Several observation suggest that the antimelanocyte autoantibodies could play a role in melanocyte destruction. Some experiments indicate that melanocyte antibodies from patients with vitiligo can kill melanocyte in vitro. In these experiments, we demonstrated that vitiligo patient's sera containing antimelanocyte antibodies can lyse cultured human melanocytes by complement activation. Melanocyte cytotoxicity was measured using the ethidium bromide/ acridine orange viability assay. Significant melanocyte cytotoxicity was seen in sera from patients with both active and inactive vitiligo(p<0.01). Melanocyte cytotoxicity measured with complement-mediated cytotoxicity decreased after systemic steroid treatment(p<0.05) ; however melanocyte cytotoxicity showed no significant change with systemic PUVA therapy.
Acridine Orange ; Antibodies ; Autoantibodies* ; Complement Activation ; Ethidium ; Humans ; Melanocytes ; PUVA Therapy ; Vitiligo*

There are substantial evidences indiacting that anesthesia and surgery produce significant suppression of immune function. It is generally recognized that immunosuppressive manifestations such as lymphopenia, granulocytosis, decreased transformation to various antigens and impaired neutrophil chemotaxis could be followed by surgical operation. anesthetic agents may also have both direct and hormone-mediated indirect effects on immune systems. Recent evidences indicate that immunosurveillance mechanisms are not only important in the management of emerging infection and malignancy, but also critical to successful elimination of microscopic residual tumor after operation. This study was done to investigate the effeets of halothane anesthesia on T-lymphocyte subpopulations in patients undergoing hysterectomy. Lymphocyte, granulocytes and T-lymphoeyte subpopulations were counted before, during and after anestesia. The results showed that the decrease in the CD4+ cells (helper/inducer T-cells) was bigger than the decrease in the CD8+ cells (suppressor/ cytotoxic T-cells). CD3+ cells (total T-cells) and CD45R+ cells were also decreased. However, these decrease turned to normal values in 5 days. The overall result of this study suggest that anesthesia with halothane may bring temporal suppressive effect on the immunologic responses.
Anesthesia* ; Anesthetics ; Chemotaxis ; Granulocytes ; Halothane* ; Humans ; Hysterectomy ; Immune System ; Lymphocyte Subsets* ; Lymphocytes* ; Lymphopenia ; Monitoring, Immunologic ; Neoplasm, Residual ; Neutrophils ; Reference Values ; T-Lymphocytes

PURPOSE: Joubert syndrome presents neonatal respiratory abnormalities and other clinical manifestations. Pathologically the patients show hypoplasia or agenesis of cerebellar vermis and other intracranial anomalies. Our purpose is to evaluate the clinical manifestations and MR findings of Joubert syndrome. MATERIALS AND METHODS: Among the patients presenting with clinical stigmata of Joubert syndrome and agenesis of vermis on MR imaging, eight patients who did not satisfied the criteria of Dandy-Walker malformation, tectocerebellar dysraphia and rhombencephalosynapsis were selected. MR findings and clinical manifestation were analyzed. RESULTS: On MR imaging, agenesis of the cerebellar vermis (all cases), hypoplasia of the cerebellar peduncle (6cases), fourth ventricular contour deformity(6cases), tentorial elevation (4cases), deformity of the lateral ventricles (4cases), dysgenesis of the straight sinus (3cases) were demonstrated. Other findings were abnormalities of corpus callosum (3cases), falx anomalies (3 cases), occipital encephalomeningocele (2 cases) and fluid collection in posterior cranial fossa (2cases). Clinical manifestations were developmental delay (5cases), abnormal eyeball movement (3cases), hypotonia (2 cases), neonatal rerspiratoy abnormality (2cases), etc. CONCLUSION: Joubert syndrome showed various clinical manifestations and intracranial anomalies. MR imaging is an useful modality in detection of the cerebellar vermian agenesis and other anomalies of the patients.
Christianity ; Congenital Abnormalities ; Corpus Callosum ; Cranial Fossa, Posterior ; Dandy-Walker Syndrome ; Humans ; Lateral Ventricles ; Magnetic Resonance Imaging* ; Muscle Hypotonia

Sunlight is one of the well-established factors which play key roles in the induction and exacerbation of lupus erythematosus. In two patients of discoid lupus erythematosus, we have experimentally reproduced skin lesions by provocative phototesting. Both UVA (100 joules/cm²) and UVB (80 millijoules/cm²) radiation induced the skin lesions. The reproduced skin lesions were clinically and histopathologically consistent with lupus erythematosus.
Humans ; Lupus Erythematosus, Discoid ; Reproduction* ; Skin ; Sunlight

To estimate the child and infant mortality rates among Korean children, a mortality survey was carried out in the province of Kyongsangnam,buk-do. The study population are the beneficiaries of Korea Medical Insurance Coorporation (KMIC), Kyongsangnam,buk-do area, among which the 3,867 and 1767 deaths occurred from January, 1989 to December, 1990 in Kyongsangnam-do area and from January, 1991 to December, 1991 in Kyongsangbuk-do area respectively. We reviewed the data to confirm the causes of death. These were based on the death certificates and medical utilization records before dying which were available through the computerized databases on medical care utility of KMIC. The survey conducted along three steps. At first, the death certificates were examined, as a second step, medical utilization records were reviewed, and finally direct contacts to the family members of the deceased were done. As a result, 115 deaths were found under 20 years of age. Using them, age specific mortalities and causes of death were estimated. Mortality rate in this area was estimated 129 per 100,000 person-years during 1 month to 11 months of age, 67 during 1 year to 4 years of age, 23 during 5 years to 9 years of age, 10 during 10 years to 14 years of age, and 29 during 15 years to 19 years of age, respectively. And the frequent causes of death were congenital anomalies, central nervous system (CNS) diseases, certain condition originating from perinatal period during 1 months of age; accidents, congenital anomalies, malignancies, CNS diseases, and pneumonia or bronchiolitis during 1 to 4 years of age; accidents, malignancies, CNS diseases, and congenital anomalies during 5 to 14 years of age; and accidents, suicide, malignancies, and CNS diseases during 15 to 19 years of age.
Bronchiolitis ; Cause of Death ; Central Nervous System ; Central Nervous System Diseases ; Child ; Child Mortality* ; Child* ; Death Certificates ; Gyeongsangbuk-do ; Gyeongsangnam-do ; Humans ; Infant ; Infant Mortality ; Insurance ; Korea ; Mortality ; Pneumonia ; Suicide

PURPOSE: The purpose of this study was to evaluate the spectrum of MR characteristics of cystic acoustic neurinomas and to correlate with pathologic findings. MATERIALS AND METHODS: We retrospectively reviewed the MR findings of 12 patients with cystic acoustic neurinomas. The signal intensity and enhancement pattern of the cystic components as well as the location relative to the tumors were analyzed. RESULTS: A total of 30 cysts were found in 15 acoustic neurinomas;28 were intratumoral cysts and the remaining two were extratumoral cysts. The signal intensity of all 28 intratumoral cysts was higher than that of CSF on Tl-weighted images, and isointense to CSF on T2-weighted images, while the signal intensity of the two extratumoral cysts was same as CSF on both Tl-weighted and T2-weighted images. Rim enhancement was seen in 27 of 28 intratumoral cysts but in none of the two extratumoral cysts. CONCLUSION: We concluded that intratumoral cyst was due to tumoral necrosis, hemorrhage or degenerative change and extratumoral cyst due to secondary arachnoid cyst formation.
Acoustics* ; Arachnoid ; Hemorrhage ; Humans ; Necrosis ; Neuroma, Acoustic* ; Retrospective Studies

No abstract available.
Female ; Magnesium Sulfate* ; Magnesium* ; Obstetric Labor, Premature* ; Pregnancy ; Ritodrine*

BACKGROUND: The clinical behavior of vitiligo has not been clearly understood and hypothesis concerning the pathogenesis of the disease has been confusing and contradictory though autoimmune mechanisms have been considered important by many authors. OBJECTIVE: The purpose of this study was to develop a better understanding of the clinical features and pathogenesis of vitiligo. METHODS: We investigated clinical features of vitiligo in 1315 patients, and also compared the clinical course and features of non-segmental type(type A) and segmental type(type B) vitiligo patients to see whether the two types of vitiligo have a different pathogenic mechanism. RESULTS: Previously reported clinical patterns of the disease were reviewed and compared with our data, and the different clinical findings between the two types which supported the hypothesis of Koga et al. that type A and type B vitiligo had a different pathogenesis and autoimmune mechanisms played a role only in type A were shown. CONCLUSION: We investigated the clinical characteristics of vitiligo in Korea and showed that the type A vitiligo might have a different pathogenic mechanism with type B.
Clinical Study* ; Humans ; Korea ; Vitiligo*

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es 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 t,he 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* ; 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 treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es 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 t,he 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* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*