BACKGROUND: Chronic cutaneous lupus erythematosus(CCLE) is a well-known disease entity. But there has been no data about its clinical behavior and histopathologic features in Korea. OBJECTIVES: This study was conducted to elucidate the clinical, laboratory, and histopathologic features of CCLE, and the relationship between CCLE and SLE. MATERIALS AND METHODS: We investigated 48 cases of CCLE that visited the department of dermatology at the Seoul National University Hospital from January 1990 to June 1997. Medical records and biopsy slides were reviewed.
Biopsy ; Dermatology ; Korea ; Lupus Erythematosus, Cutaneous* ; Medical Records ; Seoul

PURPOSE: The replacement of functional genes into cells that lack genes or mutant genes is the basis of gene therapy. In cancer, where cells often have multiple genetic defects, the replacement of critical genes may suffice to suppress cell growth or induce cell death. In malignant brain tumors, p53 mutation are among the most frequently observed genetic findings and inactivation p53 suggests that p53 plays a critical role in carcinogenesis and tumor progression. Therefore, we study the successful transfer of the wild-type p53 gene using a replicative deficient adenovirus vector into human glioma and medulloblastoma c~ell lines. Meterials and Methods: The human glioma cell line T-98G, U-87MG, U-373MG were used. To determine the efficiency of the adenovirus vector, cell lines were transfected with the Ad-p gal and analysed with X-Gal staining. Cell viability was determined by trypan blue exclusion every day after infection and Westem blot analysis was used to conform the expression of the exogenous p53 protein. RESULTS: Cell growth of the Ad-CMV-p53 infected U-373MG, and U-87MG was significantly suppressed. It appeared that exogenous p53 protein expression had an earlier ad more profound suppressive effect on U-373MG having a mutated p53 gene than on U-87MG having a wild-type p53. The expression of the exogenous p53 was more than 10 times higher than the expression of the endogenous p53. To examine the decreased viability, U-373MG was stained with Hochest 33258 and detected nuclear condensation and apoptic body. Staining results suggest that cells undergo apoptosis. CONCLUSION: The replicative deficient adenoviral vector can transfer and express p53 in human glioma cell lines in vitro, restoring wild-type p53 tumor suppressor functions. The restoration of normal p53-encoded protein in the mutant ceil lines induced cell death. The high expression of the newly transduced protein had different effects on the growth rate of the infected cell lines depending on the p53 status of the cells.
Adenoviridae* ; Apoptosis ; Brain Neoplasms ; Carcinogenesis ; Cell Death ; Cell Line* ; Cell Survival ; Genes, p53 ; Genetic Therapy ; Glioma* ; Humans ; Medulloblastoma ; Trypan Blue

The effect of induced hypotension with sodium nitroprusside(SNP) on alveolar-arterial oxygen tension difference and pulmonary shunting in 10 surgical patients with normal pulmonary function was studied under general anesthesia. Heart rate, mean arterial pressure, central venous pressure, blood gases and hemoglobin were measured before, during and after SNP infusion. Using the above data, alveolar-arterial oxygen tension difference and pulmonary shunting were calculated. The results were as follows. 1) Mean arterial pressure decreased significantly from 98+/-9.1mmHg before SNP infusion to 61+/-3.0 mmHg during SNP infusion(p<0.001), and increased to 96+/-6.7mmHg again after SNP infusion. 2) Heart rate increased significantly from 78+/-10.5 beats/min. to 101+/-11.9 beats/min.(p<0.001), and decreased to 84+/-11.5 beats/min. again. 3) Arterial oxygen tension decreased from 489+/-32.5mmHg to 480+/-25.0mmHg, but was not statistically significant. (p>0.05). 4) Alveolar-arterial oxygen tension difference increased from 188+/-29.0mmHg to 196+/-25.0mmHg, but was not statistically significant(p>0.05). 5) Pulmonary shunting increased from 9.0+/-1.83% to 9.2+/-1.50%, but was not statistically significant.(p>0.05). The above findings suggest that pulmonary shunting in patients with normal lung function will not affected during induced hypotension with SNP.
Anesthesia, General ; Arterial Pressure ; Central Venous Pressure ; Gases ; Heart Rate ; Humans ; Hypotension* ; Lung ; Nitroprusside* ; Oxygen* ; Sodium*

PURPOSE: Neuroendocrine (NE) cells of the prostate are considered to be involved in the pathogenesis of benign prostate hyperplasia (BPH). By a comparative analysis of NE cell density in BPH tissue of men who were either exposed to or not exposed to 5alpha-reductase inhibitor, we investigated the relationship between NE cells and BPH, and the effect of androgen deprivation on NE cells. MATERIALS AND METHODS: Prostate tissue specimens, obtained from 30 men by transurethral resection of the prostate or radical cystoprostatectomy, were used. Of the 30 patients, 10 had a prostate smaller than 25 ml (normal control), the other 20 had a prostate larger than 40ml, 10 of who had taken 5alpha-reductase inhibitor (finasteride) for 3 months before surgery (androgen blockade group), and 10 who had not (BPH group). The distribution of NE cells in the prostate was examined using the anti-chromogranin A (CgA) antibody, and the density of the CgA-positive cells was compared by an optical dissector method. Immunoblotting was performed using the neuron specific enolase (NSE) antibody. A Mann-Whitney U test was used in a statistical analysis. RESULTS: Most of the CgA-positive NE cells were localized between the acinar epithelial cells. The mean numbers of CgA-positive NE cells per acinus in the normal controls and the BPH groups were 1.67+/-0.78 and 4.45+/-2.54, respectively, and the difference was statistically significant (p<0.05). However, the mean number of CgA-positive NE cells in the androgen blockade group, was 4.93+/-2.17, which was similar to the BPH group. In a NSE immunoblotting study, a distinct band was observed in the BPH and androgen blockade groups, but the density of the band was higher in the androgen blockade group. CONCLUSIONS: Our results suggest that NE cells may be involved in the hyperplastic process of BPH. Inhibition of dihydrotestosterone, caused by the oral administration of the 5alpha-reductase inhibitor, failed to induce any significant change in the NE cells, probably due to the incomplete androgen blockade.
Administration, Oral ; Cell Count ; Dihydrotestosterone* ; Epithelial Cells ; Humans ; Hyperplasia ; Immunoblotting ; Male ; Neuroendocrine Cells* ; Phosphopyruvate Hydratase ; Prostate ; Prostatic Hyperplasia*

No abstract available.
Choanal Atresia*

Acoustic stimulation test(AST), is currently being used as an alternative tool of nonstress test (NST). However, there are no standard guideline for analysis of AST. Computerized numerical analysis of AST would be helpful for development of diagnostic criteria of AST. Fifty-one normal pre-term pregnancies entered to this study after conventional 20-minutes NST and 10-minutes AST. Acoustic stimulations were performed using Fetal Acoustic Stimulator (Model 146, Corometrics, US). We analyzed the FHR response after acoustic stimulation using our on-line computerized FHR analysis system, HYFM-I & II software. The changes of loss of signal, baseline FHR, variability, number of fetal movements, and number of FHR accelerations were analyzed numerically. The loss of signal was increased about 2 fold(122.61%). The baseline FHR was increased from 144.57bpm to 156.81bpm(8.5%) after acoustic stimulation. Number of fetal movements was increased about 2 fold(from 2.1 to 4.12/10 minutes). FHR variability was also increased from 17.81 bpm to 26.37 bpm. After AST, number of FHR accelaration was increased 55.47%(10sec 10bpm) and 68.42%(15sec 15bpm), respectively. In this study, we acrumulated elemental FHR data using computerized system after AST. These data would be helpful in the accurate analysis of AST and also enable us to develop the objective interpretation system for AST.
Acceleration ; Acoustic Stimulation* ; Acoustics* ; Female ; Fetal Heart* ; Fetal Movement ; Heart Rate, Fetal* ; Pregnancy ; Pregnancy*

No abstract available.
Blast Crisis* ; Leukemia*

No abstract available.
Blast Crisis* ; Leukemia*

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

No Abstract Available.
Mass Screening*