L-10 has been recognized as an irnmune suppressive cytokine which inhibits Ag-specific activation and proliferation of T cells. It also inhibits Ag presenting capacity of monocyte/macrophage and down-regulates monokine production. However it has also shown that IL-10 has stimulatory effect on immune effector cells in recent studies. This report shows that IL-10 has direct stimulatory effect on antitumor cytolytic activity suppressed by TGF-B. To assess the effect of IL-10 on cytolytic activity against tumor, spleen cells prepared from tumor-bearing mice were cultured with mitomycin C-treated MOPC-315 cells in the presence of IL-10. Unexpectedly, IL-10 was able to reverse the cytolytic activity suppressed with TGF-B. The stimulatory effect of IL-10 was dependent on the addition time of IL-10. At day 0, 4, those effects were shown higher than those of the other days. Also, the stimulatory effect of IL-10 showed specificity against MOPC-315 tumor cells. To elucidate the role of endogenous IL-10, TGF-B in MLTC cultures, anti-IL-10 and anti-TGF-B mAb were used. The inhibition of IL-10 release in MLTC cultures by using anti-IL-10 mAb resulted in the suppression of cytolytic activity against MOPC-315 tumor cells. Taken together, although IL- 10 has been recognized as a strong immunosuppressive cytokine derived of tumor cells, IL-10 showed the direct stimulatory effect on the antitumor cytolytic activity of spleen cells.
Animals ; Interleukin-10* ; Mice ; Mitomycin ; Sensitivity and Specificity ; Spleen* ; T-Lymphocytes ; Transforming Growth Factor beta

Gastric cancer cells express large amounts of galectin-3 on the cell surface. This fact may provide the possibility to use galectin-3 protein as a surface target for delivering cytotoxic anticancer agents. To investigate the possibility of application of galectin-3 protein as a target protein in delivering cytotoxic anticancer agents, we synthesized doxorubicin immunoconjugate by using maleimidocaproic acid and conjugated doxorubicin immunoconjugate to anti-galectin-3 mAb. The anticancer effect of immunotoxin was assayed on NIH3T3, AGS and KATO III cell lines. The anticancer effect of immunotoxin on AGS cell line is highest and that of KATO III is higher than that of NIH3T3. This results relate to that of flow cytometry analysis previously shown and indicate that galectin-3 protein can be used as a target protein on the surface of gastric cancer cell for delivering cytotoxic anticancer agents.
Antineoplastic Agents* ; Cell Line ; Doxorubicin ; Flow Cytometry ; Galectin 3 ; Galectins* ; Immunoconjugates ; Immunotoxins ; Staphylococcal Protein A ; Stomach Neoplasms

The authors analyzed data from 15 patients with idiopathic dilated cardiomyopathy to evaluate the hemodynamic changes and left ventricular cineangiogram as compared with normal control. Mean right atrial pressure, right ventricular systolic pressure, mean pulmonary artery pressure and mean pulmonary wedge pressure were signigicantly elevated in patients with dilated cardiomyopathy. Left ventricular enddiastolic volume was increased in idiopathic dilated cardiomyopathy(139.9+/-58.73 ml/m2). Cardiac index, left ventricular ejection fraction and circumferential fiber shortening were significantly reduced in patients with dilated cardiomyopathy as compared with normal control(p<0.001). Hypokinetic, diffuse wall motion abnormalities of left ventricle were common in idiopathic dilated cardiomyopathy. A few cases of akinetic or dyskinetic segmental wall motion abnormalities were present. Left ventricular configurations in patients with idiopathic dilated cardiomyopathy were globe shape(53.4%) as compared with pear core shape(90%) of normal control. Associated mitral regurgitations in patients with idiopathic dilated cardiomyopathy confirmed by left ventricular cineangiogram were 53.3 percent. Mild to moderate mitral regurgitations were often present(46.6%).
Atrial Pressure ; Blood Pressure ; Cardiomyopathy, Dilated* ; Heart Ventricles ; Hemodynamics* ; Humans ; Pulmonary Artery ; Pulmonary Wedge Pressure ; Pyrus ; Stroke Volume

No abstract available.
Temporomandibular Joint*

No abstract available.
Temporomandibular Joint*

The coronary artery cross sectional area (CSA) is proportional to LV mass. We have measured the cross sectional area of the left and right coronary arteries in patients with ischemic heart disease to see whether it is related to the change in the LV mass. The following results were obtained ; 1) There were no significant difference in mean CSA of coronary arteries and LV mass determined by echocardiography and cineangiography between control and ischemic heart disease. 2) There were significantly increased ratio of left ventricular mass by cineangiogram to CSA of left anterior descending coronary artery in patients with myocardial infarction as compared with control group. 3) A linear relation between LV mass by cineangiogram and CSA of left coronary artery was noted in control group (r=0.53, P<0.05) and ischemic heart disease group (r=0.51, P<0.05). 4) A linear relation between LV mass determined by echocardiography and CSA of left coronary artery was noted in control group (r=0.55, P<0.05).
Cineangiography ; Coronary Vessels* ; Echocardiography ; Humans ; Myocardial Infarction ; Myocardial Ischemia

No abstract available.

Taxol is a clinically useful anticancer drug against a variety of cancers. Although it has been known that taxol induces the apoptosis of cancer cells through cytochrome C release and the activation of caspases, the effect of taxol on dendritic cells (DCs) has not been studied. In this study, taxol enhanced the expression of MHC class II on DCs, compared to medium-treated immature DCs. Surprisingly, the viability of DCs was not decreased by taxol, whereas that of cancer cells was. It was confirmed that taxol did not induce the apoptosis of DCs based on annexin V-FITC/propidium iodide (PI) staining assay. Since previous study demonstrated that taxol induced the production of nitric oxide (NO) related to the viability of DCs, the level of NO from taxol-treated DCs was determined. Any significant amount of NO was not detected. Although taxol enhanced the expression of a maturation marker, MHC class II molecules, it strikingly inhibited the proliferation of splenic T lymphocytes activated by DCs. Taken together, this study demonstrated that taxol induced an altered maturation of DCs, the increase of MHC class II molecule but the inhibition of proliferation of splenic T lymphocytes. It is suggested that taxol may induce the immunosuppression in patients with cancer by the inhibition of DC-activated T cell proliferation, but not by the direct killing of DCs.
Animals ; Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/drug effects ; Coloring Agents/metabolism ; Dendritic Cells/cytology/*drug effects/immunology ; Female ; Flow Cytometry ; Formazans/metabolism ; Histocompatibility Antigens Class II/biosynthesis ; Lymphocyte Activation/drug effects ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Paclitaxel/*pharmacology ; T-Lymphocytes/cytology/immunology/metabolism ; Tetrazolium Salts/metabolism

Disulfiram (DSF) is an aldehyde dehydrogenase inhibitor. DSF has potent anti-cancer activity for solid and hematological malignancies. Although the effects on cancer cells have been proven, there have been few studies on DSF toxicity in bone marrow cells (BMs). DSF reduces the metabolic activity and the mitochondrial membrane potential of BMs. In subset analyses, we confirmed that DSF does not affect the proportion of BMs. In addition, DSF significantly impaired the metabolic activity and differentiation of BMs treated with granulocyte macrophage-colony stimulating factor, an essential growth and differentiation factor for BMs. To measure DSF toxicity in BMs in vivo, mice were injected with 50 mg/kg, a dose used for anti-cancer effects. DSF did not significantly induce BM toxicity in mice and may be tolerated by antioxidant defense mechanisms. This is the first study on the effects of DSF on BMs in vitro and in vivo. DSF has been widely studied as an anti-cancer drug candidate, and many anti-cancer drugs lead to myelosuppression. In this regard, this study can provide useful information to basic science and clinical researchers.

Metformin is a treatment used widely for non-insulin-dependent diabetes mellitus with few side effects and acts by inhibiting hepatic gluconeogenesis and glucose absorption from the gastrointestinal tract. Lymphoma is one of the most common hematological malignancies in dogs. Chemotherapy is used mainly on lymphoma, but further research on developing anticancer drugs for lymphoma is needed because of its severe side effects. This study examined the anticancer effects of metformin alone and in combination with 2-deoxy-D-glucose (2-DG), a glucose analog, on EL4 cells (mouse T-cell lymphoma). Metformin reduced the metabolic activity of EL4 cells and showed an additive effect when combined with 2-DG. In addition, cell death was confirmed using a trypan blue exclusion test, Hochest 33342/propidium iodide (PI) staining, and Annexin V/PI staining. An analysis of the cell cycle and mitochondria membrane potential (MMP) to investigate the mechanism of action showed that metformin stopped the G2/M phase of EL4 cells, and metformin + 2-DG decreased MMP. Metformin exhibited anticancer effects as a G2/M phase arrest mechanism in EL4 cells and showed additive effects when combined with 2-DG via MMP reduction. Unlike cytotoxic chemotherapeutic anticancer drugs, metformin and 2-DG are related to cellular glucose metabolism and have little toxicity. Therefore, metformin and 2-DG can be an alternative to reduce the toxicity caused by chemotherapeutic anticancer drugs. Nevertheless, research is needed to verify the in vivo efficacy of metformin and 2-DG before they can be used in lymphoma treatments.