No abstract available.
Animals ; Asian Continental Ancestry Group* ; Cricetinae ; Cricetulus* ; Female ; Humans* ; Ovary*

No abstract available.
Child* ; Colon* ; Humans

OBJECTIVE: Bacteroides fragilis, normal colonic inhabitant, is the most frequently isolated anaerobes in infected tissues, particularly in intraabdominal abscesses. In the acute infection model with abscesses, the response to B. fragilis infection is characterized by infiltration of neutrophils and macrophages. This study was designed to determine whether proinflammatory cytokines could be upregulated in peritoneal tissue of B. fragilis-infected mouse model. METHODS: After C57BL/6 mice were infected with abscess-inducing encapsulated B. fragilis, RNA was extracted from the intraperitoneal tissues. Cellular RNA was also extracted from mouse peritoneal macrophages (MPM) and human peripheral blood mononuclear cells (PBMC) after infection with B. fragilis. Expression of various cytokine mRNA was assessed using RT-PCR and standard RNA. Each cytokine protein was also measured by ELISA. RESULTS: B. fragilis-infected intraperitoneal tissues showed upregulated expression of IL-1u, IL-6 and TNFu mRNA. Expression of IL-1u and TNFu mRNA and protein was significantly higher in MPM or PBMC infected with B. fragilis than in those without infection. However, expression of IL-6 mRNA and protein was not increased in MPM or PBMC infected with B. fragilis compared with those without infection. CONCLUSION: These results suggest that the cytokines can be involved in immunopathologic reactions of the peritoneal tissue infected with B. jragilis.
Abscess ; Animals ; Bacteroides fragilis* ; Bacteroides* ; Colon ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-6 ; Macrophages ; Macrophages, Peritoneal ; Mice* ; Neutrophils ; RNA ; RNA, Messenger

Invasion of enteric bacteria, such as Salmonella and invasive E. coli, into intestinal epithelial cells induces proinflammatory gene responses and finally epithelial cell apoptosis. In this study, we asked whether invasive bacterial infection of human intestinal epithelial cells could upregulate cyclooxygenase-2 (COX-2) gene expression and whether increased COX-2 expression could influence intestinal epithelial cell apoptosis. Expression of COX-2 mRNA and prostaglandin (PG) E production were upregulated in HT-29 colon epithelial cells which were infected with S. dublin or invasive E. coli, as examined by quantitative RT-PCR and radioimmunoassay. Inhibition of COX-2 expression and PGE2 production using NS-398, a specific COX-2 inhibitor, showed a significant increase af epithelial cell apoptosis and caspase-3 activation in HT-29 cells infected with invasive bacteria. However, the addition of valerylsalicylate, a specific COX-1 inhibitor, did not change apoptosis in S. dublin-infected HT-29 cells. These results suggest that upregulated COX-2 expression and PGE2 production in response to invasive bacterial infection could contribute to host defense by inhibiting apoptosis of intestinal epithelial cells.
Apoptosis* ; Bacteria ; Bacterial Infections* ; Caspase 3 ; Colon ; Cyclooxygenase 2 ; Dinoprostone ; Enterobacteriaceae ; Epithelial Cells* ; Gene Expression ; HT29 Cells ; Humans ; Prostaglandin-Endoperoxide Synthases* ; Radioimmunoassay ; RNA, Messenger ; Salmonella

CTLA-4 (=CD152), a T cell activation antigen, has been known to be homologous to CD28 in its molecular and genomic structure. Both of these two molecules are sharing their counterreceptors, B7 (CDSO) and B7-2 (CD86) and are known to play a crucial role in T cell activation. In previous our study it was reported that there are 2 forms of CTLA-4 antigen in activated human T cells, 30 kD membrane-bound form and 34 kD cytosolic-sequestered form and the former was less than 5 % of total of this antigen induced. Aims of this study are to confirm previous finding by using flow cytometry and to characterize the cytoplasmic form of human CTLA-4 by using ultrafiltration and immunoprecipitation techniques. In PHA stimulated peripheral blood lymphocyte surface expression of CTLA-4 was less than 2.1% of any of CD4+, CD8+ and CD56+ subsets. And the 34 kD form of CTLA-4 was detected in CDS+ subset only. This discrepancy confirms that 34 kD antigen is the cytoplasmic form of human CTLA-4. In ultrafiltration and subsequent Western blot analysis study this 34 kD antigen was detected in >100 kD fraction only. And in non-reducing condition this antigen formed high molecular weght complex (MW > 350 kD). In immunoprecipitation study using anti-peptide A antibody it was found that this high molecular weight complex consists of the 34 kD cytoplasmic form of CTLA-4 and previously unknown 54 kD antigen and 46 kD antigen at 1:1:8-10 ratio. And none of these 3 molecules were identified in membrane fraction of activated human T cell. The result of this study implies that CTLA-4 molecule induced upon T cell activation mainly sequestered in cytoplasrn and another signal is necessary to target this antigen on the activated T cell surface.
Antigens, CD27 ; Blotting, Western ; CTLA-4 Antigen ; Cytoplasm* ; Flow Cytometry ; Humans* ; Immunoprecipitation ; Lymphocytes ; Membranes ; Molecular Weight ; T-Lymphocytes ; Ultrafiltration

No abstract available.
Bacteroides fragilis* ; Bacteroides* ; Enterotoxins* ; Epithelial Cells* ; Gene Expression* ; Humans* ; Intestinal Mucosa*

No abstract available.
HIV* ; Humans ; Humans* ; Lymphocytes* ; Zidovudine*

PURPOSE: The purpose of this study was to compare subjective symptoms of VDT between computer-addicted and non-addicted adolescents. METHOD: A descriptive survey design was used and 646 students in one middle and two high schools were selected as participants. RESULT: The VDT subjective symptoms and degree of severity differed according to whether the students were computer-addicted or not, and in all symptoms, general, musculoskeletal, eye and mental, the mean score for subjective symptoms was higher in the addicted group than in the non-addicted group. The score for VDT subjective symptoms was highest in the addicted group for girls and students who were not healthy. The most frequent physical symptom reported by students who visited the school health room for a health problem after using the computer was headache. The most frequent type of treatment at the school health room was treatment of the symptom. CONCLUSIONS: This study suggests that students must acquire correct habits in computer use and be careful not to be addicted to the computer in order to avoid VDT syndrome. For this, educational authorities should develop computer-related health education programs and start the programs from the lower grades of elementary school.
Adolescent* ; Female ; Headache ; Health Education ; Humans ; School Health Services ; Child Health

No abstract available.
Interleukin-2* ; Shock* ; Stress, Psychological*

Antigen-specific T cell activation requires interaction of the T cell with specialized antigen-presenting cells. Signaling through the TCR is necessary but not sufficient to induce antigen-specific T cell activation and cytokine secretion. This first signal, termed signal 1, is both antigen-specific and MHC-restricted. Signal 2, which is neither antigen-specific nor MHC-restricted, is necessary to induce cytokine secretion, cellular proliferation, and effector function. Recently immunological studies in T cell activation area are mainly focused on biological and molecular biological characterization of TCR/CD3 complex and accessary molecules providing costimulatory signal (signal 2). If signal 2 is not delivered, T cell enter a state of long term un-responsiveness to specific antigen-termed anergy. Monoclonal antibody technique has been especially involved in recognizing novel inducible cell surface antigens on T cell activation. This study was aimed to develop monoclonal antibodies recognizing novel cytoplasmic proteins present in activated T cells. We make 6 monoclones involved in changing pattern of T cell activated cytoplasmic proteins. Using these 6 monoclonal antibodies analyze to find novel molecules involved in T cell activation associated response, apoptosis, and/or heat shock response of the T cells in early T cell activation.
Antibodies, Monoclonal* ; Antigen-Presenting Cells ; Antigens, Surface ; Apoptosis ; Cell Proliferation ; Cytoplasm* ; Heat-Shock Proteins ; Heat-Shock Response ; Humans* ; T-Lymphocytes*