scispace - formally typeset
K

Kanji Higashio

Researcher at St. Vincent's Institute of Medical Research

Publications -  64
Citations -  14658

Kanji Higashio is an academic researcher from St. Vincent's Institute of Medical Research. The author has contributed to research in topics: Osteoprotegerin & Osteoclast. The author has an hindex of 36, co-authored 64 publications receiving 14220 citations.

Papers
More filters
Journal ArticleDOI

Basic fibroblast growth factor induces osteoclast formation by reciprocally regulating the production of osteoclast differentiation factor and osteoclastogenesis inhibitory factor in mouse osteoblastic cells.

TL;DR: It is concluded that bFGF induces osteoclast formation by stimulating ODF production through COX-2-mediated prostaglandin synthesis and by suppressing OCIF production through a mechanism independent of prostaglandsin synthesis.
Journal ArticleDOI

Hypocalcemic effect of osteoclastogenesis inhibitory factor/osteoprotegerin in the thyroparathyroidectomized rat.

TL;DR: It is suggested that OCIF not only inhibits the formation of osteoclasts but also affects the function and/or survival of mature osteoclast at doses used in this study.
Journal ArticleDOI

Structure of the mouse osteoclastogenesis inhibitory factor (OCIF) gene and its expression in embryogenesis

TL;DR: The isolation of mouse OCIF gene should facilitate studies on OCIF knock-out mice for a better understanding of the role of OCIF in vivo and the structures of these regions characterized in human OCIF are rigidly conserved.
Journal ArticleDOI

Cloning and characterization of the gene encoding mouse osteoclast differentiation factor.

TL;DR: The mouse ODF gene is a single copy gene consisting of five exons and spans approximately 40kb of the mouse genome, and the genomic organization is similar to that of other members of the TNF family, especially the CD40 ligand.
Journal ArticleDOI

Preventive effects of the deleted form of hepatocyte growth factor against various liver injuries

TL;DR: The pretreatment of rats and mice with the deleted form of HGF prevented the liver injuries and coagulopathy induced by endotoxin, dimethylnitrosamine and acetaminophen and reduced the mortality due to hepatic dysfunction induced by these hepatotoxins.