阻燃PE基木塑地板燃烧产烟毒性的动物染毒试验评价

采用动物染毒法,研究阻燃剂类别、阻燃剂添加量、主要成分配比对木塑地板燃烧产烟毒性的影响。结果表明:3种阻燃剂中,氢氧化铝[Al(OH)3]处理试样的产烟毒性较小;随着超细Al(OH)3添加量的增加,试样的产烟毒气安全等级提高。采用试验得到的较优阻燃工艺处理地板试样,产烟毒性达到GB/T 20285-2006《材料产烟毒性危险分级》要求的准安全ZA1等级。

城市轨道客车内装材料产烟毒性评价

综合介绍国内外城市轨道客车产烟毒性评价标准。根据GB 20285标准产烟装置和FTIR烟气成分分析、动物暴露染毒法,对6种城市轨道客车用内装材料的产烟毒性进行对比。结果显示:所测材料的产烟毒性均通过ZA3级;成分分析法低估了门窗密封条和阻燃泡沫的毒性,高估了有机玻璃的毒性。使用FED值与动物暴露染毒相结合的方法,对城轨客车内装材料产烟毒性进行评价更为科学。

红芪黄酮气溶胶给药与灌胃给药对COPD大鼠的影响

目的:比较红芪黄酮灌胃给药及气溶胶给药两种不同的给药方法对大鼠慢性阻塞性肺病模型(COPD)的治疗作用。方法:选取40只SPF级雄性SD大鼠,随机分为空白对照组、模型对照组、红芪黄酮灌胃给药组及红芪黄酮气溶胶给药组,每组10只。空白对照组正常饮食喂养,不加任何处理措施。其余3组每天于小动物烟雾气溶胶染毒暴露系统吸入新鲜的香烟烟雾染毒造模,每天染毒30分钟,造模28天。造模后第7天开始给药,共21天。红芪黄酮灌胃给药组每日灌胃1 mL/100 g,37.41 mg/kg,给药,红芪黄酮气溶胶给药组气溶胶给药,气溶胶浓度保持在3.5~4.0 mg/m^3,给药时间约40分钟。实验结束后,检测清醒及麻醉状态下各组动物肺功能,观察肺组织切片病理形态。结果:清醒状态及麻醉状态下造模组动物肺功能指标与空白对照组比较,均有显著性变化,差异有统计学意义(P<0.05);与模型对照组比较,各给药组显著改善肺功能相关指标,且气溶胶给药组作用更为显著。病理切片结果显示,与空白对照组比较,造模组出现不同程度的异常改变;与模型对照组比较,各给药组病理形态有显著改善,且气溶胶给药组作用更为显著。结论:气溶胶给药与灌胃给药相比,对COPD模型大鼠的治疗作用更为显著,气溶胶给药技术对于COPD的治疗具有重要意义。

Characterization of a Putative Filovirus Vaccine:Virus-Like Particles

Filoviruses are hemorrhagic fever viruses endemic to parts of Africa and the Philippines. Infection carries with it a mortality rate of up to 90% and currently there are no effective vaccines or therapeutics available to combat infection. However, the filovirus virus-like particles (VLP), which are currently under development, have been shown to be a promising vaccine candidate. They provide protection from infection in the mouse, guinea pig, and nonhuman primate models of infection, eliciting high anti-glycoprotein antibody titers and T cell responses to viral proteins. In this review, we will highlight the development of the filovirus VLP and describe the current understanding of VLP immunogenicity and correlates of protection.

Animal models for the study of hepatitis C virus infection and replication

Hepatitis C virus (HCV) hepatitis, initially termed non-A, non-B hepatitis, has become one of the leading causes of cirrhosis and hepatocellular carcinoma worldwide. With the help of animal models, our understanding of the virus has grown substantially from the time of initial discovery. There is a paucity of available animal models for the study of HCV, mainly because of the selective susceptibility limited to humans and primates. Recent work has focused modification of animals to permit HCV entry, replication and transmission. In this review, we highlight the currently available models for the study of HCV including chimpanzees, tupaia, mouse and rat models. Discussion will include methods of model design as well as the advantages and disadvantages of each model. Particular focus is dedicated to knowledge of pathophysiologic mechanisms of HCV infection that have been elucidated through animal studies. Research within animal models is critically important to establish a complete understanding of HCV infection, which will ultimately form the basis for future treatments and prevention of disease.

New animal models for hepatitis C viral infection and pathogenesis studies

Hepatitis C virus （HCV） is a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma （HCC）. In man, the pathobiological changes associated with HCV infection have been attributed to both the immune system and direct viral cytopathic effects. Until now, the lack of simple culture systems to infect and propagate the virus has hampered progress in understanding the viral life cycle and pathogenesis of HCV infection, including the molecular mechanisms implicated in HCV-induced HCC. This clearly demonstrates the need to develop small animal models for the study of HCV-associated pathogenesis. This review describes and discusses the development of new HCV animal models to study viral infection and investigate the direct effects of viral protein expression on liver disease.

Toll-like receptor 4 plays an anti-HBV role in a murine model of acute hepatitis B virus expression

AIM： Toll-like receptor 4 （TLR4） has been shown to be important for bacterial infection, especially to lipopolysaccharide signaling. Its possible role in HBV infection is studied in the present study. MATERIALS AND METHODS： pHBV3.6 plasmid, containing full-length HBV genome was used in the murine model of acute HBV expression by hydrodynamics in vivo transfection. TLR4 normal or mutant mouse strain was compared to investigate the possible role of TLR4 in acute HBV expression. RESULTS： After pHBV3.6 injection, the infiltrating leukocytes expressed TLR4 were observed nearby the HBsAg-expressing hepatocytes. The HBV antigenemia as well as the replication and transcription were higher in TLR4-mutant C3H/HeJ mice than in normal C3H/ HeN mice. The HBV-specific immune responses were impaired in the liver or spleen of the C3H/HeJ mice. Their inducible nitric oxide synthase （iNOS） expression on the hepatic infiltrating cells was also impaired. When adoptively transferring splenocytes from C3H/HeN mice to C3H/HeJ mice, the HBV replication was inhibited to the level as that of C3H/HeN. CONCLUSION： These results suggest that TLR4 plays an anti-HBV role in vivo through the induction of iNOSexpression and HBV-specific immune responses after HBV expression.

Involvement of autophagy in alcoholic liver injury and hepatitis C pathogenesis

This review describes the principal pathways of macroautophagy (i.e. autophagy), microautophagy and chaperone-mediated autophagy as they are currently known to occur in mammalian cells. Because of its crucial role as an accessory digestive organ, the liver has a particularly robust autophagic activity that is sensitive to changes in plasma and dietary components. Ethanol consumption causes major changes in hepatic protein and lipid metabolism and both are regulated by autophagy, which is significantly affected by hepatic ethanol metabolism. Ethanol exposure enhances autophagosome formation in liver cells, but suppresses lysosome function. Excessive ethanol consumption synergizes with hepatitis C virus (HCV) to exacerbate liver injury, as alcohol-consuming HCV patients frequently have a longer course of infection and more severe manifestations of chronic hepatitis than abstinent HCV patients. Alcohol-elicited exacerbation of HCV infection pathogenesis is related to modulation by ethanol metabolism of HCV replication. Additionally, as part of this mechanism, autophagic proteins have been shown to regulate viral (HCV) replication and their intracel-lular accumulation. Because ethanol induces autophagosome expression, enhanced levels of autophagic proteins may enhance HCV infectivity in liver cells of alcoholics and heavy drinkers.

Hepatic artery infusion of antisense oligodeoxynucleotide and lipiodol mixture transfect liver cancer in rats

AIM: To study the distribution and stability of antisense oligodeoxynucleotide (ASODN) in Walker-256 cells and their distribution in liver, lung and kidney tissues after being infused alone or mixed with lipiodol via hepatic artery in a rat liver tumor model.METHODS: 5'-Isothiocyananate (FITC)-labeled vascular endothelial growth factor (VEGF) ASODN was added into Walker-256 cell culture media. Its distribution in cells was observed by fluorescence microscope at different time points. Walker-256 carcinosarcoma was transplanted into Wistar rat liver to establish a liver cancer model. 5'-FITC-labeled VEGF ASODN mixed with (mixed group, n = 6) or without (TAI group, n = 6)ultra-fluid lipiodol was administrated via hepatic artery.Frozen samples of liver, lung and kidney tissue were taken from rats after 1, 3 and 6 d, respectively. The distribution of ASODN was observed under fluorescent microscope.RESULTS: ASODN could enter cytoplasm within 2 h and nuclei within 6 h. Accumulation of ASODN reached the peak point in nuclei at 12 h, and then disappeared gradually. No fluorescence could be seen in cells at 48 h. In vivo experiment, on d 1 and 3 the fluorescence staining in liver was stronger in mixed group than in TAI group and more fluorescence could be detected in lung and kidney in TAI group than in mixed group. On d 6, no fluorescence could be detected in TAI group, but faint fluorescence could be seen in mixed group. ASODN could be seen in cancer cells and normal hepatic cells. In mixed group, ASODN was mainly distributed in liver tumor tissues.CONCLUSION: ASODN can transfect Walker-256 cells.ASODN mixed with lipiodol infusion via hepatic artery can be used in the treatment of HCC.

Construction and characterization of chimeric BHIV (BIV/HIV-1) viruses carrying the bovine immunodeficiency virus gag gene

AIM:To explore the possibility of the replacement of the gag gene between human immunodeficiency virus and bovine immunodeficiency virus, to achieve chimeric virions, and thereby gain a new kind of AIDS vaccine based on BHIV chimeric viruses. METHODS: A series of chimeric BHIV proviral DNAs differing in the replacement regions in gag gene were constructed, and then were transfected into 293T cells. The expression of chimeric viral genes was detected at the RNA and protein level. The supernatant of 293T cell was ultra centrifuged to detect the probable chimeric virion. Once the chimeric virion was detected, its biological activities were also assayed by infecting HIV-sensitive MT4 cells. RESULTS: Four chimeric BHIV proviral DNAs were constructed. Genes in chimeric viruses expressed correctly in transfected 293T cells. All four constructs assembled chimeric virions with different degrees of efficiency. These virions had complete structures common to retroviruses and packaged genomic RNAs, but the cleavages of the precursor Gag proteins were abnormal to some extent. Three of these virions tested could attach and enter into MT4 cells, and one of them could complete the course of reverse transcription. Yet none of them could replicate in MT4 cells. CONCLUSION: The replacement of partial gag gene of HIV with BIV gag gene is feasible. Genes in chimeric BHIVs are accurately expressed, and virions are assembled. These chimeric BHIVs (proviral DNA together with virus particles) have the potential to become a new kind of HIV/AIDS vaccine.

Animal models for studying hepatitis C and alcohol effects on liver

Chronic consumption of ethanol has a dramatic effect on the clinical outcome of patients with hepatitis C virus (HCV) infection, but the mechanism linking these two pathologies is unknown. Presently, in vitro systems are limited in their ability to study the interaction between a productive wild-type HCV infection and chronic ethanol exposure. Mouse models are potentially very useful in dissecting elements of the HCV-ethanol relationship. Experiments in mice that transgenically express HCV proteins are outlined, as are experiments for the generation of mice with chimeric human livers. The latter models appear to have the most promise for accurately modeling the effects of chronic ethanol intake in HCV-infected human livers.

Hepatitis G virus genomic RNA is pathogenic to Macaca mulatta

AIM: To explore the pathogenicity and infectivity of hepatitis G virus (HGV) by observing replication and expression of the virus, as well as the serological and histological changes of Macaca mulatta infected with HGV genomic RNA or HGV RNA-positive serum.METHODS: Full-length HGV cDNA clone (HGVqz) was constructed and proved to be infectious, from which HGV genomic RNA was transcribed in vitro. Macaca mulatta BY1 was intra-hepatically inoculated with HGV genomic RNA, HGV RNA-positive serum from BY1 was intravenously inoculated into Macaca mulatta BM1, and then BB1 was infected with serum from BM1. Serum and liver tissue were taken regularly, and checked with RT-PCR, in situ hybridization and other immunological, serological,histological assays.RESULTS: Serum HGV RNA was detectable in all the 3Macaca mulattas, serological and histological examinations showed the experimental animals had slightly elevated alanine transaminase (ALT) and developed HGV viremia during the infectious period. The histology, immunohistochemistry, and in situ hybridization in liver tissues of the inoculated animals demonstrated a very mild hepatitis with HGV antigen expression in cytoplasm of hepatocytes.RT-PCR and quantitative PCR results showed that HGV could replicate in liver.CONCLUSION: The genomic RNA from full-length HGV cDNA is infectious to the Macaca mulatta and can cause mild hepatitis. HGV RNA-positive serum, from HGV RNA inoculated Macaca mulatta, is infectious to other Macaca mulattas. Macaca mulatta is susceptible to the inoculated HGV, and therefore can be used as an experimental animal model for the studies of HGV infection and pathogenesis.

Cytokines Expression Profile and Kinetics of Peste des petits ruminants Virus Antigen and Antibody in Infected and Vaccinated Goats

The present study deals with the co-ordination of cytokine （IL-4 and IFN-7） expression and kinetics of peste des petits ruminants （PPR） virus antigen and antibody in PPRV infected and vaccinated goats. The infected animals exhibited mixed cytokine （both TH1 and TH2） responses in the initial phase of the disease. The infected and dead goats had increased IFN-T response before their death; while IL-4 remained at the base level. The cytokine expression in recovered animals was almost similar to that of vaccinated ones, where a unique biphasic response of IL-4 expression was observed with an up-regulation of IFN-T on 7th days post vaccination （dpv）. Analysis of PPR virus antigen and antibody kinetics in different components of blood from infected and vaccinated animais revealed that the PPR virus antigen load was highest in plasma followed by serum and blood of the infected animals, whereas vaccinated animals showed only marginal positivity on 9th dpv. The antibody titer was high in serum followed by plasma and blood in both vaccinated and infected animals. Therefore, it is inferred that the presence of antigen and antibody were significant with the expression of cytokine, and that a decreased response of IL-4 was noticed during intermediate phase of the disease i.e., 7 to 12m days post infection （dpi）. This indicates the ability to mount a functional TH2 response after 14th dpi could be a critical determinant in deciding the survival of the PPR infected animal.

The Effects of Allitridin on the Expression of Transcription Factor T-bet/GATA-3 in Mice Infected by Murine Cytomegalovirus

The aim of this study is to investigate the effects of allitridin on the expression of transcription factor T-bet/GATA-3 in mice infected by murine cytomegalovirus. BALB/c mice model system of murine cytomegalovirus (MCMV) infection was established. In which 20 model mice were allocated randomly into allitridin treated group ( n =10) and infected control group ( n =10). Allitridin (25 mg·kg -1 ·d -1 ) was used in treated group at the 24 h by intraperitoneal route ( once/d ×14 d), and the same volume of saline solution was injected control mice. Normal control mice ( n =10), were only given with the same volume of 0.89% sodium chloride, without infection with MCMV. The expression levels of transcription factor T-bet/GATA-3 mRNA were measured by RT-PCR, and the expression levels of T helper 1(Th1) cytokine IFN-γ and Th2 cytokine IL-10 in supernatant of spleen cell culture were measured by ELISA. Experimental results showed MCMV infection could markedly down-modulate the expression of IFN-γ and T-bet, and significantly up-modulate the expression of IL-10 and GATA-3 mRNA. Allitridin could induce increased expression of transcription factor T-bet mRNA and Th1 cytokine IFN-γ significantly ( P <0.01), and decreased expression of transcription factor GATA-3 mRNA and Th2 cytokine IL-10 markedly ( P <0.01). It is concluded that MCMV infection leads to disequilibrium of Th1/Th2 cytokine expression: the level of Th1 cytokine IFN-γ decreases significantly and Th2 cytokine IL-10 overexpresses markedly. Allitridin can up-regulate the expression of T-bet and IFN-γ, and inhibit the expression of GATA-3 mRNA and IL-10 in MCMV infected mice, indicating a Th1 dominant state which should enhance the specific cellular immune reactions against CMV and be helpful for clearance of the cytomegalovirus in host.

EFFECT OF VERAPAMIL ONCa^（2＋） INFLUX ANDCVB3－RNA REPLICATION IN CULTURED NEONATALRAT HEART CELLS INFECTED WITH CVB3

The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<O. 01) by verapamil (1 μmol/L) after infection of heart cells for 48h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (Iμmol/L and 10 nmo/L) at the same time for 48h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<O. 05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e. g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.

Recent Advances in Animal Models of Zika Virus Infection

An infection by Zika virus(ZIKV), a mosquito-borne flavivirus, broke out in South American regions in 2015, and recently showed a tendency of spreading to North America and even worldwide. ZIKV was first detected in 1947 and only 14 human infection cases were reported until 2007. This virus was previously observed to cause only mild flu-like symptoms.However, recent ZIKV infections might be responsible for the increasing cases of neurological disorders such as GuillainBarre′ syndrome and congenital defects, including newborn microcephaly. Therefore, researchers have established several animal models to study ZIKV transmission and pathogenesis, and test therapeutic candidates. This review mainly summarizes the reported animal models of ZIKV infection, including mice and non-human primates.

Numerical Investigation of High Pressure and High Reynolds Diffusion Flame Using Large Eddy Simulation

Today,with nonstop improvement in computational power,Large-Eddy Simulation(LES) is a high demanding research tool for predicting engineering flows.Such flows on high pressure condition like diesel engines is extensively employed in ground and marine transportation,oblige the designer to control and predict toxic pollutants,while maintaining or improving their high thermal efficiency.This becomes one of the main challenging issues in decades.In the present work,numerical investigation of diffusion flame dynamics is performed in the near-field of high-Reynolds jet flow on high pressure condition encountered in diesel engine applications.This work discusses the implementation of Partially Stirred Reactor(PaSR) combustion model by the approaches of large eddy simulation(LES).The simulation results show that LES,in comparison with Reynolds-Averaged Navier-Stokes(RANS) simulation predicts and captures transient phenomena very well.These phenomena such as unsteadiness and curvature are inherent in the near-field of high Reynolds diffusion flame.The outcomes of this research are compared and validated by other researchers' results.Detailed comparisons of the statistics show good agreement with the corresponding experiments.