The advance of the immunobiology clarifies the nature of non-Hodgkin's lymphoma(NHL). In addition the proceed in the immunophenotyping renders the classification of NHL. According to the Revised European American Lymphoma(REAL) classification, classified by the etiologic factors, molecular biological characteristics, immunophenotype, cytogenetics and histologic feature, nasal T/NK-cell lymphoma(=angiocentric lymphoma) belongs to the category of peripheral T-cell and natural killer cell lymphoma. Nasal T/NK-cell lymphoma is a distinct clinicopathologic entity characterized by progressive necrotic lesions in the nasal cavity, nasopharynx, and palate. The cellular origin of this tumor has been controversial. Although most nasal T/NK-cell lymphomas are of NK-cell lineage, being CD56+, negative for surface CD3(Leu4), and unassociated with rearrangements of the T-cell receptor genes, other minor variants have been reported. This lymphoma is a rare disease and usually experienced in adult. Recently, we experienced a rare type lymphoma, nasal T/NK-cell lymphoma, in 14 years old boy. His soft mass occupied the right nasal cavity including the nasal septum and turbinate. Pathologically this nasal mass showed the infiltration into the vascular wall, illustrating angiodestructive lesion. The cellular origin was NK-cell lineage, being CD56+ and negative to CD3. Now, we report the case with a brief review of related literatures.
Adolescent ; Adult ; Classification ; Cytogenetics ; Genes, T-Cell Receptor ; Humans ; Immunophenotyping ; Killer Cells, Natural ; Lymphoma* ; Lymphoma, Non-Hodgkin ; Male ; Nasal Cavity ; Nasal Septum ; Nasopharynx ; Palate ; Population Characteristics ; Rare Diseases ; T-Lymphocytes ; Turbinates

To determine the incidence, clinical characteristics and coronary angiographic findings of postinfarction angina, clinical course and coronary angiogram were studied in 45 patients with acute myocardial infarction. During a mean follow-up period of 12 weeks, 17 patients(37.8%) developed angina. Of 5 patients with postinfarction angina within 1 week of infarction, 2 patients died during hospitalization, whereas all 12 patients with postinfarction angina which occured more than 1 week after acute myocardial infarction were discharge alive. The frequency of stenosis over 90% and multivessel disease by coronary angiography were 51.7% and 64.7% respectively in patients with postinfarction angina, and 25%, 28.5% respectively in patients without postinfarction angina.
Constriction, Pathologic ; Coronary Angiography ; Follow-Up Studies ; Hospitalization ; Humans ; Incidence ; Infarction ; Myocardial Infarction

BACKGROUND: The normal functions of the cell cycle inhibitor p16INK4a are frequently inactivated in many human cancers. Over 80% of hepatocellular carcinoma (HCC) cases lack a functional p16/Rb pathway. p16/Rb pathway, as well as p53 pathway, is considered as one of key components of tumor suppression. METHODS: To study the roles of p16INK4a in HCC, a stable cell line expressing exogenous p16 was generated from SNU-449 hepatocellular carcinoma cells lacking endogenous p16, and suppression subtractive hybridization (SSH) was performed in parallel with the control cells. RESULTS: 1) SSH identifies fibronectin (FN1), crystallin alphaB (CRYAB), Rac1, WASP, RhoGEF, and CCT3 as differentially-expressed genes. 2) Among the selected genes, the up- regulation of FN1 and CRYAB was confirmed by Northern blot, RT-PCR and by proteomic methods. CONCLUSION: These genes are likely to be associated with the induction of stress fiber and stabilization of cytoskeleton. Further studies are required to clarify the possible role of p16 in the signal transduction pathway.
Blotting, Northern ; Carcinoma, Hepatocellular* ; Cell Cycle ; Cell Line ; Crystallins ; Cytoskeleton ; Fibronectins ; Gene Expression* ; Humans ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction ; Stress Fibers ; Wasps

PURPOSE: Chemotherapeutic agents are known to induce cell death in cancer cells by apoptotic mechanisms. This study was to investigate the influence of the differentiation on the apoptotic potential of chemotherapeutic agents. METHODS: Etoposide and cytosine arabinoside (Ara-C) were chosen as chemotherapeutic agents, and human promyelocytic leukemia cell line, HL-60, was used as target cells. RESULTS: Etoposide or Ara-C treated HL-60 cells showed cytoplasmic blebbing and nuclear condensation and fragmentation under fluorescence microscope when stained with acridine orange/ethidium bromide. In addition, the cellular DNA of HL-60 cells was found to cleave into internucleosomal fragments after treatment with chemotherapeutic agents. These findings were the characteristics of apoptosis and suggested the induction of apoptotic cell death of HL-60 cells by etoposide or Ara-C treatment. HL-60 cells are known to differentiate into myeloid or monocytic lineage by retinoic acid, phorbol 12-myristate acetate (PMA) and dimethyl sulfoxide (DMSO), and this differentiation itself can activate apoptosis program, so-called 'apoptosis by terminal differentiation'. The effect of terminal differentiation by PMA or DMSO on the apoptosis induced by etoposide or Ara-C was also investigated, utilizing qualitative and quantitative DNA fragmentation assay. HL-60 cells treated with PMA (100 nM) were adherent to culture dish and formed cellular processes. DMSO (1.25%) treated HL-60 cells instead recovered the ability to reduce nitroblue tetrazolium to blue-to-purple formazan, indicating its differentiation. After induction of differentiation by PMA or DMSO, differentiated HL-60 cells were treated with etoposide (10 muM) and Ara-C (50 muM) to compare its apoptotic potential with that of undifferentiated HL-60 cells. The ladder DNA induced by etoposide and Ara-C was decreased in differentiated HL-60 cells. On quantitative analysis of DNA fragmentation, PMA reduced DNA fragmentation induced by etoposide and Ara-C to 73% and 69%, respectively, and DMSO reduced it to 74% and 56%, respectively. In western blot analysis, the expression of Bcl-2, which is known to inhibit etoposide and Ara-C induced apoptosis, decreased significantly in HL-60 cells differentiated by PMA or DMSO. CONCLUSION: These results suggest that the differentiation of HL-60 cells by PMA or DMSO prevents apoptosis by etoposide and Ara-C, but bcl-2 proto-oncogene may have only minor role in inhibiting apoptosis by chemotherapeutic agents in differentiated HL-60 cell.
Apoptosis* ; Blister ; Blotting, Western ; Cell Death ; Cell Line* ; Cytarabine ; Cytoplasm ; Dimethyl Sulfoxide ; DNA ; DNA Fragmentation ; Etoposide ; Fluorescence ; HL-60 Cells ; Humans* ; Leukemia ; Nitroblue Tetrazolium ; Proto-Oncogenes ; Tretinoin

No abstract available.
Transplantation* ; Tuberculosis*

No abstract available.
Transplantation* ; Tuberculosis*

No abstract available.
Kidney* ; Transplants* ; Tuberculosis*

BACKGROUND: AG60 is a complex of acriflavine and guanosine. Our previous study revealed that AG60 had not only in vitro antitumor activities in several human cancer cell lines, but also strong antitumor effects in animal experiments using p388 or S180 cells-implanted mice. METHODS: Antitumor effects of AG60 were compared with those of Adriamycin, acriflavine, guanosine or control group. Body weight, tumor weight change, and survival time were measured in Ehrlich carcinoma cells implanted ICR mice. RESULTS: Body weights in AG60, acriflavine, or Adriamycin treated groups were significantly lower than those in control group during 30 day observation period(p<0.05). The percent tumor growth inhibition of AG60, Adriamycin, acriflavine, or guanosine two weeks after last treatment was respectively 86% (T/C%=14), 83% (T/C%=17), 68%(T/C%=32), 41% (T/C%=59). According to above data, tumor growth inhibition in AG60 treated group was significantly stronger than that in control, acriflavine or guanosine treated group(p<0.01), but there was no significant difference between AG60 and Adriamycin treated group. Mean survival time in control, AG60, Adriamycin, acriflavine, or guanosine treated group was respectively 33+/-3.9 days, 68+/-4.2 days, 54+/-5.8 days, 36+/-3.8 days, 50+/-8.1 days. CONCLUSIONS: The anti-tumor effect of AG60 against Ehrlich tumor was significantly stronger than that of control, acriflavine or guanosine, and comparable with Adriamycin. Mean survival time in AG60 treated group was significantly longer than that in control, acrifavine, guanosine or Adriamysin treated group.
Acriflavine ; Animal Experimentation ; Animals ; Body Weight ; Cell Line ; Doxorubicin ; Guanosine ; Humans ; Mice ; Mice, Inbred ICR ; Survival Rate ; Tumor Burden

We investigated fifty four patients with spontaneous intracerebral lobar hemorrhage who were admitted to the Seoul National University Hospital Neurology Sercice during a period of five and a half years. Of these patients 25 (46.3%) had hypertension as the probable cause of hemorrhage Of the remaining cases, 12(22.2%) had other etiologies including 5 arteriovenous malforrnations. 3 aneurysms, 2 tumors, 1 Moyamoya disease and 1 superior sagittal sinus thrombosis, while 14(25.2%) had no apparent etiology. But some of them seemed to be due to cerebral amyloid angiopathy or occult vascular malformation. Parietal region was the most frequent site of hemorrage(23 cases, 42.6%). Six cases had multiple intracerebral hematoma. Common clinical manifestations were headache, vomiting, hemiparesis, seizure in order of frequency. Mortality rate was 16.7%, which was correlated with the size of hematoma (P<0.05) and consciousness level at the initial stage (p<0.05). But not with the presence of intraventricular or subarachnoid hemorrhage. Hypertension or age of onset.
Age of Onset ; Aneurysm ; Cerebral Amyloid Angiopathy ; Cerebral Hemorrhage* ; Consciousness ; Headache ; Hematoma ; Hemorrhage ; Humans ; Hypertension ; Mortality ; Moyamoya Disease ; Neurology ; Paresis ; Rabeprazole ; Seizures ; Seoul ; Subarachnoid Hemorrhage ; Superior Sagittal Sinus ; Thrombosis ; Vascular Malformations ; Vomiting

This is a case report of a sixteen-year-old boy who has been suffering from throbbing headache since thirteen years of age. Neuroimaging investigations including brain CT and MRI demonstrated the characteristic features of Sturge-Weber syndrome: intracranial calcification, enlarged choroid plexus. And gyral enhancement. However, there was no facial nevus or focal neurological abnorrnality.
Brain ; Choroid Plexus ; Headache ; Humans ; Magnetic Resonance Imaging ; Male ; Neuroimaging ; Nevus* ; Sturge-Weber Syndrome*