PURPOSE: To determine the value of bilobate anterior epidrual extension(AEE) on MRI in differential diagnosis of tuberculous spondylitis, pyogenic spondylitis and malignant tumor. MATERIALS AND METHODS: SE TI-,T2- and Gd-DTPA enhanced Tl-weighted, sagittal and axial MR images of 39 patients(40 vertebral lesions), including 16 tuberculous spondylitis, 7 pyogenic spondylitis(8 lesions, consisting of 2 separate lesion of 1 patient), and 16 malignant vertebral tumors(15 metastases,1 lymphoma) with an AEE were reviewed. The frequency of bilobate AEE shown as double-convexity in the anterior epidural space on axial scans was evaluated in the above vertebral diseases. RESULTS: The bilobate AEE on the axial scans was seen in 12 out of the 16 tuberculous spondytitis(75%) and 1 out of 8 pyogenic spondylitis(13%), and 10 out of the 16 malignant tumor including 15 metastasis and 1 lymphoma(63%). CONCLUSION: The bilobate' ^EE of vertebral lesions is suggestive of tuberculous spondylitis or malignant tumor rather than pyogenic spondylitis. This pattern seems to be related with the preservation of the structures, including midline septurn, F~LL(Posterior longitudinal ligament), lateral membrane and fibrous membrane, limiting and surrounding the extension of the tuberculous spondylitis and malignant tumor, and with the early penetration or disruption of PLL, midline septurn, lateral & fibrous membranes in the pyogenic spondylitis.
Diagnosis, Differential ; Epidural Space ; Gadolinium DTPA ; Magnetic Resonance Imaging* ; Membranes ; Neoplasm Metastasis ; Spondylitis

No abstract available.
Genes, erbB-1

PURPOSE: Bile acids were considered as a promoting factor for colon cancers. It has been suggested that bile acids could promote cellular proliferation or apoptosis according to their concentration. Therefore, we studied the expression of cell cycle and apoptosis related proteins on HCT116 colon cancer cells according to different deoxycholic acid concentrations. METHODS: HCT116 colon cancer cells were incubated with low (20 micro M) and high (250 micro M) concentrations of deoxycholic acid for 72 hours. Cellular proliferation and toxicity were then measured by MTS assay. The expression of cell cycle and apoptosis related proteins was evaluated by Western blot analysis. RESULTS: In a low concentration of deoxycholic acid, the change of expression of the cell cycle related proteins-cyclin D1, cyclin E, cyclin A and CDK2 were similar compared with cultures that were without deoxycholic acid. In a high concentration of deoxycholic acid, cyclin A and cyclin D1 proteins were not expressed and the expression of cyclin E and CDK2 were decreased. The expression of survivin protein was increased by a low concentration of deoxycholic acid but it showed no significant difference when compared with cultures without deoxycholic acid. However in a high concentration of deoxycholic acid, survivin was not expressed. Deoxycholic acid has no effect on the expression of Bcl-2 and Bax proteins. CONCLUSION: A high concentration of deoxycholic acid can inhibit HCT116 colon cancer cell proliferation by suppressing the expression of all the cell cycle related proteins and also survivin, an inhibitor of apoptosis.
Apoptosis* ; bcl-2-Associated X Protein ; Bile Acids and Salts ; Blotting, Western ; Cell Cycle ; Cell Proliferation ; Colon* ; Colonic Neoplasms* ; Cyclin A ; Cyclin D1 ; Cyclin E ; Cyclins ; Deoxycholic Acid*

No abstract available.
Drug Therapy* ; Humans

The authors have analyzed retrospectively a series of 102 consecutive patient with severe head injury who were admitted to the department of Neurosurgery, Dong Guk Univ. Hosp. between January, 1989, and December, 1989. All patients, after appropriate cardiopulmonary resuscitation, diagnostic measure, and, when required, surgical treatment, were managed in ICU with usual care method. The outcome has been analyzed 4 month later. The overall mortality rate was 36%. Of the survivors, 65% made good recovery or moderate disability, 22% remained severely disabled, and 14% were in a persistent vegetative state. Mortality rates at the variable GCS scores were 82% at 3-4, 25% at 5-6, and 14% at 7-8. The most reliable predictive factors were : Glasgow coma scale, motor response, pupillary reflex at admission.
Cardiopulmonary Resuscitation ; Craniocerebral Trauma* ; Glasgow Coma Scale ; Head* ; Humans ; Mortality ; Neurosurgery ; Persistent Vegetative State ; Reflex, Pupillary ; Retrospective Studies ; Survivors

PURPOSE: Evidence that indicates bile acid is a promoter of colon cancer exists. Deoxycholic acid (DCA) modifies apoptosis or proliferation by affecting intracellular signaling and gene expression. However, because previous studies have been based on studies on colon cancer cell lines, the effect of DCA on normal colonocytes is unknown. METHODS: Normal colonocytes and Caco-2 and HCT116 cells were treated with 20 micrometer and 250 micrometer of DCA, and the effect of different concentrations of DCA was measured based on the expression of cell-cycle-related proteins by using Western blots. RESULTS: The expressions of CDK2 and cyclin D1 for different concentrations of DCA in normal colonocytes and colon cancer cells were similar, but the expressions of cyclin E and A were significantly different. In HCT116 colon cancer cells, the expression of cyclin E increased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin E was not changed or decreased. In HCT116 colon cancer cells, the expression of cyclin A was not changed or decreased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin A was increased at a DCA concentration of 20 micrometer. CONCLUSION: The effect of DCA on stimulating cell proliferation suggests that DNA synthesis is stimulated by an increased expression of cyclin E in colon cancer cells. Our results suggest that a low dose of DCA induces cellular proliferation through increased expression of cyclin A and that a high dose of DCA induces decreased expression of cyclin E and CDK2 in normal colonocytes.
Apoptosis ; Bile ; Blotting, Western ; Caco-2 Cells ; Cell Cycle ; Cell Cycle Proteins ; Cell Line ; Cell Proliferation ; Colonic Neoplasms ; Cyclin A ; Cyclin D1 ; Cyclin E ; Cyclins ; Deoxycholic Acid ; DNA ; Gene Expression ; HCT116 Cells ; Humans ; Proteins

PURPOSE: Although oxaliplatin is one of the most widely used chemotherapeutic agents for the treatment of advanced stages of colorectal cancers in clinic, cancer cells often develop oxaliplatin drug resistance. Thus, overcoming oxaliplatin drug resistance is a major issue in the successful treatment for advanced stages of colorectal malignancy. In order to maximize oxaliplatin therapy, we examined whether resveratrol, a natural phytochemical known to have chemopreventive effects on cancers, can have a chemosensitizing effect upon cotreatment with oxaliplatin. Survivin, a small inhibitor of apoptosis protein (IAP), expression is examined using HCT116 colon cancer cells. METHODS: In order to examine resveratrol chemosensitizing effect upon oxaliplatin cotreatment, survivin transcripts and protein expression, cell proliferation, and apoptotic responses were evaluated using HCT116 cells. Reverse transcription polymerase chain reaction (RT-PCR), Western blot, crystal violet staining analyses were performed. For survivin specific inhibition, YM155 molecule was used. RESULTS: Although oxaliplatin significantly suppressed survivin transcripts and protein expression level in HCT116 cells, resveratrol cotreatment induced restoration of survivin expression level of both transcripts and protein. Apoptotic induction by oxaliplatin only treatment was nullified upon resveratrol cotreatment. Induction of survivin restoration upon resveratrol cotreatment also occurred when survivin specific inhibitor, YM155, was used. In addition to survivin restoration, resveratrol cotreatment also induced restoration of Bcl-2/caspase-3 expression suppressed by oxaliplatin only treatment. CONCLUSION: Resveratrol has an antichemosensitizing effect upon cotreatment with oxaliplatin in HCT colon cancer cells. This antichemosensitizing effect of resveratrol can be cell-type specific. However, clinical use of resveratrol cotreatment with oxaliplatin should be approached cautiously.
Blotting, Western ; Cell Proliferation ; Colon* ; Colonic Neoplasms* ; Colorectal Neoplasms ; Drug Resistance ; Gentian Violet ; HCT116 Cells ; Inhibitor of Apoptosis Proteins ; Polymerase Chain Reaction ; Reverse Transcription

PURPOSE: Cyclin E/CDK2 complexes are thought to play critical roles in multiple cell cycle events, including DNA replication, centrosome duplication, and activation of the E2F transcriptional program. Deregulation of the cell cycle control mechanism is an obligatory step in tumorigenesis. Cyclin E gene amplification and the high expression of low molecular weight (LMW) cyclin E proteins are reported to be important events in breast, and other cancers. According to recent studies, the overexpression of cyclin E protein has the role of developing chromosomal and microsatellite instability (MSI). MSI is known as one of the pathways by which colorectal cancer develops. LMW cyclin E variants are also expressed exclusively in cancer tissues. Therefore, we hypothesize that the LMW cyclin E maybe related to the MSI in sporadic colorectal cancers. METHODS: The expressions of the LMW cyclin E, CDK2 proteins and MSI stati were detected by western blot and PCR-SSCP analysis, respectively, using five Bethesda microsatellite markers in 49 sporadic colorectal cancers, which were compared with matched normal colonic mucosal tissues. RESULTS: There were 5, 10 and 34 cases of MSI-H (10.2%), MSI-L (20.4%) and MSS (69.4%), respectively. LMW cyclin E was over-expressed in 4 of the 5 MSI-H (80%) and 31 of the 44 MSI-L and MSS cases (70.5%). No correlation was found between LMW cyclin E (Fisher exact one-tailed P= 0.554), CDK2 expression (Fisher exact one-tailed P=0.569) and microsatellite instability in sporadic colorectal cancers. CONCLUSION: The expression of the LMW cyclin E variant was not associated with the MSI status in sporadic colorectal cancers.
Blotting, Western ; Breast ; Carcinogenesis ; Cell Cycle ; Cell Cycle Checkpoints ; Centrosome ; Colon ; Colorectal Neoplasms* ; Cyclin E* ; Cyclin-Dependent Kinase 2 ; Cyclins* ; DNA Replication ; Gene Amplification ; Microsatellite Instability ; Microsatellite Repeats ; Molecular Weight* ; Mucous Membrane ; Phenotype*

PURPOSE: The causes of colon cancer can be divided into genetic and environmental components. A high-fiber diet is known to reduce the risk of colon cancer. Dietary fiber is converted to short chain fatty acid, butyrate, in the colon by bacteria. Butyrate is used as an energy source for the colonic epithelial cells, and is known to induce apoptosis in colon cancer cell lines. Survivin, a recently discovered member of the IAP (inhibitor of apoptosis) family, is known to suppress apoptosis. Not only does it suppress cell apoptosis, but it also has a protective effect from disabling G2/M phase of the cell cycle by attaching to the microtubule of the mitotic spindle. The purpose of this study is to evaluate the effect of butyrate on the expression of survivin, in HCT116 colon cancer cell lines. METHODS: Cytotoxicity of butyrate was measured by MTS method. Cell cycle phase and apoptosis was analyzed by flowcytometry. Protein expression of survivin was evaluated by Western blot analysis, and the mRNA expression by RT-PCR. RESULTS: Butyrate can induce apoptosis in HCT116 colon cancer cell line at a concentration of 6 mM. Butyrate suppressed the expression of survivin mRNA and also the expression of cytosolic and nuclear survivin. In flowcytometric analysis, the apoptotic portion was increased and the proportions of S and M phase were decreased when cultured with butyrate. CONCLUSION: We concluded that butyrate could induce cellular apoptosis partially by suppressing the expression of survivin in HCT116 colon cancer cells.
Apoptosis ; Bacteria ; Blotting, Western ; Butyrates ; Cell Cycle ; Cell Division ; Cell Line ; Colon ; Colonic Neoplasms ; Cytosol ; Diet ; Dietary Fiber ; Epithelial Cells ; Humans ; Microtubules ; RNA, Messenger

Purpose: A water-soluble variant of the artemisinin called artesunate, approved as an antimalarial agent, can induce cell death on various cancer cell types. We studied the mechanism of cell death of artesunate on HCT116 colorectal cancer cells. Methods: We treated HCT116 colon cancer cells with artesunate, holo-transferrin, deferoxamine mesylate, ferrostatin, necrostatin-1, and YM155. We observed the growth inhibition of artesunate on HCT116 colon cancer cells by morphologic findings. Inhibition of cell growth was assessed by MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide) assay and long-term growth inhibition by colony-forming assay. Apoptosis was investigated by flow cytometry and Western blot analysis. Results: Artesunate inhibited the proliferation of HCT116 colon cancer cells effectively. Co-treatment with YM155, a specific survivin inhibitor, enhanced the artesunate-induced cell death. Co-treatment with the iron-chelating agent deferoxamine rescued artesunate induced cell death and increased long-term cell survival and proliferation. Conclusion In this study, we demonstrated that artesunate-induced cytotoxicity in HCT116 colon cancer cells by suppressing the expression of survivin and partially by ferroptosis. Our findings suggest that the co-treatment artesunate with YM155 can induce more potent cell death on HCT116 colon cancer cells and shows new insight for the treatment of colorectal cancer patients.