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1.
Article in Chinese | MEDLINE | ID: mdl-35439862

ABSTRACT

Objective: To analyze the epidemiological characteristics of pneumoconiosis in Qinghai Province from 2011 to 2020, and to provide a basis for the formulation of prevention and control strategy. Methods: In April 2021 , the cases of pneumoconiosis were monitored by the Occupational Disease and Health Hazard Factors Monitoring Information System in Qinghai Province from 2011 to 2020. The distribution of pneumoconiosis, the composition of diseases and the working years exposed to dust were analyzed. Results: All 1026 cases of pneumoconiosis were newly diagnosed in Qinghai Province from 2011 to 2020, silicosis and coal worker pneumoconiosis were the main diseases (78.36% ,804/1026). Stage Ⅰ pneumoconiosis were 484 (47.17%,484/1026) cases. 359 (34.99%,359/1026) cases, 315 (30.70%,315/1026) cases and 252 (24.56%, 252/1026) cases had been diagnosed respectively in Xining City, Haidong City and Haixi Prefecture; 628 (61.21%,628/1026) cases and 418 (40.74%, 418/1026) cases engaged in mining industry and large-sized enterprise, respectively. The working years exposed to dust in silicosis cases were shorter than that in coal worker pneumoconiosis and other pneumoconiosis (P <0.05). Conclusion: The pneumoconiosis area and industry focus in Qinghai Province is obvious. The supervision and adninistration of small and micro scale employers should be strengthened to protect the health rights and interests of workers, especially for the key area and industry.


Subject(s)
Anthracosis , Coal Mining , Pneumoconiosis , Silicosis , Anthracosis/epidemiology , China/epidemiology , Dust , Health Services Accessibility , Human Rights , Humans , Pneumoconiosis/diagnosis , Pneumoconiosis/epidemiology , Silicosis/epidemiology
2.
Phys Rev E ; 100(1-1): 013307, 2019 Jul.
Article in English | MEDLINE | ID: mdl-31499910

ABSTRACT

The present paper analyzes the typical unified lattice Boltzmann (LB) models for different convection-diffusion (CD) problems in multiphase systems. The CD problems in multiphase systems can be roughly classified into three groups: CD problems with a continuous scalar value and a continuous flux, a discontinuous scalar value and a continuous flux, a continuous scalar value and a discontinuous flux. The characteristics of the corresponding unified LB models for the three kinds of CD problems are analyzed and the equivalence between the LB models based on different perspectives or numerical schemes is revealed. Finally, a comprehensive multiphase LB model (CMLBM) capable of solving different isotropic and anisotropic CD problems in multiphase systems is proposed. Four typical CD problems in multiphase systems are calculated to validate the CMLBM; the results show that it performs well against the typical isotropic and anisotropic CD problems in multiphase systems.

4.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi ; 35(12): 907-910, 2017 Dec 20.
Article in Chinese | MEDLINE | ID: mdl-29495152

ABSTRACT

Objective: To investigate the relationship between occupational stress and working ability of workers in a petroleum processing enterprise in a high altitude area. Methods: A total of 728 workers in a petroleum processing enterprise at an altitude of 2850 m were subjected to a survey using Occupational Stress Inventory (OSI) , Work Ability Index (WAI) Scale, Occupational Role Questionnaire (ORQ) , Personal Strain Questionnaire (PSQ) , and Personal Resource Questionnaire (PRQ) from May 2014 to August 2016. Results: Of the 728 workers, 55 (7.6%) had a poor working ability, moderate in 262 (35.9%) , and good in 411 (56.5%). There were significant differences in WAI between the workers with different types of work, sexes, ages, and working years (P<0.05). There was a significant difference in WAI between different occupational stress groups (P<0.05). WAI was negatively correlated with ORQ score and PSQ score (r(s)=-0.387, P<0.05; r(s)=-0.467, P<0.05) and positively correlated with PRQ score (r(s)=0.343, P<0.05). The multiple linear regression analysis showed that high ORQ score and PSQ score were the inhibitory factors for high WAI (B=-0.058; B=-0.082) and high PRQ score was a contributing factor for high WAI (B=0.029) . Conclusion: Occupational stress is an influencing factor for the working ability of workers in the petroleum processing enterprise in the high altitude area. Hypoxia in high altitude area may further reduce the working ability. In order to reduce occupational stress and improve work ability, it should be considered to strengthen skills training, improve the working environment, and pay attention to mental health.


Subject(s)
Occupational Exposure/adverse effects , Occupational Stress , Petroleum , Work Capacity Evaluation , Workload , Altitude , Humans , Stress, Psychological , Surveys and Questionnaires , Task Performance and Analysis
5.
Cell Death Differ ; 20(3): 515-23, 2013 Mar.
Article in English | MEDLINE | ID: mdl-23175187

ABSTRACT

Autophagy is a lysosomal pathway for cellular homeostasis control. Both non-selective bulk autophagy and selective autophagy of specific proteins or organelles have been found. Selective autophagy prevents cells from pathogen invasion and stress damage, but its role in regulating transcriptional factors is not clear. Using a macrophage cell differentiation model, the role of autophagy in nuclear factor-κB (NF-κB) regulation is investigated. The bone marrow-derived macrophages (BMDMs) will differentiate into a M2-like phenotype in the presence of hepatoma tumor cell condition medium (CM). The TLR2 signaling drives this M2 polarization and causes NF-κB p65 degradation via lysosome-dependent pathway. The CM-induced ubiquitinated- NF-κB p65 forms aggresome-like structures (ALS) in the cytoplasm of cultured and hepatoma-associated M2 macrophages. This NF-κB p65-contained ALS is recognized by p62/SQSTM1 and degraded by selective autophagy. Treatment with the lysosomal inhibitor bafilomycin A1 or the knockdown of Atg5 can prevent CM-induced NK-κB p65 degradation and induce M2 macrophages to produce a high level of pro-inflammatory cytokines. Furthermore, TLR2 signal induces sustained phosphorylation of extracellular signal-regulated kinase 1/2 to facilitate this autophagy-dependent NF-κB regulation. Our finding provides a novel pathway of NF-κB regulation by p62/SQSTM1-mediated selective autophagy.


Subject(s)
Autophagy , Lysosomes/metabolism , Macrophages/cytology , Toll-Like Receptor 2/metabolism , Transcription Factor RelA/metabolism , Adaptor Proteins, Signal Transducing/antagonists & inhibitors , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Animals , Autophagy-Related Protein 5 , Bone Marrow Cells/cytology , Carcinoma, Hepatocellular/metabolism , Cell Differentiation , Cell Line, Tumor , Culture Media, Conditioned/pharmacology , Cytokines/metabolism , Female , Lysosomes/drug effects , Macrolides/pharmacology , Macrophages/drug effects , Macrophages/metabolism , Mice , Mice, Inbred BALB C , Mice, Knockout , Microtubule-Associated Proteins/antagonists & inhibitors , Microtubule-Associated Proteins/genetics , Microtubule-Associated Proteins/metabolism , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Phosphorylation , RNA Interference , RNA, Small Interfering/metabolism , Sequestosome-1 Protein
6.
Eur J Clin Microbiol Infect Dis ; 31(6): 1219-24, 2012 Jun.
Article in English | MEDLINE | ID: mdl-21983920

ABSTRACT

Enterovirus 71 (EV71) infection commonly strike children under the age of 3 years, with an occasionally unfavorable outcome in children. This study was designed to explore the relationship between age and the severity of complications, which may associate with antibody-dependent enhancement (ADE) in EV71. All EV71-infected patients during the outbreak of 2008 were recruited. In total, 134 patients were enrolled and categorized into two age groups, 0-12 months (n = 18) and >12 months (n = 116). Pulmonary edema/hemorrhage more commonly occur in patients younger than 12 months. No difference in the occurrence of herpangina/hand-foot-and-mouth disease (HFMD), uncomplicated brainstem encephalitis (BE), or autonomic nervous system (ANS) dysregulation was noted between the two age groups. Patients with pulmonary edema/hemorrhage (11.9 ± 14.7 months) were younger than patients with herpangina/HFMD (35.8 ± 26.4 months) or ANS dysregulation (33.9 ± 20.9 months). Our findings are in agreement with the data regarding the outbreak in Taiwan, in which a decrease in age corresponded to an increase in disease severity with regard to central nervous system complications. A reduction of maternal antibodies to the subneutralizing level within 1 year of age may be associated with the ADE of the infection. This study could provide possible clinical significance with regard to ADE phenomena in young infants infected by EV71.


Subject(s)
Communicable Diseases, Emerging/epidemiology , Communicable Diseases, Emerging/pathology , Enterovirus A, Human/isolation & purification , Enterovirus Infections/epidemiology , Enterovirus Infections/pathology , Severity of Illness Index , Age Factors , Antibodies, Viral/blood , Child , Child, Preschool , Communicable Diseases, Emerging/complications , Encephalitis, Viral/epidemiology , Encephalitis, Viral/pathology , Enterovirus Infections/complications , Female , Humans , Infant , Male , Taiwan/epidemiology
7.
J Appl Microbiol ; 108(3): 936-944, 2010 Mar.
Article in English | MEDLINE | ID: mdl-19709334

ABSTRACT

AIMS: To investigate the effect of a water-soluble Melaleuca alternifolia concentrate (MAC) on group A streptococcus (GAS; Streptococcus pyogenes)-induced necrotizing fasciitis. METHODS AND RESULTS: MAC pretreatment (1% and 2% v/v) was able to protect mice from GAS infection in an air pouch model. GAS-induced mouse death and skin injury were inhibited dose dependently by MAC. Administration of MAC at 6 h post-GAS infection partially delayed mouse death. Surveys of the exudates of the air pouch of MAC-treated mice revealed that the survival of infiltrating cells was prolonged, the bacteria were eliminated, and the production of inflammatory cytokines was inhibited. MAC could directly inhibit the growth of GAS in vitro, and the minimal inhibitory concentration (MIC) of MAC for GAS was determined as 0.05% v/v using the time-kill assay. Furthermore, a sub-MIC dose of MAC not only enhanced the bactericidal activity of RAW264.7 macrophage cells against GAS but also increased susceptibility of GAS for blood clearance. CONCLUSIONS: These results suggest that MAC may inhibit GAS-induced skin damage and mouse death by directly inhibiting GAS growth and enhancing the bactericidal activity of macrophages. SIGNIFICANCE AND IMPACT OF THE STUDY: Our results provide scientific data on the use of MAC for the treatment of GAS-induced necrotizing fasciitis in the murine model.


Subject(s)
Fasciitis, Necrotizing/drug therapy , Macrophages/immunology , Melaleuca/chemistry , Streptococcal Infections/drug therapy , Tea Tree Oil/therapeutic use , Animals , Cell Line , Fasciitis, Necrotizing/prevention & control , Female , Mice , Mice, Inbred C57BL , Microbial Sensitivity Tests , Phytotherapy , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Skin/microbiology , Skin/pathology , Streptococcal Infections/prevention & control , Streptococcus pyogenes/drug effects , Streptococcus pyogenes/growth & development , Tea Tree Oil/pharmacology
8.
J Viral Hepat ; 15(7): 490-7, 2008 Jul.
Article in English | MEDLINE | ID: mdl-18221299

ABSTRACT

The role of the p38 mitogen-activated protein kinase (MAPK) pathway in hepatitis B virus (HBV) replication was investigated in this study. After transient transfection with HBV plasmid, p38 MAPK, but not JNK or ERK1/2, was significantly phosphorylated in human hepatoma cell Huh7. Interestingly, HBV proteins and RNA synthesis were significantly inhibited by a specific inhibitor of p38 MAPK, SB203580, in a dose-dependent manner. Intracellular core-associated DNA, extracellular virion-associated DNA and covalently closed circular DNA were also significantly inhibited by SB203580. Further results showed the antiviral role of nitric oxide (NO) on the suppression of HBV replication and downregulation of p38 MAPK phosphorylation. In conclusion, these results suggested that suppression of phosphorylation of p38 MAPK by inhibitor or NO could inhibit intracellular HBV replication.


Subject(s)
Hepatitis B virus/drug effects , Liver/drug effects , Liver/virology , Nitric Oxide/pharmacology , Virus Replication/drug effects , p38 Mitogen-Activated Protein Kinases/metabolism , Antiviral Agents , Carcinoma, Hepatocellular/pathology , Cells, Cultured , Hepatitis B virus/immunology , Hepatitis B virus/physiology , Hepatocytes/virology , Humans , Liver/cytology , Liver/immunology , Virus Replication/physiology
9.
Int J Immunopathol Pharmacol ; 21(4): 817-26, 2008.
Article in English | MEDLINE | ID: mdl-19144267

ABSTRACT

Concanavalin A (Con A) is known to induce acute hepatitis that is mediated by activation of NKT and T-cell and cytokine production in immunocompetent mice. The observation of Con A-induced autophagic cell death of hepatoma cells via a Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 mediated autophagic pathway made us re-evaluate the effect of Con A-induced hepatitis in mice. Con A was administrated intravenously to BABL/c, SCID, or SCID/NOD mice at doses of 20, 30 or 40 mg/kg, respectively, to induce acute hepatitis. The levels of hepatitis and autophagy induction were both analyzed. We found that Con A can induce acute hepatitis in SCID or SCID/NOD mice with kinetics similar to that of BALB/c, but requiring a higher dose of Con A. No lymphocyte infiltrations were found in SCID or SCID/NOD mice, and the cytokine productions were different. An autophagy with microtubule-associated protein light chain 3-II conversion was demonstrated in the liver post-Con A injection in SCID/NOD mice. Due to the mannose/glucose-specific binding on cell membrane, Con A can induce a T-cell-independent acute hepatitis with autophagy in SCID/NOD mice.


Subject(s)
Autophagy , Chemical and Drug Induced Liver Injury/etiology , Concanavalin A/toxicity , Animals , Liver/pathology , Male , Mice , Mice, Inbred BALB C , Mice, Inbred NOD , Mice, SCID
10.
Kidney Int ; 72(6): 716-24, 2007 Sep.
Article in English | MEDLINE | ID: mdl-17637712

ABSTRACT

Streptococcal pyrogenic exotoxin B is an extracellular cysteine protease. Only nephritis-associated strains of group A streptococci secrete this protease and this may be involved in the pathogenesis of post-streptococcal glomerulonephritis. Mice were actively immunized with a recombinant protease inactive exotoxin B mutant or passively immunized with exotoxin B antibody. Characteristics of glomerulonephritis were measured using histology, immunoglobulin deposition, complement activation, cell infiltration, and proteinuria. None of the mice given bovine serum albumin or exotoxin A as controls showed any marked changes. Immunoglobulin deposition, complement activation, and leukocyte infiltration occurred only in the glomeruli of exotoxin B-hyperimmunized mice. One particular anti-exotoxin B monoclonal antibody, 10G, was cross-reactive with kidney endothelial cells and it caused kidney injury and proteinuria when infused into mice. This cross-reactivity may be involved in the pathogenesis of glomerulonephritis following group A streptococcal infection.


Subject(s)
Autoantibodies/immunology , Cysteine Endopeptidases/immunology , Endothelial Cells/immunology , Glomerulonephritis/immunology , Animals , Antibodies, Monoclonal/blood , Antibodies, Monoclonal/immunology , Antibodies, Monoclonal/pharmacology , Autoantibodies/blood , Autoantibodies/pharmacology , Complement Activation/immunology , Cross Reactions , Cysteine Endopeptidases/pharmacology , Disease Models, Animal , Endothelial Cells/cytology , Glomerulonephritis/pathology , Humans , Immunization , Kidney Glomerulus/immunology , Kidney Glomerulus/pathology , Leukocytes/immunology , Mice , Mice, Inbred BALB C , Proteinuria/immunology , Proteinuria/pathology , Recombinant Proteins/immunology , Recombinant Proteins/pharmacology
11.
Clin Microbiol Infect ; 13(7): 677-82, 2007 Jul.
Article in English | MEDLINE | ID: mdl-17441979

ABSTRACT

Taiwan has experienced several outbreaks of enterovirus 71 (EV71) infections since 1998. This study examined the quantitative relationship between specific cytokines in the cerebrospinal fluid (CSF) and the severity of EV71 brain stem encephalitis (BE), and investigated whether the CSF cytokine response differed from that to uncomplicated echovirus meningitis (EM). The study included 57 children with EV71 BE, of whom 24 had isolated BE, 24 had autonomic nervous system (ANS) dysregulation, and nine had pulmonary oedema (PE), and 15 children with EM. All were confirmed by virus culture. Mean CSF glucose, total protein and lactate levels were increased significantly in association with the severity of EV71 BE. The mean CSF concentration of interleukin (IL)-1beta in children with EV71 PE was significantly higher than in those with isolated BE. IL-6 and interferon (IFN)-gamma levels were significantly higher for EV71 PE and ANS dysregulation than for isolated BE. In contrast, EM was associated with high levels of IL-1beta and low levels of IFN-gamma. Cytokines in the central nervous system, as well as in blood, appear to be involved in the pathogenesis of EV71 BE.


Subject(s)
Brain Stem/physiopathology , Cytokines/cerebrospinal fluid , Encephalitis, Viral/physiopathology , Enterovirus Infections/immunology , Enterovirus/pathogenicity , Brain Stem/immunology , Brain Stem/virology , Child, Preschool , Disease Outbreaks , Echovirus Infections/epidemiology , Echovirus Infections/immunology , Echovirus Infections/physiopathology , Echovirus Infections/virology , Encephalitis, Viral/epidemiology , Encephalitis, Viral/immunology , Encephalitis, Viral/virology , Enterovirus/immunology , Enterovirus B, Human/immunology , Enterovirus B, Human/pathogenicity , Enterovirus Infections/epidemiology , Enterovirus Infections/physiopathology , Enterovirus Infections/virology , Female , Humans , Infant , Male , Meningitis, Viral/epidemiology , Meningitis, Viral/immunology , Meningitis, Viral/physiopathology , Meningitis, Viral/virology , Severity of Illness Index , Taiwan/epidemiology
12.
Clin Exp Immunol ; 141(3): 500-8, 2005 Sep.
Article in English | MEDLINE | ID: mdl-16045740

ABSTRACT

Both viral effect and immune-mediated mechanism are involved in the pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In this study, we showed that in SARS patient sera there were autoantibodies (autoAbs) that reacted with A549 cells, the type-2 pneumocytes, and that these autoAbs were mainly IgG. The autoAbs were detectable 20 days after fever onset. Tests of non-SARS-pneumonia patients did not show the same autoAb production as in SARS patients. After sera IgG bound to A549 cells, cytotoxicity was induced. Cell cytotoxicity and the anti-epithelial cell IgG level were positively correlated. Preabsorption and binding assays indicated the existence of cross-reactive epitopes on SARS-CoV spike protein domain 2 (S2). Furthermore, treatment of A549 cells with anti-S2 Abs and IFN-gamma resulted in an increase in the adherence of human peripheral blood mononuclear cells to these epithelial cells. Taken together, we have demonstrated that the anti-S2 Abs in SARS patient sera cause cytotoxic injury as well as enhance immune cell adhesion to epithelial cells. The onset of autoimmune responses in SARS-CoV infection may be implicated in SARS pathogenesis.


Subject(s)
Autoantibodies/blood , Epithelial Cells/immunology , Lung/immunology , Membrane Glycoproteins/immunology , Severe Acute Respiratory Syndrome/immunology , Severe acute respiratory syndrome-related coronavirus , Viral Envelope Proteins/immunology , Cell Adhesion , Cell Death , Cell Line, Tumor , Cross Reactions/immunology , Cytotoxicity Tests, Immunologic , Epithelial Cells/pathology , Humans , Immunoglobulin G/blood , Immunoglobulin G/immunology , Lung/pathology , Severe Acute Respiratory Syndrome/pathology , Spike Glycoprotein, Coronavirus
13.
Genes Immun ; 6(6): 493-9, 2005 Sep.
Article in English | MEDLINE | ID: mdl-15959534

ABSTRACT

The interleukin (IL)-24/melanoma differentiation associated gene-7 (mda-7) is a member of the IL-10 cytokine family. Introduction of the IL-24 gene into a variety of cancer cells suppresses their growth. It has not been shown, however, whether IL-24 can suppress the growth of hepatoma cells. The purpose of this study was to determine whether the mouse (m)IL-24 gene would suppress hepatoma cells in vivo after being delivered via intramuscular electroporation. After mice were given a subcutaneous dorsal injection of ML-1 hepatoma cells, the mIL-24 gene was delivered and suppressed tumor growth. On day 140, 60% of the mIL-24-treated mice (n=10) and 0% (n=10) of the untreated control mice had survived. We also generated a mouse-hepatoma model by injecting ML-1 cells into the spleen, which resulted in tumor metastasis in the liver. Intramuscular electroporation of mIL-24 also inhibited hepatoma-cell growth in the liver. On day 50, 90% of the experimental mice (n=10) and 40% (n=10) of the control mice had survived. Liver tumors in surviving experimental mice were 50% smaller than those in control mice. IL-24 also inhibited tumor vascularization. These results suggest that IL-24 has potential therapeutic value for hepatoma


Subject(s)
Cytokines/genetics , Genetic Therapy , Liver Neoplasms, Experimental/therapy , Animals , Electroporation , Female , Liver/blood supply , Mice , Mice, Inbred BALB C , Neovascularization, Pathologic/therapy , Receptors, Immunologic/analysis , Receptors, Immunologic/metabolism , Suppression, Genetic , Transfection
14.
Curr Pharm Des ; 10(2): 213-21, 2004.
Article in English | MEDLINE | ID: mdl-14754400

ABSTRACT

Vascular disorders, resulting from endothelial cell dysfunction, may be caused by various stimuli, including infectious pathogens, cytotoxic reagents, and pathophysiological mechanisms mediated by immune responses. Endothelial cell dysfunction characterized by apoptosis and abnormal immune activation is, at least in part, induced by anti-endothelial cell antibody (AECA) in some cases of autoimmune disease. However, the molecular mechanisms of AECA-mediated pathogenetic damage to host vascular system remain unclear. The dual role of nitric oxide (NO) both in endothelial cell apoptosis and survival has been described. In this paper, endothelial cell apoptosis caused by the presence of cross-reactive AECA via a NO-mediated mechanism is demonstrated in dengue virus infection. Endothelial cells undergo apoptosis via the mitochondria-dependent pathway that is regulated by NO production. NO-regulated endothelial cell injury thus may play a role in the disruption of vessel endothelium and contribute to the AECA-induced pathogenesis of vasculopathy. The modulation of NO may provide the therapeutic strategies for autoimmune diseases by preventing the AECA-mediated endothelial cell damage.


Subject(s)
Antibodies/physiology , Endothelial Cells/pathology , Nitric Oxide/physiology , Vascular Diseases/pathology , Animals , Autoimmune Diseases/immunology , Autoimmune Diseases/pathology , Endothelial Cells/physiology , Endothelium, Vascular/pathology , Endothelium, Vascular/physiology , Humans , Vascular Diseases/physiopathology
15.
FEMS Immunol Med Microbiol ; 32(2): 133-40, 2002 Jan 14.
Article in English | MEDLINE | ID: mdl-11821235

ABSTRACT

Bacterial penetration across the blood-brain barrier (BBB) into the central nervous system is the first step in development of meningitis. The role of tumor necrosis factor-alpha (TNF-alpha) in the penetration process was examined with peripheral infection of Streptococcus pneumoniae type 6. After intraperitoneal infection of S. pneumoniae type 6, the BBB opening was increased continuously from 6 h and the mice died of septic shock within 36 h due to bacterial overgrowth. The bacteria crossed the BBB and began to deposit in brain at 6 h post infection. There was strong staining of TNF-alpha on blood vessels of brain from 6 h to 24 h post infection. Anti-TNF-alpha antibody blocked both the BBB opening and the entrance of circulatory S. pneumoniae type 6 into brain, indicating that TNF-alpha played an important role in controlling the opening of BBB. Furthermore, an adult murine model of hematogenous pneumococcal meningitis was developed that is based on opening of the BBB by TNF-alpha and controlling the degree of bacteremia by cefazolin antibiotic. In conclusion, hematogenous meningitis developed as TNF-alpha initiated BBB opening, peripheral bacteria entered into the brain and formed bacterial emboli, and then progressed to meningitis.


Subject(s)
Blood-Brain Barrier/immunology , Meningitis, Pneumococcal/immunology , Tumor Necrosis Factor-alpha/immunology , Animals , Antibodies, Monoclonal/immunology , Brain/immunology , Brain/microbiology , Meningitis, Pneumococcal/physiopathology , Mice , Mice, Inbred C57BL , Streptococcus pneumoniae/immunology , Streptococcus pneumoniae/physiology , Tumor Necrosis Factor-alpha/biosynthesis
16.
J Med Microbiol ; 50(9): 812-821, 2001 Sep.
Article in English | MEDLINE | ID: mdl-11549183

ABSTRACT

Blood-brain barrier (BBB) permeability during sepsis with Escherichia coli or Streptococcus pneumoniae was examined in a mouse model and measured by a circulating beta-galactosidase tracer. The leakage of brain microvascular vessels during sepsis was confirmed by transmission electron microscopic examination of brain tissues stained with horseradish peroxidase. The increase of BBB permeability induced by E. coli and S. pneumoniae, which was maximal at 3 h and 12 h after injection, respectively, was transient because of rapid clearance of the bacteria from the blood. Tumour necrosis factor-alpha (TNF-alpha) was stained on microvascular vessels of the brain during sepsis and intravenous injection of recombinant TNF-alpha also increased the BBB permeability. The increase in BBB permeability induced by either E. coli or S. pneumoniae could be inhibited by anti-TNF-alpha antibody. It was concluded that circulating TNF-alpha generated during sepsis induced the increase in BBB permeability.


Subject(s)
Blood-Brain Barrier/physiology , Escherichia coli Infections/metabolism , Pneumococcal Infections/metabolism , Sepsis/metabolism , Tumor Necrosis Factor-alpha/physiology , Animals , Brain/immunology , Brain/ultrastructure , Disease Models, Animal , Escherichia coli/physiology , Escherichia coli Infections/immunology , Female , Humans , Immunohistochemistry , Mice , Mice, Inbred C57BL , Microscopy, Electron , Pneumococcal Infections/immunology , Sepsis/immunology , Streptococcus pneumoniae/physiology , Tumor Necrosis Factor-alpha/analysis , beta-Galactosidase/metabolism
17.
J Biomed Sci ; 8(5): 377-88, 2001 Sep.
Article in English | MEDLINE | ID: mdl-11549879

ABSTRACT

Dengue virus infection causes dengue fever (DF), dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS), whose pathogeneses are not clearly understood. Current hypotheses of antibody-dependent enhancement, virus virulence, and IFN-gamma/TNFalpha-mediated immunopathogenesis are insufficient to explain clinical manifestations of DHF/DSS such as thrombocytopenia and hemoconcentration. Dengue virus infection induces transient immune aberrant activation of CD4/CD8 ratio inversion and cytokine overproduction, and infection of endothelial cells and hepatocytes causes apoptosis and dysfunction of these cells. The coagulation and fibrinolysis systems are also activated after dengue virus infection. We propose a new hypothesis for the immunopathogenesis for dengue virus infection. The aberrant immune responses not only impair the immune response to clear the virus, but also result in overproduction of cytokines that affect monocytes, endothelial cells, and hepatocytes. Platelets are destroyed by crossreactive anti-platelet autoantibodies. Dengue-virus-induced vasculopathy and coagulopathy must be involved in the pathogenesis of hemorrhage, and the unbalance between coagulation and fibrinolysis activation increases the likelihood of severe hemorrhage in DHF/DSS. Hemostasis is maintained unless the dysregulation of coagulation and fibrinolysis persists. The overproduced IL-6 might play a crucial role in the enhanced production of anti-platelet or anti-endothelial cell autoantibodies, elevated levels of tPA, as well as a deficiency in coagulation. Capillary leakage is triggered by the dengue virus itself or by antibodies to its antigens. This immunopathogenesis of DHF/DSS can account for specific characteristics of clinical, pathologic, and epidemiological observations in dengue virus infection.


Subject(s)
Dengue Virus/pathogenicity , Dengue/immunology , Dengue/physiopathology , Animals , Antiviral Agents/therapeutic use , Biomarkers , Blood/virology , Dengue/drug therapy , Dengue Virus/immunology , Disease Models, Animal , Endothelium, Vascular/pathology , Endothelium, Vascular/virology , Humans , Interleukin-6/metabolism , Liver/virology
18.
Clin Exp Allergy ; 31(4): 652-62, 2001 Apr.
Article in English | MEDLINE | ID: mdl-11359435

ABSTRACT

BACKGROUND: Increasing evidence suggests that pulmonary surfactant protein A (SP-A) and D (SP-D) participate in the lung defence against pathogens. However, the role of surfactant proteins in the pathogenesis of allergen-induced airway inflammation has not been elucidated. In this study we examined the levels and distributions of SP-A and SP-D in a dust mite (Dermatophagoides pteronyssinus, Der p) allergen-induced murine model of asthma. METHODS: The concentration of SP-A and SP-D in the bronchoalveolar lavage fluid (BALF) and the distribution of surfactant proteins in the lung were assayed by ELISA and immunohistochemistry methods, respectively. The effect of surfactant proteins on allergen-induced pulmonary lymphocyte proliferation was also studied. RESULTS: We demonstrated that there were marked reductions of SP-A and SP-D levels in the BALF of Der p-sensitized BALB/c mice at 48-72 h after allergen challenge (AC). Both purified SP-A and SP-D were able to suppress, in a dose dependent manner, Der p-stimulated intrapulmonary lymphocyte proliferation of naïve mice with saline or allergen challenge, or of Der p-sensitized mice with saline challenge. On the contrary, this suppressive effect was mild (< 9%) on lymphocytes from sensitized mice after AC. CONCLUSION: These results indicated the involvement of pulmonary surfactant proteins in the allergic bronchial inflammation of sensitized mice.


Subject(s)
Allergens/adverse effects , Asthma/metabolism , Bronchitis/immunology , Glycoproteins/pharmacology , Mites/immunology , Proteolipids/metabolism , Pulmonary Surfactants/metabolism , Pulmonary Surfactants/pharmacology , Animals , Bronchial Provocation Tests , Bronchoalveolar Lavage Fluid/cytology , Dust/adverse effects , Humans , Immunoblotting , Immunohistochemistry , Lymphocytes/drug effects , Mice , Pulmonary Surfactant-Associated Protein A , Pulmonary Surfactant-Associated Protein D , Pulmonary Surfactant-Associated Proteins
19.
Antimicrob Agents Chemother ; 45(6): 1788-93, 2001 Jun.
Article in English | MEDLINE | ID: mdl-11353626

ABSTRACT

The effect of a water-soluble trimalonic acid derivative of fullerene, carboxyfullerene, against Streptococcus pyogenes infection was tested. Pretreatment with carboxyfullerene was able to protect mice from S. pyogenes infection in an air pouch model. S. pyogenes-induced death and skin injury were inhibited dose dependently by carboxyfullerene. Administration of carboxyfullerene via the peritoneum and air pouch at 3 h post-S. pyogenes infection was able to protect 33% of mice from death. Surveys of exudates of the air pouch of carboxyfullerene-treated mice revealed that survival of infiltrating neutrophils was prolonged and that the bacteria were eliminated as a result of enhanced bactericidal activity of the neutrophils. Furthermore, carboxyfullerene was able to directly inhibit in vitro growth of S. pyogenes. These data suggest that carboxyfullerene can be considered an antimicrobial agent for group A streptococcus infection.


Subject(s)
Carboxylic Acids/therapeutic use , Free Radical Scavengers/therapeutic use , Skin/pathology , Streptococcal Infections/prevention & control , Streptococcus pyogenes/drug effects , Animals , Carboxylic Acids/pharmacology , Free Radical Scavengers/pharmacology , Injections, Intraperitoneal , Mice , Mice, Inbred C57BL , Neutrophils/drug effects
20.
J Med Virol ; 64(2): 104-8, 2001 Jun.
Article in English | MEDLINE | ID: mdl-11360241

ABSTRACT

Hepatitis A, the predominant reported etiologic form of viral hepatitis in Taiwan, continues to be a disease primarily of children and young adults. A seroepidemiologic study was performed to assess the seroprevalence of hepatitis A (HAV) antibodies in the southern Taiwan general population in 1998 and is compared with results of a similar study in 1992. A total of 948 subjects (477 male and 471 female) with ages ranging from 0.3 to 63 years were stratified into 14 age-specific groups. The presence of anti-HAV antibodies was detected using a commercially available radioimmunoassay. Fifteen percent of the subjects were positive for anti-HAV antibodies, which is lower than that in 1992 (P < 0.001). Seroprevalences were 14.1% for males and 22.6% for females (P = 0.006). The pattern of anti-HAV seroprevalence was distinguishable from that found in 1992; minimum seroconversion occurred at ages ranging from 1 to 30 years. Prevalence of seropositive subjects decreased markedly for the < 1, 13-15, 16-19, 20-24, 25-29, and 30-39 year age groups in comparing 1998 with 1992. The current study demonstrates a continuing decline in the prevalence of HAV among children, adolescents, and young adults. The findings can be ascribed to the improvement of socioeconomic status and modernization of environmental sanitation. As a consequence of this changing trend of endemicity and the resulting lack hepatitis A antibodies among the general population in Taiwan, the risk of sudden major outbreaks is increased because of increasing international travel and immigration, particularly during and after natural disasters. HAV vaccination will be important for the prevention and control of HAV outbreaks in the community.


Subject(s)
Hepatitis A Virus, Human/immunology , Hepatitis A/epidemiology , Hepatitis Antibodies/blood , Adolescent , Adult , Child , Child, Preschool , Female , Hepatitis A/immunology , Humans , Infant , Male , Middle Aged , Seroepidemiologic Studies , Taiwan/epidemiology
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