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The role of glucocorticoid receptor and gene expression in the anti-inflammatory action of dexamethasone
TLDR
The results reported here suggest that a glucocorticoid receptor and the induction of gene expression are involved in the anti-inflammatory action of dexamethasone.
The effect of CYP2C19 polymorphism on the safety, tolerability, and pharmacokinetics of tivantinib (ARQ 197): results from a phase I trial in advanced solid tumors.
TLDR
Neutropenia, leukopenia, anemia, fatigue, and anorexia were the frequent adverse events related to tivantinib and were commonly observed in both EMs and PMs.
Effects of luseogliflozin, a sodium–glucose co‐transporter 2 inhibitor, on 24‐h glucose variability assessed by continuous glucose monitoring in Japanese patients with type 2 diabetes mellitus: a
TLDR
After 7 days of treatment, the mean 24‐h glucose level was significantly lower with luseogliflozin than with placebo, and the decrease in glucose levels was accompanied by reductions in serum insulin levels throughout the day.
The effect of CYP2C19 polymorphism on the tolerability of ARQ 197: Results from phase I trial in Japanese patients with metastatic solid tumors.
TLDR
ARQ 197 monotherapy showed a clear sign of activity and was well tolerated in PM pts as well as EM pts, and CYP2C19 genotype clearly affected the exposure to ARQ 197 which led to different RP2Ds, 360mg bid for EM pts and 240 mg bid for PM pts.
Comparative study between steroidal and nonsteroidal anti-inflammatory drugs on the mode of their actions on vascular permeability in rat carrageenin-air-pouch inflammation.
TLDR
Prostaglandin E level in the exudate of the acute stage inflammation was suppressed by either dexamethasone or indomethacin in accordance with the inhibition of the vascular permeability, suggesting significant role of prostaglandsin E in the acute exudative inflammation.
Vascular permeability responses and the role of prostaglandin E2 in an experimental allergic inflammation of air pouch type in rats
TLDR
It is suggested that in this model, endogenous PGE2 does not affect oedema formation measured at 4 h, however, oedma formation measured over the period 0–4 h may be dependent on P GE2 generation.
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