The DAOA gene is associated with schizophrenia in the Taiwanese population.

The gene D-amino acid oxidase activator (DAOA), which has a former name of G72, and the D-amino acid oxidase (DAO) gene have been suggested as candidate genes of schizophrenia. However, association studies have so far yielded equivocal results. We analyzed one single nucleotide polymorphism (SNP) for DAO (rs3741775) and seven SNPs for G72 (rs3916956, rs2391191, rs9558562, rs947267, rs778292, rs3918342, and rs1421292) in this study enrolling 248 schizophrenia cases and 267 controls in the Taiwanese samples. In SNP-based single locus association analyses, the rs778292 in the DAOA gene showed significant association with schizophrenia. The rs3741775 in the DAO gene could not withstand statistically significant after multiple corrections. Additionally, a three-SNP haplotype (rs778292-rs3918342-rs1421292) in the DAOA gene were observed to be significantly associated with schizophrenia. Among them, the TCT haplotype presented higher prevalence in controls than in cases whereas the TTT and CTT haplotype were significantly more frequent in cases than in controls. The study also provides significant evidence for epistatic interactions among DAOA and DAO gene in the development of schizophrenia. These results provide additional evidence and indicate that the DAOA gene and DAOA-DAO gene-gene interactions might play a role for schizophrenia in a Taiwanese sample.

Fear of falling (FF): Psychosocial and physical factors among institutionalized older Chinese men in Taiwan.

Fear of falling (FF) can have multiple adverse consequences in the elderly. Although there are various fall prevention programs, little is known of FF and its associated characteristics. This study examined FF-associated physical and psychosocial factors in older Chinese men living in a veterans home in southern Taiwan. Subjects with a recent episode of delirium, of bed-ridden or wheelchair-bound status, severe hearing impairment or impaired cognition were excluded. Overall, 371 residents (mean age 82.1 ± 5.11 years, all males) participated. The prevalence of FF was 25.3%. Univariate analysis revealed that subjects in the FF group were older age, having lower education level, poorer sitting and standing balance, poorer activities of daily living (ADL), more depressive symptoms, higher chances of using walking aids, neurologic diseases, and a history of fall within the past 6 months. Logistic regression showed that depressive symptoms (odds ratio = OR = 6.73, 95%CI: 3.03-14.93, p < 0.001), activities of daily living (OR = 2.48, 95%CI: 1.08-5.71, p = 0.033), history of fall in the past 6 months (OR = 2.47, 95%CI: 1.04-5.9, p = 0.041), and neurological diseases (OR = 2.75, 95%CI: 1.15-6.56, p = 0.023) were all independent risk factors for FF.

Effect of 17beta-estradiol on intracellular Ca(2+) levels in renal tubular cells.

The effect of 17beta-estradiol on intracellular Ca(2+) concentrations ([Ca(2+)](i)) in Madin Darby canine kidney cells was investigated by using the fluorescent dye fura-2. 17Beta-estradiol (5-100 micromol/l) induced instantaneous increases in [Ca(2+)](i) in a concentration-dependent manner. Ca(2+) removal inhibited 45 +/- 15% of the Ca(2+) signal. In Ca(2+)-free medium, pretreatment with 50 micromol/l 17beta-estradiol abolished the [Ca(2+)](i) increases induced by 2 micromol/l carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler), 1 micromol/l thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) and 50 micromol/l brefeldin A (an antibiotic which disperses the Golgi complex), but pretreatment with brefeldin A, CCCP and thapsigargin only partly inhibited the 17beta-estradiol-induced [Ca(2+)](i) signal. Adding 3 mmol/l Ca(2+) increased [Ca(2+)](i) in cells pretreated with 5-100 micromol/l 17beta-estradiol in Ca(2+)-free medium. Pretreatment with 1 micromol/l U73122 to abolish the formation of inositol-1,4,5-trisphosphate inhibited 50% of the Ca(2+) release induced by 50 micromol/l 17beta-estradiol. 17Beta-estradiol (20 micromol/l) also increased [Ca(2+)](i) in human bladder cancer cells and prostate cancer cells. Collectively, this study shows that 17beta-estradiol evoked a significant internal Ca(2+) release and external Ca(2+) entry possibly in a nongenomic manner.