No abstract available.
Hearing* ; Humans ; Tinnitus*

No abstract available.
Female ; Fetomaternal Transfusion* ; Pregnancy

PURPOSE: To evaluate the possibility that human muscle derived stem cells (hMDSCs) can be differentiated into neurons in vitro. MATERIAL AND METHODS: Muscle derived stem cells were isolated from the hamstring muscles during the anterior cruciate ligament reconstruction by preplate technique. For the characterization of these cells, desmin staining, CD 34, Sca-1, CD 29 using the Flow cytometry were performed. In the experimental group, neuronal induction media was added to differentiate hMDSCs to neuronal cells. These cells were evaluated by neuronal markers such as neuron-specific enolase (NSE), neurofilament (NF), TrkA using immunocytochemistry. For the control group, no induction media was added. Statstical analyses were performed by use of Kruskal-Wallis H test and Student-Newman-Keuls test (P<0.01). RESULT: Desmin staining was positive in 92.3+/-6%. Flow cytometry was negative for CD 34 and Sca-1. However it was positive for CD 29. (69.4+/-10%). The immunocytochemical result revealed NSE, NF and TrkA positive with 63.2+/-2.3%, 59.2+/-2.5%, 55+/-2.4% respectively. However, these were negative in the control group. CONCLUSION: Our observations indicate that hMDSCs have the capacity to differentiate into neurons in a specialized culture media.
Anterior Cruciate Ligament Reconstruction ; Culture Media ; Desmin ; Flow Cytometry ; Humans* ; Immunohistochemistry ; Muscles ; Neurons* ; Phosphopyruvate Hydratase ; Stem Cells*

3-Deazaadenosine (DZA), a cellular methylation blocker was reported to induce the caspase-3-like activities-dependent apoptosis in U-937 cells. In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases. In the U-937 cells treated with DZA, cytochrome c release from mitochondria and subsequent activation of caspase-9, -8 and -3 were observed before the induction of apoptosis. zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways. zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9. Moreover, ZB4, an antagonistic Fas-antibody, exerted no effect on the activation of caspase-8 and induction of apoptosis by DZA. In addition, zVAD-Fmk and mitochondrial permeability transition pore (MPTP) inhibitors such as cyclosporin A (CsA) and bongkrekic acid (BA) did not block the release of cytochrome c from mitochondria. Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction. And caspase-3 seems to be activated by other caspses including IETDase-like enzyme and caspse-9 seems to be activated by cytochrome c released from mitochondria without the involvement of caspases and CsA- and BA- inhibitory MPTP.
Amino Acid Chloromethyl Ketones/pharmacology ; Apoptosis/*drug effects ; Bongkrekic Acid/pharmacology ; Caspases/*metabolism ; Cell Line ; Cyclosporine/pharmacology ; Cytochrome c/drug effects/metabolism ; Enzyme Activation ; Human ; Leukocytes, Mononuclear/cytology ; Ligands ; Membrane Glycoproteins/metabolism ; Tubercidin/*pharmacology ; U937 Cells

3-Deazaadenosine (DZA), a cellular methylation blocker was reported to induce the caspase-3-like activities-dependent apoptosis in U-937 cells. In this study, we analyzed the activation pathway of the caspase cascade involved in the DZA-induced apoptosis using specific inhibitors of caspases. In the U-937 cells treated with DZA, cytochrome c release from mitochondria and subsequent activation of caspase-9, -8 and -3 were observed before the induction of apoptosis. zDEVD-Fmk, a specific inhibitor of caspase-3, and zLEHD-Fmk, a specific inhibitor of caspase-9, prevented the activation of caspase-8 but neither caspase-3 nor caspase-9, indicating that caspase-8 is downstream of both caspase-3 and caspase-9, which are activated by independent pathways. zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9. Moreover, ZB4, an antagonistic Fas-antibody, exerted no effect on the activation of caspase-8 and induction of apoptosis by DZA. In addition, zVAD-Fmk and mitochondrial permeability transition pore (MPTP) inhibitors such as cyclosporin A (CsA) and bongkrekic acid (BA) did not block the release of cytochrome c from mitochondria. Taken together, these results suggest that in the DZA-induced apoptosis, caspase-8 may serve as an executioner caspase and be activated downstream of both caspase-3 and caspase-9, independently of Fas receptor-ligand interaction. And caspase-3 seems to be activated by other caspses including IETDase-like enzyme and caspse-9 seems to be activated by cytochrome c released from mitochondria without the involvement of caspases and CsA- and BA- inhibitory MPTP.
Amino Acid Chloromethyl Ketones/pharmacology ; Apoptosis/*drug effects ; Bongkrekic Acid/pharmacology ; Caspases/*metabolism ; Cell Line ; Cyclosporine/pharmacology ; Cytochrome c/drug effects/metabolism ; Enzyme Activation ; Human ; Leukocytes, Mononuclear/cytology ; Ligands ; Membrane Glycoproteins/metabolism ; Tubercidin/*pharmacology ; U937 Cells

Cyclopentenone prostaglandins (PGs) have antiproliferative activity on various tumor cell growth in vitro. Particularly, 9-deoxy-(9,12)-13,14-dihydro PGD2( delta12-PGJ2) was reported for its antineoplastic and apoptotic effects on various cancer cells, but its mechanism inducing apoptosis is still not clear. In this study, we have characterized apoptosis induced by delta12-PGJ2in HeLa cells. Treatment of delta12-PGJ2induced apoptosis as indicated by DNA fragmentation, chromatin condensation, and formation of apoptotic body. We also observed release of cytochrome c from mitochondria and activation of caspase cascade including caspase-3, -8, and -9. And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH2-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta12-PGJ2 showing participation of caspases in this process. However, protein expression level of Bcl-2 family was not altered by delta12-PGJ2, seems to have no effect on HeLa cell apoptosis. And ZB4, an antagonistic Fas-antibody, exerted no effect on the activation of caspase 8 indicating that Fas receptor-ligand interaction was not involved in this pathway. Treatment of delta12-PGJ2 also leads to suppression of nuclear factor kappaB (NF-kappaB) as indicated by nuclear translocation of p65/RelA and c-Rel and its DNA binding ability analyzed by EMSA. Taken together, our results suggest that delta12-PGJ2-induced apoptosis in HeLa cell utilized caspase cascade without Fas receptor-ligand interaction and accompanied with NF-kappaB inactivation.
Antigens, CD95/metabolism ; Apoptosis/*physiology ; Caspases/metabolism ; Cytochromes c/*metabolism ; Hela Cells ; Human ; NF-kappa B/metabolism ; Prostaglandin D2/*analogs & derivatives/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism

PURPOSE: Vascular endothelial growth factor (VEGF) known as an angiogenic factor is a potent inducer of pathologic neovascularization. The purpose of this study is identifying the relationship between serum PSA, invasiveness and VEGF expression in prostatic cancer. MATERIALS AND METHODS: Ex-vivo study with immunohistochemical stain analysis for VEGF expression was performed on 18 paraffin embedded specimens of prostatic cancer patients who were treated with radical prostatectomy. VEGF expressions were classified by three groups (1+ , 2+ , 3+ ) according to the degree of staining of cancer cell. Biochemical failure and recurrence were determined by Takayama's IMx PSA assay criterion (>0.1ng/ml) following radical prostatectomy. RESULTS: Immunohistochemical studies demonstrated that each group contained 1, 2, 8 patients in advanced disease (n=11), and 3, 2, 2 patients in localized disease (n=7), respectively. All cases in strong positive (3+ ) group had Gleason sum higher than 7 and nadir PSA values were lower than 0.1ng/ml except one case. We found no correlation between initial PSA and VEGF expression (p=0.361). Three biochemical recurrent patients were identified as strong positive VEGF expression. CONCLUSIONS: Our study indicates that patients with advanced stage and higher Gleason sum have a trend with more VEGF expression than patients with localized disease. Identifying the angiogenesis factors especially, VEGF involved in prostatic cancer growth and understanding their regulation will lead to the developement of anti-angiogenic strategies useful for diagnostic studies and therapeutic interventions.
Angiogenesis Inducing Agents ; Humans* ; Neovascularization, Pathologic ; Paraffin ; Prostate-Specific Antigen* ; Prostatectomy ; Prostatic Neoplasms* ; Recurrence ; Vascular Endothelial Growth Factor A*

Mature cystic teratoma of the ovary is the most common ovarian germ cell tumor and almost benign, but malignant transformation occurs in less than 2% of benign mature teratoma. Of the malignancies arising in teratomas, squamous cell carcinoma is the most common (70-80%). The presentation in stage I disease dose not differ from that of benign cystic teratoma. In the early stage, the treatment is possible through surgical intervention alone. We experienced a case of squamous cell carcinoma of the ovary arising in mature cystic teratoma, which is presented with a brief review of literature.
Carcinoma, Squamous Cell* ; Female ; Neoplasms, Germ Cell and Embryonal ; Ovary* ; Teratoma*

Bailey and Cushing described the oligodendroglioma firstly in 1926. The oligodendroglioma is rare tumor and involves the ventricular system in 7% to 10% of all cases. The authors present a case of intraventricular oligodendroglioma associated with arterio venous malformations in a 34 year old male who had the history of visual disturbance and mental deterioration, for one month. The diagnosis was confirmed by operation and autopsy.
Adult ; Autopsy ; Diagnosis ; Humans ; Male ; Oligodendroglioma*

BACKGROUND: Early reperfusion therapy with thrombolytic agents or primary PTCA is most important to salvage ischemic myocardium in acute myocardial infarction(AMI). Timely reperfusion of jeopardized myocardium clearly improves hemodynamics, decreases infarct size and improves survival. The extent of protection appears to be directly related to the rapidity of reperfusion after onset of coronary occlusion. Although the intravenous thrombolysis is a feasible therapy in the patients with evolving AMI, the benifit of thrombolytic therapy decreases because of the time delay after onset of symptom. This study was perfomed to analyze the factors time delay between onset of symptom and the thrombolytic therapy with retrospective and prospective questionaire in the patients with AMI. METHOD: Eighty one patients with AMI were included in this study who came to the emergency room(ER) of Chungnam National University Hospital(CNUH) from Feburary 1995 to October 1996. Delay between door and thrombolytic therapy was defined as hospital time delay. RESULTS: Thrombolytic therapy(rt-PA or urokinase iv) was done in 60 patients(74.1%) and mean prehopital time delay was significantly decreased in the patients with thrombolytic therpapy when compared with those without thormbolytic threapy(462+/-90 vs 1375+/-473 minutes, p=0.005). There were no singificant factors for prehospital time delay such as age, sex, redsidence, ER near residence, transfer time to ER near residence, family status, family history of AMI, severity of chest pain, presence of risk factors of cardiovascular disease(CVD), previous CVD, degree of education, history of other disease and routine check, transfer methods. The only 8 patients(9.8%) knew about AMI and 7 patients among these patient came to ER earlier and received thrombolytic therapy. From 57 referred patients, 40 patients(70.2%) received reperfusion therapy and only 30 patients(52.6%) had recored EKG in the referred hospital. In the analysis of hospital delay from patient's arrival to the thrombolytic therapy, the arrival time at weekdays and weekend had no differences, but hospital delay were significantly prolonged when patients arrived at ER in the night. CONCLUSION: Since prehospital time delay is a most important factor of time delay for the effective thrombolytic therapy in AMI, the pubic education program and effective transport system are needed. And routine record of EKG in patient with chest pain in the local hospital is very helpful to start effective thromolytic therapy at ER. The well designed prospective study with more patinets in our local region is essential to get more accurate information about transport system and to improve survival rate in patients with AMI.
Chest Pain ; Chungcheongnam-do ; Coronary Occlusion ; Education ; Electrocardiography ; Emergencies ; Fibrinolytic Agents ; Hemodynamics ; Humans ; Myocardial Infarction* ; Myocardium ; Prospective Studies ; Reperfusion ; Retrospective Studies ; Risk Factors ; Survival Rate ; Thrombolytic Therapy* ; Urokinase-Type Plasminogen Activator