M Nishida

The University of Tokyo, Tōkyō, Japan

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Publications (9)20.2 Total impact

  • K Mori · Y Yamagata · S Aikou · M Nishida · T Kiyokawa · K Yagi · H Yamashita · S Nomura · Y Seto ·
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    ABSTRACT: Transthoracic esophagectomy (TTE) is believed to have advantages for mediastinal lymphadenectomy in the treatment of resectable esophageal cancer despite its association with a greater incidence of pulmonary complications and postoperative mortality. Transhiatal esophagectomy is regarded as less invasive, though insufficient in terms of lymph node dissection. With the aim of achieving lymph dissection equivalent to that of TTE, we have developed a nontransthoracic esophagectomy (NTTE) procedure combining a video-assisted cervical approach for the upper mediastinum and a robot-assisted transhiatal approach for the middle and lower mediastinum. We prospectively studied 22 accumulated cases of NTTE and verified feasibility by analyzing perioperative and histopathological outcomes. We compared this group's short-term outcomes with outcomes of 139 equivalent esophageal cancer cases operated on at our institution by conventional TTE (TTE group). In the NTTE group, there were no procedure-related events and no midway conversions to the conventional surgery; the mean operation time was longer (median, 524 vs. 428 minutes); estimated blood loss did not differ significantly between the two groups (median, 385 mL vs. 490 mL); in the NTTE group, the postoperative hospital stay was shorter (median, 18 days vs. 24 days). No postoperative pneumonia occurred in the NTTE group. The frequencies of other major postoperative complications did not differ significantly, nor were there differences in the numbers of harvested mediastinal lymph nodes (median, 30 vs. 29) or in other histopathology findings. NTTE offers a new radical procedure for resection of esophageal cancer combining a cervical video-assisted approach and a transhiatal robotic approach. Although further accumulation of surgical cases is needed to corroborate these results, NTTE promises better prevention of pulmonary complications in the management of esophageal cancer.
    Diseases of the Esophagus 03/2015; DOI:10.1111/dote.12345 · 1.78 Impact Factor
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    ABSTRACT: Either palliative distal gastrectomy or gastrojejunostomy are the initial treatment options for locally advanced gastric cancer with outlet obstruction when curative-intent resection is not feasible. Since chemotherapy is the mainstay for unresectable gastric cancer, the clinical value of palliative distal gastrectomy is controversial. We retrospectively reviewed the clinical data of patients with gastric cancer with outlet obstruction treated at our institution between January 2002 and December 2012. We compared the clinical outcomes of palliative distal gastrectomy with those of gastrojejunostomy patients and the factors affecting overall survival were evaluated. Elective palliative distal gastrectomy and gastrojejunostomy were performed in 18 and 25 patients, respectively. The median overall survival times in the gastrojejunostomy and palliative distal gastrectomy groups were statistically equivalent at 8.8 and 8.3 months, respectively (P = 0.73), despite the more locally advanced tumors in the gastrojejunostomy as compared with the palliative distal gastrectomy group. A multivariate Cox regression analysis showed absence of postoperative chemotherapy and higher postoperative complication grade to be associated with worse clinical outcomes. Palliative distal gastrectomy offers neither survival nor palliative benefit as compared to gastrojejunostomy. Minimizing the morbidity of intervention for outlet obstruction, followed by chemotherapy, appears to be the optimal initial strategy for incurable gastric cancer with outlet obstruction.
    World Journal of Surgical Oncology 11/2014; 12(1):364. DOI:10.1186/1477-7819-12-364 · 1.41 Impact Factor
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    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 06/2014; 7(5):2690-4. · 1.89 Impact Factor
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  • Shouji Shimoyama · Takashi Kiyokawa · Masato Nishida · Yasuyuki Seto ·
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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: Endothelial cell injury/dysfunction is considered to play a critical role in the pathogenesis of severe sepsis and septic shock. Although it is considered that endothelial cell apoptosis is involved in endothelial injury/dysfunction, physiological involvement remains ambiguous since the induction of apoptosis requires the inhibition of endogenous apoptosis inhibitors. Here we show that caspase-3 activation, a biological indicator of apoptosis, is observed in response to lipopolysaccharide (LPS) stimulation even under the influence of endogenous apoptosis inhibitors, and that activated caspase-3 is rapidly released from human umbilical vein endothelial cells (HUVEC). In the presence of cycloheximide (CHX), an increase in intracellular caspase-3/7 activity in response to LPS was not detected in HUVEC up to 24 h following stimulation even in the presence of LPS-binding protein (LBP), soluble CD14 and soluble MD-2, whereas the decrease in cell viability and increase in release of the cellular enzyme lactate dehydrogenase (LDH) were observed in a soluble CD14/LBP-dependent manner. On the other hand, even in the absence of CHX, a significant increase in caspase-3/7 activity and a cleaved caspase-3 fragment with a slight increase in LDH release was observed in culture supernatants in response to LPS. This increase in caspase-3/7 activity was observed even when LDH release was undetected. These results indicate that caspase-3 is activated by LPS under physiological conditions and suggest that HUVEC escape from cell death by rapidly releasing activated caspase-3 into extracellular space. Failure of this escape mechanism may result in endothelial injury/dysfunction.
    Biochimica et Biophysica Acta 07/2009; 1792(10):1011-8. DOI:10.1016/j.bbadis.2009.06.006 · 4.66 Impact Factor
  • T Hoashi · H Okochi · T Kadono · K Tamaki · M Nishida · S Futami · K Maekawa ·
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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. DOI:10.1111/j.1365-2133.2008.08475.x · 4.28 Impact Factor
  • T Himi · M Ikeda · T Yasuhara · M Nishida · I Morita ·
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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. DOI:10.1007/s00702-003-0049-z · 2.40 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. DOI:10.1038/sj.bmt.1703568 · 3.57 Impact Factor
  • M Nishida · S Futami · I Morita · K Maekawa · S I Murota ·
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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. · 1.91 Impact Factor
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    K Maekawa · S Futami · M Nishida · T Terada · H Inagawa · S. and Suzuki · K Ono ·
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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. DOI:10.1097/00005373-199707000-00088 · 2.96 Impact Factor

Publication Stats

178 Citations
20.20 Total Impact Points


  • 2014
    • The University of Tokyo
      Tōkyō, Japan
  • 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