[Assessment of clinical usefulness of Eviprostat for benign prostatic hyperplasia--comparison of Eviprostat tablet with a formulation containing two-times more active ingredients].

We compared the usefulness of Eviprostat tablet, a therapeutic agent for benign prostatic hyperplasia (BPH), and EVI-F tablet, a new formulation of Eviprostat containing two times more active ingredients (Chimaphila umbellata extract, Populus tremula extract, Pulsatilla pratensis extract, Equisetum arvense extract and purified wheat germ oil) and consequently designed to reduce the number of tablets per dose by half. In this study, patients with BPH were randomly assigned to either Eviprostat group (6 tabs/day) or EVI-F group (3 tabs/day) using the envelope method. The clinical efficacy of these two drugs were evaluated by the International Prostate Symptom Score (IPSS) and QOL score at the end of the treatment period, and their safety was evaluated by the incidence of side effects. Based on the clinical study guidelines for dysuria, the change in the IPSS total score and QOL score were comparable to the previously reported data for other treatment agents for BPH, and these indices showed gradual improvement with the treatment period. Both treatments were well tolerated. The clinical usefulness of the monotherapy with EVI-F tablet or Eviprostat tablet was reasonably demonstrated in this study. Furthermore, both treatments reduced nocturia, which has an impact on the QOL of patients with BPH.

Cirp protects against tumor necrosis factor-alpha-induced apoptosis via activation of extracellular signal-regulated kinase.

Mild hypothermia shows protective effects on patients with brain damage and cardiac arrest. To elucidate the molecular mechanisms underlying these effects, we analyzed the effects of low culture temperature (32 degrees C) and cold-inducible RNA-binding protein (Cirp) expression on apoptosis in vitro. In BALB/3T3 cells treated with tumor necrosis factor (TNF)-alpha and cycloheximide, the down-shift in temperature from 37 degrees C to 32 degrees C increased the expression of Cirp and suppressed the apoptosis. Activation of caspase-8 was suppressed, and the level of phosphorylated extracellular signal-regulated kinase (ERK) was increased. Transduction of Cirp into the Cirp-deficient mouse fibroblasts increased the level of phosphorylated ERK and suppressed the TNF-alpha-induced apoptosis both at 37 degrees C and 32 degrees C. The ERK-specific inhibitor PD98059 decreased the cytoprotective effect of Cirp as well as that of low culture temperature. These data suggest that mild hypothermia protects cells from TNF-alpha-induced apoptosis, at least partly, via induction of Cirp, and that Cirp protects cells by activating the ERK pathway.