Papers - Takahashi, Takao

Successful haploidentical BMT with post-transplant cyclophosphamide for refractory autoimmune pancytopenia after cord blood transplant in pediatric myelodysplastic syndrome.

Shima H, Isshiki K, Yamada Y, Yamazaki F, Takahashi T, Shimada H.

Bone Marrow Transplant 52   653 - 655 2017

Research paper (scientific journal), Joint Work

Changeability of the fully methylated status of the 15q11.2 region in induced pluripotent stem cells derived from a patient with Prader-Willi syndrome.

Okuno H, Nakabayashi K, Abe K, Ando T, Sanosaka T, Kohyama J, Akamatsu W, Ohyama M, Takahashi T, Kosaki K, Okano H.

Congenit Anom (Kyoto) 57   96 - 103 2017

Research paper (scientific journal), Joint Work

Randomized controlled trial of oral immunotherapy for egg allergy in Japanese patients.

Akashi M, Yasudo H, Narita M, Nomura I, Akasawa A, Ebisawa M, Takahashi T, Ohya Y.

Pediatr Int 59   534 - 539 2017

Research paper (scientific journal), Joint Work

A sedation protocol with fasting and shorter sleep leads to MRI success.

Kimiya T, Sekiguchi S, Yagihashi T, Arai M, Takahashi H, Takahashi T.

Pediatr Int  2017

Research paper (scientific journal), Joint Work

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Childhood Sjögren syndrome presenting as acute brainstem encephalitis.

Matsui Y, Takenouchi T, Narabayashi A, Ohara K, Nakahara T, Takahashi T.

Brain Dev 38   158 - 162 2016

Research paper (scientific journal), Joint Work

Trivalent inactivated influenza vaccine effective against influenza A(H3N2) variant viruses in children during the 2014/15 season, Japan.

Sugaya N, Shinjoh M, Kawakami C, Yamaguchi Y, Yoshida M, Baba H, Ishikawa M, Kono M, Sekiguchi S, Kimiya T, Mitamura K, Fujino M, Komiyama O, Yoshida N, Tsunematsu K, Narabayashi A, Nakata Y, Sato A, Taguchi N, Fujita H, Toki M, Myokai M, Ookawara I, Takahashi T.

Euro Surveill 21 ( 42 )  2016

Research paper (scientific journal), Joint Work

Conservative follow-up of fractured percutaneously inserted central venous catheter.

Kobayashi H, Mizuno Y, Takahashi T.

Pediatr Int 58 ( 12 ) 1369 - 1370 2016

Research paper (scientific journal), Joint Work

In Utero Exposure to Valproic Acid Induces Neocortical Dysgenesis via Dysregulation of Neural Progenitor Cell Proliferation/Differentiation.

Fujimura K, Mitsuhashi T, Shibata S, Shimozato S, Takahashi T.

J Neurosci 36   10908 - 10919 2016

Research paper (scientific journal), Joint Work, Accepted

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Association Between Invisible Basal Ganglia and ZNF335 Mutations: A Case Report.

Sato R, Takanashi J, Tsuyusaki Y, Kato M, Saitsu H, Matsumoto N, Takahashi T.

Pediatrics 138 ( 3 )  2016

Research paper (scientific journal), Joint Work

Hirschsprung disease as a yet undescribed phenotype in a patient with ARID1B mutation.

Takenouchi T, Yoshihashi H, Sakaguchi Y, Uehara T, Honda M, Takahashi T, Kosaki K, Miyama S.

Am J Med Genet 170   3249 - 3252 2016

Research paper (scientific journal), Joint Work

Keio Pediatric Influenza Research Group. Effectiveness of trivalent inactivated influenza vaccine in children estimated by a test-negative case-control design study based on influenza rapid diagnostic test.

Shinjoh M, Sugaya N, Yamaguchi Y, Tomidokoro Y, Sekiguchi S, Mitamura K, Fujino M, Shiro H, Komiyama O, Taguchi N, Nakata Y, Yoshida N, Narabayashi A, Myokai M, Sato M, Furuichi M, Baba H, Fujita H, Sato A, Ookawara, I , Tsunematsu K, Yoshida M, Kono M, Tanaka F, Kawakami C, Kimiya T, Takahashi T, Iwata S.

PLOS ONE 10   e0136539 2015

Research paper (scientific journal), Joint Work

Assessment of Developing Speech Perception in Preterm Infants Using Near-Infrared Spectroscopy.

Arimitsu T, Minagawa Y, Takahashi T, Ikeda K.

NeoReviews 16   e481 - e489 2015

Research paper (scientific journal), Joint Work

Successful lung transplantation in a case with diffuse pulmonary arteriovenous malformations and hereditary hemorrhagic telangiectasia

H. Fukushima, T. Mitsuhashi, T. Oto, Y. Sano, K. F. Kusano, K. Goto, M. Okazaki, H. Date, Y. Kojima, H. Yamagishi and T. Takahashi

American Journal of Transplantation 13 ( 12 ) 3278 - 81 2013.12

Research paper (scientific journal), Joint Work, Accepted,  ISSN  1600-6143

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Diffuse pulmonary arteriovenous malformations (AVMs) are associated with a poor prognosis and the therapeutic strategy remains controversial. We describe a pediatric patient with diffuse pulmonary AVMs associated with hereditary hemorrhagic telangiectasia (HHT), who presented with two cerebral AVMs in the parietal and occipital lobes as well. Of note, successful bilateral lung transplantation not only improved the hypoxemia but also resulted in size reduction of the cerebral AVMs. Although it is essential to consider involvements other than pulmonary AVMs, especially brain AVMs, to decide the indication, lung transplantation can be a viable therapeutic option for patients with diffuse pulmonary AVMs and HHT.

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情報通信技術を活用した大学病院・地域中核病院間連携小児科研修

三橋隆行、高木優樹、三春晶嗣、肥沼悟郎、野村寿博、福島裕之、小崎健次郎、高橋孝雄

日本小児科学会雑誌 115 ( 4 ) 823 - 827 2011.04

Research paper (scientific journal), Joint Work, Accepted,  ISSN  0001-6543

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地域中核病院と大学病院とをインターネットで結合し、双方の教育環境の共有化を実施した。遠隔カンファレンスは、20ヵ月間に12関連施設と接続して合計11回の公演会を開催し、延べ約1000名が参加した。ストリーミング配信は、20ヵ月間に合計471個の学習内容を作成し、e-learningサイトへの総アクセス数は2083回、延べ1205名がストリーミングを視聴した。情報通信技術(ICT)を用いることにより、地域中核病院や大学病院の教育内容を他の研修施設に提供可能となった。さらに、休職中・留学中の医師・医学生への提供も可能になった。e-learningの長所と限界を認識しつつ、ICTを活用することにより、教育関連施設と大学病院の特徴の補完、かつ臨床研修教育者の負担軽減が可能に成り得ると思われた。

In utero exposure to dioxin causes neocortical dysgenesis through the actions of p27Kip1

T. Mitsuhashi, J. Yonemoto, H. Sone, Y. Kosuge, K. Kosaki and T. Takahashi

Proc Natl Acad Sci U S A 107 ( 37 ) 16331 - 5 2010.09

Joint Work, Accepted,  ISSN  1091-6490

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Dioxins have been reported to exert various adverse effects, including cell-cycle dysregulation in vitro and impairment of spatial learning and memory after in utero exposure in rodents. Furthermore, children born to mothers who are exposed to dioxin analogs polychlorinated dibenzofurans or polychlorinated biphenyls have developmental impairments in cognitive functions. Here, we show that in utero exposure to dioxins in mice alters differentiation patterns of neural progenitors and leads to decreased numbers of non-GABAergic neurons and thinner deep neocortical layers. This reduction in number of non-GABAergic neurons is assumed to be caused by accumulation of cyclin-dependent kinase inhibitor p27(Kip1) in nuclei of neural progenitors. Lending support to this presumption, mice lacking p27(Kip1) are not susceptible to in utero dioxin exposure. These results show that environmental pollutants may affect neocortical histogenesis through alterations of functions of specific gene(s)/protein(s) (in our case, dioxins), exerting adverse effects by altering functions of p27(Kip1).

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Embryonic expression profile of chicken CHD7, the ortholog of the causative gene for CHARGE syndrome

M. Aramaki, T. Kimura, T. Udaka, R. Kosaki, T. Mitsuhashi, Y. Okada, T. Takahashi and K. Kosaki

Birth defects research. Part A, Clinical and molecular teratology 79 ( 1 ) 50 - 7 2007.01

Research paper (scientific journal), Joint Work, Accepted,  ISSN  1542-0752

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BACKGROUND: CHARGE syndrome represents a constellation of malformations: C, coloboma of the iris or retina; H, heart defects; A, atresia of the choanae; R, retardation of growth and/or development; G, genital anomalies; and E, ear abnormalities. Recently, the Chromodomain helicase DNA-binding protein-7 (CHD7) at chromosome 8q12.1 was identified as a causative gene for CHARGE syndrome. Because CHD7 was identified as a causative gene using a positional cloning approach, the role of CHD7 in early embryogenesis needs to be further investigated. METHODS: Fertilized chick eggs were incubated to Hamburger and Hamilton stages 4-20 and were studied using whole mount in situ hybridization. Chicken EST clones corresponding to the chicken CHD7 (cChd7) sequence were identified using the chicken EST sequence database. From the EST clones, a digoxigenin-labeled RNA probe was synthesized and hybridized in situ to the embryonic specimens. RESULTS: The expression of cChd7 was pan-neuronal at stages 8-20. It was expressed throughout the rostral neural ectoderm and along the rostrocaudal axis but was absent from the more lateral, non-neuronal ectoderm. Adjacent to the neural tube, cChd7 transcripts were detected at the optic and otic placodes. At stage 20, cChd7 expression was observed in the branchial arches and olfactory placodes in addition to brain and optic and otic placodes. CONCLUSIONS: cChd7 was expressed in the neural epithelium, the otic placodes, the optic placodes, the branchial arches, and the olfactory placodes, which are the primordial tissues that give rise to organs affected in human CHARGE syndrome patients.

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Genome-wide screening of dioxin-responsive genes in fetal brain: bioinformatic and experimental approaches

H. Fujita, H. Samejima, N. Kitagawa, T. Mitsuhashi, T. Washio, J. Yonemoto, M. Tomita, T. Takahashi and K. Kosaki

Congenital Anomalies 46 ( 3 ) 135 - 43 2006.09

Research paper (scientific journal), Joint Work, Accepted,  ISSN  0914-3505

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Many of the effects of dioxins, which are potent environmental pollutants and teratogens, are mediated through the aryl hydrocarbon receptor, also known as the dioxin receptor. The purpose of the present study was to characterize dioxin-responsive genes in a comprehensive manner using two complementary approaches: bioinformatic analysis and microarray analysis. First, we characterized the overall distribution of the cis-regulatory element for the dioxin-responsive element sequence (DRE) 'gcgtg' within putative promoter regions. We assembled the upstream sequences 10 kb from the transcription start site and evaluated their location and frequency in the human and mouse genomes. Second, we characterized the expression profile of mouse embryonic day 12 fetal brain exposed to 2,3,7,8-tetrarchlorodibenzo-p-dioxin. The distributions of 26,680 DREs among 2,843 human genes and 98,711 DREs among 18,541 mouse genes were examined. In both species, the DREs tended to be located close to the transcription start site. Forty genes exhibited significant induction or repression following dioxin exposure in fetal mice. The set of genes exhibited a strong functional coherence, with statistically significant enrichment in organogenesis and the DNA-dependent regulation of transcription, according to Gene Ontology annotations. In both humans and mice, DREs were preferentially distributed close to transcription start sites. Evolutionary conservation of this unique DRE distribution pattern suggests that DREs may be involved in transcriptional regulation. In mice, prenatal dioxin exposure altered the expression of 10 transcription factors, many of which have been documented to play a role in organogenesis. These genes may represent potential mediators of dioxin's effects in fetal tissues.

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The RNA-binding protein HuD regulates neuronal cell identity and maturation

W. Akamatsu, H. Fujihara, T. Mitsuhashi, M. Yano, S. Shibata, Y. Hayakawa, H. J. Okano, S. Sakakibara, H. Takano, T. Takano, T. Takahashi, T. Noda and H. Okano

Proc Natl Acad Sci U S A 102 ( 12 ) 4625 - 30 2005.03

Research paper (scientific journal), Joint Work, Accepted,  ISSN  0027-8424

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Neural Hu proteins (HuB/C/D) are RNA-binding proteins that have been shown to induce neuronal differentiation activity when overexpressed in immature neural progenitor cells or undifferentiated neuronal tumors. Newly generated HuD-deficient mice exhibited a transient impaired-cranial-nerve-development phenotype at an early embryonic stage. Adult HuD-deficient mice exhibited an abnormal hind-limb reflex and poor rotarod performance. Analysis of neurosphere formation revealed that the number and self-renewal capacity of the neural stem/progenitor cells were increased in HuD-deficient mice. HuD-deficient primary neurospheres also generated a smaller number of neurons. Cohort analysis of the cellular proliferative activity by using BrdUrd and iododeoxuridine labeling revealed that the number of differentiating quiescent cells in the embryonic cerebral wall was decreased. Long-term administration of BrdUrd revealed that the number of slowly dividing stem cells in the adult subventricular zone was increased in the HuD-deficient mice. Taken together, the results suggest that HuD is required at multiple points during neuronal development, including negative regulation of proliferative activity and neuronal cell-fate acquisition of neural stem/progenitor cells.

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クロバザム極少量投与により副作用を回避し得たCYP2C19*2*3複合ヘテロ接合体の1例

高橋孝雄、三橋隆行、下郷幸子、佐藤玲子、谷川原祐介、田村和代、小崎健次郎

小児科臨床 58 ( 3 ) 407 - 410 2005.03

Research paper (scientific journal), Joint Work, Accepted,  ISSN  0021-518X

Colocolic intussusception associated with pneumatosis cystoides intestinalis after cord blood stem cell transplantation.

'TAKAHASHI TAKAOSugita M, Mori T, Shimada H, Shimasaki N, Morikawa Y, Takahashi T'

J Pediatr Gastroenterol Nutr 38 ( 5 ) 549-551 2004.05

Research paper (scientific journal), Joint Work