Metabolomic analysis of the serum and urine of rats exposed to diazinon, dimethoate, and cypermethrin alone or in combination.

BACKGROUND: Multiple pesticides are often used in combination for plant protection and public health. Therefore, it is important to analyze the physiological changes induced by multiple pesticides exposure. The objective of this study was to investigate the combined toxicity of the widely-used organophosphorus and pyrethroid pesticides diazinon, dimethoate, and cypermethrin. METHODS: Male Wistar rats were administrated by gavage once daily with the three pesticides individual or in combination for consecutive 28 days. The metabolic components of serum and urine samples were detected by using 1H nuclear magnetic resonance (NMR)-based metabolomics method. Histopathological examination of liver and kidneys and serum biochemical determination were also carried out. RESULTS: The results showed that after the 28-day subacute exposure, serum glutamic transaminase and albumin were significantly increased and blood urea nitrogen was significantly decreased in the rats exposed to the mixture of the pesticides compared with the control rats, suggesting that the co-exposure impaired liver and kidney function. Metabolomics analysis indicated that the indicators 14 metabolites were statistically significant altered in the rats after the exposure of the pesticides. The increase in 3-hydroxybutyric acid in urine or decrease of lactate and N-acetyl-L-cysteine in serum could be a potentially sensitive biomarker of the subchronic combined effects of the three insecticides. The reduction level of 2-oxoglutarate and creatinine in urine may be indicative of dysfunction of liver and kidneys. CONCLUSION: In summary, the exposure of rats to pesticides diazinon, dimethoate, and cypermethrin could cause disorder of lipid and amino acid metabolism, induction of oxidative stress, and dysfunction of liver and kidneys, which contributes to the understanding of combined toxic effects of the pesticides revealed by using the metabolomics analysis of the urine and serum profiles.

Long-term low-dose exposure of permethrin induces liver and kidney damage in rats.

BACKGROUND: Permethrin is one of the pyrethroid insecticides, which is widely used in agriculture and public health. Although acute toxicity of the insecticide has been studied, the chronic toxicity upon the long-term exposure has not been clear yet. The purpose of the current study is to investigate the organ toxicities of permethrin following its long-term low-dose exposure. METHODS: Male Wistar rats were daily administrated orally with permethrin (75 mg/kg body weight/day, gavage) for 90 days, and then the samples of biofluids (blood and urine) and organs including liver and kidney were collected. The serum and urine samples were measured by biochemical assay and the tissues of kidney and liver were examined and analyzed by histopathological method. RESULTS: The results showed that no change was found in serum and urine biochemical parameters for the toxicity; however, significant changes including hyperchromatic nuclei swollen in the hepatic parenchymal cells and the swelling proximal tubules in the kidneys were observed in the tissue structures of liver and kidneys in the histopathological sections. CONCLUSION: These results indicate that low-dose long-term exposure of permethrin can cause chronic toxicity with slight liver and kidney damage.

Very Early Corona Treatment-Mediated Artificial Incubation of Silkworm Eggs and Germline Transformation of Diapause Silkworm Strains.

Diapause is an important biological characteristic for many insect species to adapt to adverse environmental conditions and maintain the continuity of the race. Compared with the traditional hydrochloric acid or/and cold storage treatment methods, the artificial corona incubation technology of silkworm (Bombyx mori) eggs has many advantages including, the absence of pollution, easy operation and safety. However, this technology has not yet been applied in sericulture. In this study, we developed a novel artificial corona instrument to successfully disrupt the diapause of newly laid and refrigerated eggs from various Chinese and Japanese lineage silkworm strains. Subsequently, we invented a very early corona treatment (VECT) strategy to prevent the diapause of newly laid silkworm eggs within 4 h of oviposition. The hatching rates of the larvae were more than 95% in all diapause silkworm strains, which was comparable to the effect of the traditional HCl treatment strategy. In addition, we developed a combination strategy of VECT and pre-blastoderm microinjection and successfully created transgenic silkworms in various diapause strains. The results of the current study can aid in improving the corona artificial incubation technology and promote its application in sericulture.

Circular RNA expression profiles in human bronchial epithelial cells treated with beryllium sulfate.

Circular RNAs (circRNAs), is a novel type of endogenous non-coding RNAs (ncRNAs) participated in the pathogenesis of many diseases. Beryllium is one of the carcinogenesis elements. However, the mechanism and function of circRNAs in human bronchial epithelial cells (16HBE) induced by beryllium sulfate (BeSO4) was rarely reported. Therefore, the high-throughput RNA sequencing analysis was performed to detect the circRNA profiles between control groups and BeSO4-induced groups. Furthermore, circRNA-miRNA-mRNA network, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and PPI network analysis were used for bioinformatics analysis. CircRNA sequencing analysis revealed that 36 circRNAs were up-regulated and 35 circRNAs were down-regulated in the BeSO4-exposed groups. The selected circRNAs were verified by real-time fluorescent quantitative PCR (qRT-PCR). Hsa_circ_0004214 and hsa_circ_0003586 were validated to be up-regulated, hsa_circ_0047958, hsa_circ_0001944, and hsa_circ_0008982 were down-regulated. The circRNA-miRNA-mRNA network annotated the key signaling pathway including cellular senescence, TNF signaling pathway, NF-kappa B signaling pathway, HIF-1 signaling pathway, and Hippo signaling pathway. The PPI network indicated the most circRNAs might participate in the BeSO4 toxicity by acting as a sponge for the miR-663b through JAK-STAT signaling pathway. In summary, our study suggests that circRNAs may play roles in the mechanism of beryllium toxicity.

Body fluids from the rat exposed to chlorpyrifos induce cytotoxicity against the corresponding tissue-derived cells in vitro.

BACKGROUND: This study aims to establish an in vitro monitoring approach to evaluate the pesticide exposures. We studied the in vitro cytotoxicity of three different body fluids of rats to the respective corresponding tissue-derived cells. METHODS: Wistar rats were orally administrated daily with three different doses of chlorpyrifos (1.30, 3.26, and 8.15 mg/kg body weight/day, which is equal to the doses of 1/125, 1/50, and 1/20 LD50, respectively) for consecutive 90 days. Blood samples as well as 24-hour urine and fecal samples were collected and processed. Then, urine, serum, and feces samples were used to treat the correspondent cell lines, i.e., T24 bladder cancer cells, Jurkat lymphocytes, and HT-29 colon cancer cells respectively, which derived from the correspondent tissues that could interact with the respective corresponding body fluids in organism. Cell viability was determined by using MTT or trypan blue staining. RESULTS: The results showed that urine, serum, and feces extract of the rats exposed to chlorpyrifos displayed concentration- and time-dependent cytotoxicity to the cell lines. Furthermore, we found that the cytotoxicity of body fluids from the exposed animals was mainly due to the presence of 3, 4, 5-trichloropyrindinol, the major toxic metabolite of chlorpyrifos. CONCLUSIONS: These findings indicated that urine, serum, and feces extraction, especially urine, combining with the corresponding tissue-derived cell lines as the in vitro cell models could be used to evaluate the animal exposure to pesticides even at the low dose with no apparent toxicological signs in the animals. Thus, this in vitro approach could be served as complementary methodology to the existing toolbox of biological monitoring of long-term and low-dose exposure to environmental pesticide residues in practice.

The Threshold Effects of Low-Dose-Rate Radiation on miRNA-Mediated Neurodevelopment of Zebrafish.

The biological effects and regulatory mechanisms of low-dose and low-dose-rate radiation are still rather controversial. Therefore, in this study we investigated the effects of low-dose-rate radiation on zebrafish neurodevelopment and the role of miRNAs in radiation-induced neurodevelopment. Zebrafish embryos received prolonged gamma-ray irradiation (0 mGy/h, 0.1 mGy/h, 0.2 mGy/h, 0.4 mGy/h) during development. Neurodevelopmental indicators included mortality, malformation rate, swimming speed, as well as the morphology changes of the lateral line system and brain tissue. Additionally, spatiotemporal expression of development-related miRNAs (dre-miR-196a-5p, dre-miR-210-3p, dre-miR-338) and miRNA processing enzymes genes (Dicer and Drosha) were assessed by qRT-PCR and whole mount in situ hybridization (WISH). The results revealed a decline in mortality, malformation and swimming speed, with normal histological and morphological appearance, in zebrafish that received 0.1 mGy/h; however, increased mortality, malformation and swimming speed were observed, with pathological changes, in zebrafish that received 0.2 mGy/h and 0.4 mGy/h. The expression of miRNA processing enzyme genes was altered after irradiation, and miRNAs expression was downregulated in the 0.1 mGy/h group, and upregulated in the 0.2 mGy/h and 0.4 mGy/h groups. Furthermore, ectopic expression of dre-miR-210-3p, Dicer and Drosha was also observed in the 0.4 mGy/h group. In conclusion, the effect of low-dose and low-dose-rate radiation on neurodevelopment follows the threshold model, under the regulation of miRNAs, excitatory effects occurred at a dose rate of 0.1 mGy/h and toxic effects occurred at a dose rate of 0.2 mGy/h and 0.4 mGy/h.

Association of Early-Phase In-Hospital Glycemic Fluctuation With Mortality in Adult Patients With Coronavirus Disease 2019.

OBJECTIVE: To investigate the association of in-hospital early-phase glycemic control with adverse outcomes among inpatients with coronavirus disease 2019 (COVID-19) in Wuhan, China. RESEARCH DESIGN AND METHODS: The study is a large case series, and data were obtained regarding consecutive patients hospitalized with COVID-19 in the Central Hospital of Wuhan between 2 January and 15 February 2020. All patients with definite outcomes (death or discharge) were included. Demographic, clinical, treatment, and laboratory information were extracted from electronic medical records. We collected daily fasting glucose data from standard morning fasting blood biochemistry to determine glycemic status and fluctuation (calculated as the square root of the variance of daily fasting glucose levels) during the 1st week of hospitalization. RESULTS: A total of 548 patients were included in the study (median age 57 years; 298 [54%] were women, and n = 99 had diabetes [18%]), 215 suffered acute respiratory distress syndrome (ARDS), 489 survived, and 59 died. Patients who had higher mean levels of glucose during their 1st week of hospitalization were older and more likely to have a comorbidity and abnormal laboratory markers, prolonged hospital stays, increased expenses, and greater risks of severe pneumonia, ARDS, and death. Compared with patients with the lowest quartile of glycemic fluctuation, those who had the highest quartile of fluctuation magnitude had an increased risk of ARDS (risk ratio 1.97 [95% CI 1.01, 4.04]) and mortality (hazard ratio 2.73 [95% CI 1.06, 7.73]). CONCLUSIONS: These results may have implications for optimizing glycemic control strategies in COVID-19 patients during the early phase of hospitalization.

The role of protein kinase C alpha in tri-ortho-cresyl phosphate-induced autophagy in human neuroblastoma SK-N-SH cells.

As an organophosphorus ester, tri-ortho-cresyl phosphate (TOCP) has been widely used in agriculture and industry. It is reported that TOCP can induce organophosphate-induced delayed neuropathy (OPIDN) in sensitive animal and human species. However, the exact molecular mechanisms underlying TOCP-induced neurotoxicity are still unknown. In this study, we found that TOCP could induce autophagy by activating protein kinase C alpha (PKCα) signaling in neuroblastoma SK-N-SH cells. PKCα activators could positively regulate TOCP-induced autophagy by increasing the expression levels of neighbor BRCA1 gene protein 1 (NBR1), LC3 and P62 autophagic receptor protein. Furthermore, PKCα activation impaired the ubiquitin-proteasome system (UPS), resulting in inhibition of proteasome activity and accumulation of ubiquitinated proteins. UPS dysfunction could stimulate autophagy to serve as a compensatory pathway, which contributed to the accumulation of the abnormally hyperphosphorylated tau proteins and degradation of impaired proteins of the MAP 2 and NF-H families in neurodegenerative disorders.

Intraoperative blood transfusion volume is an independent risk factor for postoperative acute kidney injury in type A acute aortic dissection.

BACKGROUND: Type A acute aortic dissection is a life-threatening disease associated with adverse clinical outcomes. Acute kidney injury (AKI) is common after surgery. However, the relationship between intraoperative blood transfusion and postoperative AKI remains unclear. METHODS: The records of 130 patients who underwent type A acute aortic dissection surgery from January 2015 to December 2018 were retrospectively analyzed. According to the Kidney Disease Improving Global Outcomes criteria, postoperative AKI was defined based on serum creatinine concentration. Multivariable logistic regression analysis was applied to estimate the independent association between intraoperative blood transfusion volume and the risk of postoperative AKI. RESULTS: Postoperative AKI was observed in 82 patients (63.08%). The in-hospital mortality was 16.15% (n = 21). Multivariate logistic regression showed that the amount of intraoperative blood transfusion was independently associated with the risk of postoperative AKI in a dose-dependent manner. Every 200 ml increment of blood transfusion volume was associated with a 31% increase in AKI risk (odds ratio 1.31 and 95% confidence interval 1.01-1.71). CONCLUSIONS: Intraoperative transfusion volume may increase the incidence of postoperative AKI. The mechanism and influence of transfusion thresholds on AKI need to be explored in the future.

Role of neutrophil chemoattractant CXCL5 in SARS-CoV-2 infection-induced lung inflammatory innate immune response in an in vivo hACE2 transfection mouse model.

Understanding the pathogenesis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and clarifying antiviral immunity in hosts are critical aspects for the development of vaccines and antivirals. Mice are frequently used to generate animal models of infectious diseases due to their convenience and ability to undergo genetic manipulation. However, normal adult mice are not susceptible to SARS-CoV-2. Here, we developed a viral receptor (human angiotensin-converting enzyme 2, hACE2) pulmonary transfection mouse model to establish SARS-CoV-2 infection rapidly in the mouse lung. Based on the model, the virus successfully infected the mouse lung 2 days after transfection. Viral RNA/protein, innate immune cell infiltration, inflammatory cytokine expression, and pathological changes in the infected lungs were observed after infection. Further studies indicated that neutrophils were the first and most abundant leukocytes to infiltrate the infected lungs after viral infection. In addition, using infected CXCL5-knockout mice, chemokine CXCL5 was responsible for neutrophil recruitment. CXCL5 knockout decreased lung inflammation without diminishing viral clearance, suggesting a potential target for controlling pneumonia.

Characteristics of Atmospheric Fine Particulate Matter (PM 2.5) Induced Differentially Expressed Proteins Determined by Proteomics and Bioinformatics Analyses.

OBJECTIVE: To screen the differentially expressed proteins (DEPs) in human bronchial epithelial cells (HBE) treated with atmospheric fine particulate matter (PM 2.5). METHODS: HBE cells were treated with PM 2.5 samples from Shenzhen and Taiyuan for 24 h. To detect overall protein expression, the Q Exactive mass spectrometer was used. Gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG), and Perseus software were used to screen DEPs. RESULTS: Overall, 67 DEPs were screened in the Shenzhen sample-treated group, of which 46 were upregulated and 21 were downregulated. In total, 252 DEPs were screened in the Taiyuan sample-treated group, of which 134 were upregulated and 118 were downregulated. KEGG analysis demonstrated that DEPs were mainly enriched in ubiquitin-mediated proteolysis and HIF-1 signal pathways in Shenzhen PM 2.5 samples-treated group. The GO analysis demonstrated that Shenzhen sample-induced DEPs were mainly involved in the biological process for absorption of various metal ions and cell components. The Taiyuan PM 2.5-induced DEPs were mainly involved in biological processes of protein aggregation regulation and molecular function of oxidase activity. Additionally, three important DEPs, including ANXA2, DIABLO, and AIMP1, were screened. CONCLUSION: Our findings provide a valuable basis for further evaluation of PM 2.5-associated carcinogenesis.

Clinical Course and Mortality of Stroke Patients With Coronavirus Disease 2019 in Wuhan, China.

BACKGROUND AND PURPOSE: No studies have reported the effect of the coronavirus disease 2019 (COVID-19) epidemic on patients with preexisting stroke. We aim to study the clinical course of COVID-19 patients with preexisting stroke and to investigate death-related risk factors. METHODS: We consecutively included 651 adult inpatients with COVID-19 from the Central Hospital of Wuhan between January 2 and February 15, 2020. Data on the demography, comorbidities, clinical manifestations, laboratory findings, treatments, complications, and outcomes (ie, discharged or death) of the participants were extracted from electronic medical records and compared between patients with and without preexisting stroke. The association between risk factors and mortality was estimated using a Cox proportional hazards regression model for stroke patients infected with severe acute respiratory syndrome coronavirus 2. RESULTS: Of the 651 patients with COVID-19, 49 with preexisting stroke tended to be elderly, male, had more underlying comorbidities and greater severity of illness, prolonged length of hospital stay, and greater hospitalization expenses than those without preexisting stroke. Cox regression analysis indicated that the patients with stroke had a higher risk of developing critical pneumonia (adjusted hazard ratio, 2.01 [95% CI, 1.27-3.16]) and subsequent mortality (adjusted hazard ratio, 1.73 [95% CI, 1.00-2.98]) than the patients without stroke. Among the 49 stroke patients, older age and higher score of Glasgow Coma Scale or Sequential Organ Failure Assessment were independent risk factors associated with in-hospital mortality. CONCLUSIONS: Preexisting stroke patients infected with severe acute respiratory syndrome coronavirus 2 were readily predisposed to death, providing an important message to individuals and health care workers that preventive measures must be implemented to protect and reduce transmission in stroke patients in this COVID-19 crisis.

Association between platelet parameters and mortality in coronavirus disease 2019: Retrospective cohort study.

BACKGROUND: Thrombocytopenia has been implicated in patients infected with severe acute respiratory syndrome coronavirus 2, while the association of platelet count and changes with subsequent mortality remains unclear. METHODS: The clinical and laboratory data of 383 patients with the definite outcome by March 1, 2020 in the Central Hospital of Wuhan were reviewed. The association between platelet parameters and mortality risk was estimated by utilizing Cox proportional hazard regression models. RESULTS: Among the 383 patients, 334 (87.2%) were discharged and survived, and 49 (12.8%) died. Thrombocytopenia at admission was associated with mortality of almost three times as high as that for those without thrombocytopenia (P < 0.05). Cox regression analyses revealed that platelet count was an independent risk factor associated with in-hospital mortality in a dose-dependent manner. An increment of per 50 × 109/L in platelets was associated with a 40% decrease in mortality (hazard ratio: 0.60, 95%CI: 0.43, 0.84). Dynamic changes of platelets were also closely related to death during hospitalization. CONCLUSIONS: Baseline platelet levels and changes were associated with subsequent mortality. Monitoring platelets during hospitalization may be important in the prognosis of patients with coronavirus disease in 2019.

Dysbiosis of gut microbiome affecting small intestine morphology and immune balance: a rhesus macaque model.

There is a growing appreciation for the specific health benefits conferred by commensal microbiota on their hosts. Clinical microbiota analysis and animal studies in germ-free or antibiotic-treated mice have been crucial for improving our understanding of the role of the microbiome on the host mucosal surface; however, studies on the mechanisms involved in microbiome-host interactions remain limited to small animal models. Here, we demonstrated that rhesus monkeys under short-term broad-spectrum antibiotic treatment could be used as a model to study the gut mucosal host-microbiome niche and immune balance with steady health status. Results showed that the diversity and community structure of the gut commensal bacteria in rhesus monkeys were both disrupted after antibiotic treatment. Furthermore, the 16S rDNA amplicon sequencing results indicated that Escherichia-Shigella were predominant in stool samples 9 d of treatment, and the abundances of bacterial functional genes and predicted KEGG pathways were significantly changed. In addition to inducing aberrant morphology of small intestinal villi, the depletion of gut commensal bacteria led to increased proportions of CD3 + T, CD4 + T, and CD16 + NK cells in peripheral blood mononuclear cells (PBMCs), but decreased numbers of Treg and CD20 + B cells. The transcriptome of PBMCs from antibiotic-treated monkeys showed that the immune balance was affected by modulation of the expression of many functional genes, including IL-13, VCAM1, and LGR4.

Association of CFH polymorphism with susceptibility to sepsis caused by Pseudomonas aeruginosa in Chinese Han populations: A multi-center study.

Complement factor H (CFH) serves as a major down-regulator in the complement system, often utilized by bacterial pathogens to evade complement attack. Yet, little is currently known about the genetic correlation of CFH polymorphisms with sepsis due to various microbial infections. A case-control method (488 septic patients and 527 healthy individuals) was carried out in this study to investigate the genetic relationship between CFH polymorphisms (rs3753394 C/T, rs1065489 G/T and rs1061170 C/T) and susceptibility to sepsis caused by bacterial infections in Chinese Han populations. Our findings indicated that the frequency of rs3753394 CT/TT genotype in the septic patients with P. aeruginosa was significantly higher than that in the control individuals (P = 0.033, OR = 2.668, 95%CI = 1.072-6.334). The rs3753394 T allele frequency in the P. aeruginosa-infected patients was significantly increased, compared to that in the healthy controls (P = 0.014, OR = 1.68, 95%CI = 1.118-2.538). Moreover, these significant differences of rs3753394 genotype and allele frequencies remained after multiple testing corrections [P (corr.) = 0.033 for genotype; P (corr.) = 0.033 for allele]. The current study highlighted the significance of CFH polymorphism rs3753394 as a potential biomarker for targeting P. aeruginosa infection in critically ill patients.

The progressive alteration of urine metabolomic profiles of rats following long-term and low-dose exposure to permethrin.

Background: Permethrin is a type of widely used pyrethroid pesticide. Although acute toxicity of permethrin has been well-characterised, the non-acute toxicity of permethrin upon long-term exposure at low dose has been seldom studied yet. The current study investigates the time-course change of the metabolomic profiles of urine following the low level long-term exposure of permethrin and identified biomarkers of the chronic toxicity of permethrin.Methods: Male Wistar rats were administrated orally with permethrin (75 mg/kg body weight/day, 1/20 LD50) daily for consecutive 90 days. The urine samples from day 30, day 60, and day 90 after the first dosing were collected and analysed by 1H NMR spectrometry. Serum biochemical analysis was also carried out.Results: Permethrin caused significant changes in the urine metabolites such as taurine, creatinine, acetate, lactate, dimethylamine, dimethylglycine, and trimethylamine-N-oxide. These biological markers indicated prominent kidney and liver toxicity induced by permethrin. However, there was no change in serum biochemical parameters for the toxicity, indicating that metabolomic approach was much more sensitive in detecting the chronic toxicity.Conclusion: The time-course alteration of metabolomic profiles of the urine based on 1H NMR reflects the progressive development of the chronic toxicity with the long-term low-level exposure of permethrin.

Time-Course Changes in Urine Metabolic Profiles of Rats Following 90-Day Exposure to Propoxur.

As a major kind of carbamate insecticide, propoxur plays an important role in agriculture, veterinary medicine, and public health. The acute toxicity of propoxur is mainly neurotoxicity due to the inhibition of cholinesterase. However, little is known regarding the toxicity of propoxur upon long-term exposure at low dose. In this study, Wistar rats were orally administrated with low dose (4.25 mg/kg body weight/day) for consecutive 90 days. And the urine samples in rats treated with propoxur for 30, 60, and 90 days were collected and analyzed by employing 1H NMR-based metabolomics approach. We found that propoxur caused significant changes in the urine metabolites, including taurine, creatinine, citrate, succinate, dimethylamine, and trimethylamine-N-oxide. And the alteration of the metabolites was getting more difference compared with that of the control as the exposure time extending. The present study not only indicated that the changed metabolites could be used as biomarkers of propoxur-induced toxicity but also suggested that the time-course alteration of the urine metabolomic profiles could reflect the progressive development of the toxicity following propoxur exposure.

Study of Catalytic Combustion of Dioxins on Ce-V-Ti Catalysts Modified by Graphene Oxide in Simulating Iron Ore Sintering Flue Gas.

Ce-V-Ti and Ce-V-Ti/GO catalysts synthesized by the sol-gel method were used for the catalytic combustion of dioxins at a low temperature under simulating sintering flue gas in this paper. The catalytic mechanism of Ce-V-Ti catalysts modified with graphene oxides (GO) at a low temperature was revealed through X-ray diffractometer (XRD), Brunauer-Emmett-Teller (BET), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), H2-temperature-programmed reduction (H2-TPR) and Fourier transform infrared (FTIR). During the tests, chlorobenzene (CB) was used as a model reagent since the dioxins are poisonous. The results showed that introducing GO to Ce-V-Ti catalysts can improve the specific surface area and promote the CB adsorption on the surface of catalysts. Simultaneously, the Ce-V-Ti with 0.7 wt % GO support showed the high activity with the conversion of 60% at 100 °C and 80% at 150 °C. The adsorb ability of catalysts is strengthened by the electron interaction between GO and CB through π-π bond. In the case of Ce-V-Ti catalysts, Ce played a major catalytic role and V acted as a co-catalytic composition. After GO modification, the concentration of Ce3+ and V4+ were enlarged. The synergy between Ce3+ and V3+ played the critical role on the low-temperature performance of catalysts under sintering flue gas.

Urokinase-type plasminogen activator protects human umbilical vein endothelial cells from apoptosis in sepsis.

The aim of this study was to investigate the effect of urokinase-type plasminogen activator (uPA) on cell viability, apoptosis, and inflammatory cytokine levels in septic human umbilical vein endothelial cells (HUVECs). Lipopolysaccharides (LPS) were added to construct septic HUVECs, then the septic HUVECs were treated by uPA, and cell viability, apoptosis, TNF-α, IL-6, GMCSF and uPAR levels were evaluated by CCK-8, AV/PI, qPCR, western blot and ELISA, respectively. Subsequently, uPA shRNA was transferred into septic HUVECs, and the cells viability, cell apoptosis and the expressions of TNF-α, IL-6, GMCSF, as well as uPAR were assessed by the same methods. uPA promoted viability while reducingapoptosis in septic HUVECs. However, uPA had no effect on the regulation of TNF-α or IL-6 expression in septic HUVECs. In addition, uPA elevated the expressions of GMCSF and uPAR in septic HUVECs. After the transfection of uPA shRNA, cell viability was decreased, apoptosis was enhanced, and GMCSF and uPAR expressions were reduced, while TNF-α or IL-6 expression did not vary in septic HUVECs. In conclusion, uPA promotes cell viability, represses apoptosis,and has no effect on regulating inflammatory cytokines in septic HUVECs.