Esophageal tunnel formation after endoscopic variceal sclerotherapy.
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Biomedical subjects
Publications and source records attributed to S Muranaka.
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To clarify the clinicopathological features of tumors with submucosal invasion, especially superficial elevated and sessile ones, histological architectures of 32 cases of submucosal invasive cancers were analyzed. They were classified into 3 types based on cross-section view: PG and NPG of Shimoda's classification and PG'. Histological architectures were drawn in accordance with these findings. In 7 PG-Ca which consisted of PG only, no apparent correlation was found between the tumor sizes and invasion depth of submucosal layer. However, 12 NPG-Ca which consisted of NPG only and 12 Mixed-Ca which include various cross-section views both showed massive invasion into the submucosa with 1 cm or more in tumor size. Therefore these two types were similar in biological behavior in terms of invasion depth. And degree of submucosal invasion tended to increase in the order of PG-Ca, Mixed-Ca and NPG-Ca. Examinating histological architectures of the Mixed-Ca tumors in details, all of these cancers were consisted of both PG and PG'. Of the 12 Mixed-Ca, 91.7% were proved to be PG dominant type. Macroscopically, I s and II a contained 88.9% and 40.0% of Mixed-Ca, respectively. In conclusion, these results suggest that PG' is a subtype of PG, and PG-Ca have a correlation between tumor invasion and alteration from PG to PG' in histological architectures among submucosal cancers. It is important to clarify morphological features of PG' in margin of I s and II a tumors in diagnosing the depth of early colorectal cancers.
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Ten children between the ages of five and fifteen years old with leukemia (two with acute nonlymphocytic leukemia in first remission, four with acute lymphocytic leukemia in first or second remission, one with acute lymphocytic leukemia in relapse, and one with chronic myelocytic leukemia in chronic phase), malignant lymphoma (one) or severe aplastic anemia (one) were given transplants from HLA-matched or mismatched family members between March, 1982 and April, 1984. Two patients died of leukemia relapses on days 107 and 257 following transplantation. One patient died of cardiac failure on day 157. One patient who received HLA-mismatched marrow from his father died of pulmonary edema and acute graft versus host disease on day 32. Six are alive 268-843 days post transplantation. None of the ten patients developed interstitial pneumonia due to cytomegalovirus which is one of the major causes of death reported in other published studies.
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Several genetic markers, HLA-A, B and DR antigens, Gm and Km types, and ABO blood types, were studied on 78 rubella seronegative schoolgirls immunized with "TO336" rubella vaccine. A marked association was found between an HLA haplotype, HLA-Aw24-Bw52-DRHO, and the low antibody responsiveness to rubella virus. The association with the DR antigen was thought to be primary to those with the HLA-A or B antigens, suggesting that the gene(s) controlling the low responsiveness to rubella might be located near the HLA-DR locus in the human 6th chromosome. There was no statistically significant association between Gm, Km or ABO blood types and the rubella specific immune responsiveness as far as the primary in vivo antibody response was concerned.
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Properties of delta-aminolevulinic acid synthetase in erythroblasts of patients with pyridoxine-responsive anemia were investigated with special reference to the protease in mitochondria of erythroblasts. delta-Aminolevulinic acid synthetase activity in erythroblasts of patients with this disease before treatment was extremely decreased, whereas it gradually increased in parallel with the improvement of anemia by the therapy with pyridoxal phosphate. The amount of apo-delta-aminolevulinic acid synthetase in erythroblasts before treatment was also extremely diminished. Apparent affinity to pyridoxal phosphate of the apo-delta-aminolevulinic acid synthetase obtained from erythroblasts of the patients was almost the same as that of normal controls. The activity of a new protease which is considered to be engaged in the regulation of delta-aminolevulinic acid synthetase levels in mitochondria of erythroblasts was shown to be in normal range in erythroblasts of the patients. On the other hand, apo-delta-aminolevulinic acid synthetase obtained from the patients was extremely sensitive to the protease. These results indicate that disturbance of heme synthesis characteristic to pyridoxine-responsive anemia could be ascribed to the hypercatabolism of delta-aminolevulinic acid synthetase caused by the increased susceptibility to the controlling protease in erythroblasts.
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We examined the response of T lymphocytes activated with specific alloantigens following Fas-mediated apoptosis; using a mixed lymphocyte culture (MLC) system. Cells obtained from an MLC after 6 or 7 days of culture were incubated for are additional 24 hours in the presence or absence of the agonistic monoclonal antibody (MoAb), 7C11, or the antagonistic MoAb, ZB4. We assessed DNA fragmentation/specific cytotoxiy of the MoAb-treated cells. Cells harvested after 4 days of culture were sensitive to apoptosis induced by 7C11 with maximum DNA fragmentation observed on day 6. ZB4 slightly inhibited apoptosis of the cells compared with controls. The simultaneous addition of recombinant interleukin-2 (rIL-2) with the MoAbs significantly inhibited DNA fragmentation in control and ZB4-treated cells, but had little effect on the 7C11-treated cells. Control and ZB4-treated MLC cells showed cytotoxic activities against specific target cells, namely >10%. In contrast, the 7C11-treated cells showed <5% cytotoxicity. Although the addition of rIL-2 increased specific percentage cytotoxicity of control and ZB4-treated cells, it had little effect on the specific cytotoxic activity of the 7C11-treated MLC cells. These results suggest that specific cytotoxic T lymphocytes may be eliminated via apoptosis mediated by the Fas/Fas ligand system.
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