A case of bilateral absence of vas deference with sterility is reported. By new 15O cases of congenital absence of the vas deference, rather a rare congenital anomaly, were reported.
Infertility

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

Thirty one free vascularized fibula bone grafts were performed for treatment of osteonecrosis of the femoral head in 26 patients, 24 men and 2 women aged from 16 to 48(mean:32 years). Twenty one patients had unilateral disease. Five patients had bilateral disease underwent staged bilateral free vascularized fibula grafts three months apart. Associated etiological factors included alcohol(9 patients), steroid(7 patients), and trauma(one patient). The condition was considered idiopathic in the remaining 9 patients. Radiologic staging by Ficat included stage 1 in one hip, stage II in 15 hips, stage III in 14 hips, and stage IV in one hip. A skin island flap was used for monitoring purpose for the grafted fibula. One monitoring, flap was necrotized due to vascular occlusion but the fibula bone graft was left in place to use as a nonvascularized bone graft. Average follow-up period was 21 months in 31 hips. Pain was relieved in 28 hips(93.3 percent) and aggravated in 2 hips(6.7 per cent). On radiographic evaluation, 26 hips(86.7 per cent) demonstrated excellent preservation of the femoral head contour. Progressive collapse of the femoral head (greater than 1-2 mm) occurred in 2 hips, i mm depression in one hip with stage III and 2 mm collapse in one hip with stage IV. In conclusion, the free vascularized fibula bone graft is an excellent treatment modality for preserving the femoral head and relieving symptoms in cases of the osteonecrosis of the femoral head.
Depression ; Female ; Fibula* ; Follow-Up Studies ; Head* ; Hip ; Humans ; Male ; Osteonecrosis* ; Skin ; Transplants

No abstract available.
Congenital Hypothyroidism* ; Thyroid Dysgenesis*

No abstract available.
Endocarditis* ; Lupus Erythematosus, Systemic*

Supravalvular aortic stenosis may be defined as an obstructive congenital deformity of the ascending aorta which originates just distal to the level of the origins of the coronary arteries. It may be localized or diffuse, and includes a wide spectrum of pathologic changes. A 16 years old school boy was admitted because of exertional dyspnea for 6 years. Clinical diagnosis of supravalvular and valvular aortic stenosis with bicuspid aortic valves and myocardial hypertrophy was made by echocardiography and angiocardiography. Surgical correction was performed successfully. We presented a case of supravalvular and valvular aortic stenosis with a review of literatures.
Adolescent ; Angiocardiography ; Aorta ; Aortic Stenosis, Supravalvular ; Aortic Valve ; Aortic Valve Stenosis* ; Bicuspid ; Congenital Abnormalities ; Coronary Vessels ; Diagnosis ; Dyspnea ; Echocardiography ; Humans ; Hypertrophy ; Male

The index on myocardial contractility of pure mitral regurgitation(MR) after mitral valve replacement is believed to be useful in determining proper operation time before irreversible myocardial damage by volume overload. Thus the authors examined pre and post-operative echocardiographic results of 20 cases of pure MR patients who had been admitted to Pusan National University hospital and compared the usefulness of each index. Pre and post-operative echocardiographic results were as follows respectively ; 1) Left ventricular internal dimension in diastole(LVIDd) were 6.49+/-0.19cm and 5.51+/-0.17cm. 2) Left ventricular internal dimension in systole(LVIDs) were 4.26+/-0.12 and 3.79+/-0.18cm. 3) Ejection fraction were 71.28+/-1.57% and 59.24+/-3.05%. 4) Fractional shortening(FS) were 34.09+/-1.18% and 27.21+/-1.84%. 5) Mean Vcf were 1.53+/-0.08cm/sec and 1.18+/-0.09cm/sec. 6) Left ventricular end-diastolic volume index(EDVI) were 196.35+/-18.33cc/m2 and 98.46+/-9.96cc/m2. 7) Left ventricular end-systolic volume index(ESVI) were 55.28+/-5.12cc/m2 and 41.88+/-6.07cc/m2. 8) Left ventricular end-systolic wall stress/ESVI(ESS/ESVI) were 2.3+/-0.21 and 3.91+/-0.83. ESS/ESVI showed significantly(p<0.05) elevated postoperative change, LVIDd, LVIDs, EF, FS, EDVI, ESVI revealed significantly(p<0.05) reduced postoperative change whereas Mean Vcf had no postoperative change. After examining correlation between preoperative and postoperative results of each index, it is believed that LVIDd, LVIDs, and ESS/ESVI were useful prognostic indices but were unrelated to postoperative ejection phase indices such as EF, FS, and MEan Vcf. Especially in case of LVIDd>6cm, LVIDs>4cm, and ESS/ESVI<2, the prognosis was poor due to myocardial damage by mitral regurgitation.
Busan ; Echocardiography ; Humans ; Mitral Valve Insufficiency* ; Mitral Valve* ; Prognosis ; Stroke Volume

Profound reduction of anterograde coronary flow with concomitant ischemia is seen occasionally during percutaneous coronary intervention despite technically successful procedure. We found interesting coronary flow pattern in a patient with acute myocardial infarction, showing angiographic no reflow phenomenon after direct PTCA. The coronary blood flow pattern of the angiographic no-reflow phenomenon in this case was characterized by minimal systolic flow and sharp deceleration of diastolic flow. Coronary flow reserve calculated by the ratio of adenosine induced maximal hyperemic velocity and basal velocity was reduced. The Dopplertipped guide wire was useful for observation of phasic coronary flow pattern of angiographic no-reflow phenomenon.
Adenosine ; Deceleration ; Humans ; Ischemia ; Myocardial Infarction* ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention

Deliberately induced hypotension reduces bleeding in operative fields, therby facilitating the surgical manipulation of a highly vascularized lesion and enabling a better dissection to be made. Hypocapnia is a technique by which the regional cerebral blood flow is reduced, effecting a decrease in the intracranial volume. The monitoring of end-tidal CO2 tension(PECO2) is widely done since the amount of end-tidal CO2 tension reflects indirectly the value of the degree of arterial CO2 tension(PaCO2). During hypotension, increased physiologic dead space my produce the widened PaCO2-PECO2 gradient and this large gradient makes PECO2 an unreliable indication of PaCO2. There are many reports on hypotensive agents and techniques. Induced hypotension with halothane has been reported to be a relatively safe and useful method by Murtagh(1960) and Schettini, et al (1967). We reported 100 cases of halothane induce hypotensive anesthesia for intracranial aneurysm surgery in 1979. The present study reports concerning the hypotensive anesthesia for 259 cases of intracranial aneurysm surgery, which were performed at Severance Hospital of the Yonsei University College of Medicine from 1972 to 1985. We evaluated prospectively the PaCO2-PECO2 gradient with modern infrared capnographs during the induced hypotension of 25 cases, which was performed for intracranial aneurysm surgery at this hospital. The result of the retrospective and prostpective studies were as follows. A. Retrospective study 1) Halothane and enflurane were used as the primary anesthetics in 246 and 13 cases, respectively. Hydralasine, nitroprusside, and trimetaphan were supplementarily used for inducing hypotension in 29, 19 and 15 cases, respectively. 2) The mean arterial blood pressure of the lowest blood pressure in the induced hypotension group was 57.2+/-9.3 mmHg, and the mean arterial blood pressure of the highest blood pressures during the induction fo anesthesia was 111.3+/-20.8mmHg. 3) There was no significant difference in the perioperative hemoglobins, hematocrits, and serum electrolytes. 4) In the introperative period gas analysis revealed respiratory alkalosis(arterial CO2 tension and pH were 29.7+/-6.7mmHg and 7.485+/-0.078, respectively). In other values there was no significant change. 5) The mortality rate in 259 cases of intracranial aneurysm surgery was 6.2%. B. Prospective study There was no significant difference in the PaCO2-PECO2 gradients between in the hypotensive period (5.5+/-3.8 mmHg) and in the normotensiveperiod(4.3+/-3.4mmHg). In conclusion, the technique of using induced hypotension with the inhalation anesthetics, halothane or enflurane, is a safe and useful one to use in performing surgery for intracranial aneurysm, and end-tidal carbon dioxide tension can be used as an indirect measure of arterial carbon dioxide during the induced hypotension.
Anesthesia* ; Anesthetics ; Anesthetics, Inhalation ; Arterial Pressure ; Blood Pressure ; Carbon Dioxide ; Electrolytes ; Enflurane ; Halothane ; Hematocrit ; Hemorrhage ; Hydrogen-Ion Concentration ; Hypocapnia ; Hypotension ; Intracranial Aneurysm* ; Mortality ; Nitroprusside ; Prospective Studies ; Retrospective Studies ; Trimethaphan