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.
Adult* ; Humans ; Risk Factors*

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

No abstract available.
Caroli Disease*

The exact composition of urinary stone is clinically important. Reliable analytical information is fundamental for a study of the etiology of calculus formation and absolutely necessary for planning medical regimens. Infrared absorption utilizing potassium bromide pressed-disk preparations is a newer approach to the analysis of inorganic and organic calculi The speed and accuracy combined with the convenience of infrared spectrometer strongly recommend their application in the clinical laboratory. We have analyzed 121 urinary calculi of Korean people by infrared spectrometer. The following results were obtained: 1. Mixed calculus (66.9%) is much more than single calculus(33.1%), The most common type of calculi is calcium oxalate-dibasic calcium phosphate (37.2%). The most common type of components is calcium oxalate (53.2%) 2. Component of the most common calculus is calcium oxalate-dibasic calcium phosphate in the kidney (44.4%), ureter (37.3%) and bladder(33.3%). 3. Of 6 staghorn calculi, there are 2 calcium oxalate calculi, 2 calcium oxalate-dibasic calcium phosphate, 1 magnesium ammonium phosphate and I magnesium phosphate-calcium carbonate. 4. Only 3 cases of 10 laminated calculi contained the different component in nucleus and outermost layer. 5. Above the age of 20, calcium oxalate-dibasic calcium phosphate calculi is most common, and under the age of 20` all are the calcium oxalate calculi. 6. Calcium oxalate calculus is the most common over a pH range from 5.5 to 5.9 and calculus having other components is most common over a pH range from 6.5 to 6.9. 7. Percentage of urinary infection is 36.4% in the calcium oxalate and more than 80% in the calculi having other components.
Absorption ; Ammonium Compounds ; Calcium ; Calcium Oxalate ; Calculi ; Carbon ; Hydrogen-Ion Concentration ; Kidney ; Magnesium ; Potassium ; Spectrum Analysis* ; Ureter ; Urinary Calculi* ; Urolithiasis

No abstract available.
Humans* ; Retroviridae*

No abstract available.
Aneurysm* ; Angiography* ; Circle of Willis*

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: Conventional echocardiography provides fundamental information about mitral valve morphology and function but is often subjective and has a relatively low specificity in evaluating valve calcific deposit, which is critical information for the preoperative decision. We hypothesized that mitral valvular calcification could be detected in standard two-dimensional echocardiograms of mitral valve in vivo by evaluating regional gray level(echo amplitude) using computerized image analysis so that we could overcome the subjectivity and low specificity of conventional echocardiography. METHODS: We tested this hypothesis by performing standard 2.5MHz two-dimensional echoes on mitral valve and myocardium in 30 patients with mitral stenosis, scheduled to undergo mitral valve replacement. We compared gray level of each region of interest in mitral valve and myocardium in stop-frame images with the degree of calcifications identified by pathologic and radiographic examinations. RESULTS: Ratio of mean gray level of mitral valve to mean gray level of myocardium was the most reliable value in evaluating degree of calcification. Quantitatively, region of calcification displayed the ratio of significantly higher value than that of no calcification. In case of anterior mitral valve, the ratio of the evident calcified region was greater than 3.11, that of the region without calcification was less than 2.42 and that of microcalcification was betwwn 2.42 and 3.11. For posterior mitral valve, the ratio of the evident calcified region was greater than 3.50, that of the region without calcification was less than 2.19 and that of microcalcification was between 2.19 and 3.50. The sensitivity and specificity of this method for assessment of degree of calcification was 75% and 100% for anterior mitral valve and 9% and 87.5% for posterior mitral valve. CONCLUSION: Mitral valvular calcification could be detected quantitatively in standard two dimensional echocardiograms of mitral valve in vivo by evaluating regional gray level(echo amplitude) using computerized image analysis.
Echocardiography ; Humans ; Mitral Valve ; Mitral Valve Stenosis* ; Myocardium ; Sensitivity and Specificity