Adult wounds heal with scar formation, whereas fetal wounds heal without scarring and with a lesser inflammatory and cytokine response. Recently connective tissue growth factor (CTGF) is known to play an important role in wound healing. We reasoned that a strategy employing antisense oligodeoxynucleotides (ODN) complementary to CTGF mRNA by topical application of the ODN on the skin wound. Phosphorothioation of ODN to retard their degradation. When antisense CTGF ODN were applied on the wound site, there was a marked reduction of scarring compared with a control wound site. This effect of antisense CTGF ODN on scar forrnation was associated with decreased expression of the CTGF gene. However, sense CTGF ODN had no effect on the expression of the CTGF gene. In addition, control wounds healed with excessive fibrosis compared with the antisense-treated wounds. In conclusion, our results indicate that antisense CTGF ODN could be used for ameliorating scar formation during wound healing.
Adult* ; Cicatrix* ; Connective Tissue Growth Factor* ; Connective Tissue* ; Fibrosis ; Humans ; Oligodeoxyribonucleotides ; RNA, Messenger ; Skin ; Wound Healing ; Wounds and Injuries*

No Abstract Available.

No abstract available.
GRB2 Adaptor Protein*

No abstract available.
Cytokines* ; Macrophages*

Normal C3WHeN strain mice exposed to topical 8inethoxypsomlen plus long wave ultraviolet (PUVA) showed a reduction in contact hypersensitivity, (CH) which was localized to the skin in the area of PUVA treatment (local suppression), whereas systemic PUVA treatment caused diffuse suppression of CH reaction, regardless of the application site of 2,4-dinitro-1-fluorobenzene (DNFB). There seem to be two different mechanisms responsible for CH reduction by PUVA. Local suppression by topical PUVA treatment was thought to be a result of blocking the afferent phase of immune response, it was associated with a lack of CH effector cells in the peripheral lymph nodes and could not be reversed by indomethacin treatment. Diffuse suppression induced by systemic PUVA treatment seemed to be associated with blocking of egress of effector cells from the regional lymph nodes, this depressed CH response was prevented when indomethacin was administered before PUVA treatment.
Animals ; Dermatitis, Contact* ; Indomethacin ; Lymph Nodes ; Mice ; Skin

The immunocompetence is important not only to kill the neoplastic cells but also to keep the neoplastic cells from growing further. T lymphocyte is plays the most important role in maintaining the tumor immunity efficiently. T lymphocyte has its specific functions depending in the subset of T lymphocytes. The author analyzed the T lymphocyte subsets in 31 brain tumor patients using anti-CD3, anti-CD4, anti-CD8 monoclonal antibodies and flow cytometry to determine the immunological status of brain tumor patients. All CD3, CD4 and CD8 subsets were reduced in both benign and malignant brain tumor patients but more signigicantly reduced in malignant tumor group. But in benign tumor group, the subtypes of T lymphocytes were not so different from those of normal healthy controls except the pituitary tumor patients, who showed the significant decrease in all the subtypes. In malignant tumor group, each subtype was signigicantly reduced and CD8 subtypes was markedly reduced in metastatic tumor patients, These analyses were considered to have the possibility to be contributable to planning the further immunotherapy and also the possibility to moniter the brain tumor patients clinically.
Antibodies, Monoclonal ; Brain Neoplasms* ; Brain* ; Flow Cytometry ; Humans ; Immunocompetence ; Immunotherapy ; Lymphocytes ; Pituitary Neoplasms ; T-Lymphocyte Subsets* ; T-Lymphocytes*

No abstract available.
T-Lymphocytes* ; Transplantation*

We investigated the acute effect of recombinant human growth hormone (rhGH) on the activity of polymorphoneuclear leukocyte (PMN). We selected 6 patients of growth hormone deficient and 5 normal control children. In both groups, 0.15 IU/kg of rhGH was administered subcutaneously. The plasma growth hormone level were measured by radioimmunoassay on 0, 2, and 6 hours after administration of rhGH. To determined PMN activity, peripheral blood PMN were separated by discontinuous density-gradient centrifigation. Isolated PMN were stimulated hy fMLP and PMA and then respiratory burst activity of PMN was determined. The average growth hormone level of growth horrnone deficient and normal group were increased to the level of 41.6+/-23.7 and 96.3+/-46.5 ng/ml respectively, 2 hours after rhGH injection and decreased to the level of 18.5+/-10.6 and 42.2+/-5.5 ng/ml respectively, 6 hours after rhGH injection. Superoxide (O ) production by PMN which was stimulated by PMA was increased from 9.98+/-5.18 to 38.67+/-19.19 (x 10'cpm) after 6 hours of rhGH injection in control group children. It seemed that administration of the rhGH do not made a any effects acutely on PMN activity in growth hormone deficient group. But in a normal control children, extemal administration of rhGH acutely increased activity of PMN.
Child* ; Growth Hormone ; Human Growth Hormone* ; Humans* ; Leukocytes ; Neutrophils* ; Plasma ; Radioimmunoassay ; Respiratory Burst ; Superoxides

It is well established that mast cell proliferation and maturation are regulated by two principle cytokines, IL-3 and the c-kit ligand stem cell factor (SCF). Previous reports have demonstrated that bone marrow-derived IL-3-dependent mast cells exhibit the characteristic apoptosis on removal of IL-3. To know how the number of mast cells is controlled, we observed the effects of nitric oxide (NO) on the murine bone marrow-derived cultured mast cells (BMCMC). Apoptosis was measured by the analysis of flow cytometric data and electrophoretic evidence of DNA fragmentation. Our data showed that sodiurn nitroprusside (SNP)-a NO releasing substance- induced apoptosis in BMCMC. Cell cycle analysis showed that the number of the G,/G, and S phase decreased markedly, while the percentage of cell in G,/M phase was increased. Also, SNP alone induced cell death, whereas SNP in combination with SCF markedly decreased cell death of BMCMC. SNP-induced apoptosis was partially inhibited by the treatment of BMCMC with SCF. Our results suggest that NO might have sorne role in the regulation of the number of mast cells.
Apoptosis ; Bone Marrow* ; Cell Cycle ; Cell Death ; Cytokines ; DNA Fragmentation ; Interleukin-3 ; Mast Cells* ; Nitric Oxide* ; Nitroprusside ; S Phase ; Stem Cell Factor

Nitric oxide (NO) has been emerged as an important intracellular and intercellular regulatory molecule having functions as diverse vasodilatation, neural communication, and host defense. In the immune system, NO produced by activated macrophage or neutrophil is known to kill tumor cells as a defense molecule. In addition, recent reports demonstrated that NO could interact with superoxide to generate peroxynitrite (ONOO-), an anion and a potent oxidant, in macrophages or other cellular systems. The production of peroxynitrite has been recognized to be associated with the activation and expression of inducible NO synthase (iNOS). In this study, to evaluate the role of NO and peroxynitrite in murine bladder tumor cells, the author investigate the effect of NO and peroxynitrite on the viability, cytotoxicity, and DNA fragmentation of MBT-2 cells. The results are as followings: 1. Activated macrophages treated with INF-r, LPS, or INF-r+ LPS showed increment of nitrite (NO2) production and cytotoxicity against MBT-2 cells in a dose dependent manner. However, treatment with NGMMA, a NOS inhibitor, decreased NO2- production and cytotoxicity. 2. Treatment with SNP, a nitric oxide donor, increased NO2 production and DNA fragmentation (%), but decreased viability (%) of MBT-2 cells in a concentration dependent manner. 3. Treatment with peroxynitrite increased cytotoxicity and DNA fragmentation, but decreased viability of MBT-2 cells in a concentration dependent manner. 4. NO- and peroxynitrite-mediated increment of cytotoxicity in MBT-2 cells was corresponded to the programmed cell death, apoptosis. Taken together, these data indicate that NO and peroxynitrite elaborated from macrophages or other cellular systems may increase the cytotoxicity of MBT-2 cells via the mechanism of apoptosis.
Apoptosis* ; Cell Death ; Cell Line* ; DNA Fragmentation ; Humans ; Immune System ; Macrophages ; Neutrophils ; Nitric Oxide Synthase ; Nitric Oxide* ; Peroxynitrous Acid* ; Superoxides ; Tissue Donors ; Urinary Bladder Neoplasms ; Urinary Bladder* ; Vasodilation