There are many kinds of instrumentation systems for posterior operation in the treatment of scoliosis. Cotrel-Dubousset (C-D) system is most widly used for its excellent correction potential and stability. However there were some problems in C-D hook system such as hook dislodgement and correction loss. So, in order to reduce these problems we use transpedicular screw system and compare the results between two systems. We studied 44 cases of scoliosis ( hook 19 cases, screw 25 cases) who were operated with C-D instrumentation from February 1988 to August 1995. The average follow-up period was 54 months in hook group and 23 months in screw group. 1. Operation time was 241 minutes in hook group and 223 minutes in screw group. Average amount of transfusion was 5.0 pints in hook group and 4.6 pints in screw group. 2. Involved segments of main curvature were 7.0 in hook group and 6.6 in screw group. 3. Scoliotic curve was changed from 49degrees to 13degrees (73%) in hook group and from 47degrees to 12degrees (74%) in screw group. Loss of correction during follow up period was 7degrees in hook group and 3 in screw group. 4. Thoracic kyphosis was changed from 24degrees to 26degrees in hook group and from 27degrees to 30degrees in screw group. Lumbar lordosis was changed from 26degrees to 29degrees in hook group and from 26degrees to 31degrees in screw group. 5. Correction rate of rotation of apex vertebrae by Pedriolle method was 43% (from 20degrees to 12degrees) in hook group and 50% (from 22degrees to 11degrees) in screw group. 6. Complications were two cases of hook dislodgement, one delayed deep infection and four cases of progression of curvature in hook group and one case of malinsertion of screw and two cases of progression of curvature in screw group. In conclusion, these results suggested that screw system is more effective than hook system on rotational correction of apex vertebra and prevention of loss of correction.
Animals ; Follow-Up Studies ; Kyphosis ; Lordosis ; Scoliosis* ; Spine

No abstract available.
Colorectal Neoplasms*

No abstract available.
Humans ; Hysterectomy*

No abstract available.
Meconium* ; Peritonitis*

CD44 is a cell adhesion molecule with numerous isoforms created by mRNA alternative splicing. Expression of CD44 variants has been suggested to play a potential role in tumor progression and metastasis. We designed primers CD44V, CD44V6/7, CD44R1 and CD44V6-10 to analyze and compare the roles of each CD44 variants. Expressions of CD44 variants were investigated in normal colonic mucosa, the lymph nodes which was histopathologically free of cancer cell, and cancer tissues of 44 human colorectal cancer patients by RT-PCR method. The expression of CD44V was observed in 28 out of 39 (71.8%) tumors and 7 out of 11 (63.6%) N1 normal regional lymph nodes, and CD44V6/7 was observed in 28 out of 39 (71.8%) tumors and 9 out of 11 (81.8%) N1 normal regional lymph nodes. The expressions of CD44V and CD44V6/7 were most frequently observed compared with any other CD44 variants. In normal colonic mucosa, the expression of CD44 variants are low but in cancer tissue and its regional lymph node, the expression of CD44V and CD44V6/7 were significantly higher and more frequent than any other CD44 variants (p<0.05). These results suggest that CD44V and CD44V6/7 can be a molecular marker for colorectal cancer and its micrometastasis to the regional normal lymph node.
Alternative Splicing ; Antigens, CD44/genetics* ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/immunology* ; Gene Expression ; Human ; Lymph Nodes/pathology ; Lymph Nodes/immunology* ; Protein Isoforms/genetics

PURPOSE: Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, have been known to take a role in signal transduction pathway of angiogenesis. The authors confirmed that PKC is the most noticeable mediator for abnormal proliferation of vascular endothelial cells through in vitro study model using the inhibitors, targeting the formation of three co-enzymes. In this study, we would investigate which isoform of PKC play an important role in abnormal angiogenesis of vascular endothelial cell. METHODS: In 96 well plates, 10(4) HUVECs(human umbilical vein endothelial cells) were evenly distributed. Two groups were established; the control group without administration of DMH(1,2-dimethylhydrazine) and the DMH group with administration of 7.5x10(-9)M DMH. RNA was extracted from vascular endothelial cell of each group and expression of the PKC isoform was analyzed by RT-PCR(reverse transcriptase-polymerase chain reaction) method. RESULTS: RT-PCR analysis showed that PKCalpha, -betaI, -betaII, -eta, -micron and -zeta were expressed in vascular endothelial cells of each group. DMH incresed the expression of PKCalpha and PKCmicron, and decreased PKCbetaI, PKCbetaII expression dominantly. CONCLUSION: Based on the result of this study, it was suggested that PKCalpha and PKCmicron may have significant role in abnormal proliferation of vascular endothelial cell.
1,2-Dimethylhydrazine* ; Cell Proliferation ; Dimenhydrinate ; Endothelial Cells* ; Oxidoreductases ; Protein Kinase C* ; Protein Kinases* ; RNA ; Signal Transduction ; Tyrosine ; Umbilical Veins

BACKGROUND AND OBJECTIVES: QT dispersion (QTd) is defined as the difference between the maximum and minimum QT interval in any of the 12 leads of the surface ECG. QTd has been shown to reflect regional variations in ventricular repolarization. Ischemic dilated cardiomyopathy (DCM) may lead to more spatial and temporal dispersion in ventricular repolarization than idiopathic DCM. The purpose of this study was to determine the difference of QTd between patients who had ischemic and idiopathic DCM. MATERIALS AND METHODS: The study population included 30 patients with ischemic DCM and 30 with idiopathic DCM. All standard 12-lead ECGs were examined prospectively by two observers who were unware of the patient's details. RESULTS: QTd in ischemic DCM was significantly higher than that in idiopathic DCM (63+/-32 vs. 44+/-26 msec, p=0.012) and JTd in ischemic DCM was significantly higher than that in idiopathic DCM (48+/-21 vs. 36+/-22 msec, p=0.036). Results did not change when Bazett's QTc and JTc was substituted for QT (QTcd:69+/-33 vs. 52+/-28 p=0.039) and JT (JTcd:56+/-21 vs. 41+/-25 p=0.043). CONCLUSION: Ischemic DCM has increased spatial inhomogeneity of repolarization probably due to more regional myocardial damages compared with idiopathic DCM. The value of QT dispersion as an easily accessible, non-invasive method in predicting the risk of life threatening arrhythmia and overall mortality in patients with dilated cardiomyopathy must be confirmed in prospective trials.
Arrhythmias, Cardiac ; Cardiomyopathy, Dilated* ; Electrocardiography ; Heart Failure ; Humans ; Mortality ; Prospective Studies

The purposes of this study are to establish standard model in which endothelial cell proliferations are induced by DMH stimulation in vitro, and to analyze the gene expressions of proliferative HUVECs using DNA chip technique which could evaluate the mechanisms of angiogenesis, and the development of vascular tumors. To perform the MTT assay in 96-well microplates, 104 cells were seeded in each well which were cultured in medium. On the third day, the cells were treated with 5 different concentrations of diluted DMH from 10 to 10-3 ng/ml. Five DMH-treated groups were compared with the control group which was not treated with DMH. The optical densities in each group were measured at the time of 0, 6, 12, 24, 36, 48, and 72 hours after DMH treatment. The same experiment was repeated 9 times. Statistically significant cell proliferations were observed in 1 and 10-1ng/ml group. The RNAs were isolated from HUVECs of control group and 1ng/ml DMH-treated group, and they were used to analyze the gene expressions using DNA chip technique. One hundred and seventy-seven genes(142 of up-retulated genes and 35 down-regulated genes) were identified, and several genes were associated with VEGF and FGF production. Also DMH could affect expression of genes that involve oncogenesis. Further study should be performed to evaluate the processes of angiogenesis and morphogenesis of vascular tumors, which could be utilized in the development of new therapeutic approaches.
Carcinogenesis ; Dimenhydrinate ; Dimethylhydrazines ; Endothelial Cells ; Gene Expression Profiling* ; Gene Expression* ; Human Umbilical Vein Endothelial Cells* ; Humans* ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; RNA ; Umbilical Veins ; Vascular Endothelial Growth Factor A

Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, take a significant role in signal transduction pathway of angiogenesis. The authors utilized the inhibitors, targeting the formation of three co-enzyme in signal transduction pathway in order to quantify the suppression of abnormal vascular endothelial cell proliferation induced by DMH, to compare the level suppression in each up-regulated growth factors, CTGF, CYR61, ITGbeta1, FHL2, and to identify the relationship between abnormal cell proliferation and signal transduction pathway. Five groups were established; Control group, Group of DMH, Group of DMH-mixed Herbimycin, inhibitor of protein tyrosine kinase, Group of DMH-mixed Calphostin C, inhibitor of protein kinase C, Group Of Dmh-Mixed 10U Catalase, Inhibitor Of oxidase. The rise of vascular endothelial cell was compared by MTT assay, and four growth factors were analysed with RT-PCR method, at pre-administration, 4, 8, 12, and 24 hours after administration. In comparison of abnormal proliferation of vascular endothelial cell induced by DMH, suppression was noticed in Herbimycin and Calphostin C group, and Calphostin C group revealed higher suppression effect. Nevertheless, Catalase group did not have any suppression. In manifestation of four growth factors, Herbimycin and Calphostin C group presented similar manifestation with control group, except in ITGbeta. Catalse group had similar manifestation with DMH group in all four growth factors. Abnormal proliferation of vascular endothelial cell induced by DMH have a direct relationship with PTK and PKC, more specifically to PKC. Oxidase was confirmed not to have any relevance.
Catalase ; Cell Proliferation ; Dimenhydrinate ; Endothelial Cells* ; Intercellular Signaling Peptides and Proteins ; Oxidoreductases ; Protein Kinase C ; Protein Kinases ; Protein-Tyrosine Kinases ; Signal Transduction* ; Tyrosine

PURPOSE: DMH(1,2-dimethylhydrazine) has been known to induce vascular neoplasm such as malignant endothelioma in animal experiment, through induction of abnormal proliferation of HUVECs. In our previous studies, 11 types of PKC isoenzymes were determined by RT-PCR and the expression of PKCalpha, and mu was more prominent than other PKC isoenzymes in the DMH-treated group. However, this result was not based on objective assessment. In this study, we further evaluated the role of PKCalpha on the DMH-induced abnormal proliferation of HUVECs by two different methods to identify its presence with high relevance in objective view. PKCmu will be investigated in further study. METHODS: The study was conducted with the cultured HUVECs group(control) and the 0.75x10(-9)M DMH-treated group. After processing protein extraction in 0 and 24 hour, extracted protein was treated of quantitative test through BCA protein assay. In the western blot analysis, electrophoresis was performed in the order of gel preparation, sample preparation, and gel running. Electrotransfer to nitrocellulose membrane and reaction with antibody were done. Detection of PKCalpha was achieved through "Gel Image Analysis System". In the fluorescence immunocytochemical analysis, the grading of radiance of the intracellular PKCalpha particles was detected with confocal microscope after treating with primary and fluorescent secondary antibody in 0 and 24 hours. RESULTS: The Western blot analysis showed increased PKCalpha expression from the specimen obtained in 24 hour of the DMH treatment group when compared to those in control group. Under confocal fluorescence microscope, the emitting radiance in the DMH treated group was brighter at 24 hours as well. CONCLUSION: We believe that PKCalpha plays a role in DMH-induced abnormal proliferation of the vascular endothelium, which may provide insights in understanding the vascular neoplasm.
Animal Experimentation ; Blotting, Western ; Collodion ; Dimenhydrinate ; Electrophoresis ; Endothelium, Vascular ; Fluorescence ; Isoenzymes ; Membranes ; Protein Kinase C ; Running ; Vascular Neoplasms