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Koji Y. Arai

Researcher at Tokyo University of Agriculture and Technology

Publications -  54
Citations -  924

Koji Y. Arai is an academic researcher from Tokyo University of Agriculture and Technology. The author has contributed to research in topics: Luteinizing hormone & Ovulation. The author has an hindex of 18, co-authored 54 publications receiving 854 citations. Previous affiliations of Koji Y. Arai include University of Kansas & University of Tokushima.

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Adverse effects of environmental toxicants, octylphenol and bisphenol A, on male reproductive functions in pubertal rats.

TL;DR: It is demonstrated that OP and BPA can reduce sperm counts resulting from lowered plasma testosterone in male rats just after puberty, raising the possibility of a link between these chemicals and prostate diseases because IGF-I has been implicated in the pathogenesis of human prostate cancers.
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Novel factors in regulation of activin signaling

TL;DR: Data indicate that ARIP2 is a novel factor regulating cell surface ActRII expression and activin function, and that follistatin and FLRG likely play distinct roles as activin/GDF binding proteins in vivo.
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Expression of Nerve Growth Factor and Its Receptors NTRK1 and TNFRSF1B Is Regulated by Estrogen and Progesterone in the Uteri of Golden Hamsters

TL;DR: Results suggest that NGF may play important roles in action of steroids on uterine function and changes in uterine weights induced by estradiol-17β and/or progesterone showed the same profile with that of NGF, suggesting that a proliferative act of N GF may be involved in uterusine growth.
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A New Alternative Method for Superovulation Using Passive Immunization Against Inhibin in Adult Rats

TL;DR: Results indicate that immunoneutralization of endogenous inhibin is a new practical alternative for induction of superovulation as a substitution for eCG-hCG method in the adult rat.
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Tumor Necrosis Factor α (TNF) Increases Granulosa Cell Proliferation: Dependence on c-Jun and TNF Receptor Type 1

TL;DR: It is demonstrated that TNF increased c-Jun by activating stress-activated protein kinase/c-Jun-NH(2)-teminal kinase signaling via TNFR1 in mouse granulosa cells, and the induced c- Jun resulted in increased cell proliferation.