No abstract available.
Chorionic Gonadotropin* ; Gonadotropin-Releasing Hormone* ; Gonadotropins* ; Humans* ; Progesterone* ; Superovulation*

No abstract available.
Fertilization in Vitro* ; Superovulation*

PURPOSE: The cause and pathogenesis of lower urinary tract symptoms (LUTS) in elderly men is unclear. We analyzed the clinical and urodynamic findings of elderly patients with LUTS to search for accurate diagnosis and effective treatments. MATERIALS AND METHODS: We performed a retrospective chart review of 154 male patients older than 65 years old with LUTS who underwent urodynamic studies between January 2002 and December 2008. The patients were divided into irritative and obstructive symptom groups according to their chief complaints. The urodynamic findings between two groups were compared. And the prevalence of detrusor dysfunction (either detrusor underactivity; DU or detrusor overactivity; DO) according to age, history of urinary retention, the presence of an indwelling urethral catheter, neurologic disease, or diabetes was estimated. RESULTS: The mean age of men was 70.8+/-4.5 years. On urodynamics, detrusor dysfunction was detected in 116 (75.4%) of 154 patients. Seventy eight (50.6%) patients showed demonstrable evidence of DU of whom 33 (21.4%) had concomitant DO, while 18 (11.7%) had concomitant bladder outlet obstruction (BOO). BOO and DO was identified in 67 (43.5%) and 71 (46.1%) patients, respectively. The prevalence of was significantly greater in the presence of history of acute urinary retention and an indwelling urethral catheter. CONCLUSION: One hundred forty one (91.6%) elderly patients with LUTS showed urodynamic abnormalities such DO, DU and BOO. Urodynamic study would play a important role in establishing a correct diagnosis in elderly patients with LUTS and deciding on additional treatments.
Aged ; Diagnosis ; Humans ; Lower Urinary Tract Symptoms* ; Male ; Multiple Endocrine Neoplasia Type 1 ; Prevalence ; Retrospective Studies ; Urinary Bladder Neck Obstruction ; Urinary Catheters ; Urinary Retention ; Urinary Tract ; Urodynamics*

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*

No abstract available.
Leiomyoma*

No abstract available.
Family Practice* ; Fatigue* ; Humans ; Pilot Projects* ; Prospective Studies*

No abstract available.

No abstract available.
Follicle Stimulating Hormone* ; Gonadotropin-Releasing Hormone* ; Humans ; Superovulation*

BACKGROUND: Macrophage migration inhibitory factor(MIF) was discovered in 1960s as a T-cell cytokine which inhibited random migration of macrophages. MIF is a multifunctional protein acting as cytokine, hormone, or enzyme. It plays a pivotal role in innate and adaptive immune responses and early phase of inflammatory response, as well as cell proliferation, differentiation, and tumor progression. Many inflammatory diseases and cancers show increased activity and serum concentration. The purpose of this study was to measure the normal serum MIF concentration of Korean people to be utilized as base data for future MIF research. METHODS: Sera of 20 healthy adults from each groups of 20's to 60's(total 100 persons) who visited the Health Promotion center of Inha university Hospital were collected. The MIF concentration in each serum was measured by enzyme-linked immunosorbent assay(ELISA). RESULTS: The average serum MIF concentration was 1.49 ng/ml(ranging from 0 to 3.33), and there was no significant difference between age groups. CONCLUSION: The normal serum MIF concentration of Korean people is 1.49 ng/ml, and seems to be unchanged with aging.
Adult ; Aging ; Cell Proliferation ; Health Promotion ; Humans ; Macrophages* ; T-Lymphocytes