No abstract available.
Dwarfism*

No abstract available.
Beckwith-Wiedemann Syndrome*

No abstract available.
Gastroenteritis* ; Humans* ; Rotavirus*

The HUMACTBP2 locus was investigated to collect population genetic data in the Korean population and to evaluate the applicability for the forensic field. An Automatic fluorescent-based sequencer (377 automatic DNA sequencer, ABI) was used to detect amplified fragments of the HUMACTBP2 locus electrophoresed on 4% denaturing polyacrylamide sequencing gels. ACTBP2 allelic ladder consisting of different sizes of 18 alleles was constructed and employed as an internal size standard in combination with a GS-350 size standard for precision of allele-band sizing. By utilizing different fluorescent dyes, both the allelic ladders and samples were able to be analyzed in the same lane by 99% orecision of allele-band sizing. Among the Korean population (n=224), 26 alleles in the range of 239-313 bp are determined. allele No. 6 is found 45 times (0.100) which is mostly frequent, and the rest of allele is distributed with their relative frequency of 0.002-0.100. The comparison between observed and expected numbers of homozygous and heterozygous individuals confirms that ACTBP2 locus is in the state of Hardy-Weinberg equilibrium among the Korean population. The heterozygosity is 0.9389+/-0.0034(93.89%), and the power of discrimination(PD) and power of exclusion(PEX) are calculated to be 0.991(99.1%)and 0.890(89.0%), respectively, showing the high informativeness for individual identification. Thus, these results mean that the HUMACTBP2 locus can effectively be used for the forensic application.
Alleles ; DNA ; Fluorescent Dyes ; Gels ; Genetic Variation*

No abstract available.
Membranes* ; Pregnancy* ; Rupture*

A Case of Goldenhar's Syndrome. The authors experienced a case of Goldenhar's syndrome which is characterized by epibulbar dermoid, preauricular appendage and pretragal blind fistula. The patient was a 7-month old korean boy who had epibulbar dermoid, preauricular appendages, and hemifacial microsomia. We reviewed the available literatures regarding this syndrome.
Dermoid Cyst ; Fistula ; Goldenhar Syndrome ; Humans ; Infant ; Male

No abstract available.
Animals ; Horns* ; Kidney*

During the 6 year period, frorn May 1, 1989 to August 31, 1995, 40 cases of endometrial carcinoma were encountered at College of Medicine, University of Ulsan, Asan Medical Center. The purpose of this study is to investigate the patient's clinical characteristics and to correlate these findings with the there histopathologic results. The results were as follows : 1. There was an increasing tendency of endometrial carcinoma during 3-year time interval between May 1, 1989 and August 31, 1995. 2. Age distribution of the patients with endometrial cancer showed; 10% for the 31s ages<40, 27.5% for the 41.
Age Distribution ; Chungcheongnam-do ; Endometrial Neoplasms* ; Female ; Humans ; Ulsan

OBJECTIVES: To investigate the role of ATP-sensitive potassium channel (KATP) during sustained ventricular fibrillation (VF), the effects of gliburide, a specific blocker of KATP channel and PCO400, an KATP opener, were studied in isolated and perfused swine right ventricular free walls (n=). METHODS: Recording of single cell transmembrane potentials was performed and constructed action potential duration restitution (APDR) curve by plotting APD 90%(APD90) versus preceding diastolic interval (DI). RESULTS: All isolated tissues fibrillated spontaneously. In this preparation, stable VF could persist over a 4-hour period if it was allowed to continue undisturbed (n=). Gliburide (1-5 uM) increased DI without significant changes in APD90 during VF, resulting in more regularization of VF. Higher concentration (10-20 uM) increased both APD90 and DI, and converted to monomorphic ventricular tachycardia (MVT) through the transitional period characterized by APD alternans. PCO400 (1-2.5 uM) caused a significant shortening of APD during MVT and a period of APD alternans became more evident before conversion from MVT to VF. Gliburide eliminated profibrillatory effect of PCO400. This antifibrillatory action of gliburide was accompanied by gradual decrease in the maximum slope of APDR curve during VF. CONCLUSION: KATP channel blockade causes a transition from VF to MVT via lengthening of DI and APD alternans, concomitantly with a reduction of the slope of APD restitution curve.
Action Potentials ; Membrane Potentials ; Potassium Channels ; Swine ; Tachycardia, Ventricular ; Ventricular Fibrillation*

Vorinostat (VOR) has been reported to enhance the cytotoxic effects of doxorubicin (DOX) with fewer side effects because of the lower DOX dosage in breast cancer cells. In this study, we investigated the novel mechanism underlying the synergistic cytotoxic effects of VOR and DOX co-treatment in cervical cancer cells HeLa, CaSki and SiHa cells. Co-treatment with VOR and DOX at marginal doses led to the induction of apoptosis through caspase-3 activation, poly (ADP-ribose) polymerase cleavage and DNA micronuclei. Notably, the synergistic growth inhibition induced by the co-treatment was attributed to the upregulation of the pro-apoptotic protein Bad, as the silencing of Bad expression using small interfering RNA (siRNA) abolished the phenomenon. As siRNA against p53 did not result in an increase in acetylated p53 and the consequent upregulation of Bad, the observed Bad upregulation was mediated by acetylated p53. Moreover, a chromatin immunoprecipitation analysis showed that the co-treatment of HeLa cells with VOR and DOX increased the recruitment of acetylated p53 to the bad promoter, with consequent bad transactivation. Conversely, C33A cervical cancer cells containing mutant p53 co-treated with VOR and DOX did not exhibit Bad upregulation, acetylated p53 induction or consequent synergistic growth inhibition. Together, the synergistic growth inhibition of cervical cancer cell lines induced by co-treatment with VOR and DOX can be attributed to the upregulation of Bad, which is induced by acetylated p53. These results show for the first time that the acetylation of p53, rather than histones, is a mechanism for the synergistic growth inhibition induced by VOR and DOX co-treatments.
Acetylation ; Antineoplastic Agents/*pharmacology ; Apoptosis/drug effects ; Cell Survival/drug effects ; Chromatin/metabolism ; Doxorubicin/*pharmacology ; Drug Synergism ; Female ; HeLa Cells ; Humans ; Hydroxamic Acids/*pharmacology ; Transcriptional Activation ; Tumor Suppressor Protein p53/genetics/*metabolism ; Uterine Cervical Neoplasms/metabolism ; bcl-Associated Death Protein/genetics/*metabolism