M Nishida

Tokyo Medical University, Edo, Tōkyō, Japan

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Publications (10)20.01 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Esophageal complications occur after hematopoietic stem cell transplantation (HSCT). There are, however, only limited reports on the etiology or management of esophageal complications. Here, we report the occurrence of intramucosal hematoma presenting continuous esophageal hemorrhage in a 34 year-old man following the second peripheral blood stem cell transplantation for acute myeloid leukemia. His hematemesis started 2 months after HSCT and was repeated in supportive care. On day 156, he underwent total esophagectomy as a result of uncontrollable massive hematemesis. Histopathological testings of the resected esophagus confirmed intramucosal hematoma as a cause of hematemesis. This case highlights intramucosal hematoma as one of the important etiologies of esophageal complications following HSCT.
    International journal of clinical and experimental pathology. 01/2014; 7(5):2690-4.
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    ABSTRACT: We report a gastric cancer patient with positive peritoneal lavage cytology (CY1) who achieved 20-month progression free survival by S-1 monotherapy. An 82-year-old male patient who underwent distal gastrectomy with residual disease for type 4 scirrhous gastric cancer manifesting pyloric stenosis, direct invasion to the pancreas, and CY1. He received S-1 monotherapy postoperatively. His ECOG performance status (PS) was 0. The initial treatment schedule was 100mg/day, twice daily for 4 weeks with a 2-week rest, repeated every 6 weeks. Grade 2 thrombocytopenia at the end of the 5th course of treatment required discontinuation of one course of treatment, and subsequent treatment was continued with a dose reduction to 80mg/day. Afterwards, although treatment was temporarily postponed for 2 weeks, the dose modification enabled him to receive S-1 for 20 months, leading to a relative dose intensity of 81%. There was no evidence of disease progression. The most severe adverse events were transient grade 3 neutropenia as well as leukocytopenia, anemia, and thrombocytopenia, grade 2 each, without gastrointestinal toxicities. His PS was not deteriorated. Although survivalrates of CY1 gastric cancer patients are still poor, our case suggests that S-1 monotherapy is effective against CY1, even for patients aged over 80, if the relative dose intensity is maintained by comprehensive patient management and appropriate dose modification.
    Gan to kagaku ryoho. Cancer & chemotherapy 09/2012; 39(9):1411-4.
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    ABSTRACT: Accidental whole-body overexposure of radiation occurs very rarely. Radiation exposure causes DNA breaks in the cells and shows various clinical features, which are time dependent, dose dependent and tissue dependent. Neutron rays are more destructive than gamma rays but their actual effect on humans have been under-reported. We observed the time-dependent and the dose-dependent dermatological changes in a patient who was severely irradiated by neutron and gamma rays, with the aim of clarifying the clinicopathological features of severely irradiated skin. The detection of DNA breaks in keratinocytes was performed by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling technique. The degenerative changes of the skin and the re-epithelialization varied in a time dependent and dose dependent manner. DNA breaks were significantly higher in irradiated keratinocytes. Neutron rays caused depth-dependent degeneration of the skin. Evaluation of DNA breaks in the skin cells might be a clue to estimate local dosimetry.
    British Journal of Dermatology 04/2008; 158(3):597-602. · 3.76 Impact Factor
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    ABSTRACT: Cysteine uptake is the rate-limiting process in glutathione synthesis. Previously we have shown that the inhibitors of excitatory amino acid transporters (EAATs) significantly enhance glutamate toxicity via depletion of intracellular glutathione. In this study we show evidence that the neuronal glutamate transporter EAAT3 is directly enrolled in cysteine uptake in cultured neurons. Neuronal cysteine uptake was dependent on the extracellular sodium, and was suppressed by EAAT inhibitors. Cysteine uptake was suppressed by extracellular glutamate and aspartate, substrates of EAATs, and not by substrates of cysteine transporters. Intracellular glutathione levels were reduced by EAAT inhibitors, and not by inhibitors of cysteine transporters. Knock down of EAAT3 expression using antisense oligonucleotide significantly reduced cysteine uptake, intracellular glutathione level, and neuronal viability against oxidative stress. These facts indicate that EAAT3 functions as a cysteine transporter, and this function seems to be unique and distinct from cysteine transporters that have been reported.
    Journal of Neural Transmission 01/2004; 110(12):1337-48. · 3.05 Impact Factor
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    ABSTRACT: Accidental exposure to acute high-dose total body neutron radiation is rare. We report a 35-year-old man exposed to a total body dose of 5.4 Gy neutron- and 8.5-13 Gy gamma-radiation in a radiation criticality accident. He received a blood stem cell transplant from his HLA-identical sister. There was bone marrow recovery with complete donor chimerism. Random chromatid breaks were observed in donor cells suggesting a bystander effect of neutron exposure. The subject died 82 days after the accident (75 days post transplant) from multi-organ failure.
    Bone Marrow Transplantation 07/2002; 29(11):935-9. · 3.54 Impact Factor
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    ABSTRACT: Patient A who was exposed to a critical dose of radiation developed skin lesions throughout the body surface, gastrointestinal disorder with massive diarrhea and prominent bleeding, which caused severe loss in body fluids. Gastrointestinal bleeding due to the deteriorated intestinal mucosa was considered to be one of the major causes of death, although infection did not develop, possibly because of SDD and aseptic intensive care, until terminal stages. Patient A ultimately developed respiratory and renal failure in addition to skin exudate and gastrointestinal bleeding, and died of multiple organ failure on the 83rd day after exposure. The extreme unevenness of the dose distribution and the neutron versus y-ray component made the clinical manifestation very complicated. Initially, the mean absorbed dose was calculated as 16-20 GyEq for Patient A, mainly based on neutron-activated 24Na in the blood. However, a very recent calculation showed that the absorbed skin dose was highest at the upper-right abdomen reaching 61.8 Gy (27.0 as neutron plus 34.8 Gy as y-ray). The dorsal side was calculated to have received one eighth of the value of the abdominal side, and much smaller neutron component. His absorbed-dose distribution throughout the body was very inhomogeneous because of the closeness of the standing point to the mixing tank. Despite prolonged survival because of intensive care with massive fluids and blood transfusion, peripheral blood stem-cell transplantation, cultured skin-cell grafts, and the administration of cytokines for marrow, the patient was not saved. Restoration of the bone marrow function, prevention of skin fibrosis, radiation lung damage, and repair of gastrointestinal mucosa, and final recovery of the patient were elusive. Abundant personnel and resources were also a prerequisite to allow for the comprehensive and collective intensive care. A further understanding of the effects of high-dose radiation as well as the basic and clinical development of regeneration medicine are important issues for the future.
    Journal of Radiation Research 10/2001; 42 Suppl:S167-82. · 1.45 Impact Factor
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    ABSTRACT: We studied the change in gap junctional intercellular communication (GJIC) on human umbilical vein endothelial cells (HUVEC) under hypoxia-reoxygenation (H-R) conditions by the fluorescence redistribution after photobleaching (FRAP) method. Confluent HUVEC monolayers were exposed to hypoxia (pO2<0.1%) for 12 hours, and then were returned to normal atmospheric conditions for reoxygenation. Contrast microscopic observation showed no significant changes in the morphology of the HUVEC at any times after H-R. Reoxygenation following hypoxia caused time-dependent decrease in GJIC, that is, GJIC reduction was induced after 2 hours and reached maximum at 4-6 hours which recovered to normal levels after 18 hours. Oxidant sensitive fluorescence dye assay revealed that the generation of intracellular free radicals increased during the first 2 hours after reoxygenation. Hydroxyl radical scavengers (MCI-186, DMSO) and an iron chelator (deferoxamine) abolished the reduction of GJIC due to H-R. However, SOD, catalase and probucol were essentially inactive on this reduction. These data suggest that ischemia-reperfusion injury may be caused by a functional defect of GJIC induced by reactive oxygen radicals.
    Endothelium 02/2000; 7(4):279-86. · 1.65 Impact Factor
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    ABSTRACT: Vascular endothelial cells (EC), communicating with one another across gap junctions, are usually made dysfunctional by hypoxia and reoxygenation (H/R); however, very limited information exists regarding the effects of H/R on the endothelial gap junctions. We investigated whether H/R interferes with endothelial gap junctional intercellular communication (GJIC). After human umbilical vein EC had grown to confluence, they were exposed to hypoxia (pO2 < 0.1%) for 12-16 h and then returned to normal atmospheric conditions for reoxygenation. At 0-, 2-, 4-, 6-h reoxygenation, GJIC was detected by means of a fluorescence recovery after a photobleaching technique. The results demonstrated that a GJIC reduction (about 20% less than that under normoxia) was induced after 2 h of reoxygenation; after 4 h of reoxygenation, it began to recover (to about 10% less than that under normoxia); and after 6 h of reoxygenation, GJIC was restored to the normal level. Calphostin C (1 x 10(-7) mol/l), a specific protein kinase C inhibitor, partially inhibited the reduction in GJIC (resulting in a level about 10% less than that under normoxia), whereas the tyrosine kinase inhibitor genistein (10 micromol/L) completely blocked the reduction in GJIC. Vanadate (1.5 mmol/l), a tyrosine phosphatase inhibitor, amplified the inhibitory effect of H/R on GJIC (to about 40% less than that under normoxia). Immunofluorescence and immunoprecipitation showed that 2-h reoxygenation significantly stimulated tyrosine protein phosphorylation, and this phosphorylation event was obviously enhanced by vanadate. The results of Western blotting showed that the gap junctional protein connexin 43 (Cx43) was phosphorylated by H/R; moreover, immunoprecipitation demonstrated that 2-h reoxygenation induced a prominent increase of tyrosine phosphorylation of Cx43 compared with that under normoxia. These data indicate that H/R induces a transient endothelial GJIC dysfunction through the activation of tyrosine kinase and phosphorylation of tyrosine residues of Cx43.
    Journal of Cellular Physiology 10/1999; 180(3):305-13. · 4.22 Impact Factor
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    ABSTRACT: To examine (1) the effects of trauma on changes in neutrophil L-selectin and CD11b expression and on the levels of soluble L-selectin and (2) whether these alterations are different on leukocyte subpopulations in those patients who develop multiple organ dysfunction syndrome. Twenty patients with Injury Severity Score (ISS) > or = 16 and 15 patients with ISS score < 16 were studied. Arterial blood were collected serially after injury. The staining of leukocyte surface adhesion molecules was performed with antibodies against L-selectin and CD11b. Positive cell count and mean fluorescence intensity were determined by flow cytometry. Soluble L-selectin was measured using enzyme-linked immunosorbent assay. In patients with ISS > or = 16, neutrophil L-selectin expression showed an immediate increase, reaching peak levels between 3 to 4 hours after injury (p < 0.05 vs. patients with ISS < 16), followed by a gradual decrease. Plasma levels of soluble L-selectin reached peak levels at 6 hours after injury. However, in patients with ISS < 16, minimal changes in L-selectin expression and soluble L-selectin were observed. Neutrophil CD11b expression showed an immediate increase for the first 3 hours followed by a gradual increase up to 24 hours after injury. In patients who developed multiple organ dysfunction syndrome, CD11b both on neutrophils and lymphocytes remained elevated for 120 hours. These findings suggest that acute neutrophil activation is an early event after trauma and may be implicated as "a vulnerable window" for leukocyte-mediated end organ injury.
    The Journal of trauma 03/1998; 44(3):460-8. · 2.35 Impact Factor

Publication Stats

186 Citations
20.01 Total Impact Points

Institutions

  • 2013–2014
    • Tokyo Medical University
      • Division of Hematology
      Edo, Tōkyō, Japan
  • 2004
    • Teikyo University Hospital
      Edo, Tōkyō, Japan
  • 2000
    • Tokyo Medical and Dental University
      • Department of Cellular Physiological Chemistry
      Edo, Tōkyō, Japan