No abstract available.
Colon* ; Colonic Neoplasms* ; Humans ; Sparganosis* ; Ultrasonography*

No abstract available.
Nevus*

We report a false positive case of I-131 scan due to a sialolithiasis in right submandibular gland. I-131 images showed not only remnant thyroid tissues and functional metastases in the anterior neck but also a hot uptake near right submandibular gland. We confirmed the sialolithiasis by radiologic studies. Sialolithiasis should be regarded as a false positive cause when I-131 scan shows a hot spot near salivary bed.
Neck ; Neoplasm Metastasis ; Salivary Gland Calculi* ; Submandibular Gland ; Thyroid Gland* ; Thyroid Neoplasms*

In general, the long head of the biceps brachii originates from the superior glenoid labrum and the supraglenoid tubercle, crosses the rotator cuff interval, and extends into the bicipital groove. However, rare anatomic variations of the origins of the long head have been reported in the past. In this report, we review the clinical history, radiologic findings, and arthroscopic identifications of 3 anatomic variants of the biceps tendon long head. As the detection of long head of biceps tendon pathology during preoperative radiologic assessment can be difficult without prior knowledge, surgeons should be aware of such possible anatomic variations.
Anatomic Variation ; Head* ; Pathology ; Rotator Cuff ; Shoulder ; Tendons

Myocardial scintigraphy is a widely used noninvasive procedure with high sensitivity for the detection of patients with suspected coronary artery disease. The purpose of this study was to determine the prognostic value of a normal myocardial scintigraphy in 292 patients (150 males, 142 females, mean age 53+/-12 years) with chest pain who were followed from 7 to 58 (mean 25) months. Myocardial SPECT was performed with Tc-99m MIBI in 173 patients, with Tc-99m tetrofosmin in 74 patients and with T1-201 in 45 patients. During the follow-up period, there were 2 cardiac deaths and 2 nonfatal myocardial infarctions resulting in cardiac event rate of 1.37% (0.66% per year). The cardiac event rate was not different in patients with angiographically normal coronary arteries (1/30, 3.3%) and in those who had significant coronary a disease (2/27, 7.4%) (p=0.60). In conclusion, patients with chest pain and normal myocardial scintigraphy have a low cardiac event rate, and there was no significant difference of cardiac event rates between patients with normal and abnormal coronary angiograms.
Chest Pain* ; Coronary Artery Disease ; Coronary Vessels ; Death ; Female ; Follow-Up Studies ; Humans ; Male ; Myocardial Infarction ; Myocardial Perfusion Imaging ; Perfusion Imaging* ; Perfusion* ; Prognosis ; Thorax* ; Tomography, Emission-Computed, Single-Photon

It has been shown that both rest and stress myocardial perfusion imagings with technetium agents can be performed on the same day using two different doses injected within few hours. The purpose of this study was to compare the two protocols (stress-rest and rest-stress) in detecting coronary artery diseases. One hundred and sixty patients (101 males, 59 females, mean age 57+/-9 years) and 120 patients (79 males, 41 females, mean age 59+/-10 years) underwent stress-rest myocardial perfusion SPECT and rest-stress myocardial perfusion SPECT, respectively All of them underwent both myocardial perfusion SPECT and coronary angiography within 1 month. A coronary stenosis was considered significant when it compromised the luminal diameter by> or =50%. The chi square test was used to compare differences in sensitivity, specificity and accuracy between the two groups. The overall sensitivity, specificity and accuracy of stress-rest protocol were 99%, 35%and 68%, respectively. Those of rest-stress protocol were 96%, 47%, and 78%, respectively. There was no difference between the two protocols in identifying individual diseased coronary artery branches. Therefore, one day stress-rest and rest-stress myocardial SPECT using Tc-99m agents were comparable and were very sensitive tests in detecting coronary artery diseases.
Coronary Angiography ; Coronary Artery Disease* ; Coronary Stenosis ; Coronary Vessels* ; Female ; Humans ; Male ; Perfusion Imaging ; Perfusion* ; Phenobarbital ; Sensitivity and Specificity ; Technetium ; Tomography, Emission-Computed, Single-Photon

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

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*

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*