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Articles by Y Maeda
Total Records ( 4 ) for Y Maeda
  S Nomura , Y Kurata , Y Tomiyama , T Takubo , M Hasegawa , K Saigo , M Nishikawa , S Higasa , Y Maeda and K. Hayashi
 

Immune thrombocytopenic purpura (ITP) is an acquired hemorrhage condition involving accelerated platelet consumption caused by antiplatelet autoantibodies. Although various therapeutic strategies are used to treat patients with ITP, the standard treatment method is steroid therapy. The most important problem with steroid administration may be a prolonged use tendency in many cases, because there are many refractory chronic patients. To elucidate the effects of glucocorticoid on bone mineral density (BMD) in patients with ITP, we retrospectively evaluated the relationship between BMD and the total dose of glucocorticoid or the mean daily dose given. We observed decreased BMD in 66.7% of the patients with ITP to whom glucocorticoid was given, although normal bone BMD was observed in 28.6% of patients with ITP treated without steroids. The mean level of BMD was markedly decreased in steroid-treated patients compared with nonsteroid-treated patients (P < .01). The relationship between BMD and the total dose of glucocorticoid (P = .023) or the mean daily dose revealed a negative correlation (P = .022). Administration of bisphosphonate revealed a significant increase in bone mass in patients at 6 and 12 months after the start of bisphosphonate treatment, despite the aggravation of thrombocytopenia. In conclusion, glucocorticoid-induced osteoporosis was observed in patients with ITP, similar to situation seen in patients with other diseases. Bisphosphonate may be an effective agent for the prevention and treatment of glucocorticoid-induced osteoporosis in patients with ITP scheduled to receive long-term steroid treatment.

  T Bando , T Mito , Y Maeda , T Nakamura , F Ito , T Watanabe , H Ohuchi and S. Noji
  Tetsuya Bando, Taro Mito, Yuko Maeda, Taro Nakamura, Fumiaki Ito, Takahito Watanabe, Hideyo Ohuchi, and Sumihare Noji

An amputated cricket leg regenerates all missing parts with normal size and shape, indicating that regenerating blastemal cells are aware of both their position and the normal size of the leg. However, the molecular mechanisms regulating this process remain elusive. Here, we use a cricket model to show that the Dachsous/Fat (Ds/Ft) signalling pathway is essential for leg regeneration. We found that knockdown of ft or ds transcripts by regeneration-dependent RNA interference (rdRNAi) suppressed proliferation of the regenerating cells along the proximodistal (PD) axis concomitantly with remodelling of the pre-existing stump, making the regenerated legs shorter than normal. By contrast, knockdown of the expanded (ex) or Merlin (Mer) transcripts induced over-proliferation of the regenerating cells, making the regenerated legs longer. These results are consistent with those obtained using rdRNAi during intercalary regeneration induced by leg transplantation. We present a model to explain our results in which the steepness of the Ds/Ft gradient controls growth along the PD axis of the regenerating leg.

  K Izumi , K Narimoto , K Sugimoto , Y Kobori , Y Maeda , A Mizokami , E Koh , T Yamada , S Yano and M. Namiki
  Objective

The safety and accuracy of active percutaneous needle biopsy for small renal tumors have been reported. However, there have been few reports of passive biopsy for renal tumors without clear pretreatment histological characterization based on imaging studies due to the rarity of these tumors. In this study, we examined the background, accuracy, adverse events and patient prognosis associated with such biopsies.

Methods

Japanese patients with renal tumors histological characteristics of which were unclear on imaging prior to treatment were enrolled in this study and analyzed retrospectively. The study population consisted of 24 renal cell carcinoma patients and 13 non-renal cell carcinoma patients.

Results

Although the percentage of hypervascularity was significantly higher in clear cell renal cell carcinoma compared with the other neoplasms (P < 0.001), there were no significant differences between renal cell carcinoma and non-renal cell carcinoma with regard to hypervascularity, hydronephrosis, venous thrombus, hematuria or metastasis. The histological results in eight of nine (89%) nephrectomy patients were in accordance with those of biopsies. The median survival time of all 37 patients was 21 months and the 5-year survival rate was 31.1%. The 5-year survival rates of nephrectomy patients and non-nephrectomy patients were 75 and 0%, respectively. The overall survival of nephrectomy patients was significantly better than that of non-nephrectomy patients (P = 0.003).

Conclusions

Biopsy of renal tumors is safe and accurate regardless of the type of guidance and nephrectomy after appropriate diagnosis by biopsy contributed to longer survival.

  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.

 
 
 
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