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Articles by T Fujita
Total Records ( 6 ) for T Fujita
  T Shinohara , S Kanaya , K Taniguchi , T Fujita , K Yanaga and I. Uyama

Objective  To evaluate the safety and effectiveness of laparoscopic total gastrectomy with D2 lymphadenectomy for gastric cancer.

Design  Review of findings from a prospectively acquired institutional database.

Setting  University hospital.

Patients  Fifty-five consecutive patients operated on by the same surgeon between October 1997 and March 2008.

Main Outcome Measures  Blood loss, complication rate, and survival.

Results  All operations were accomplished without conversion to open laparotomy. The median operative time was 406 minutes. The median blood loss was 102 mL. A median of 46 lymph nodes were harvested. The TNM stages of the tumor were I in 17 patients (31%), II in 12 (22%), III in 16 (29%), and IV in 10 (18%). A total of 21 complications occurred in 18 patients (33%) with no postoperative mortality. At last follow-up, 44 of the 55 patients were alive without tumor recurrence and 3 with recurrence at a median follow-up of 16 months, whereas 8 had died of recurrence or another cause.

Conclusions  The mortality rate of zero and acceptable morbidity of our series indicate that laparoscopic total gastrectomy with D2 lymphadenectomy is technically feasible and safe in the hands of experienced surgeons. Long-term follow-up is mandatory to validate oncologic outcome.

  T Fujita , K Teramoto , Y Ozaki , J Hanaoka , N Tezuka , Y Itoh , T Asai , S Fujino , K Kontani and K. Ogasawara

Tumor-draining lymph nodes (DLN) are the most important priming sites for generation of antitumor immune responses. They are also the location where an immunosuppressive cytokine, transforming growth factor-β (TGF-β), plays a critical role in suppressing these antitumor immune responses. We focused on TGF-β–mediated immunosuppression in DLNs and examined whether local inhibition of TGF-β augmented antitumor immune responses systemically in tumor-bearing mice models. For inhibition of TGF-β–mediated immunosuppression in DLNs, C57BL/6 mice subcutaneously bearing E.G7 tumors were administered plasmid DNA encoding the extracellular domain of TGF-β type II receptor fused to the human IgG heavy chain (TGFR DNA) i.m. near the established tumor. In DLNs, inhibition of TGF-β suppressed the proliferation of regulatory T cells and increased the number of tumor antigen-specific CD4+ or CD8+ cells producing IFN-. Enhancement of antitumor immune responses in DLNs were associated with augmented tumor antigen-specific cytotoxic and natural killer activity in spleen as well as elevated levels of tumor-specific antibody in sera. The growth of the established metastatic as well as primary tumors was effectively suppressed via augmented antitumor immune responses. Inhibition of TGF-β–mediated immunosuppression in DLNs is significantly associated with augmented antitumor responses by various immunocompetent cell types. This animal model provides a novel rationale for molecular cancer therapeutics targeting TGF-β. [Cancer Res 2009;69(12):5142–50]

  J Hirahashi , K Hishikawa , S Kaname , N Tsuboi , Y Wang , D. I Simon , G Stavrakis , T Shimosawa , L Xiao , Y Nagahama , K Suzuki , T Fujita and T. N. Mayadas

Background— Inflammation and thrombosis coexist in several disorders. Although it is recognized that leukocytes may induce a procoagulant state at sites of inflammation, the critical molecular determinants of this process remain largely unknown.

Methods and Results— To examine mechanisms of inflammation-induced thrombosis, we developed a murine model of thrombotic glomerulonephritis (TGN), a known cause of acute renal failure in patients. This model, induced by lipopolysaccharide and antibody to the glomerular basement membrane, led to rapid glomerular neutrophil recruitment, thrombotic glomerular lesions with endothelial cell injury, and renal dysfunction. In mice immunodepleted of neutrophils or lacking the leukocyte-specific integrin Mac-1, neutrophil recruitment, endothelial injury, glomerular thrombosis, and acute renal failure were markedly attenuated despite the robust generation of renal cytokines. Neutrophil elastase is a likely effector of Mac-1 because its activity was reduced in Mac-1–deficient mice and the phenotype in mice deficient in Mac-1 or neutrophil elastase was similar. Platelets accumulated in glomerular capillaries within 4 hours of TGN before evidence of thrombosis. Platelet immunodepletion before TGN markedly exacerbated hematuria (hemorrhage), inflammation, and injury, whereas thrombocytopenic Mac-1–deficient mice remained resistant to disease, indicating that initial glomerular platelet deposition protects the vessel wall from neutrophil-mediated sequelae. The subsequent thrombosis relied on the interaction of Mac-1 on recruited neutrophils with glycoprotein Ib on platelets as antibody-mediated disruption of this interaction attenuated TGN without affecting renal neutrophil accumulation.

Conclusions— These observations establish Mac-1 on neutrophils as a critical molecular link between inflammation and thrombosis and suggest it as an attractive target for antithrombotic therapy.

  T Fujita , M Nakano , J Ohtani , T Kawata , M Kaku , M Motokawa , N Tsuka , H Hayashi and K. Tanne

The present study was designed to examine the expression of Sox 9 and type II and X collagens in regenerated condyle resulting from the use of a functional appliance. Ninety, 3-week-old, mice were divided equally into the following groups: two experimental groups (condylectomy group and condylectomy with functional appliance group) and the corresponding control group. In the condylectomy group, a unilateral condylectomy was performed on the right side. In the condylectomy with appliance group, the mandible was repositioned in a forward direction using a functional appliance after unilateral condylectomy. The expression of Sox 9 and type II and X collagens in the condyle was determined immunohistochemically 4 weeks after surgery.

In mice with a condylectomy, the expression was minimal. On the other hand, these factors were highly expressed in the condylectomized side with the appliance. It is thus speculated that cartilaginous regeneration is due to the expression of chondrogenic factors, such as Sox 9 and type II and X collagens. It is also suggested that condyle regeneration results from an optimal intra-articular environment with appropriate joint spaces achieved by condylar repositioning.

  T Fujita and M. Chen

We demonstrate quantitative electron holographic tomography using a latex sphere as a simple example. Although a simple object is used, we believe that the observations made in this study will lead to further developments in electron holographic tomography. In particular, we make the quantitative interpretation of artifacts caused by incomplete angular information, i.e. a ‘missing wedge’.

  K Takahasi , H Kumeta , N Tsuduki , R Narita , T Shigemoto , R Hirai , M Yoneyama , M Horiuchi , K Ogura , T Fujita and F. Inagaki

The RIG-I like receptor (RLR) comprises three homologues: RIG-I (retinoic acid-inducible gene I), MDA5 (melanoma differentiation-associated gene 5), and LGP2 (laboratory of genetics and physiology 2). Each RLR senses different viral infections by recognizing replicating viral RNA in the cytoplasm. The RLR contains a conserved C-terminal domain (CTD), which is responsible for the binding specificity to the viral RNAs, including double-stranded RNA (dsRNA) and 5'-triphosphated single-stranded RNA (5'ppp-ssRNA). Here, the solution structures of the MDA5 and LGP2 CTD domains were solved by NMR and compared with those of RIG-I CTD. The CTD domains each have a similar fold and a similar basic surface but there is the distinct structural feature of a RNA binding loop; The LGP2 and RIG-I CTD domains have a large basic surface, one bank of which is formed by the RNA binding loop. MDA5 also has a large basic surface that is extensively flat due to open conformation of the RNA binding loop. The NMR chemical shift perturbation study showed that dsRNA and 5'ppp-ssRNA are bound to the basic surface of LGP2 CTD, whereas dsRNA is bound to the basic surface of MDA5 CTD but much more weakly, indicating that the conformation of the RNA binding loop is responsible for the sensitivity to dsRNA and 5'ppp-ssRNA. Mutation study of the basic surface and the RNA binding loop supports the conclusion from the structure studies. Thus, the CTD is responsible for the binding affinity to the viral RNAs.

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