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*

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*

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

No Abstract Available.

Normal C3H/HeN strain mice exposed to low-dose ultraviolet radiation(4 * 400 J/m) demonstrated a reduction in contact sensitization potential which locaiized to the skin area of direct UVR exposure(local suppression), where high-dose exposure of UVR(1*30.000 J/m) caused systemic suppression of CH induction, regardless of the application site of 2,4-dinitro-l-fluorobenzene(DNFB). There seemed to be two different mechanisms that are responsible for CH reaction induced by UVR. One of them, local suppression of low-dose UVR resulted from blocking the afferent phase of immune response by the functiona] inactivation of the epidermal Langerhans cells ; it was associated with lack of CH effector cells in the peripheral lymph nodes, an enhanced splenic suppressor cell acitvity, and could not be reversed by indomethacin treatment. The other, systemic suppression of high-dose UVR was mediated by enhancement of prostaglandin E(PGE); it was associated with prevention of the egress of effector cells within the regional lymph node which was caused by blocking the efferent lymphatics, and elevated plasma level of PGE. And depressed CH response was reversed when treated by indomethacin.
Animals ; Dermatitis, Contact* ; Indomethacin ; Langerhans Cells ; Lymph Nodes ; Mice* ; Plasma ; Prostaglandins E ; Skin

No abstract available.
Lymphocytes* ; Macrophages* ; Nitric Oxide*

No abstract available.
Deoxyglucose* ; Shock*