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Your search keyword '"Inokuchi K"' showing total 101 results
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101 results on '"Inokuchi K"'

17. Mouse containing a human chromosome 21 models Downs syndrome

Author

Oshimura, M., Shinohara, T., Tomizuka, K., Miyabara, S., Kazuki, Y., Ikegami, S., Inokuchi, K., and Ishida, I.

Subjects
Human chromosome 21 -- Research, Down syndrome -- Models, Genetic disorders -- Models, Biological sciences
Published
2001

25. Regulated expression of an actin-associated protein, synaptopodin, during long-term potentiation.

Author

Yamazaki, M., Matsuo, R., Fukazawa, Y., Ozawa, F., and Inokuchi, K.

Subjects
PROTEINS, NEUROPLASTICITY
Abstract

We report NMDA receptor-dependent expression of synaptopodin mRNA in the dentate granule cells of the hippocampus following induction of long-term potentiation (LTP) in vivo. Synaptopodin did not belong to immediate-early genes, as de novo protein synthesis was required for the induction of synaptopodin gene transcription. An increased level of synaptopodin mRNA was observed at 75 min and 3.5 h after the onset of LTP. Importantly, there was correlation between the induction of mRNA expression and the persistence of LTP. Synaptopodin immunoreactivity was elevated specifically in synaptic layers, middle and outer molecular layers of dentate gyrus where LTP was induced. As synaptopodin is an actin-associated protein present in spine neck and implicated in the modulation of cell morphology, our results suggest that synaptopodin, by regulating the dynamics of the actin cytoskeleton, contributes to the morphological change in spine shape considered to be important for the maintenance of synaptic plasticity. [ABSTRACT FROM AUTHOR]

Published
2001
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29. Chemotherapy for minimally differentiated acute myeloid leukemia (AML-M0). A report on five cases and review of the literature.

Author

Yokose, N., Ogata, K., Ito, T., Miyake, K., An, E., Inokuchi, K., Yamada, T., Gomi, S., Tanabe, Y., Ohki, I., Kuwabara, T., Hasegawa, S., Shinohara, T., Dan, K., and Nomura, T.

Abstract

With the objective of establishing the optimal therapy for minimally differentiated acute myeloid leukemia (AML-M0), we examined the therapeutic results of five AML-M0 cases and reviewed the literature. In a series of 63 patients with newly diagnosed acute leukemia who were admitted to the Main Hospital of Nippon Medical School, five patients fit the criteria for AML-M0: negative myeloperoxidase (MPO) and Sudan black B reaction by light microscopy, negative for B- and T-lineage markers, and positive for myeloid markers. They were treated by means of AdVP [adriamycin, vincristine, and prednisolone (PSL)] therapy and/or BHAC-DMP [behenoylcytosine arabinoside (BHAC), daunorubicin (DNR), 6-mercaptopurine (6-MP), and PSL] therapy. The AdVP therapy was unsuccessful in the two patients who received it, while a complete remission (CR) was achieved with the BHAC-DMP therapy in three of four patients. Although one patient treated with BHAC-DMP did not achieve CR, his blasts were apparently sensitive to the therapy. In assessable cases in the literature where leukemic blasts were MPO-negative, myeloid marker-positive and B- and T-lineage marker-negative, CR was achieved in 54.5% and 44.4% with anti-acute myeloid leukemia therapy and anti-acute lymphocytic leukemia therapy, respectively. Five cases in the literature were treated with a chemotherapeutic regimen containing BHAC [or cytosine arabinoside (Ara-C)], DNR, and 6-MP, and all achieved CR. The regimen containing BHAC (or Ara-C), DNR, and 6-MP may be useful as induction chemotherapy for AML-M0. [ABSTRACT FROM AUTHOR]

Published
1993
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