Redundant publication in hepatology.
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Alcohol Dehydrogenase↗
Biomedical subjects
M Ohata
Publications and source records attributed to M Ohata.
[Chest wall reconstruction after the resection of primary chest wall tumors].
Between April 1983 and June 1994, we performed chest wall reconstructions on 9 patients (7 males and 2 females) out of 27 all of whom underwent the radical resection for the primary chest wall tumors. Histological diagnosis of tumors included 6 chondrosarcomas, 1 Ewing's sarcoma, 1 plasmacytoma and 1 giant cell tumor. Six lesions were located on the rib and 3 on the sternum. For the materials for reconstruction of the chest wall use a polyethylene plate in 2 patients, a Marlex mesh in 5 patients and a Marlex mesh with a methyl methacrylate utilizing the sandwich method in 2 patients. The polyethylene plate proved to be satisfactory for maintaining stability of the chest wall. However, our experience using this plate showed intensive foreign body reactions, and discovering these we have not use the polyethylene plate. Marlex mesh had an affinity with human tissue and was very easy to use and produced no complications. We use Marlex mesh for flat surfaces on the anterior or posterior chest wall. Marlex mesh and methyl methacrylate utilizing the sandwich method, combined the solidity and shaping of methyl methacrylate with the benefit such as easy fixation and excellent incorporation of the mesh.
Adult↗
[Five cases of myelodysplastic syndrome treated with cytarabine ocfosfate].
Five cases of myelodysplastic syndrome were treated with cytarabine ocfosfate. Ocfosfate (100-200 mg) was orally administered for 14 days with 14 days' interval. Etoposide was combined in one case, and nartograstim was added in two cases. Two of the five cases achieved remission, one case having complete remission, and another case showing a good response. Their remission durations were 141 and 112 days, respectively. Further improvement of therapy is needed to achieve a higher remission rate and a longer remission duration.
Administration, Oral↗
[Usefulness of the modified Greipp's morphological classification of multiple myeloma cells].
In order to clarify the clinical usefulness of the morphological classification of multiple myeloma (MM) originally proposed by Greipp, et al. and modified by us, Giemsa-stained MM cells in bone marrows obtained from 61 untreated patients were analyzed. According to the original classification, there was no significant difference in survival time between the patients with plasmablastic MM and those with other types. However, the mean survival time of each type of MM according to the modified classification was 2014 days in mature MM, 1564 days in intermediate MM, 967 days in immature MM, and 254 days in plasmablastic MM. The survival time of plasmablastic MM was significantly shorter than those of other types. DNA aneuploidy was observed more frequently in plasmablastic MM than in other types. Furthermore, PCNA- and Ki-67-positive rates were higher in plasmablastic MM than in other ones. Four of five patients with plasmablastic MM who were treated with VAD(vincristine, doxorubicin, dexamethasone) regimen showed no significant effect, and most patients with the type died of sepsis or renal failure. From these results, it was concluded that patients with plasmablastic MM have a poor prognosis. Moreover, our modified classification is recommended as a clinically useful approach for selecting treatment strategy and predicting an accurate prognosis.
Adult↗
Enhanced interaction between tubulin and microtubule-associated protein 2 via inhibition of MAP kinase and CDC2 kinase by paclitaxel.
Paclitaxel, an anti-mitotic anti-cancer agent, is active against solid tumors. The inhibition of depolymerization and promotion of microtubular assembly are essential for the anti-tumor activity of paclitaxel. Microtubule-associated proteins (MAPs) co-polymerize with tubulin and play some roles in microtubular dynamics. We examined the effect of paclitaxel on the interaction between tubulin and MAPs. Human lung-cancer cells, PC-14, were synchronized to G1/S border by the thymidine-double-block technique. After release from exposure to thymidine, the cells were treated briefly with 2 nM paclitaxel and the levels of alpha and beta tubulins and MAPs were examined after various times. Immunoblot analysis of paclitaxel-treated cells showed no changes in the overall expression of alpha and beta tubulins, microtubule-associated protein 2 (MAP2) or MAPs in comparison with controls. The samples were immunoprecipitated with anti-alpha- and anti-beta-tubulin antibodies and reblotted with an anti-MAP2 antibody, which showed that the amount of co-immuno-precipitated MAP2 in the synchronized cells, were increased by the brief paclitaxel treatment. These results suggest that paclitaxel treatment enhances the interaction between alpha and beta tubulins and MAP2. Since the phosphorylation state of MAP2 regulates the affinity of MAP2 for tubulins, and mitogen-activated protein (MAP) kinase is considered to be one of the kinases responsible for MAP2 phosphorylation, the effect of paclitaxel treatment on the MAP-kinase activity of synchronized PC-14 cells was examined. Two bands with molecular masses of 42 and 44 kDa were detected by an "intra-gel" MAP-kinase assay using myelin basic protein as the substrate. Paclitaxel treatment inhibited the MAP-kinase activity of PC-14 cells and inhibition was maximal at the G2/M phase of the cell cycle. Similar, concentration-dependent inhibition by paclitaxel of cellular MAP kinase of human synchronized small-cell lung carcinoma, H69, was observed. No inhibition of the MAP kinase of the paclitaxel-resistant sub-line H69/Txl by paclitaxel was observed, suggesting that some change of the MAP-kinase cascade had occurred in these cells. No direct inhibition of MAP-kinase activity by paclitaxel was observed in the cell-free assay (in vitro), suggesting that paclitaxel did not inhibit MAP kinase directly. Since it has been speculated that p34cdc2 kinase is also a kinase that phosphorylates MAP2, the effect of paclitaxel treatment on the p34cdc2-kinase activity of synchronized PC-14 and PC-9 cells was examined. Paclitaxel inhibited p34cdc2-kinase activation at the G2/M phase. These results suggest that paclitaxel inhibited MAP kinase and p34cdc2 kinase in vivo indirectly. These actions of paclitaxel may be responsible for the increased affinity between MAP2 and tubulins that it induces.
Amino Acid Sequence↗
Polymorphisms in alcohol metabolizing enzyme genes and alcoholic cirrhosis in Japanese patients: a multivariate analysis.
Alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and P450IIE1 are the primary enzymes that catalyze the conversion of ethanol to acetaldehyde and then to acetate. Genetic polymorphisms have been reported in ADH2, ADH3, ALDH2, and the 5'-flanking region of P450IIEI. In this study, we used multivariate analysis to determine which genetic polymorphisms in alcohol metabolizing enzymes were independently associated with the development of alcoholic cirrhosis. Thirty-four noncirrhotic alcoholic patients, including 27 with fatty liver and 7 with nonspecific changes, and 46 patients with alcoholic liver cirrhosis were studied. Restriction fragment length polymorphisms (RFLPs) in the ADH2 and P450IIE1 genes were detected by digestion of polymerase chain reaction (PCR)-amplified DNA with MaeIII and RsaI, respectively. In the ALDH2 gene, RFLPs were detected by differences in the MboII site after PCR amplification. By multivariate analysis of four significant factors including total alcohol intake, ADH, ALDH, and P450IIE1 using the multiple logistic regression model, genotype ADH2(2)/ADH2(2) (P = .029) and genotype c1/c1 of P450IIE1 (P = .013) were found to be independently associated with alcoholic cirrhosis. The odds ratios for ADH2(2)/ADH2(2) genotype and the type A genotype of P450IIE1 (c1/c1) were 4.600 and 4.006, respectively. These results suggest that ADH2 and P450IIE1 gene polymorphisms may be independently associated with the development of alcoholic liver cirrhosis in Japan.
Adult↗
Stimulatory effect of 1 alpha,25-dihydroxyvitamin D3 on mouse alveolar macrophage tumor necrosis factor-alpha production in vitro: involvement of protein kinase C and Ca2+/calmodulin-dependent kinase.
1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3, calcitriol] has been shown to modulate the immune function of peripheral monocytes and peritoneal macrophages. However, its effect on alveolar macrophage (AM) cytokine secretion has not been reported. We therefore investigated the influence of calcitriol on tumor necrosis factor (TNF-alpha) production by murine AMs and attempted to elucidate changes in the signal transduction system involved in such effects. Calcitriol significantly enhanced TNF-alpha secretion by AM stimulated with either lipopolysaccharide (LPS; 10 micrograms/ml; p < 0.005) or phorbol 12-myristate 13-acetate (PMA; 100 ng/ml; p < 0.05) at low doses (between 10(-11) and 10(-9) M). However the protein kinase C (PKC) inhibitor, H7 (10 microM), and the Ca2+/calmodulin inhibitor, W7 (25 microM), reversed such calcitriol effects. Calcitriol increased the total PKC activity of AMs. These findings indicate that calcitriol enhances both LPS- and PMA-stimulated TNF-alpha secretion through PKC- or Ca2+/calmodulin-dependent pathways.
Animals↗
[A case of chronic hypersensitivity pneumonitis due to long term exposure to toluene diisocyanate].
A 55-year-old paint sprayer, who had been working with paint containing toluence diisocyanate since age 20, was admitted to our hospital with a complaint of exertional dyspnea. Physical examination revealed clubbed fingers, and fine crackles were audible in both lower lung fields. The thoracic CT film showed diffuse linear and ringed shadows in both lung fields. Open lung biopsy disclosed alveolitis and fibrosis as well as infiltration of mononuclear cells, but no Masson bodies or granulomas. Toluene diisocyanate-specific antibody was positive. Based on these results, we diagnosed chronic hypersensitivity pneumonitis due to the chemical. To our knowledge, there has been no previously reported case of chronic hypersensitivity pneumonitis due to isocyanate.
Alveolitis, Extrinsic Allergic↗
Systemic management of cerebral edema based on a new concept in severe head injury patients.
Cerebral hypothermia treatment of critical brain injury patients was studied based on the management and control of cerebral thermo-pooling, synaptic excitation, hypermetabolic demand, and the systemic critical condition of the metabolic reserve. The initial pathophysiological changes after trauma included a progressive increase in brain tissue temperature. Such cerebral thermo-pooling, which reached a maximum of 43.8 degrees C, can change or damage the vascular proteins directly. The brain tissue temperature was influenced by four factors: 1. the cerebral metabolism, 2. the systemic excess energy metabolism, 3. the CPP that carries the systemic energy to the brain tissue, and 4. the cerebral blood flow that leads to washout of brain tissue temperature. Mild cerebral hypothermia (32-33 degrees C) managed by the whole body compartment cooling technique in the critical conditions of diffuse brain injury patients (GCS < 4) produced a good recovery in 8 of 10 patients. Continuous monitoring of the jugular venous oxygen saturation and BTT/TMT was effective for evaluating cerebral ischemia and oxygen metabolic disturbances even during cerebral hypothermia treatment.
Blood-Brain Barrier↗
Effect of ageing on erythrocyte aldose reductase and sorbitol dehydrogenase activity.
We measured erythrocyte aldose reductase and sorbitol dehydrogenase activity in erythrocytes in healthy individuals aged from 16 to 91 years to determine the mechanism of age-dependent sorbitol accumulation. Erythrocyte aldose reductase activity increased significantly with age but ageing had no effect on sorbitol dehydrogenase activity. Age and the aldose reductase/sorbitol dehydrogenase ratio were positively correlated. These findings suggest that an increase in the ratio of aldose reductase to sorbitol dehydrogenase may contribute to the tissue accumulation of sorbitol in the elderly and may be a mechanism of a disease that is common in elderly individuals.
Adolescent↗
Effect of aging on plasma 1,5-anhydroglucitol levels in humans and rats.
Since normal reference values change with age in some clinical parameters, we measured the plasma levels of 1,5-anhydroglucitol (AG), a new marker of glycemic control in diabetes mellitus, in healthy subjects and in rats. Our results showed a significantly negative correlation of the marker with age in humans and that the plasma AG levels of older rats were markedly lower than those of younger counterparts. This remarkable reduction of AG in the older rat group can be partially explained by our finding that aged animals excreted AG more rapidly in the urine than younger ones, besides a decrease in food intake. We therefore suggest that normal clinical reference values for plasma AG levels should be modified according to age.
Adolescent↗
Effect of chronic tobacco smoke exposure on the function of alveolar macrophages in mice.
We evaluated the effect of chronic tobacco smoke exposure on the function of the alveolar macrophage (AM) in mice. Tumor necrosis factor-alpha production of the AM triggered by lipopolysaccharides was smaller in smoke-exposed mice as compared to control mice but did not reach statistical significance (27.3 +/- 4.0 vs. 34.8 +/- 4.9 U/ml). The percentage of AM which did not phagocytize latex particles in the smoke-exposed mice was significantly larger than that in control mice (33.9 +/- 2.3 vs. 20.8 +/- 2.1%; p < 0.05). Ia antigen expression of the AM was significantly larger in smoke-exposed mice (cytotoxicity index: 0.180 +/- 0.033 vs. 0.038 +/- 0.0118; p < 0.01). The asialo-GM1 antigen expression was similar in both groups (0.949 +/- 0.007 vs. 0.961 +/- 0.011). Although the precise mechanisms of these functional changes of the AM by tobacco smoke exposure are not clear, they may have some immunological effects on the alveolar space.
Animals↗
[Influence of age on mouse pulmonary alveolar macrophage clonal growth].
Although monocyte influx has been suggested as the primary source of pulmonary alveolar macrophages (AM), increasing evidence from recent studies has indicated that AM may be sustained through a self-renewal mechanism. We evaluated the age-related changes of the clonal growth (colony formation) of AM in mice (C57BL/6N mice and senescence accelerated mice). The colony forming unit (CFU) of AM of 24 month old C57BL/6N mice was lower than that of AM of 4-month-old mice (p < 0.05). In SAMP6 (senescence accelerated mice), CFU of AM was decreased with aging (p < 0.05). In SAMR1 (controls for SAMP6), CFU of AM was decreased with aging (p < 0.001). In SAMR1, CFU of bone marrow (BM) adherent cells of 12-month-old mice was similar to that of 4-month-old mice. In SAMP6, CFU of BM adherent cells of 12-month-old mice was larger than that of 4-month-old mice (P < 0.005). It was concluded that the CFU of AM declined with aging, but the CFU of the BM adherent cells did not. The decline of the AM CFU may be partly responsible for the defect of the immune response of the alveolar space in the elderly.
Aging↗
[Hemangiopericytoma].
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Diagnosis, Differential↗
[Hemangioendothelioma].
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Diagnosis, Differential↗
[Neurofibroma, neurinoma].
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Diagnosis, Differential↗