Zobrazeno 1 - 10
of 42
pro vyhledávání: '"Shunichi Murakami"'
Publikováno v:
JA Clinical Reports, Vol 6, Iss 1, Pp 1-4 (2020)
Abstract Background Excessive dynamic airway collapse (EDAC) is an uncommon cause of high airway pressure during mechanical ventilation. However, EDAC is not widely recognized by anesthesiologists, and therefore, it is often misdiagnosed as asthma. C
Externí odkaz:
https://doaj.org/article/5a3ae602a7f64cf9ad952e9a016b7b1a
Publikováno v:
JA Clinical Reports, Vol 6, Iss 1, Pp 1-4 (2020)
JA Clinical Reports
JA Clinical Reports
Background Excessive dynamic airway collapse (EDAC) is an uncommon cause of high airway pressure during mechanical ventilation. However, EDAC is not widely recognized by anesthesiologists, and therefore, it is often misdiagnosed as asthma. Case prese
Autor:
Michiyasu Suzuki, Satoshi Yamashita, Takayuki Okamura, Kazuyoshi Ishida, Hiroshi Kurazumi, Mishiya Matsumoto, Hideyuki Ishihara, Atsuo Yamashita, Tetsuro Oda, Shunichi Murakami, Ryo Suzuki
Publikováno v:
Journal of cardiothoracic and vascular anesthesia. 34(5)
Autor:
Iva Vesela, Petr Dvorak, Miroslav Varecha, Vitezslav Bryja, Iveta Cervenkova, Alois Kozubík, Marcela Buchtová, Iva Jelínková, Anie Aklian, Petr Matula, Zaneta Konecna, Tereza Spoustova, Pavel Krejci, Tereza Pospisilova, Ivan Duran, Tereza Obadalova, Lukas Balek, Iva Gudernova, Shunichi Murakami, Veronika Oralova, Jan Masek, Zhufeng Ouyang
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1852:839-850
Aberrant fibroblast growth factor (FGF) signaling disturbs chondrocyte differentiation in skeletal dysplasia, but the mechanisms underlying this process remain unclear. Recently, FGF was found to activate canonical WNT/β-catenin pathway in chondrocy
Publikováno v:
Journal of Bone and Mineral Research. 30:765-774
Chondrocytes in the epiphyseal cartilage undergo terminal differentiation prior to their removal through apoptosis. To examine the role of ERK1 and ERK2 in chondrocyte terminal differentiation, we generated Osterix (Osx)-Cre; ERK1–/–; ERK2flox/fl
Autor:
Michael D. Schneider, Soma Biswas, Baojie Li, Shafiquzzaman, Hongguang Wu, Shunichi Murakami, Ping Li, Yuji Mishina, Jing Li
Publikováno v:
Scientific Reports
Scientific Reports, Vol 8, Iss 1, Pp 1-14 (2018)
Scientific Reports, Vol 8, Iss 1, Pp 1-14 (2018)
Bone morphogenetic proteins (BMPs) activate the canonical Smad1/5/8 and non-canonical Tak1-MAPK pathways via BMP receptors I and II to regulate skeletal development and bone remodeling. Specific ablation of Bmpr1a in immature osteoblasts, osteoblasts
Autor:
Ruggero Pardi, Shunichi Murakami, Bojian Liang, Guang Zhou, Dongxing Chen, Zhijun Chen, Lindsay A. Bashur
Publikováno v:
Journal of Cellular Physiology. 229:1607-1617
The transcriptional cofactor Jab1 controls cell proliferation, apoptosis, and differentiation in diverse developmental processes by regulating the activity of various transcription factors. To determine the role of Jab1 during early limb development,
Autor:
Abdus Sattar, Adriana Ortiz-Lopez, Shunichi Murakami, Cynthia F. Bartels, Matthew L. Warman, Fozia Khan, Tariq M. Haqqi, Hulya Bukulmez
Publikováno v:
Arthritis & Rheumatology (Hoboken, N.j.)
Objective The C-type natriuretic peptide (CNP) signaling pathway is a major contributor to postnatal skeletal growth in humans. This study was undertaken to investigate whether CNP signaling could prevent growth delay and cartilage damage in an anima
Autor:
Xin Chen, Guangbin Luo, Guang Zhou, Edward M. Greenfield, Bryan S. Hausman, Shunichi Murakami, Janet Rubin
Publikováno v:
Stem Cells. 31:2789-2799
The protein kinase inhibitor (Pki) gene family inactivates nuclear protein kinase A (PKA) and terminates PKA-induced gene expression. We previously showed that Pkig is the primary family member expressed in osteoblasts and that Pkig knockdown increas
Publikováno v:
Epstein's Inborn Errors of Development: The Molecular Basis of Clinical Disorders of Morphogenesis
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::47527d69664fc17e2a366ebd5f220195
https://doi.org/10.1093/med/9780199934522.003.0013
https://doi.org/10.1093/med/9780199934522.003.0013