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

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

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

No abstract available.
Child* ; Colon* ; Humans

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.
HIV* ; Humans ; Humans* ; Lymphocytes* ; Zidovudine*

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

No abstract available.
Antigen-Antibody Complex* ; Humans ; Interleukin-2* ; Ovarian Neoplasms*

PURPOSE: The purpose of this study was to develop a specialized education curriculum aimed at helping nurses prepare for running and managing a Maternal-Child Health Center (Postpartum Care Center). METHOD: This study was conducted by an academy and industry joint research group consisting of professors of Nursing, and nurses actually running a Postpartum Care Center. The group compiled job descriptions of nursing through document research, interviews and observation during site visits, surveys, and seminars. They then performed a feasibility study and developed the final curriculum. RESULT: The education curriculum is a 32-week (2semester) program compromised of a theory part (12 credits, 180 hours) covering maternal and infant care and business start-up and field practice (3 credits, 45 hours). Courses in the theory part include an antenatal care, overview and details of maternal care, starting a business and its management. Of these courses, the overview of a maternal care course was developed with web-based contents. Field practice is designed to give students opportunities to visit Postpartum Care Centers, observe the care provided, and get hands-on experience. CONCLUSION: The specialized education curriculum is a 32-week course comprised of 12 credits on theory of antenatal care, overview and details of maternal care, infant care, starting and operating a business and 3 credits of field practice.
Child ; Commerce ; Curriculum* ; Education* ; Feasibility Studies ; Humans ; Infant ; Infant Care ; Job Description ; Joints ; Maternal-Child Health Centers* ; Nursing ; Postnatal Care ; Running

Programrned cell death (PCD), or apoptosis, is a process by which cells die in response to specific physiological and toxicological signals. This genetically programmed form of cellular suicide is intirnately involved in many biological processes including growth, metamorphosis, embryogenesis, and oncogenesis. Cells undergoing PCD in normal and neoplasmic tissues display the following biochemical and morphological features: internucleosomal DNA fragmentation, reduced cell volume, condensed chromatin in nucleus, zeiosis and generation of apoptotic bodies containing intact organelles and plasma rnembrane. Hybridoma cell production, resulting from the fusion of myeloma cells with antibody producing spleen cells, is widely used in various fields of life science. This technique requires hypoxanthine guanine phosphoribosyl transferase (HGPRT) deficient mutant myeloma cell line as a fusion partner. When these mutants cell is treated with aminopterin plus hypoxanthine-thymidine (HAT) after the cell fusion they are selectively and efficiently eliminated remaining fused hybridoma celis. But there hasn't been any report regarding the selective elimination mechanism of this HGPRT mutant myeloma cell. By using HGPRT myeloma P3-X 63-Ag8.653 (V653) as a model system, this study demonstrated that PCD was induced by aminopterin treatment of this V653 cell line. And the sequential ultrastructural changes during this death process were observed by using electron microscope. When V653 cells were incubated with 0.4 uM aminopterin, DNA fragmentation was detectable after 3 hours and peaked between 12 and 18 hours of aminopterin treatment and the cell viability decreased in a time dependant manner. V653 cells incubated with amiopterin showed following ultrastructural changes during the death process. Dilatation of rough endoplasmic reticulum (RER) and detachment of ribosomes were the earliest ultrastructural changes and first seen after 30 minute incubation. Dilatation of perinuclear cisternae began to appear after 1 hour and deformation of nucleoplasm such as decreased electron density of perinuclear heterochromatin and increased electron density of euchromatin were seen after 3 hours. Increased electron density of cytoplasm, decreased cell volume, condensation of chromatin and apoptotic bodies were observed in many cells after 9 hours but vacuolation by severe dilatation of RER was seen in some cells. 24 hours after incubation with aminopterin, many cells showed typical form of apoptosis characterized by cell shrinkage, increased electron density of cytoplasm and apoptotic bodies. On the contrary, some cells showed different type of cell death characterized by increased cell volume, decreased electron density of cytoplasm, severely dilated RER and apoptotic bodies. In both types of cells, mitochondrial cristae and limiting membrane of mitochondria are comparatively well preserved. In other cells, nuclei did not show significant changes but there were deformations of mitochondria such as markedly increased electron density and formation of lamella bodies. The death process of V653 cell was not synchronized among cells. The results of this study proved that aminopterin-induced selective elimination of fusion partner V653 myeloma cell is due to PCD. The earliest ultrastructural changes observed in this process were dilatation of RER and detachment of ribosomes. And there were two distinct morphological types in the PCD.
Aminopterin* ; Animals ; Apoptosis* ; Biological Processes ; Biological Science Disciplines ; Carcinogenesis ; Cell Death ; Cell Fusion ; Cell Line ; Cell Size ; Cell Survival ; Chromatin ; Cytoplasm ; Dilatation ; DNA Fragmentation ; Embryonic Development ; Endoplasmic Reticulum, Rough ; Euchromatin ; Female ; Guanine ; Heterochromatin ; Hybridomas ; Hypoxanthine ; Hypoxanthine Phosphoribosyltransferase ; Membranes ; Mice* ; Mitochondria ; Organelles ; Plasma ; Pregnancy ; Ribosomes ; Spleen ; Suicide ; Transferases