No abstract available.
Adult* ; Humans ; Risk Factors*

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

No abstract available.
Burns* ; Hand* ; Humans ; Infant*

No abstract available.
Caroli Disease*

We report a case of subungual solitary glomus tumor in a 28-year-old female, who has suffered from pain and tenderness of the left 4th finger tip for about 5 years. Simple surgical excision was performed for removal of the tumor mass and for the relief of the subjective symptoms. No recurrence has been observed for 5 months following excision of the tumor.
Adult ; Female ; Fingers ; Glomus Tumor* ; Humans ; Recurrence

In order to evaluate the efficiency of serological typing of A. baumannii in practical application, a total of 63 strains of A. baumannii and 234 strains of Gram-negative, lactose non-fermenting bacteria were tested with polyclonal rabbit immunized sera (RIS) against heat-killed A. baumannii strains by slide agglutination tests. Six typing sera of RIS were finally obtained after the checkerboard agglutination test and reciprocal cross-absorption. Species identification of sixty-three strains of A. baumannii were confirmed by ribotyping. Forty-seven (74.6%) of the 63 strains of A. baumannii showed strong positive reaction by slide agglutination tests. Thirty-nine strains could be serotypable and thus classified into 6 distinct serovars of A. baumannii, but 8 strains were unable to classify into specific serovar. Serovar 4 was the most frequent arbitrary serovar and included 17 strains among the 39. When slide agglutination tests were performed with 50-fold diluted pooled polyclonal RIS, there was no cross-reactions except one of E. coli strain among 234 strains of various Gram-negative lactose non-fermenting. Although each profile of LPS-gel electrophoresis of A. baumannii appeared to be unrelated with serovar, the patterns of western-blot of LPS after immunostaining with homologous RIS showed serovar-specificity. Several fractions of low molecular weight LPS showed cross-reaction with antisera of other serovars. In conclusion, the sensitivity and specificity of serological identification of A. baumannii strains were 74.6% and 99.6%, respectively. This result suggests that serotyping is a useful method for the identification of A. baumannii strains as well as is the epidemiological tool to trace back the source of the nosocomial outbreaks.
Acinetobacter baumannii* ; Acinetobacter* ; Agglutination Tests ; Bacteria ; Disease Outbreaks ; Electrophoresis ; Immune Sera ; Lactose ; Molecular Weight ; Ribotyping ; Sensitivity and Specificity ; Serotyping

BACKGROUND: The pathogenesis of atopic dermatitis is still unknown. Many reports have suggested that the house dust mite antigen may play a role in the pathogenesis of atopic dermatitis. The IgG4 allergen-specific subclass has been considered to be involved both in allergic reactions and associated with the appropriate response to allergen-specific immunotherapy. OBJECT: The purpose of this study was to evaluate the positive rate of the allergic prick test to D. farinae and the levels of D. farinae-specific IgE and Ig64. METHODS: We performed the allergy prick test, RAST for D. farinae-specific IgE and ELISA for D. farinae-specific IgG subclasses and compared the values between atopic dermatitis patients and normal controls. RESULTS: 1. D. farinae was the most common allergen in patients with atopic dermatitis and the positive rate of the allergic prick test was 61.0%. The positive rate of the allergic prick test and the positive rate to D. farinae increased as c]inical grading increased. 2. The Positive reaction rate of D. farinae-specific IgE(RAST) in those with atopic dermatitis was 68.8% and increased as the positive reactions of the allergic prick test to D. farinae and chnical grading increased. 3. Among the IgG subclasses, only the level of D. farinae-specific IgG4 was significantly higher in atopic dermatitis than normal controls. 4. The level of D. farinae-specific IgG4 showed a tendency to decrease in accordance with the clinical severity grades. CONCLUSION: These results suggested that D. farinae might play an important role in the development of atopic dermatitis and well-designed studies should continue to be performed in order to delineate the biological significance of IgG4.
Antibodies* ; Dermatitis, Atopic* ; Enzyme-Linked Immunosorbent Assay ; Humans ; Hypersensitivity ; Immunoglobulin E* ; Immunoglobulin G* ; Immunotherapy ; Pyroglyphidae*

No abstract available.
Female ; Perinatal Mortality* ; Pregnancy ; Pregnancy, Multiple*

Predominant type of serum prostate specific antigen (PSA) is a complexed-form which is bound to alpha-1-antichymotrypsin (ACT). Major fraction of serum ACF is derived from the liver and ACT has recently been demonstrated to be produced by PSA-producing prostatic epithelium as well. However, the feature and significance of prostate-derived ACT remain ill-defined. We herein immunohistochemically studied prostatic tissues in 40 patients with prostate cancer and 20 patients with benign prostatic hyperplasia (BPH) using antibody to ACT, cytokeratin AE3 and chromogranin A. In normal portion of prostate, secretory epithelia of central zone and peripheral zone, and basa1 cells and neuroendocrine cells of peripheral zone showed positive staining for ACT. Benign hyperplastic prostatic gland did not stain for ACT. On the study of prostate cancer tissues, relatively increased staining for ACT were found in solid and infiltrative type of cancer cells and high grade cancer cells. High intensity staining for ACT were observed in normal prostatic tissues adjacent to invasive cancer cells. In conclusions, basal cells as well as secretory epithelia of the normal prostate gland may be the source of serum ACT production by prostate cancer may be closely related with its malignant and invasive potential.
Chromogranin A ; Epithelium ; Humans ; Immunohistochemistry ; Keratins ; Liver ; Neuroendocrine Cells ; Prostate* ; Prostate-Specific Antigen ; Prostatic Hyperplasia ; Prostatic Neoplasms*