1.The effects of insulin-like growth factors on the proliferation of endometrial stromal cells from patients with and without endometriosis.
Myung Hee KIM ; Gue Wha LEE ; Yong Hee LEE ; Jung Gu KIM
Korean Journal of Obstetrics and Gynecology 2000;43(2):286-294
OBJECTIVES: To test the hypothesis that the endometrial stromal cells from patients with endometriosis responds differently to the insulin-like growth factor (IGF) compared with those from patients without endometriosis. METHODS: IGFs in peritoneal fluid (PF) from patients with endometriosis(n=18) and without endometriosis(n=12;control patients) were measured by radioimmunoassay. Endometrial stromal cells from patients with endometriosis and control patients were cultured in serum free media(SFM) in the presence or absence of PF or IGF-I(0.25-25 ng/ml) or IGF-II(5-50 ng/ml) and the proliferation of endometrial stromal cells were evaluated by [3H] thymidine incorporation test. All statistics were performed by ANOVA test and student's t-test. RESULTS: When added to SFM, IGF-I(1-25 ng/ml) increased thymidine incorporation in both endometrial stromal cells from patients with endometriosis and control patients in dose dependent manner and IGF-II(5-25 ng/ml) gave similar response in latter cells but not in former cells. Within low IGF-I(less than 100 ng/ml) PF group or high IGF-I(more than 100ng/ml) PF group, the type of endometrial stromal cells did not result in any difference in thymidine incorporation. However, regardless of the source of stromal cells, high IGF-I PF group produced a greater extent of thymidine incorporation than low IGF-I PF group in patients with endometriosis but not in control patients. Also, thymidine incorporation was higher in high IGF-I PF group of former patients than in the same group of latter patients. PF induced higher thymidine incorporation in endometrial stromal cells than the same levels(0.25-2.5 ng/ml) of IGF-I directly added to SFM. CONCLUSIONS: The effects of IGF-I in PF on endometrial stromal cells are similar regardless of their source and IGF-I is one of several growth factors that may participate in the growth of endometrial stromal cells in pelvic endometriosis.
Ascitic Fluid
;
DNA
;
Endometriosis*
;
Female
;
Humans
;
Insulin-Like Growth Factor I
;
Intercellular Signaling Peptides and Proteins
;
Radioimmunoassay
;
Somatomedins*
;
Stromal Cells*
;
Thymidine
2.Prognostic factors influencing the recurrence of thyroid cancer.
Jung Hyun YANG ; Seo Gue YOON ; Bong Wha LEE ; Ze Hong WOO
Journal of the Korean Surgical Society 1993;45(3):324-334
No abstract available.
Recurrence*
;
Thyroid Gland*
;
Thyroid Neoplasms*
3.Follicle stimulating hormone receptor gene mutation in Korean women with premature ovarian failure and normal karyotype.
Young Min CHOI ; Seok Hyun KIM ; Jeong Koo KIM ; Shin Yong MOON ; Jin Yong LEE ; Gue Wha LEE
Korean Journal of Obstetrics and Gynecology 2000;43(5):836-841
OBJECTIVE: To determine whether the follicle stimulating hormone(FSH) receptor gene mutation (C566T point mutation) is present in Korean women with premature ovarian failure and normal karyotype. METHODS: Genomic deoxyribonucleic acid(DNA) obtained from 40 patients with chromosomally competent premature ovarian failure and from 30 normal fertile women(control group) was amplified by polymerase chain reaction(PCR). PCR products were digested by the enzyme BsmI and polyacrylamide gel(PAG) elctrophoretic patterns of these enzyme-digested products were analyzed. The direct sequencing of PCR products was also performed. RESULTS: All patients with premature ovarian failure and 30 normal control women demonstrated homozygous, normal alleles with 51- and 27- base pairs fragments in PAG elctrophoresis. The absence of C566T point mutation in both group was confirmed by direct DNA sequencing. CONCLUSIONS: A C566T mutation in FSH receptor gene is rare in Korean women with premature ovarian failure and normal karyotype.
Alleles
;
Base Pairing
;
Female
;
Follicle Stimulating Hormone*
;
Humans
;
Karyotype*
;
Point Mutation
;
Polymerase Chain Reaction
;
Primary Ovarian Insufficiency*
;
Receptors, FSH*
;
Sequence Analysis, DNA