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Articles by M Nakamura
Total Records ( 10 ) for M Nakamura
  N Yamada , S Ota , Ying Liu , C. M Chang , S Thaker , M Nakamura and M. Ito
 

Risk factors for pulmonary embolism (PE) have been identified among populations in Western countries but have not been well characterized in Japan. A hospital-based case-control design employed cases with PE, which diagnosed by standard imaging techniques; controls were individuals drawn by systematic random sampling from the hospital admission register. A total of 100 (38 males and 62 females) and 199 controls were identified. Patients with PE were younger (56.5 vs 60.9 years) and more likely to be female. The odds ratio ([OR] adjusted for other factors) and 95% confidence interval (CI) for risk of PE was elevated for the following: female gender, prolonged immobilization, history of prior venous thromboembolism (VTE), lower extremity varicose veins, body mass index (BMI) ≥ 25 kg/m 2, extremity paralysis, and gout/hyperuricemia. Inherited thrombophilia was found in 14 patients with PE (14%). Risk factors for PE in Japan are comparable in magnitude to those in Western countries; only one third of PE cases had received VTE prophylaxis.

  Y Ohya , H Jono , M Nakamura , S Hayashida , M Ueda , K Obayashi , S Misumi , K Asonuma , Y Ando and Y. Inomata
  Background

Some familial amyloidotic polyneuropathy (FAP) patients show the post-transplant progression of the clinical symptoms. Although the presence of recipient-derived cells in transplanted livers has been reported, no studies investigating the functional significance of this post-transplant chimerism in transplanted FAP patients were performed. The aims of this study were to evaluate amyloidogenic transthyretin (ATTR) production of recipient-derived cells and the relationship between the protein from recipient-derived cells and the progression of FAP symptoms after liver transplantation (LT).

Methods

Seven FAP ATTR Val30Met patients who underwent LT were included in this study. In one male patient with sex-mismatched donor, fluorescence in situ hybridization (FISH) method was performed on a liver biopsy sample using DNA probes for visualizing X and Y chromosomes to detect the recipient-derived cells. In three patients including the FISH-analysed patient, ATTR mRNA expression in transplanted livers was evaluated by the polymerase chain reaction (PCR)–restriction fragment length polymorphism method and realtime quantitative reverse transcription–PCR. In five of the seven patients, ATTR in serum protein expression was measured by mass spectrometry.

Results

One FAP patient has 3.1% recipient-derived cells in the transplanted liver. The ATTR mRNA was not expressed in any of the three transplanted livers. The ATTR was not detected in any sera of the sampled patients.

Conclusion

Although the FAP patient had recipient-derived cells in the transplanted liver, the recipient-derived cells did not contribute to the production of ATTR in our specific case. The effect of recipient-derived cells on the post-transplant progression of FAP symptoms may be negligible.

  M Nakasuji , M Nakamura , N Imanaka , M Tanaka , M Nomura and S. H. Suh
  Background

Remifentanil is associated with increased incidence of post-anaesthetic shivering (PAS). The aim of this study was to compare the effects of intraoperative high and low doses of remifentanil on PAS.

Methods

We investigated 50 consecutive patients, aged <60 yr, who underwent gynaecological laparotomy. Patients who underwent prolonged surgery (>4 h) were excluded from the study. Anaesthesia throughout surgery was maintained with i.v. propofol and remifentanil, and epidural ropivacaine, and no nitrous oxide was used. Fifty patients were randomly assigned to receive intraoperative remifentanil at 0.1 µg kg–1 min–1 (low-dose group, n=25) or 0.25 µg kg–1 min–1 (high-dose group, n=25) until the end of surgery. Intraoperative analgesia was achieved by a fixed infusion rate of remifentanil and titrated epidural ropivacaine. PAS was evaluated by nursing stuff over the first hour after surgery.

Results

PAS occurred more frequently in the high-dose group than in the low-dose group (60% vs 20%, P=0.009). None of the patients complained of pain during the observation period due to epidural analgesia. There were no significant differences in rectal or palm skin temperature after extubation between the two dose groups.

Conclusions

Remifentanil-induced PAS is not a phenomenon of intraoperative hypothermia. The higher incidence of PAS with higher doses of remifentanil probably reflects acute opioid tolerance and stimulation of N-methyl-d-aspartate receptors, similar to hyperalgesia. We conclude that patients administered high doses of remifentanil are sensitive to shivering after sudden drug withdrawal.

  M Ueda , Y Misumi , M Mizuguchi , M Nakamura , T Yamashita , Y Sekijima , K Ota , S Shinriki , H Jono , S. i Ikeda , O. B Suhr and Y. Ando
 

Background: Mass spectrometric analyses are valuable for detection of transthyretin (TTR) variants, which cause familial amyloidotic polyneuropathy (FAP). However, those methods require an immunoprecipitation step with an anti-TTR antibody and are not suitable for quantitative detection. We investigated the usefulness of SELDI-TOF mass spectrometry (MS) without an immunoprecipitation step.

Methods: We used ProteinChips with chromatographic capture formats to detect TTRs. We attempted to correlate the intensity of mixed samples of amyloidogenic TTR (ATTR) V30M to wild-type (WT) TTR. We analyzed the proportion of ATTR V30M in amyloid-laden cardiac tissues from FAP patients, and also evaluated samples from FAP patients with 16 other TTR mutations.

Results: Detection of ATTR required only 3 h of SELDI-TOF MS analysis. We determined that SELDI-TOF MS was suitable for quantitative detection of ATTR V30M and demonstrated that the proportion of ATTR V30M to WT TTR was 46.6% in amyloid-laden cardiac tissue from an FAP patient who died 10 years after liver transplantation. With this method, we identified 12 of 17 TTR variants. Small mass shifts and low concentrations of variants prevented ATTR detection. By changing the analytical conditions, we achieved detection of low concentrations of ATTR Y114C in serum.

Conclusions: SELDI-TOF MS is a reliable tool for quantitative evaluation of TTR variants, in both tissue amyloid deposits and body fluids. This method is useful for the diagnosis and investigation of the pathogenesis of FAP.

  Z Xing , C Lu , D Hu , Y. y Yu , X Wang , C Colnot , M Nakamura , Y Wu , T Miclau and R. S. Marcucio
  Zhiqing Xing, Chuanyong Lu, Diane Hu, Yan-yiu Yu, Xiaodong Wang, Celine Colnot, Mary Nakamura, Yalei Wu, Theodore Miclau, and Ralph S. Marcucio

Bone injury induces an inflammatory response that involves neutrophils, macrophages and other inflammatory cells. The recruitment of inflammatory cells to sites of injury occurs in response to specific signaling pathways. The CC chemokine receptor type 2 (CCR2) is crucial for recruiting macrophages, as well as regulating osteoclast function. In this study, we examined fracture healing in Ccr2–/– mice. We first demonstrated that the expression of Ccr2 transcripts and the filtration of macrophages into fracture calluses were most robust during the early phases of fracture healing. We then determined that the number of macrophages at the fracture site was significantly lower in Ccr2–/– mice compared with wild-type controls at 3 days after injury. As a result, impaired vascularization, decreased formation of callus, and delayed maturation of cartilage were observed at 7 days after injury in mutant mice. At day 14, Ccr2–/– mice had less bone in their calluses. At day 21, Ccr2–/– mice had larger calluses and more bone compared with wild-type mice, suggesting a delayed remodeling. In addition, we examined the effect of Ccr2 mutation on osteoclasts. We found that a lack of Ccr2 did not affect the number of osteoclasts within fracture calluses at 21 days after injury. However, Ccr2–/– osteoclasts exhibited a decreased ability to resorb bone compared with wild-type cells, which could contribute to the delayed remodeling of fracture calluses observed in Ccr2–/– mice. Collectively, these results indicate that a deficiency of Ccr2 reduces the infiltration of macrophages and impairs the function of osteoclasts, leading to delayed fracture healing.

  Y Chen , Y Yamaguchi , Y Tsugeno , J Yamamoto , T Yamada , M Nakamura , K Hisatake and H. Handa
 

Transcription elongation factor DSIF/Spt4–Spt5 is capable of promoting and inhibiting RNA polymerase II elongation and is involved in the expression of various genes. While it has been known for many years that DSIF inhibits elongation in collaboration with the negative elongation factor NELF, how DSIF promotes elongation is largely unknown. Here, an activity-based biochemical approach was taken to understand the mechanism of elongation activation by DSIF. We show that the Paf1 complex (Paf1C) and Tat-SF1, two factors implicated previously in elongation control, collaborate with DSIF to facilitate efficient elongation. In human cells, these factors are recruited to the FOS gene in a temporally coordinated manner and contribute to its high-level expression. We also show that elongation activation by these factors depends on P-TEFb-mediated phosphorylation of the Spt5 C-terminal region. A clear conclusion emerging from this study is that a set of elongation factors plays nonredundant, cooperative roles in elongation. This study also shows unambiguously that Paf1C, which is generally thought to have chromatin-related functions, is involve directlyd in elongation control.

  M Nakamura and T. Hashimoto
 

Plant cortical microtubules are mainly nucleated on previously established microtubules, grow at a narrow range of angles to the wall of mother microtubules, and eventually are released from the nucleation sites. These nucleation events are thought to be regulated by -tubulin-containing complexes. We here show that a null mutation of Arabidopsis GCP2, a core subunit of the -tubulin-containing complex, severely impaired the development of male and female gametophytes. However, a missense mutation in the conserved grip1 motif, called spiral3, caused a left-handed helical organization of cortical microtubule arrays, and severe right-handed helical growth. The spiral3 mutation compromises interaction between GCP2 and GCP3, another subunit of the complex, in yeast. In the spiral3 mutant, microtubule dynamics and nucleation efficiency were not markedly affected, but nucleating angles were wider and more divergently distributed. A spiral3 katanin double mutant had swollen and twisted epidermal cells, and showed that the microtubule minus ends...

  U Tagami , N Shimba , M Nakamura , K. i Yokoyama , E. i Suzuki and T. Hirokawa
 

Transglutaminases (TGases) are used in fields such as food and pharmaceuticals. Unlike other TGases, microbial transglutaminase (MTG) activity is Ca2+-independent, broadening its application. Here, a three-dimensional docking model of MTG binding to a peptide substrate, CBZ-Gln-Gly, was simulated. The data reveal CBZ-Gln-Gly to be stretched along the MTG active site cleft with hydrophobic and/or aromatic residues interacting directly with the substrate. Moreover, an oxyanion binding site for TGase activity may be constructed from the amide groups of Cys64 and/or Val65. Alanine mutagenesis verified the simulated binding region and indicated that large molecules can be widely recognized on the MTG cleft.

  K Migita , T Koga , T Torigoshi , Y Maeda , T Miyashita , Y Izumi , Y Aiba , A Komori , M Nakamura , S Motokawa and H. Ishibashi
 

Objective. Although serum amyloid A (SAA) has been used as a marker of inflammation, its role in leucocyte recruitment and angiogenesis has not been well established in RA. CCL20 is a chemokine involved in the migration of CCR6-expressing Th17 cells. To study the contribution of SAA to the recruitment of Th17 cells, we investigated the effects of SAA on CCL20 production by RA synoviotytes.

Methods. Synoviocytes isolated from RA patients were stimulated with recombinant SAA and cellular supernatants were analysed by CCL20-specific ELISA. CCL-20 mRNA expression was analysed by RT–PCR.

Results. SAA is a most potent inducer of CCL20 secretion in RA synoviocytes compared with other inflammatory cytokines (IL-1β, TNF- and IL-17A). SAA stimulation induced CCL20 mRNA expression in RA synoviocytes, which was not affected by polymyxin B pre-treatment. SAA-induced CCL20 production was down-regulated by NF-B inhibition and partially by c-jun N-terminal kinase (JNK) inhibition. SAA-induced CCL20 production was also suppressed by dexamethasone or FK506.

Conclusion. These findings suggest that SAA may be implicated in the recruitment of lymphocytes, including CCR6-expressing Th17 cells, in RA synovium by up-regulating CCL20 production in synoviocytes.

  Y Yamanishi , J Kitaura , K Izawa , A Kaitani , Y Komeno , M Nakamura , S Yamazaki , Y Enomoto , T Oki , H Akiba , T Abe , T Komori , Y Morikawa , H Kiyonari , T Takai , K Okumura and T. Kitamura
 

Leukocyte mono-immunoglobulin (Ig)–like receptor 5 (LMIR5)/CD300b is a DAP12-coupled activating receptor predominantly expressed in myeloid cells. The ligands for LMIR have not been reported. We have identified T cell Ig mucin 1 (TIM1) as a possible ligand for LMIR5 by retrovirus-mediated expression cloning. TIM1 interacted only with LMIR5 among the LMIR family, whereas LMIR5 interacted with TIM4 as well as TIM1. The Ig-like domain of LMIR5 bound to TIM1 in the vicinity of the phosphatidylserine (PS)-binding site within the Ig-like domain of TIM1. Unlike its binding to TIM1 or TIM4, LMIR5 failed to bind to PS. LMIR5 binding did not affect TIM1- or TIM4-mediated phagocytosis of apoptotic cells, and stimulation with TIM1 or TIM4 induced LMIR5-mediated activation of mast cells. Notably, LMIR5 deficiency suppressed TIM1-Fc–induced recruitment of neutrophils in the dorsal air pouch, and LMIR5 deficiency attenuated neutrophil accumulation in a model of ischemia/reperfusion injury in the kidneys in which TIM1 expression is up-regulated. In that model, LMIR5 deficiency resulted in ameliorated tubular necrosis and cast formation in the acute phase. Collectively, our results indicate that TIM1 is an endogenous ligand for LMIR5 and that the TIM1–LMIR5 interaction plays a physiological role in immune regulation by myeloid cells.

 
 
 
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