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Start Over Author "Yutaka, N." Journal scientific reports
3 results on '"Yutaka, N."'

1. CCL2 enhances pluripotency of human induced pluripotent stem cells by activating hypoxia related genes

Author

Hasegawa, Y., Tang, D., Takahashi, N., Hayashizaki, Y., Forrest, A.R.R., Hideya, K., Michael, R., J Kenneth Baillie, Michiel J, L.D.H., Vanja, H., Timo, L., Ivan, V.K., Marina, L., Masayoshi, I., Robin, A., Christopher, J.M., Terrence, F.M., Sebastian, S., Nicolas, B., Mette, J., Emmanuel, D., Erik, A., Christian, S., Ulf, S., Yulia, A.M., Charles, P., Morana, V., Jessica, S., Colin, A.S., Yuri, I., Robert, S.Y., Margherita, F., Intikhab, A., Davide, A., Gabriel, M.A., Takahiro, A., John A, C.A., Peter, A., Magda, B., Sarah, B., Piotr, J.B., Anthony, G.B., Swati, P., Judith, A.B., Antje, B., Bodega, B., Alessandro, B., James, B., Frank, B., A Maxwell Burroughs, Andrea, C., Carlo, V.C., Daniel, C., Yun, C., Marco, C., Yari, C., Hans, C.C., Emiliano, D., Carrie, A.D., Michael, D., Alexander, D.D., Taeko, D., Finn, D., Albert S, B.E., Matthias, E., Karl, E., Mitsuhiro, E., Hideki, E., Michela, F., Lynsey, F., Hai, F., Mary, C.F., Geoffrey, J.F., Alexander, V.F., Malcolm, E.F., Martin, C.F., Rie, F., Shiro, F., Cesare, F., Masaaki, F., Jun-ichi, F., Teunis, B.G., Andrew, G., Thomas, G., Daniel, G., Julian, G., Sven, G., Reto, G., Stefano, G., Thomas, J.H., Masahide, H., Mitsuko, H., Matthias, H., Jayson, H., Akira, H., Yuki, H., Takehiro, H., Meenhard, H., Kelly, J.H., Shannan, J.H.S., Oliver, M.H., Ilka, H., Fumi, H., Lukasz, H., Kei, I., Tomokatsu, I., Boris, R.J., Hui, J., Anagha, J., Giuseppe, J., Bogumil, K., Chieko, K., Kaoru, K., Kaiho, A., Kazuhiro, K., Mutsumi, K., Artem, S.K., Takeya, K., Shintaro, K., Sachi, K., Shuji, K., Hiroshi, K., Yuki, I.K., Tsugumi, K., Judith, S.K., Tony, J.K., Juha, K., Levon, M.K., Toshio, K., S Peter Klinken, Alan, J.K., Miki, K., Soichi, K., Naoto, K., Haruhiko, K., Shigeo, K., Sarah, K., Atsutaka, K., Andrew, T.K., Jeroen F, J.L., Weonju, L., Andreas, L., Kang, L., Berit, L., Leonard, L., Alan, M., Ri-ichiroh, M., Jessica, C.M., Benoit, M., Anthony, M., Niklas, M., Alison, M., Yosuke, M., David, A.D.L.M., Hiromasa, M., Mitsuru, M., Kazuyo, M., Efthymios, M., Hozumi, M., Christine, L.M., Mitsuyoshi, M., Sayaka, N., Yutaka, N., Fumio, N., Toshiyuki, N., Yukio, N., Kenichi, N., Erik van Nimwegen, Noriko, N., Hiromi, N., Shohei, N., Tadasuke, N., Soichi, O., Naganari, O., Hiroko, O., Hiroshi, O., Mitsuhiro, O., Mariko, O., Yasushi, O., Valerio, O., Dmitry, A.O., Arnab, P., Robert, P., Margaret, P., Helena, P., Silvano, P., James G, D.P., Owen J, L.R., Jordan, A.R., Mamoon, R., Timothy, R., Patrizia, R., Marco, R., Sugata, R., Morten, B.R., Eri, S., Antti, S., Akiko, S., Shimon, S., Mizuho, S., Hiroki, S., Hironori, S., Suzana, S., Alka, S., Claudio, S., Erik, A.S., Gundula, G.S., Anita, S., Thierry, S., Guojun, S., Hisashi, S., Yishai, S., Jay, W.S., Christophe, S., Daisuke, S., Takaaki, S., Masanori, S., Naoko, S., Rolf, K.S., Peter A, C.'.H., Michihira, T., Naoko, T., Jun, T., Hiroshi, T., Hideki, T., Zuotian, T., Mark, T., Hiroo, T., Tetsuro, T., Eivind, V., Marc van de Wetering, Linda, M.V.D.B., Roberto, V., Dipti, V., Ilya, E.V., Wyeth, W.W., Shoko, W., Christine, A.W., Louise, N.W., Ernst, W., Emily, J.W., Yoko, Y., Masayuki, Y., Misako, Y., Yohei, Y., Shigehiro, Y., Suzan, E.Z., Peter, G.Z., Xiaobei, Z., Silvia, Z., Kim, M.S., Harukazu, S., Carsten, O.D., Jun, K., Peter, H., Winston, H., Tom, C.F., Boris, L., Vladimir, B.B., Martin, S.T., Vsevolod, J.M., Albin, S., David, A.H., Piero, C., Yoshihide HayashizakSuzuki, H., Hjelt Institute (-2014), Forensic Medicine, PaleOmics Laboratory, Amsterdam institute for Infection and Immunity, Infectious diseases, Experimental Immunology, and Hubrecht Institute for Developmental Biology and Stem Cell Research

Subjects
Stage-Specific Embryonic Antigens, Chromosomal Proteins, Non-Histone, Cellular differentiation, Basic fibroblast growth factor, Gene Expression, LINES, OXYGEN, chemistry.chemical_compound, 0302 clinical medicine, Piperidines, Phosphorylation, STAT3, Induced pluripotent stem cell, Cells, Cultured, Chemokine CCL2, 0303 health sciences, Multidisciplinary, biology, Reverse Transcriptase Polymerase Chain Reaction, PROLIFERATION, Cell Differentiation, 319 Forensic science and other medical sciences, Nanog Homeobox Protein, Immunohistochemistry, Cell Hypoxia, Cell biology, HUMAN EMBRYONIC STEM, GROUND-STATE, Fibroblast Growth Factor 2, INACTIVATION, Signal transduction, Stem cell, Signal Transduction, Pluripotent Stem Cells, STAT3 Transcription Factor, EXPRESSION, Immunoblotting, Induced Pluripotent Stem Cells, Kruppel-Like Transcription Factors, Settore BIO/11 - Biologia Molecolare, Alkenes, Article, Kruppel-Like Factor 4, 03 medical and health sciences, Humans, Janus Kinases, 030304 developmental biology, Homeodomain Proteins, Proteins, Janus Kinase 1, CAP ANALYSIS, SELF-RENEWAL, chemistry, Epiblast, INDUCIBLE FACTOR-I, Immunology, biology.protein, 030217 neurology & neurosurgery
Abstract

Standard culture of human induced pluripotent stem cells (hiPSCs) requires basic Fibroblast Growth Factor (bFGF) to maintain the pluripotent state, whereas hiPSC more closely resemble epiblast stem cells than true naïve state ES which requires LIF to maintain pluripotency. Here we show that chemokine (C-C motif) ligand 2 (CCL2) enhances the expression of pluripotent marker genes through the phosphorylation of the signal transducer and activator of transcription 3 (STAT3) protein. Moreover, comparison of transcriptomes between hiPSCs cultured with CCL2 versus with bFGF, we found that CCL2 activates hypoxia related genes, suggesting that CCL2 enhanced pluripotency by inducing a hypoxic-like response. Further, we show that hiPSCs cultured with CCL2 can differentiate at a higher efficiency than culturing with just bFGF and we show CCL2 can be used in feeder-free conditions in the absence of LIF. Taken together, our finding indicates the novel functions of CCL2 in enhancing its pluripotency in hiPSCs.

Published
2014
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2. Three-year outcome following neonatal encephalopathy in a high-survival cohort.

Author

Tsuda K, Shibasaki J, Isayama T, Takeuchi A, Mukai T, Sugiyama Y, Ioroi T, Takahashi A, Yutaka N, Iwata S, Nabetani M, and Iwata O

Subjects
Child, Preschool, Cohort Studies, Humans, Infant, Infant, Newborn, Intensive Care Units, Neonatal, Treatment Outcome, Brain Diseases etiology, Hypothermia, Induced adverse effects, Hypoxia-Ischemia, Brain therapy, Infant, Newborn, Diseases etiology
Abstract

This study investigated the 3-year clinical outcomes in relation to the severity of encephalopathy in high-survival infants who underwent therapeutic hypothermia. This retrospective observational study was conducted in level II/III neonatal intensive care units in Japan. The nationwide cohort included 474 infants registered in the Baby Cooling Registry of Japan between January 2012 and December 2016. Clinical characteristics, mortality rate and severe neurological impairment at age 3 years were evaluated. Of the infants, 48 (10.4%), 291 (63.1%) and 122 (26.5%) had mild, moderate and severe encephalopathy, respectively, upon admission. By age 3, 53 (11.2%) infants died, whereas 110 (26.1%) developed major disabilities. The mild group survived up to age 3. In the moderate group, 13 (4.5%) died and 44 (15.8%) developed major disabilities. In the severe group, 39 (32.0%) died by age 3. Adverse outcomes were observed in 100 (82.0%) infants. Mortality was relatively low in all subgroups, but the incidence of major disabilities was relatively high in the severe group. The relatively low mortality and high morbidity may be due to Japanese social and ethical norms, which rarely encourage the withdrawal of intensive life support. Cultural and ethical backgrounds may need to be considered when assessing the effect of therapeutic interventions., (© 2022. The Author(s).)

Published
2022
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3. Therapeutic hypothermia for neonatal encephalopathy: a report from the first 3 years of the Baby Cooling Registry of Japan.

Author

Tsuda K, Mukai T, Iwata S, Shibasaki J, Tokuhisa T, Ioroi T, Sano H, Yutaka N, Takahashi A, Takeuchi A, Takenouchi T, Araki Y, Sobajima H, Tamura M, Hosono S, Nabetani M, and Iwata O

Subjects
Adult, Female, Gestational Age, Humans, Infant, Newborn, Japan, Registries, Treatment Outcome, Brain Diseases epidemiology, Brain Diseases therapy, Hypothermia, Induced
Abstract

Therapeutic hypothermia is recommended for moderate and severe neonatal encephalopathy, but is being applied to a wider range of neonates than originally envisaged. To examine the clinical use of therapeutic hypothermia, data collected during the first 3 years (2012-2014) of the Baby Cooling Registry of Japan were analysed. Of 485 cooled neonates, 96.5% were ≥36 weeks gestation and 99.4% weighed ≥1,800 g. Severe acidosis (pH < 7 or base deficit ≥16 mmol/L) was present in 68.9%, and 96.7% required resuscitation for >10 min. Stage II/III encephalopathy was evident in 88.3%; hypotonia, seizures and abnormal amplitude-integrated electroencephalogram were observed in the majority of the remainder. In-hospital mortality was 2.7%; 90.7% were discharged home. Apgar scores and severity of acidosis/encephalopathy did not change over time. The time to reach the target temperature was shorter in 2014 than in 2012. The proportion undergoing whole-body cooling rose from 45.4% to 81.6%, while selective head cooling fell over time. Mortality, duration of mechanical ventilation and requirement for tube feeding at discharge remained unchanged. Adherence to standard cooling protocols was high throughout, with a consistent trend towards cooling being achieved more promptly. The mortality rate of cooled neonates was considerably lower than that reported in previous studies.

Published
2017
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