Introduction In Korea, although male sexual problems have been relatively well addressed, few surveys have been conducted on female sexual dysfunction (FSD) in the general population. In the present study, we investigated the prevalence and identified the risk factors of sexual dysfunction in young Korean women. Aim To evaluate the prevalence and to identify the risk factors of FSD in young Korean women. Methods A total of 47,000 women were initially approached. All received an e-mail requesting that they participate in a Web-based survey. The participants were asked to complete a questionnaire requesting detailed medical and sexual histories, which included the questions contained in the Korean version of the Female Sexual Function Index questionnaire. Main Outcome Measures The prevalence of FSD in young Korean women in the different age groups and risk factors for developing FSD. Results A total of 504 women of average age 28.5 years (18–52 years) were evaluated during this survey. Setting the cutoff score for FSD using a receiver operating characteristic curve of our data as 25.0 points, 43.1% of women under 40 years old reported FSD. FSD was detected as a desire problem in 44.0% of women, an arousal problem in 49.0%, a lubrication problem in 37.0%, an orgasm problem in 32.0%, a satisfaction problem in 37.0%, and a pain problem in 34.6%. Risk factors for FSD as determined by logistic regression analysis were increasing age, a low frequency of sex, depression, a sexually abused history, and voiding dysfunction. Conclusions The prevalence of FSD in Korean young women was common and comparable to those reported worldwide.

T cell stimulation via glucocorticoid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR) elicits antitumor activity in various tumor models; however, the underlying mechanism of action remains unclear. Here we demonstrate a crucial role for interleukin (IL)-9 in antitumor immunity generated by the GITR agonistic antibody DTA-1. IL-4 receptor knockout (Il4ra(-/-)) mice, which have reduced expression of IL-9, were resistant to tumor growth inhibition by DTA-1. Notably, neutralization of IL-9 considerably impaired tumor rejection induced by DTA-1. In particular, DTA-1-induced IL-9 promoted tumor-specific cytotoxic T lymphocyte (CTL) responses by enhancing the function of dendritic cells in vivo. Furthermore, GITR signaling enhanced the differentiation of IL-9-producing CD4(+) T-helper (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-κB-dependent manner and inhibited the generation of induced regulatory T cells in vitro. Our findings demonstrate that GITR co-stimulation mediates antitumor immunity by promoting TH9 cell differentiation and enhancing CTL responses and thus provide a mechanism of action for GITR agonist-mediated cancer immunotherapies.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Atenolol is an antihypertensive drug, of which negligible amounts are metabolized. • Fruit juices may decrease the oral absorption of drugs by inhibiting intestinal drug transporters, as demonstrated in vitro and in vivo. WHAT THIS STUDY ADDS • The pharmacokinetic characteristics of atenolol were determined according to the SLCO2B1 genotype after apple juice administration in healthy Korean volunteers. • Apple juice ingestion markedly reduced the systemic exposure to atenolol, but genetic variations in SLCO2B1 were unlikely to contribute substantial variability to the pharmacokinetics of atenolol. AIM Fruit juice reduces the plasma concentrations of several β‐adrenoceptor blockers, likely by inhibiting OATP2B1‐mediated intestinal absorption. The aim of this study was to investigate the effects of apple juice on the pharmacokinetics of atenolol. METHODS Twelve healthy Korean volunteers with genotypes of SLCO2B1 c.1457C> T (*1/*1 (n= 6) and *3/*3 (n= 6)) were enrolled in this study. In a three‐phase, one‐sequence crossover study, the pharmacokinetics (PK) of atenolol was evaluated after administration of 50 mg atenolol. Subjects received atenolol with either 300 ml water, 1200 ml apple juice or 600 ml apple juice. RESULTS Apple juice markedly reduced the systemic exposure to atenolol. The geometric mean ratios (95% confidence intervals) of apple juice : water were 0.18 (0.13, 0.25, 1200 ml) and 0.42 (0.30, 0.59, 600 ml) for the AUC(0,tlast). In this study, the PK parameters of atenolol responded in a dose‐dependent manner to apple juice. CONCLUSIONS Apple juice markedly reduced systemic exposure to atenolol. The genetic variation of SLCO2B1 c.1457C>T had a minimal effect on the pharmacokinetics of atenolol when the drug was administered with water or apple juice.

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