scispace - formally typeset
N

Natsuo Yasui

Researcher at University of Tokushima

Publications -  232
Citations -  8028

Natsuo Yasui is an academic researcher from University of Tokushima. The author has contributed to research in topics: Spondylolysis & Distraction osteogenesis. The author has an hindex of 44, co-authored 230 publications receiving 7432 citations. Previous affiliations of Natsuo Yasui include Tokyo Medical and Dental University & Osaka University.

Papers
More filters
Journal ArticleDOI

Repair of rabbit articular surfaces with allograft chondrocytes embedded in collagen gel

TL;DR: Allogenic transplantation of isolated chondrocytes embedded in collagen gel appears to be one of the most promising methods for the restoration of articular cartilage.
Journal ArticleDOI

A RUNX2/PEBP2αA/CBFA1 mutation displaying impaired transactivation and Smad interaction in cleidocranial dysplasia

TL;DR: It is shown that signal transducers of transforming growth factor beta superfamily receptors, Smads, interact with RUNX2 in vivo and in vitro and enhance the transactivation ability of this factor.
Journal ArticleDOI

Transcriptional regulation of osteopontin gene in vivo by PEBP2alphaA/CBFA1 and ETS1 in the skeletal tissues

TL;DR: It is suggested that PEBP2αA and ETS1 cooperate in vivo to regulate expression of the opn gene in the skeletal tissue and the specific spatial arrangement of both sites and direct interaction between PEBP1 and Ets1, were essential for promoter function.
Journal ArticleDOI

Mechanical Tension-Stress Induces Expression of Bone Morphogenetic Protein (BMP)-2 and BMP-4, but Not BMP-6, BMP-7, and GDF-5 mRNA, During Distraction Osteogenesis

TL;DR: The present results suggest that excellent and uninterrupted bone formation during distraction osteogenesis owes to enhanced expression of B MP‐2 and BMP‐4 genes by mechanical tension‐stress.
Journal ArticleDOI

Skeletal muscle gene expression in space-flown rats.

TL;DR: It is postulate that mitochondrial dislocation during spaceflight has deleterious effects on muscle fibers, leading to atrophy in the form of insufficient energy provision for construction and leakage of reactive oxygen species from the mitochondria.