Effect of sex and polymorphisms of CYP2B6 and UGT1A9 on the difference between the target-controlled infusion predicted and measured plasma propofol concentration.

Introduction: To examine whether sex and polymorphisms of cytochrome P450 (CYP) 2B6 and UDP-glucuronosyltransferase (UGT) 1A9 affect the difference between predicted and measured plasma propofol concentration during continuous infusion by target-controlled infusion.

Results: Blood samples of 69 patients (48 men and 21 women) were obtained at 4 h after initial propofol infusion. Percentage performance error (PE) was calculated to assess the difference between measured and predicted propofol concentration.

Differential effects of organic nitrates on arterial diameter among healthy Japanese participants with different mitochondrial aldehyde dehydrogenase 2 genotypes: randomised crossover trial.

Objectives: To determine whether polymorphisms at codon 487 (*1, GAA=Glu; *2, AAA=Lys) of mitochondrial aldehyde dehydrogenase 2 (ALDH2) influence nitroglycerine (glyceryl trinitrate (GTN))-induced vasodilation, and whether GTN or isosorbide dinitrate (ISDN) is a more effective antianginal agent in each ALDH2 genotype.

Design: A randomised, open-label, crossover trial with 117 healthy Japanese (20-39 years) whose genotypes were determined (*1/*1, n=47; *1/*2, n=48; *2/*2, n=22) was performed at Kyushu University Hospital, Fukuoka, Japan. Participants were randomly assigned to treatment: sublingual spray of GTN (0.

DIF-1 inhibits the Wnt/β-catenin signaling pathway by inhibiting TCF7L2 expression in colon cancer cell lines.

We previously reported that differentiation-inducing factor-1 (DIF-1), a morphogen in Dictyostelium discoideum, inhibits the proliferation of human cancer cell lines by inducing β-catenin degradation and suppressing the Wnt/β-catenin signaling pathway. To determine whether β-catenin degradation is essential for the effect of DIF-1, we examined the effect of DIF-1 on human colon cancer cell lines (HCT-116, SW-620 and DLD-1), in which the Wnt/β-catenin signaling pathway is constitutively active. DIF-1 strongly inhibited cell proliferation and arrested the cell cycle in the G(0)/G(1) phase via the suppression of cyclin D1 expression at mRNA and protein levels without reducing β-catenin protein.

β(1)-Adrenergic receptor gene polymorphisms and the acute response to atenolol in healthy young Japanese subjects.

Polymorphisms at codons 49 and 389 of the β(1)-adrenergic receptor gene have been shown to alter the receptor function in vitro, whereas it remains controversial whether they influence the response to β-blocker in vivo. In the present study, we investigated whether these polymorphisms influence the acute changes of heart rate and blood pressure induced by the β(1)-adrenergic receptor-selective blocker atenolol in healthy young Japanese. A double-blind study was conducted with 307 subjects randomly allocated 2:1 to atenolol (50 mg) or placebo groups.

Anti-angiogenic effects of differentiation-inducing factor-1 involving VEGFR-2 expression inhibition independent of the Wnt/β-catenin signaling pathway.

Background: Differentiation-inducing factor-1 (DIF-1) is a putative morphogen that induces cell differentiation in Dictyostelium discoideum. DIF-1 inhibits proliferation of various mammalian tumor cells by suppressing the canonical Wnt/β-catenin signaling pathway. To assess the potential of a novel cancer chemotherapy based on the pharmacological effect of DIF-1, we investigated whether DIF-1 exhibits anti-angiogenic effects in vitro and in vivo.

Development of a comb needle with five needles for securing access to large blood vessels during emergency resuscitation.

Purpose: Animal tests have indicated that providing venous-arterial (V-A) bypass extracorporeal circulation immediately after cardiac arrest is a useful resuscitation technique for achieving resumption of a normal cardiac function and brain resuscitation. However, pulsation of the femoral artery cannot be felt in the case of cardiac arrest, and it takes a long time to puncture the femoral artery and vein. We developed a comb needle that has five 18-gauge metallic needles fixed in parallel on a plastic board.

Celecoxib induces apoptosis by inhibiting the expression of survivin in HeLa cells.

The effect of celecoxib, a cyclooxygenase-2 selective inhibitor, on a human cervical cancer cell line, HeLa cells, was examined. We found that celecoxib increased DNA ladder formation and the activity of caspase-3, indicating that celecoxib induced apoptosis in HeLa cells. Celecoxib suppressed the expression of an anti-apoptotic protein, survivin, in both protein and mRNA levels.

Celecoxib inhibits the expression of survivin via the suppression of promoter activity in human colon cancer cells.

We investigated the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on human colon cancer cell lines to clarify the mechanisms underlying the chemopreventive effect of NSAIDs. Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, induced apoptosis and strongly reduced the expression of an anti-apoptotic protein, survivin, in both protein and mRNA levels in HCT-116 cells. Subsequently, we conducted luciferase reporter assay using a reporter gene driven by the human survivin promoter.

Glycogen synthase kinase-3beta is tyrosine-phosphorylated by MEK1 in human skin fibroblasts.

Glycogen synthase kinase-3beta (GSK-3beta) can be associated with several proteins in cell. We analyzed the immunoprecipitates by an anti-GSK-3beta antibody from cell lysate of human fibroblasts and found that this protein was co-precipitated with mitogen-activated protein kinase kinase (MEK1/2). U0126, a MEK1/2 inhibitor, inhibited tyrosine phosphorylation of GSK-3beta, suggesting that MEK1/2 was involved in the phosphorylation of Tyr(216) in GSK-3beta.

Periodic binding of troponin C.I and troponin I to tropomyosin-actin filaments.

We investigated the distribution of troponin C.I and troponin I along tropomyosin-actin filaments by immunoelectron microscopy and found that anti-troponin I antibody formed transverse striations at 38 nm intervals along the bundle of filaments of both troponin C.I-tropomyosin-actin and troponin I-tropomyosin-actin.