No abstract available.
Mass Screening* ; Uterine Cervical Neoplasms*

Background: This study was conducted to identify the level of gender sensitivity and gender equality consciousness among dental hygiene students and to confirm the necessity of gender equality programs in the curriculum. Methods: A self-report questionnaire was conducted with some dental hygiene students using the Gender Sensitivity tool and Korean Gender Egalitarianism Scale for Adolescents (KGES-A). Results: First, the gender equality consciousness of the students who took women’s studies was high in the areas of educational life and socio-cultural life, and that of the subjects of grandparent families and Catholic was found to be high in the domestic life area. Second, the gender sensitivity of the subjects who took women’s studies was found to be high in all sub-areas. In addition, the gender sensitivity of females was higher in the areas of sexual identity, non-violence, and self-reflection than that of males. That of 4-year college students was higher in the areas of sexual identity, openness to gender roles, and non-violence than that of 3-year college students. In addition, the gender sensitivity of Catholic students was high in the areas of sexual identity and openness to gender roles. Third, gender equality consciousness was found to have an effect depending on whether subjects took women’s studies, family type, family type, and religion, and gender sensitivity was found to have an effect depending on whether subjects took women’s studies or gender. Conclusion Since dental hygienist is a profession that targets humans, education that can instill equal awareness and values of humans is important. To inspire gender sensitivity and gender equality consciousness in a prospective professional, it is necessary to conduct programs and education related to gender intelligence within dental hygiene curriculum.

No abstract available.
Gonadotropin-Releasing Hormone* ; Humans

It hae been well established that, specifi alterations in members of the ras gene family, H-ras, K-ras and N-ras, can convert them into active oncogenes. These alterations are either point mutations occurirg in either codon 12, 13 or 61, or alternatively, a 5- to 50-fold amplification of the wfld-type gene. Activated ras oncogenes have been found in a significant proportion of all turnors, but the incidence varies considerably with the tumor type : it is frequent (20~40%) in colarectal eancer and acute myeloid leukemia, but absent or preaent rarely in breast and atomach cancer. But the role of c-K-ras point mutatio in the development of cancers in the female genital tract has not been extensively studied. Polymerase chain reaction followed by gel electrophoresis was performed respectively using wild-type normal and specific point mutation primers{GGT->GAT, GGT->AGT, GGT->TGT and GGT->GTT) to detect, point, mutation of codon 12 of c-K-ras oncogene. The c-K-ras oncogene point mutation was confirmed by Southern blot hybridization using synthetic oligonucleatide probe. 3'-end Iabelled with digoxigenin -dUTP. With this method, the frequency of point mutation on codon 12 of c-K-ras oncogene was examined the tissues in 37 casea of ovarian cancer, 7 cases of endometrial cancer, 36 cases of the gestational trophoblastic tumor, 60 cases of cervical cancer. The relationship between the presence of a c-K-ras point mutation and clinicopathological characteristics of the female genital tract cancers were also analysed. The results were as follows; 1. The incidence of four point mutations on codon 12 of c-K-ras oncogene in 37 ovarian cancers was 45.9% (17/37) and distribution were 43.2% (16/37), 2.7% (1/37) and 0% (0/37) in GGT-->GAT, GGT-->AGT, GGT-->TGT, and GGT-->GTT, respectively. According to histological type, in ovarian cancers, The point mutation of K-ras oncogene waspositive in 45 % (10/22) of serous cystadenocarcinomas. The incidence of four point mutations on codon 12 among 37 patients with ovarian cancer according to histological type was 45.5 % (10/22) with serous cystadenocarcinoma, 57.1% (4/7) of mucinous cystadenocarcinoma. Comparing the positive rate of point mutations of K-ras oncogen among 37 patients with ovarian cancer with the clinical stage, point mutation was detected in 28.5% (2/7) of patients with stage I, 40.0% (2/5) with stage II, and 52.0% (13/25) with stage III/IV. There was no statistically significant increasement of point mutations with the advance of the clinical stage of ovarian cancer. Comparing the positive rate of point mutations of K-ras oncogen among 37 patients with ovarian cancer according to the histologic grade point mutation was detected in 50.0 % (2/4) 0f patients with grade I, 451.7 % (5/12) with grade II and 47.6 % (10/21) with grade III. 2. The incidence of point mutations of K-ras oncogen among 33 patients with ovarian cancer who were performed pelvic lymph node dissection was 57.1 % (12/21) of the patients with pelvic lymph node metastases and 16.7% (2/12) of the patients without pelvic lymph node metastases. There was statistically significant difference between the positive rate of c-K-ras point mutations and the pelvic lymph nodal status(P<0.05). 3. In 7 cases of endometrial cancer, positive rate of K-ras point was 42.8 % (3/7). Point mutations were also detected in 2 cases from 4 choriocarcinomas, but, the point mutation was only detected in 1 case from 60 cervical carcinomas. From these results, we may suggest that the point mutation on codon 12 c-K-ras oncogene are considered to be one of the important genetic change in the tumor formation and progression of ovarian of c-K-ras oncogene seems to be the one stop in the multistep process of tumor formation in ovarian cancer. Furthermore, the point mutation of c-k-ras gene could occur more frequently in the patients of ovarian cancer with pelvic lymph node metastases than in those without pelvic metastases, suggesting the orle in tumor progression. And we concluded that point mutation on codon 12 is comparable frequent in uterine endometrial carcinomas and have significance as an event that contributes to progrssion of endometrial cancers and choriocarcinoma, but cervical carcinoma do not appear to have c-K-ras point mutation in general. More studies will be necessary, but the detection of c-k-ras point mutation as the possibility of biological tumor marker to predict clinical outcome may be utilized in female malignancies.
Blotting, Southern ; Breast ; Choriocarcinoma ; Codon ; Cystadenocarcinoma, Mucinous ; Cystadenocarcinoma, Serous ; Digoxigenin ; Electrophoresis ; Endometrial Neoplasms ; Female* ; Genes, ras ; Humans ; Incidence ; Leukemia, Myeloid, Acute ; Lymph Node Excision ; Lymph Nodes ; Neoplasm Metastasis ; Oncogenes* ; Ovarian Neoplasms ; Point Mutation* ; Polymerase Chain Reaction ; Pregnancy ; Trophoblastic Neoplasms ; Biomarkers, Tumor ; Uterine Cervical Neoplasms

No abstract available.
Endometrial Neoplasms* ; Female

No abstract available.
Animals ; Macrophages* ; Mice*

No abstract available.
Cell Line, Tumor* ; Gonadal Steroid Hormones* ; Gonadotropin-Releasing Hormone* ; Gonads*

HLA A, B, C and DR were typed in 73 Korean patients with Tourette disorder meeting the diagnostic criteria of DSM III-R and compared with 291 normal subjects. Relatively higher frequencies were found in HLA A11 and A26(10) with lower incidences in HLA A24(9) and B13. A family history of tic disorders was associated with a lower frequency of HLA A24(9).
Adolescent ; Adult ; Child ; Child, Preschool ; Female ; HLA Antigens/*analysis ; HLA-DR Antigens/*analysis ; Human ; Male ; Tourette Syndrome/*genetics/immunology

OBJECTIVE: In an effort to develop a more effective therapeutic strategy for ovarian cancer, we examined whether the restoration of the wild-type p53 gene can enhance the therapeutic effect of chemotherapy. METHODS: In this study, Ov-ca-2774 cells, which are known to have p53 point mutation and cisplatin-resistance, were selected and currently used chemotherapeutic agents including cisplatin, carboplatin, paclitaxel, etoposide, topotecan, and doxorubicin were added concurrently or sequentially with adenovirus-mediated p53 gene transfer (Ad5CMV-p53). RESULTS: Transfer of the wild-type p53 cDNA gene into Ov-ca-2774 cells showed 55% cell killing in vitro at a multiplicity of infection (MOI) of 40. Although the combination of carboplatin or paclitaxel followed by p53 gene transfer with an interval of 48 h manifested no enhanced cell killing compared with cells infected with Ad5CMV-p53 alone, the other combinations of chemotherapeutic agents and p53 gene transfer resulted in 15% to 37% further cell killing (P<0.05). Furthermore, p53 gene transfer followed by doxorubicin with an interval of 24 h and concurrent combination of etoposide with p53 gene transfer showed significant difference in cell killing in contrast to the other combination strategies in the respective chemotherapeutic agent exposure groups (P<0.05). CONCLUSION: Our data demonstrated that combination of p53 gene transfer and chemotherapeutic agents had higher cell killing than either of these two modality alone.
Carboplatin ; Cisplatin ; DNA, Complementary ; Doxorubicin ; Drug Therapy* ; Etoposide ; Genes, p53 ; Homicide ; Humans* ; Ovarian Neoplasms* ; Paclitaxel ; Point Mutation ; Topotecan

Flow cytometry, a useful tool for measuring DNA content and cell differentiation as expressed by cell surface markers, is utilized to measure multiple antigens, especially surface antigen, intracellular oncoprotein, and DNA content, simultaneously. For this simultaneous detection, several methods off ixation and permeabilization have been used with limited values. In this study, 20 ng/ml of lysolecithin in 1% paraformaldehyde solution was utilized for fixation and permeabilization of cultured promyelocytic leukemic cells(HL 60). The cells were first stained with phycoerythrin (PE)-conjugated monoclonal antibody to the cell surface My 7 antigen and then were fixed and permeabilized with 20 ng/ml of lysolecithin in 1% partormaldehyde solution. After incubation, the fixed and permeabilized cells were stained with monoclonal antibody to intracellular c-myc antigen, which were followed by fluorescein isothiocyanate (FITC)-conjugated secondary antibody. The c-myc stained cells were finally stained for DNA content with 7-amino-actinomycin D(7-AAD). This procedure permits excellent staining for intracellular oncoproteins and preservation of surface antigens with relatively low cofficients of variation (CV) for the G0G1 peak of the DNA histograms and suggests that the sequential staining procedure of surface antigen, intracellular antigen, and DNA content will be extended for the study of correlations with cellular differentiation, expression of oncoproteins, and cell cycle analysis in the cells which are obtained from human malignant diseases using a 488 nm single laser flow cytometry.
Antigens, Surface* ; Cell Cycle ; Cell Differentiation ; DNA* ; Flow Cytometry* ; Fluorescein ; Humans ; Oncogene Proteins ; Phycoerythrin