay were performed to detect effects on human umbilical vein endothelial cells (HUVECs) treated with Aldo and/or Ox-LDL. Quantitative polymerase chain reaction (qPCR) and Western blot analysis were performed to figure out critical genes in the process of endothelial cells dysfunction induced by Aldo and/or Ox-LDL. Results We found that the Aldo level had a positive correlation with the TG/HDL-C ratio. Endothelial cell growth, angiogenesis, senescence, and apoptosis were significantly affected, and eNOS/Sirt1, the value of Bcl-2/Bax and Angiopoietin1/2 were significantly affected when cells were co-treated by Aldo and Ox-LDL. Conclusion Elevated Aldo with high Ox-LDL together may accelerate the dysfunction of HUVEC, and the Ox-LDL, especially for those patients with high Aldo should be well controlled. The assessment of the role of Aldo may provide a theoretical basis for the effective prevention and investigation of a new treatment of AS.

BACKGROUND Severe acute pancreatitis (SAP) is a common condition in the intensive care unit (ICU) and has a high mortality. Early evaluation of the severity and prognosis is very important for SAP therapy. Recently, red blood cell distribution (RDW) was associated with mortality of sepsis patients and could be used as a predictor of prognosis. Similarly, RDW may be associated with the prognosis of SAP patients and be used as a prognostic indicator for SAP patients. AIM To investigate the prognostic value of RDW for SAP patients. METHODS We retrospectively enrolled SAP patients admitted to the ICU of the First Affiliated Hospital of China Medical University from June 2015 to June 2017. According to the prognosis at 90 d, SAP patients were divided into a survival group and a non-survival group. RDW was extracted from a routine blood test. Demographic parameters and RDW were recorded and compared between the two groups. The receiver operator characteristic (ROC) curve was constructed and Cox regression analysis was performed to investigate the prognostic value of RDW for SAP patients. RESULTS In this retrospective cohort study, 42 SAP patients were enrolled, of whom 22 survived (survival group) and 20 died (non-survival group). The baseline parameters were comparable between the two groups. The coefficient of variation of RDW (RDW-CV), standard deviation of RDW (RDW-SD), Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and Sequential Organ Failure Assessment (SOFA) score were significantly higher in the non-survival group than in the survival group (P < 0.05). The RDW-CV and RDW-SD were significantly correlated with the APACHE II score and SOFA score, respectively. The areas under the ROC curves (AUCs) of RDW-CV and RDW-SD were all greater than those of the APACHE II score and SOFA score, among which, the AUC of RDW-SD was the greatest. The results demonstrated that RDW had better prognostic value for predicting the mortality of SAP patients. When the RDW-SD was greater than 45.5, the sensitivity for predicting prognosis was 77.8% and the specificity was 70.8%. Both RDW-CV and RDW-SD could be used as independent risk factors to predict the mortality of SAP patients in multivariate logistic regression analysis and univariate Cox proportional hazards regression analysis, similar to the APACHE II and SOFA scores. CONCLUSION The RDW is greater in the non-surviving SAP patients than in the surviving patients. RDW is significantly correlated with the APACHE II and SOFA scores. RDW has better prognostic value for SAP patients than the APACHE II and SOFA scores and could easily be used by clinicians for the treatment of SAP patients.

The seasonal variations of blood lipids have recently gained increasing interest in this field of lipid metabolism. Elucidating the seasonal patterns of blood lipids is particularly helpful for the prevention and treatment of cardiovascular and cerebrovascular diseases. However, the previous results remain controversial and the underlying mechanisms are still unclear. This mini-review is focused on summarizing the literature relevant to the seasonal variability of blood lipid parameters, as well as on discussing its significance in clinical diagnoses and management decisions.

Semi-supervised learning is an efficient method to augment training data automatically from unlabeled data. Development of many natural language understanding (NLU) applications has a challenge where unlabeled data is relatively abundant while labeled data is rather limited. In this work, we propose transductive graph-based semi-supervised learning models as well as their inductive variants for NLU. We evaluate the approach’s applicability using publicly available NLU data and models. In order to find similar utterances and construct a graph, we use a paraphrase detection model. Results show that applying the inductive graph-based semi-supervised learning can improve the error rate of the NLU model by 5%.

Japanese encephalitis virus (JEV) is a viral zoonosis that can cause viral encephalitis, death and disability whose primary vector is the Culex mosquito. Viral infection induces a series of antimicrobial peptide responses in mosquitoes, and the effector defensin enhances JEV replication in mosquitoes. However, the underlying mechanisms by which defensin enhances JEV are not fully understood. Here, we found that mosquito defensin could downregulate the antiviral protein HSC70B and enhance virus infection in mosquitoes. The cell-surface protein HSC70B was significantly downregulated by JEV infection and defensin treatment. Low levels of HSC70B were beneficial to JEV infection in mosquitoes. Taken together, these findings show that defensin and HSC70B axis facilitates JEV infection in the mosquito.

Random pore model was employed to calculate the reaction kinetics parameters of SH bituminous coal and Shenmu semi-coke blended fuels under high-temperature entrained flow combustion, and the reaction kinetics parameters was modified by the intrinsic reaction Arrhenius curve obtained from low temperature thermogravimetric experiments. Then the combustion reaction rate and intrinsic reaction order at different blending ratios of semi-coke were determined. The reaction kinetics parameters and carbon conversion rate of blended fuels were investigated based on the pore structure of fuel, the effects of blending ratio of semi-coke, initial partial pressure of oxygen and reaction temperature. The reaction order decreases with the increasing of semi-coke blended ratio except 100% semi-coke combustion has higher reaction order approximately as char pure burning. The distribution of oxygen alone the radius of particle was also calculated in this study. In the low oxygen reduction zone, the blending ratio of semi-coke has little effect on the carbon conversion of blended fuel, and the blending effect is enhanced with the increasing of oxygen content. Carbon conversion rate decreases with the increasing of blending ratio and increases with reaction temperature.

A novel health hazard assessment model of fine particles generated from five groups of coal-fired boilers is built based on AHP. In our assessment model, some important factors are taken into account, including the number from uncontrolled emission, and mass from uncontrolled emission, the particle size distribution of Rosin-Rammler function of fine particles, and the total content of toxic chemical compositions (including Cr, V, Mn, Ni, Pb, Cd, As, Se, Hg, OC and EC). By calculation, PM2.5 from the industrial grate-fired boilers are much more harmful to human health than those from the other types of coal-fired boilers, which is not recommended to choose grate-fired burners as a burner of a new boiler or a modification boiler. PM2.5 from industrial fluidized-bed boilers are more harmful to human health than that of utility CFB boilers; PM2.5 from the large-capacity utility pulverized coal boilers (⩾450MW) are more harmful to human health than those from the small-capacity utility pulverized coal boilers (

The SD12-F120 is a live-attenuated genotype I strain of Japanese encephalitis virus (JEV) and was obtained by serial passage of wild-type strain SD12 on BHK-21 cells combined with multiple plaque purification and virulence selection in mice. The large scale production and vast clinical trials always demand ideal safety and efficacy profile of live-attenuated vaccines. In the present study, SD12-F120VC has undergone serial passaging of P1-P30 in WHO qualified Vero cells to assess the potential effect of adaptation to growth on Vero cells. The series of experiments showed that vaccine SD12-F120VC (Vero cell adapted) variants have consistently increased in peak virus titer compared to early passages and have good adaptation to growth in Vero cells. The animal experiments showed that Vero cell adapted SD12-F120VC variants have attenuation phenotype in suckling mice and the plaque morphology for all SD12-F120VC variants was small. Vaccination of mice with SD12-F120VC vaccine produced complete protection for homologous SD12 genotype I strain, but failed to give the complete protection of vaccinated mice against the challenge of heterologous N28 genotype III strain. In response to immunization of SD12-F120VC in mice, the neutralizing antibodies titer against homologous SD12-F120VC and SD12 (GI) was higher than heterologous N28 (GIII) strain. The prM protein has 6 amino acid substitutions, of which 5 amino acid changes were confined at the start of the pr domain in the ∼40 amino acids, and some mutations in the pr domain of prM might contribute to Vero cell adaptation. Our findings in this study are important for validation, evaluation and quality control study of live attenuated flaviviruses vaccines and show that Vero cells are a suitable substrate for the production of a safe and stable live-attenuated JEV vaccine.

Objective Natural orifice transluminal endoscopic surgery (NOTES) is an endoscopic technique whereby surgical interventions can be performed with a flexible endoscope passed through a natural orifice (mouth, vulva, urethra, anus) then through a transluminal opening of the stomach, vagina, bladder, or colon. Although in the early stage of research and development, NOTES has been clinically applied across the globe, above all the transvaginal cholecystectomy is among the most frequently performed procedures. In the existing 2 types of transvaginal routes, the hybrid NOTES cholecystectomy (NC) is more likely to be accepted. However, there has been controversy regarding the safety outcomes of hybrid NC in comparison with classical laparoscopic cholecystectomy (LC). The primary objective of this meta-analysis is to compare the characteristics between NC and classical LC. Materials and methods A meta-analysis of eligible studies comparing NC with classical LC was performed to evaluate the safety outcomes including wound complications, other postoperative complications and intraoperative conversion between the 2 groups. Results Pooling 3 randomized controlled trials (n=157) and 7 nonrandomized trial (n=593) demonstrated that the rates of wound complications and other postoperative complications in NC group did not significantly differ from those of classical LC group [wound complications: ratio difference (RD)=-0.02, 95% confidence interval (CI) -0.04to 0.01, P=0.23; other postoperative complication: RD=-0.01; 95% CI, -0.03 to 0.02; P=0.6]. The intraoperative conversion rate in NC groups was higher than that of LC groups (RD=0.03; 95% CI, 0.01-0.06; P=0.02). Conclusions There is no significate difference between the safety of NC and laparoscope cholecystectomy. NC is associated with a higher rate of intraoperative conversion when compared with LC. It is worthy of further promotion and validation in clinical settings.

OBJECT This study aimed at exploring what level of the microcirculation alteration could weaken the decrease of ScvO2 (or the increase of O2ER) and further result in an abnormally elevated ScvO2. METHODS Beagles were randomly assigned into control (n = 5) and shock group (n = 5). The canines in shock group were intravenously injected with live E. coli (3.5×108 cfu/kg), and the ones in control group were injected with sterile saline. The experiment continued to the animals' death or for a maximum of 24 hours. Hemodynamic parameters, blood gas and inflammatory cytokines level were collected. Microcirculatory parameters were assessed with Sidestream Dark Field (SDF) imaging. The correlation between the microcirculation and oxygen metabolism or inflammatory cytokine, meanwhile the correlation between the oxygen metabolism and inflammatory cytokine was assessed. RESULTS E. coli infusion induced hypodynamic shock. The correlation between microcirculation and oxygen metabolism or inflammatory cytokine, and The correlation between the oxygen metabolism and inflammatory cytokine (O2ER vs. MFI: r = -0.700, P

Exploring stable and highly efficient bifunctional electrocatalysts for oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) is critical for the novel energy conversion and storage devices including fuel cells and metal-air batteries. Herein, the core-shell structured Co3Fe7@Fe2N nanoparticles supported on reduced graphene oxide (rGO) nanosheets (Co3Fe7@Fe2N/rGO) is designed though the simple annealing of MOFs. The as-fabricated samples present an excellent electrocatalytic performance for ORR and OER due to the synergistic effect of electrode materials. The Co3Fe7@Fe2N/rGO exhibits an onset potential of 0.98 V (vs. Reversible hydrogen electrode), peak current intensity of 1.531 A g−1 and long-term stability for ORR, which is close to that of the benchmark Pt/C (20%) in 0.1 M KOH. It also shows good oxygen evolution reaction (OER) performance with an overpotential of 371 mV (at 10 mA cm−2). When used as a bifunctional air electrode in Zn-air batteries, the core-shell materials enabled an excellent mass power density of 60 W cm−2 g−1 at 0.57 V and stable cycling performance for over 100 cycles.

A 600MW supercritical direct-current (DC) utility boiler co-firing bituminous coal with lignite, has the problems from over-large desuperheating water yield in the reheater and over-high NO x emission concentration. In this paper, the causes of the problems are analyzed through, the initial tests of pulverization system and combustion system, the adjustment of combustion, etc. The results show that the combustion in furnace lagged behind to some extent after co-firing the bituminous coal with the lignite and the center of the flame was elevated, which shortened the relative distance between the flame of the main burners and over fire air(OFA), enlarged the absorbed heat amount of the reheater and reduced the residence time of flame in the reduction zone prominently. The much less residence time would increase NO x emission. Based on the calculations of the actual operation conditions of the burners, a series of improvement measures were proposed. After performing numerical simulation and cold test verification for the improvement measures, the corresponding transformations of the power plant were carried out. The desuperheating water yield in the reheater decrease, obviously, and over-high NO x emission is controlled effectively.

Under the industrial demand of energy saving, weight loss has become one of the current concerns. By increasing the strength of Mg-Li alloy with high lithium content, the industrial demand can be met by higher specific strength. Mg-16Li-2.5Zn-2.5Er (LZ162-2.5Er) alloy is extruded at 100 °C and cold rolled subsequently. The microstructures and mechanical properties of as-cast, as-extruded and cold-rolled LZ162-2.5Er alloys were investigated. A highest specific strength of 178 kNm/kg was obtained. During extrusion, fine-grain strengthening is stimulated by dynamic recrystallization. The subsequent cold rolling increases the dislocation density and uniformizes the distribution of the second phases further, causing work hardening and dispersion strengthening. In this paper, a process of high specific strength Mg-Li alloys for lightweight industry is provided as a reference.

Background Endothelial barrier dysfunction is central to the pathogenesis of sepsis-associated acute lung injury (ALI). Microtubule (MT) dynamics in vascular endothelium are crucial for the regulation of endothelial barrier function. Unfractionated heparin (UFH) possesses various biological activities, such as anti-inflammatory activity and endothelial barrier protection during sepsis. Methods Here, we investigated the effects and underlying mechanisms of UFH on lipopolysaccharide (LPS)-induced endothelial barrier dysfunction. C57BL/6 J mice were randomized into vehicle, UFH, LPS and LPS + UFH groups. Intraperitoneal injection of 30 mg/kg LPS was used to induce sepsis. Mice in the LPS + UFH group received intravenous UFH 0.5 h prior to LPS injection. Human pulmonary microvascular endothelial cells (HPMECs) were cultured for analyzing the effects of UFH on LPS-induced and nocodazole-induced hyperpermeability, F-actin remodeling, and LPS-induced p38 MAPK activation. Results UFH pretreatment significantly attenuated LPS-induced pulmonary histopathological changes, and increased the lung W/D ratio and Evans blue accumulation in vivo. Both in vivo and in vitro studies showed that UFH pretreatment blocked the LPS-induced increase in guanine nucleotide exchange factor (GEF-H1) expression and myosin phosphatase target subunit 1 (MYPT1) phosphorylation, and microtubule (MT) disassembly in LPS-induced ALI mouse model and human pulmonary microvascular endothelial cells (HPMECs). These results suggested that UFH ameliorated LPS-induced endothelial barrier dysfunction by inhibiting MT disassembly and GEF-H1 expression. In addition, UFH attenuated LPS-induced hyperpermeability of HPMECs and F-actin remodeling. In vitro, UFH pretreatment inhibited LPS-induced increase in monomeric tubulin expression and decrease in tubulin polymerization and acetylation. Meanwhile, UFH ameliorates nocodazole-induced MTs disassembly and endothelial barrier dysfunction.Additionally, UFH decreased p38 phosphorylation and activation, which was similar to the effect of the p38 MAPK inhibitor, SB203580. Conclusions UFH exert its protective effects on pulmonary microvascular endothelial barrier dysfunction via microtubule stabilization and is associated with the p38 MAPK pathway.

The dissemination of extended spectrum beta-lactamases (ESBL) genes through gene transfer attracts wide attention. Bentonite is widely used as a feed additive in an animal-breeding environment. In order to obtain a better understanding of the effect of bentonite on Escherichia coli carrying ESBL gene, proteomic analysis was carried out to screen the key proteins. The results showed that a total of 31 proteins were differentially expressed, including 21 up-regulated proteins and 10 down-regulated proteins. These proteins were involved in biosynthetic process, metabolic process, stress response, transport, anaerobic respiration, proteolysis, hydrolase, protein folding, transcription, salvage, and other. The transcriptional level of four genes (mipA, gntY, tldD, and arcA) was in consensus with proteomic results. This study revealed the differentially expressed proteins involved when E. coli was incubated under bentonite and PBS condition, which implied the possibility that bentonite may promote the transfer of ESBL gene between E. coli.

Background: The aim of this study was to investigate the efficacy and safety of (125)I particle implantation for treating advanced non-small cell lung cancer (NSCLC). Methods: Data from 56 patients with advanced NSCLC between January 2013 and May 2016 were retrospectively analyzed. The changes of tumor size, objective response rate (ORR), disease control rate (DCR), survival rate of patients and occurrence rate of complications were calculated, and the levels of carcinoembryonic antigen (CEA) and cytokerantin-19-fragment (CYFRA21-1) before and after the treatment were evaluated. Results: The (125)I particles implantation therapy significantly inhibited the tumor local growth of NSCLC (from 7.75±6.69 to 3.39±2.12 cm) (P

Catheter-associated urinary tract infection (CAUTI) occurs frequently in critical illness with signifi-cant morbidity, mortality, and additional hospital costs. The epidemiology of symptomatic ward-acquired CAUTI (within 48 hours of intensive care unit [ICU] admission) has not been carefully examined. The objective of our study was to identify the patient characteristics and microbiology of symptomatic CAUTI in critical illness.A 4-year retrospective observational study (2013-2016) was conducted at a single adult ICU with 30 beds in a tertiary hospital in Northeast China. The enrolled patients were over 18 years of age and had been diagnosed as having symptomatic CAUTIs in the ICU from January 2013 to December 2016. The infor-mation of clinicopathological characteristics (such as age, sex, underlying diseases, hospital admission diagnosis, ICU admission source, severity of illness, duration of urinary catheterization, use of antibiotics, duration of ICU stay, and ICU mortality) was recorded in an electronic database by senior clinicians who were blinded to the study purpose and design. Microbiological data were retrieved from the computerized hospital database.Between January 2013 and December 2016, 4115 patients were admitted to the ICU. Ninety-eight symp-tomatic CAUTI cases were enrolled in this study, including 29 patients who had ward-acquired CAUTI and 69 pa-tients who had ICU-acquired CAUTI. Patients with ward-acquired symptomatic CAUTI had significantly shorter overall ICU length of stay and shorter urinary catheterization time, and the overall ICU mortality was significantly higher in patients who had ICU-acquired symptomatic CAUTI. More third-generation cephalosporins and carbap-enems were used prior to CAUTI in the patients with ICU-acquired symptomatic CAUTI. Escherichia coli and Acinetobacter baumannii were the most common bacteria causing ward-acquired and ICU-acquired CAUTI, re-spectively. There were a higher number of cases of non-Candida albicans infections in patients with ICU-acquired symptomatic CAUTI than in patients with ward-acquired symptomatic CAUTI.Clinical characteristics, microbiological characteristics, and prognosis were different between ward-acquired and ICU-acquired symptomatic CAUTI. Patients with ICU-acquired symptomatic CAUTI had higher overall ICU mortality.

Round-end concrete-filled steel tube (RCFST) columns have been applied to bridge structures. There is not the formula of RCFST under axial load in code. Based on the unified theory, the basic form of strength and stability capacity correlation equations of concrete-filled steel tube under axial load is obtained through the theoretical derivation. The formula results compared with finite element simulation results show results are in good agreement.

Background Unfractionated heparin (UFH) has been shown to ameliorate lung edema and lung vascular leakage in lipopolysaccharide-induced lung injury. Impaired tight junction (TJ) function is a sign of sepsis-induced acute respiratory distress syndrome (ARDS) and acute lung injury (ALI), which is closely related to the downregulated expression of TJ-specific proteins or the upregulated expression of inflammatory cytokines. Because UFH has been intensively studied in modulating inflammation, we hypothesize that UFH may play a positive role in treating sepsis-induced ARDS/ALI by protecting TJs. Material and methods Rat sepsis-induced lung injury was induced by cecal ligation and puncture and treated with UFH. Hematoxylin and eosin staining, lung wet/dry weight (W/D) ratio, and pulmonary microvascular leakage were evaluated to assess lung injury. Cytokines in bronchoalveolar lavage fluid were detected to determine lung inflammation. A transendothelial electrical resistance assay, a Transwell permeability assay, and transmission electron microscopy were used to study endothelial TJs in human lung microvascular endothelial cells. TJ protein expression was measured by western blotting or immunohistochemistry. Results UFH treatment alleviated lung injury in vivo by reducing IL-6 in bronchoalveolar lavage fluid and protecting TJs in LMVECs. UFH also protected TJs against lipopolysaccharide-stimulated damage and functioned upstream by inhibiting the ERK1/2 MAPK pathway to attenuate endothelial hyperpermeability and downregulating the expression of TJ proteins such as claudin-5, occludin, and ZO-1. Conclusions These findings suggested that UFH has therapeutic potential for sepsis-induced ARDS or ALI through protecting TJs in LMVECs.

Recently, new criteria for sepsis-induced coagulopathy (SIC) were developed, including the sequential organ failure assessment (SOFA) criteria. The objective of this study was to evaluate the new SIC criteria in patients diagnosed with sepsis 3.0. Data from patients diagnosed with sepsis 3.0 after ICU admission were retrospectively obtained from July 2013 to June 2014. Relevant demographic, clinical, and laboratory parameters were noted. This study included 252 patients. The International Society on Thrombosis and Haemostasis (ISTH) disseminated intravascular coagulation (DIC), modified ISTH-DIC, and SIC scores were higher among nonsurvivors (P 0.0001). The Acute Physiology and Chronic Health Evaluation II (P 0.001), ISTH (P = 0.001), modified ISTH (P = 0.001), and SIC scores (P = 0.007) were independent predictors of ICU mortality. Using the receiver operating characteristic curve, SOFA had the greatest power for predicting ICU mortality; ISTH or modified ISTH score had greater predictive power than the SIC score. There were strong correlations between SIC score and ISTH (P 0.0001), modified ISTH (P 0.0001), the Acute Physiology and Chronic Health Evaluation II (P = 0.012), and SOFA (P 0.0001) scores. More nonsurvivors were diagnosed with DIC using the ISTH and modified ISTH criteria (P 0.001). In contrast, there was no significant difference in the proportion of patients with SIC between both groups (P = 0.055). ISTH score, modified ISTH score, and SIC score were independent risk factors for ICU mortality. Compared with the ISTH and modified ISTH scores, SIC score showed no advantage in diagnosing sepsis-associated coagulopathy or DIC. The application of these three criteria in patients with sepsis 3.0 needs further evaluation.

This paper presents a heating method based on planned complex trajectories of a line heating mechanical arm, and studies the complex trajectory planning for a mechanical arm. Starting from the inverse motion algorithm of the mechanical arm, the task priority control method is adopted to realize the tracking control of the complex trajectory at the end of the mechanical arm. In addition, according to the requirements of the actual working conditions, a smooth trajectory of the mechanical arm is planned, and the method is validated by a simulation system that combines the kinematics and dynamics of the mechanical arm. The simulation results show that the trajectory planning and control strategy used in this method can effectively guarantee the completion of the tasks in line heating.

Coagulopathy is very common in patients in intensive care unit (ICU) and often indicates organ dysfunction or underlying diseases.The application of traditional methods assessing the patients' coagulation status in ICU is limited because they can not reflect the whole process of coagulation.Thromboelastography (TEG),a point-of-care (POC) assay of coagulation,fibrinolysis and platelet function,developed in recent years has been widely used in organ transplant and cardiovascular surgery and so on.However,there is no standard for the use of TEG in ICU.The development and application of TEG in sepsis,multiple trauma,guiding blood transfusion,extracorporeal membrane oxygenation (ECMO),and anticoagulation monitoring were addressed in this review,and its value and application prospect in ICU were analyzed.

To investigate the effect of unfractionated heparin (UFH) on the expression of heme oxygenase-1 (HO-1) in intestinal mucosa of mice with sepsis.Thirty-six male C57BL/6J mice were randomly divided into sham group, cecal ligation and puncture (CLP) group and UHF group, n =12 in each group. Model of intestinal injury in sepsis was induced by CLP. In sham group, the mice were exposed without ligation of cecum. In UFH group, the mice were treated intravenously with 8 U of UFH via the tail vein half an hour before the operation and 12 hours after the surgery respectively. Six mice in each group were randomly chosen at 4 hours and 24 hours after operation to collect inferior vena venous blood samples and terminalileum tissues. The serum levels of interleukins (IL-1 β,IL-6),and tumor necrosis factor-α (TNF-α) were determined by enzyme linked immunosorbent assay (ELISA).The serum level of D-lactate was determined by colorimetry.Pathological changes of ileum tissue and Chiu score were observed after hematoxylin eosin (HE) staining. The HO-1 expression was detected immunohistochemically.In sham group, no significant changes in the serum levels of IL-1 β,IL-6,TNF-α and D-lactate were observed. Twenty-four hours after the operation, the structure of intestinal mucosa was basically normal without obvious pathology change and no HO-1 positive cells were found. The serum levels of IL-1 β,IL-6,TNF-α,and D-lactate in CLP group were gradually increased, and they were significantly increased as compared with sham group [IL-1 β (ng/L):40.87±2.88 vs.22.60±2.05 at 4 hours,113.73±3.96 vs.22.07±2.74 at 24 hours;IL-6 (ng/L):63.89±3.26 vs.44.89±3.38 at 4 hours,176.56±5.45 vs.45.76±4.02 at 24 hours; TNF-α (ng/L):194.62± 14.13 vs.152.05±6.22 at 4 hours,599.62± 10.20 vs.155.90± 14.18 at 24 hours; D-lactate (mmol/L):0.24± 0.02 vs.0.19 ± 0.01 at 4 hours,0.33 ± 0.04 vs.0.20 ± 0.02 at 24 hours, all P ＜ 0.05].Twenty-four hours after the operation, edema and inflammation in ileal mucosa, intestinal villi structural damage were observed, the Chiu score was significantly higher than those in the sham group [4.5 (3.0-5.0) vs.0 (0-1.0),P ＜ 0.05],and a small amount of HO-1 positive cells were localized in the intestinal mucosa. Compared with CLP group, the serum levels of IL-1 β,IL-6,TNF-α,and D-lactate of UFH group were significantly decreased [IL-1 β (ng/L):31.53 ± 2.90 vs.40.87 ± 2.88 at 4 hours,61.13 ± 2.80 vs.113.73 ± 3.96 at 24 hours;IL-6 (ng/L):51.16 ± 5.68 vs.63.89 ± 3.26 at 4 hours,81.16 ± 4.54 vs.176.56 ± 5.45 at 24 hours; TNF-α (ng/L):171.76± 5.60 vs.194.62± 14.13 at 4 hours,328.48 ± 10.79 vs.599.62± 10.20 at 24 hours; D-lactate (mmol/L):0.21 ±0.01 vs.0.24±0.02 at 4 hours,0.24±0.02 vs.0.33±0.04 at 24 hours, all P ＜ 0.05]. Twenty-four hours after the operation, intestinal injury was ameliorated, the Chiu score was significantly lower [1.5 (1.0-5.0) vs.4.5 (3.0-5.0),P ＜ 0.05],and HO-1 positive cells in the intestinal mucosa was remarkably increased.UFH can enhance the expression of HO-1 in intestinal mucosa, reduce the release of inflammatory factors, ameliorate the intestinal inflammatory response, and thus play a protective role in intestinal tissue in mice with sepsis.

The aim of the present study was to investigate the protective role of hyperoxia liquid in regulating cardiopulmonary bypass (CPB)‑induced myocardial damage and its possible underlying mechanism. In the CPB‑induced rat model, hyperoxia liquid enhanced left ventricular ejection fraction (LVEF), reduced the left ventricular internal dimension systole (LVIDs) level, inhibited malondialdehyde levels, increased superoxide dismutase, glutathione (GSH) and GSH peroxidase levels, suppressed heart cell apoptosis, and induced the nuclear factor erythroid 2‑related factor 2 (Nrf2) and heme oxygenase‑1 (HO‑1) signaling pathway. Then, ML385, a Nrf2 inhibitor, was used to attenuate the effect of hyperoxia liquid on LVEF and LVIDs levels, oxidative stress and heart cell apoptosis in the CPB‑induced rat model. Collectively, the results of the present study demonstrated that the protective role of hyperoxia liquid may regulate oxidative stress in a CPB‑induced rat model through the Nrf2‑antioxidant response element signaling pathway.

A growing body of evidence has suggested the genetic association of ORMDL3 gene (ORMDL Sphingolipid Biosynthesis Regulator 3) polymorphisms with a diverse set of inflammatory disorders that include bronchial asthma, inflammatory bowel disease, ankylosing spondylitis and atherosclerosis. Gene functional investigations have revealed the particular relevance of ORMDL3 in endoplasmic reticulum stress, lipid metabolism and inflammatory reactions. Additionally, several reports have recently added a new dimension to our understanding of the modulation of ORMDL3 gene expression in inflammation. This mini-review summarizes the pertinent publications regarding the genetic association studies and mechanistic exploration of ORMDL3 in common inflammatory disorders.

Background Aorto-left ventricular tunnel (ALVT) is a rare congenital extracardiac channel that connects the ascending aorta to the left ventricle. To our knowledge, no case has been thus far reported as ALVT with both anomalous origin of right coronary artery (AORCA) and bicuspid aortic valve (BAV). Case presentation We reported a case of a 5-year-old female diagnosed as ALVT with accompanying AORCA and BAV which had been previously misdiagnosed as aortic regurgitation (AR) triggered by BAV. Additionally, a special modality of ALVT was confirmed in this case during the surgery in which the tunnel was formed by the separation between the roots of two aortic leaflets during the diastolic period. Conclusions ALVT with both AORCA and BAV is clinically uncommon and the aberrant tunnel in ALVT can be formed by the gap between the roots of two aortic leaflets. Besides, ALVT with BAV might easily lead to an inaccurate diagnose as aortic regurgitation caused by BAV. Cardiac surgeons should be alerted for differential diagnosis of ALVT with BAV and isolated bicuspid aortic valve (BAV) causing aortic regurgitation (AR).

To observe the effect of heparin on the cellular morphology and the expressions of nitric oxide (NO) and reactive oxygen species (ROS) in renal microvascular endothelial cells (RMVECs) stimulated by lipopolysaccharide (LPS).The three step gradient screen method was used to primarily culture rat RMVECs, and the 3rd and 4th generation cells with excellent growth were collected. The cells were divided into blank control group, 10 mg/L LPS treatment group and 2.5, 5, 10 kU/L heparin pretreatment groups (the corresponding dose of heparin was given 0.5 hour before LPS stimulation). The morphology of the cells at 24 hours after LPS stimulation was observed by transmission electron microscope, the expression of ROS in RMVECs was determined by immunofluorescence at 5, 15, 30, 45 minutes after LPS stimulation, and the expression of NO in RMVECs was determined by nitrate reductase method.(1) In blank control group, the RMVECs membrane was intact, and the mitochondria and endoplasmic reticulum in cells were clearly visible. The nuclear membrane was complete, and nucleolus was obvious. Cell bubble deformation was obvious at 24 hours after LPS stimulation, especially in the mitochondria and cell membrane. After 10 kU/L heparin pretreatment, the vacuolar degeneration of organelles was significantly reduced, and the cell membrane morphology was stable. (2) The increases in ROS and NO in RMVECs could be detected at 5 minutes after LPS stimulation, showed an increase tendency with time prolongation, ROS expression peaked at 30 minutes, NO expression peaked at 45 minutes, which showed significant differences as compared with those of blank control group [30-minute ROS (mean density): 76.2±5.8 vs. 1.5±0.1, 45-minute NO (μmol/L): 70.3±8.6 vs. 1.8±0.1, both P0.01]. The expression of ROS and NO production in RMVECs were significantly reduced by heparin, showed a decrease tendency with heparin dose elevation, and the most obvious effect was 10 kU/L of heparin, with significant difference as compared with those of LPS treatment group [30-minute ROS (mean density): 16.8±1.7 vs. 76.2±5.8, 45-minute NO (μmol/L): 11.8±8.6 vs. 70.3±8.6, both P0.01].Unfractionated heparin ameliorates LPS induced expressions of NO and ROS in RMVECs and protects the cell morphology. The effect of 10 kU/L heparin is most obvious.

To study unfractionated heparin (UFH) effect on the expression of HOXA9 in activation of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS).HUVECs were cultured and they were randomly divided into four groups (n = 5) for the challenge respectively: (1) control group (with an equal volume of phosphate buffer saline); (2) LPS group (LPS 10 mg/L); (3) UFH group (UFH 10 kU/L); (4) UFH+LPS group (10 kU/L UFH 30 minutes + LPS 10 mg/L). After treatment for 3 hours, the expressions of HOXA9, E-selectin and nuclear factor-κB (NK-κB) in endothelial cells were detected by Western Blot.Compared with the control group, the expression of HOXA9 in LPS group was significantly decreased, the expressions of E-selectin and NF-κB were significantly increased (HOXA9/β-actin: 0.082±0.009 vs. 0.199±0.067, E-selectin/β-actin: 0.113±0.055 vs. 0.047±0.030, NF-κB/β-actin: 0.845±0.025 vs. 0.664±0.092, all P0.05). Compared with LPS group, the expression of HOXA9 in UFH+LPS group was significantly increased, the expressions of E-selectin and NF-κB were significantly decreased (HOXA9/β-actin: 0.190±0.096 vs. 0.082±0.009, E-selecin/β-actin: 0.057±0.017 vs. 0.113±0.055, NF-κB/β-actin: 0.544±0.060 vs. 0.845±0.025, all P0.05). Each protein expression of UFH group were in accordance with the control group.In LPS stimulated endothelial cells, HOXA9 expression is down regulated, E-expression is reduced, and endothelial cell activation is inhibited. UFH can inhibit the activation of endothelial cells by decreasing the degree of HOXA9 reduced expression.

In sepsis-3, in contrast with sepsis-1, the definition “systemic inflammatory response” has been replaced with “dysregulated host response”, and “systemic inflammatory response syndrome” (SIRS) has been replaced with “sequential organ failure assessment” (SOFA). Although the definition of sepsis has changed, the debate regarding its nature is ongoing. What are the fundamental processes controlling sepsis-induced inflammation, immunosuppression, or organ failure? In this review, we discuss the heterogeneity of sepsis-3 and address the central role of inflammation in the pathogenesis of sepsis. An unbalanced pro- and anti-inflammatory response, inflammatory resolution disorder, and persistent inflammation play important roles in the acute and/or chronic phases of sepsis. Moreover, powerful links exist between inflammation and other host responses (such as the neuroendocrine response, coagulation, and immunosuppression). We suggest that a comprehensive evaluation of the role of the inflammatory response will improve our understanding of the heterogeneity of sepsis.

Background: Due to a scarcity of national epidemiologic data on sepsis, we performed a national cross-sectional survey to determine the epidemiologic characteristics of patients with sepsis in intensive care units (ICUs) in China. Methods: A national survey was performed in 44 hospitals which were selected by randomization according to the population from each province in mainland China. All septic patients in participating ICUs from December 1, 2015 to January 31, 2016 were included in the analysis. We recorded demographic, physiological and bacteriological data and followed up for 90 days or until death after inclusion. The incidence of and mortality due to sepsis in the ICU was calculated. The relationship between gross domestic product (GDP) and incidence of sepsis was also determined. Findings: Of 2,322 patients with sepsis included in the analysis, 786 (33.85%) patients had hospital-acquired sepsis with the most common infection site being the lung. The incidence of sepsis in the ICU was 20.6[95%CI 15.83-25.37] cases per 100 ICU admissions were diagnosed as sepsis. There was significant variation in the incidence of sepsis in the ICUs of different geographic regions. Ninety-day mortality due to sepsis was 35.49%, which yielded about 81,876 deaths in patients with ICU-treated sepsis every year in the mainland China. There was a significant relationship between the incidence of sepsis in the ICU and GDP per capita (R2=0.304, p=0.001) and the ratio of ICU beds to hospital beds (R2=0.270, p=0.003). Interpretation: Sepsis is a frequently occurring, life-threatening syndrome in the ICU with a high mortality in the mainland of China. Clinical Trial Number: This study was also registered in ClinicalTrials.gov (https://clinicaltrials.gov/show/NCT02448472). Funding Statement: This study was supported by a grant from the Development Center for Medical Science and Technology National Health and Family Planning Commission of the People’s Republic of China (WH2015-01-01), a grant from Jiangsu Provincial Key Medical Discipline (grant number: ZDXKA2016025) and a grant from Jiangsu Provincial Medical Talent (grant number: ZDRCA2016082). Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The protocol of this study was approved by the ethics committees of Zhongda Hospital, School of Medicine, Southeast University (No. 2015ZDSYLL044.0), and every enrolled hospital. Patients admitted into the ICU were enrolled in this study following informed consent from the patient or their guardian.

To investigate the effect of unfractionated heparin on the expression of serum and liver tissue heparanase (HPA) in mice with liver injury induced by sepsis.Forty-eight healthy male C57BL/6 mice aged 6-8 weeks were divided into groups according to random number table method. Twenty-four septic mice models (CLP group) were established by cecal ligation and puncture (CLP); the other 24 mice underwent sham operation (sham group), only laparotomy and abdominal closure were performed without ligation. Twelve mice in sham group and CLP group received heparin pretreatment (sham+UFH group, CLP+UFH group), and 8 U heparin unfractionated heparin (diluted to 200 μL) was injected into the tail vein of the mice at 30 minutes and 12 hours after operation respectively. The other 12 mice were injected with the same amount of normal saline. The serum and liver tissues of mice were collected at 4 and 24 hours after CLP. The levels of serum HPA, interleukin (IL-6, IL-1β), tumor necrosis factor-α (TNF-α), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured by enzyme linked immunosorbent assay (ELISA). The pathological changes of liver tissue were observed with hematoxylin eosin (HE) staining. The expression of HPA in liver tissue was detected by immunohistochemistry.Compared with the sham group, the levels of serum HPA, IL-6, IL-1β, TNF-α, ALT and AST in the CLP group were increased significantly, and increased further over time. The histopathology examination was performed, and abnormal structure, inflammatory cell infiltration, liver cell necrosis could be found in the tissue. The expression level of HPA in liver tissue was detected by immunohistochemistry, which was increased after CLP. This indicated that the animal model of sepsis was successfully prepared. Compared with CLP group, serum HPA, inflammatory factors and transaminase levels were significantly decreased at 4 hours after operation in group CLP+UFH [HPA (ng/L): 76.72±2.75 vs. 101.55±7.54, IL-6 (ng/L): 51.16±5.68 vs. 63.89±3.26, IL-1β (ng/L): 31.53±2.90 vs. 40.87±2.88,TNF-α (ng/L): 171.76±5.60 vs. 194.62±14.13, ALT (μg/L): 0.26±0.09 vs. 0.62±0.17, AST (μg/L): 1.03±0.22 vs. 1.45±0.08, all P0.05]. At 24 hours, it was significantly higher than that of 4 hours, but they were significantly lower than those in CLP group [HPA (ng/L): 125.30±7.80 vs. 302.50±17.81, IL-6 (ng/L): 81.16±4.54 vs. 176.56±5.45, IL-1β (ng/L): 61.13±2.80 vs. 113.73±3.96, TNF-α (ng/L): 328.47±10.79 vs. 599.62±10.20, ALT (μg/L): 0.38±0.17 vs. 0.91±0.26, AST (μg/L): 1.16±0.15 vs. 1.88±0.08, all P0.05]. It was shown by HE staining that the edema of liver tissue decreased and inflammatory cell infiltration decreased. It was shown by immunohistochemistry that the expression level of HPA in liver tissue was significantly decreased [A value (×10The expression of HPA was significantly increased during sepsis in mice. Unfractionated heparin may mitigate liver injury by inhibiting HPA.

Nitrogen mustards are chemical agents that are similar to sulfur mustards, with similar toxicities. The present study describes a case of nitrogen mustard-induced acute respiratory failure and myelosuppression in a 33-year-old man. The patient, who was accidentally exposed to nitrogen mustard hydrochloride in a pharmaceutical factory, exhibited severe inhalation injury and respiratory symptoms. Laboratory tests revealed reduced white blood cell counts and lowered platelet levels during the first 6 days after the skin exposure to nitrogen mustard. Following treatment with mechanical ventilation, immunity-enhancing agents and nutritional supplements for 1 month, the patient successfully recovered and was released from hospital.

Unfractionated heparin (UFH) is largely used as anti-thrombotic drug. While UFH has been shown to suppress lipopolysaccharide (LPS)-induced nuclear factor-κB (NF-κB) activation, intracellular upstream events that cause NF-κB down-regulation in response to UFH remain unclear. Thus, we investigated the involvement of phosphoinositide-3-OH kinase (PI3K)/Akt in the inhibition of LPS-activated NF-κB pathway by UFH in human pulmonary microvascular endothelial cells (HPMECs). Pretreatment with UFH (0.1-1U/ml) significantly inhibited LPS (10μg/ml)-stimulated interleukin (IL)-6 and IL-8 production in HPMECs. LPS activated Akt and NF-κB, whereas UFH suppresses LPS-induced Akt phosphorylation and NF-κB nuclear translocation, which were required for IL-6 and IL-8 gene transcription. Inhibition studies by using wortmannin abrogated NF-κB-mediated IL-6 and IL-8 expression, suggesting the requirement of PI3K/Akt pathway. Our data provided the first evidence that UFH might repress LPS-activated PI3K/Akt pathway, leading to inhibitory effect of NF-κB activation with diminished IL-6 and IL-8 expression in HPMECs.

High mobility group box 1 (HMGB1) is a systemic inflammation‑associated cytokine mediator. The aim of the present study was to examine the effect of the downregulation of HMGB1 in a lipopolysaccharide (LPS)‑induced mouse model of acute lung injury (ALI). It was identified that serum levels of tumor necrosis factor‑α and interleukin‑1β, lung myeloperoxidase activity and malondialdehyde content, as well as lung wet/dry weight ratios were all increased following LPS challenge. However, LPS‑mediated increases in these parameters were significantly downregulated in HMGB1 small interfering (si)RNA‑treated mice versus the negative control siRNA‑treated mice. In addition, the administration of HMGB1 siRNA in LPS‑treated mice resulted in a decreased DNA binding activity of nuclear factor‑κB (NF‑κB) in the lung. It was demonstrated that downregulation of HMGB1 decreases inflammation and the severity of sepsis associated with ALI, possibly via inhibiting the NF‑κB DNA‑binding activity. The present data support HMGB1 as a contributor to the pathogenesis of LPS‑induced sepsis and ALI.

Activation of protein C is greatly enhanced by the presence of thrombomodulin (TM) and endothelial protein C receptor (EPCR) on the endothelial surface. Impairment of the anticoagulant protein C system occurs during endotoxemia and contributes to sepsis-associated hypercoagulability. Previous studies have demonstrated that unfractionated heparin (UFH) can attenuate coagulation in endotoxemic mice. However, whether UFH has an effect on the protein C system remains to be elucidated. The current study evaluated the therapeutic effect of UFH on the protein C system in a mouse model of lipopolysaccharide (LPS)-induced sepsis, and further investigated the effect of UFH on the expression of TM and EPCR in vitro using human umbilical vein endothelial cells (HUVECs). The in vivo data indicated that UFH preconditioning attenuated the decline in circulating activated protein C following LPS administration, and also reduced LPS-induced shedding of TM and EPCR. In HUVECs, LPS stimulation led to the downregulation of TM and EPCR expression, and UFH dose-dependently restored the mRNA and protein levels of TM and EPCR. In addition, UFH inhibited the LPS-induced activation of mitogen-activated protein kinase 14, proto-oncogene tyrosine-protein kinase Src and nuclear factor κB signaling in HUVECs. In summary, these results suggest that UFH has a protective effect on the protein C system during sepsis. Thus, UFH may be a candidate therapeutic agent for the treatment of patients with sepsis.

Line Heating (LH) is the main method for forming ship-hull plates in most of shipyards all over the world, which is called “heated bending” usually. The accuracy of final shapes and productivity of plates solely depend on skilled workers’ experiences for LH process is mainly operated manually. A new expert system is developed in order to determine the processing parameters which can effectively improve the productivity.

Neutrophil extracellular traps (NETs) are net-like structure composed of DNA and nuclear proteins, which are produced by activated neutrophils under the circumstances of a variety of pathogens or drugs. As part of defensive mechanism, NETs have been proved to restrict the spread of pathogens and release of antimicrobial molecules. NETs can not only strengthen the adhesion between neutrophils and platelets, promote platelet mediated procoagulant reaction, but also lead to endothelial cell damage and coagulopathy in sepsis. In addition, NETs also plays an important role in pathophysiological processes of venous thrombosis. Therefore, NETs may become the biomarkers of evaluating coagulation dysfunction and potential therapy target in sepsis.

To investigate the changes of neutrophil extracellular traps (NETs) level in plasma of sepsis patients and judge its clinical value for early diagnosing of sepsis.A prospective observational study was conducted. The patients after surgery aged18 years and expected to stay in the ICU24 hours admitted to intensive care unit (ICU) of the First Affiliated Hospital of China Medical University from November 2014 to February 2015 were enrolled. According to the criteria of sepsis diagnosis in 1991, patients were divided into non-sepsis group and sepsis group. The healthy people who taken a physical examination were enrolled in the healthy control group. 3 mL peripheral venous blood was collected at 1 hour after admission to ICU. A fasting blood was collected in the healthy control group in the morning. The plasma free DNA (cf-DNA/NETs) was determined by using the fluorescence microplate reader, white blood cell (WBC), neutrophil ratio (NEU), procalcitonin (PCT), C-reactive protein (CRP) in peripheral blood of the patients were detected, and acute physiology and chronic health evaluation II (APACHE II) and sequential organ failure assessment (SOFA) scores were calculated. The correlation between plasma NETs and the risk factors in sepsis patients was analyzed by Spearman correlation analysis. The value of cf-DNA/NETs and WBC level in the diagnosis of sepsis was analyzed by using the receiver operating characteristic curve (ROC).Twenty-three sepsis patients, 20 non-sepsis patients, and 22 healthy persons were enrolled. There were no differences in baseline variables including gender and age among three groups, which indicated baseline data equalization. The plasma concentration of cf-DNA/NETs in sepsis group was significantly higher than that in non-sepsis group and healthy control group (μg/L: 453.44±185.37 vs. 188.35±29.66, 203.83±43.25, both P0.05), and there was no significant difference between last two groups (P0.05). WBC, NEU, PCT, CRP, APACHE II and SOFA score in sepsis group were significantly higher than those of non-sepsis group [WBC (×10The plasma cf-DNA/NETs levels increased significantly in sepsis patients. In the diagnosis of sepsis, plasma NETs levels had better advantages over WBC. NETs can be used as a biomarker for early diagnosis of sepsis.

To investigate the influence of heparin pretreatment on serum and lung tissue level of neutrophil extracellular traps (NETs) in septic mice model and its molecular mechanism.Ninety male C57BL/6J mice were randomly divided into control group (n = 30), lipopolysaccharides (LPS) group (n = 30, 30 mg/kg LPS in 100 ?L normal saline was intraperitoneally injected) and LPS+heparin group (n = 30, 8 U of heparin in 20 ?L normal saline was subcutaneously injected 30 minutes before the injection of LPS). Six hours later of LPS injection, blood was collected and lung tissue was harvested. Enzyme linked immunosorbent assay (ELISA) was used to assess the concentration of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and histones 2AX (H2AX), neutrophil elastase (NE), which reflected NETs concentration. PicoGreen fluorescent dyes was used to detect serum circulating free DNA (cf-DNA/NETs) concentration. The protein expression levels of H2AX and NE in lung tissue were examined by Western Blot.The serum concentrations of TNF-α, IL-6, H2AX, NE, cf-DNA/NETs, and the protein expression levels of H2AX and NE in lung tissue of septic mice were significantly higher than those of control group [TNF-α (ng/L): 133.0±14.1 vs. 2.7±1.0, IL-6 (ng/L): 3 911.2±189.2 vs. 298.9±52.5, H2AX (ng/L): 545.5±40.0 vs. 21.9±8.3, NE (μg/L): 6.48±0.12 vs. 0.47±0.15, cf-DNA/NETs (μg/L): 846.3±137.5 vs. 152.7±36.4, H2AX protein (gray value): 1.14±0.09 vs. 0.68±0.04, NE protein (gray value): 0.56±0.03 vs. 0.32±0.04, all P0.05]. After heparin pretreatment, levels of serum TNF-α, H2AX, NE, cf-DNA/NETs, and protein expression levels of H2AX and NE in lung tissue were significantly reduced [TNF-α (ng/L): 83.2±7.6 vs. 133.0±14.1, H2AX (ng/L): 435.0±39.0 vs. 545.5±40.0, NE (μg/L): 4.26±0.17 vs. 6.48±0.12, cf-DNA/NETs (μg/L): 606.5±73.9 vs. 846.3±137.5, H2AX protein (gray value): 0.91±0.03 vs. 1.14±0.09, NE protein (gray value): 0.42±0.03 vs. 0.56±0.03, all P0.05], but no significant change was found in IL-6 (ng/L: 3 919.9±166.6 vs. 3 911.2±189.2, P0.05).Heparin pretreatment could significantly decrease the level of NETs in serum and lung tissue, and can be the potential mechanism of its organ protection in sepsis.