Prevalence of insomnia and its risk factors in older individuals: a community-based study in four cities of Hebei Province, China.

OBJECTIVE: To examine the epidemiology of sleep problems and insomnia among the community older individuals in Hebei Province, China, and to investigate the potential sociodemographic and clinical correlates and medication use. METHODS: This cross-sectional study was conducted with community adults, aged 60 years or older, who resided in four major cities in Hebei province. Basic sociodemographic and clinical data were collected and analyzed. A total of 3176 older adults (1292 men, 70.2 ± 6.8 years; 1884 women, 68.8 ± 6.7 years) were interviewed. All of the participants were interviewed with a standardized questionnaire and underwent insomnia screening. RESULTS: The prevalence of insomnia was 37.75%. The most common type of sleep disturbance was difficulty maintaining sleep, followed by difficulty initiating sleep and early morning awakening. Never smoking, experiencing the loss of a parent, a history of coronary heart disease, and depression symptoms were independent risk factors for insomnia in men. Occasional drinking was an independent protective factor against insomnia in men. Older age, depression symptoms, a history of cerebral hemorrhage, hyperlipidemia, living without a spouse, and having mild cognitive impairment were independent risk factors for insomnia in women. Only 11.1% of the sample with insomnia were taking sleeping medications regularly. CONCLUSION: Insomnia is highly prevalent among the community older population in Hebei Province. The percentage of individuals regularly taking sleeping medication is low among those with insomnia. Individuals with complaints of insomnia frequently have poor physical and mental health and may need more medical attention. Comprehensive measures that involve psychosocial and personal behaviors should be implemented to alleviate insomnia in older individuals.

Delayed noradrenergic activation in the dorsal hippocampus promotes the long-term persistence of extinguished fear.

Fear extinction has been extensively studied, but little is known about the molecular processes that underlie the persistence of extinction long-term memory (LTM). We found that microinfusion of norepinephrine (NE) into the CA1 area of the dorsal hippocampus during the early phase (0 h) after extinction enhanced extinction LTM at 2 and 14 days after extinction. Intra-CA1 infusion of NE during the late phase (12 h) after extinction selectively promoted extinction LTM at 14 days after extinction that was blocked by the ß-receptor antagonist propranolol, protein kinase A (PKA) inhibitor Rp-cAMPS, and protein synthesis inhibitors anisomycin and emetine. The phosphorylation levels of PKA, cyclic adenosine monophosphate response element-binding protein (CREB), GluR1, and the membrane GluR1 level were increased by NE during the late phase after extinction that was also blocked by propranolol and Rp-cAMPS. These results suggest that the enhancement of extinction LTM persistence induced by NE requires the activation of the ß-receptor/PKA/CREB signaling pathway and membrane GluR1 trafficking. Moreover, extinction increased the phosphorylation levels of Erk1/2, CREB, and GluR1, and the membrane GluR1 level during the late phase, and anisomycin/emetine alone disrupted the persistence of extinction LTM, indicating that the persistence of extinction LTM requires late-phase protein synthesis in the CA1. Propranolol and Rp-cAMPS did not completely disrupt the persistence of extinction LTM, suggesting that another ß-receptor/PKA-independent mechanism underlies the persistence of extinction LTM. Altogether, our results showed that enhancing hippocampal noradrenergic activity during the late phase after extinction selectively promotes the persistence of extinction LTM.

ErbB2 dephosphorylation and anti-proliferative effects of neuregulin-1 in ErbB2-overexpressing cells; re-evaluation of their low-affinity interaction.

Neuregulin-1 binds to ErbB3 and ErbB4 and regulates cancer proliferation and differentiation. Neuregulin-1 had been suggested to also react with ErbB2, but this argument becomes controversial. Here, we re-evaluated the cellular responses and ErbB2 interaction of neuregulin-1 in ErbB2 overexpressing cell lines. In a competitive ligand-binding assay, we detected significant replacement of [(35)S]-labeled neuregulin-1 with nano molar ranges of cold neuregulin-1 in L929 cells expressing ErbB2 alone and SKOV3 cells carrying sulf-1 cDNA but not in these parental cells. The concentration of neuregulin-1 significantly decreased thymidine incorporation and phosphorylation of ErbB2 (Tyr877, Tyr1396, and Tyr1121) in ErbB2-overexpressing cancer cells as well as in L929 cells expressing ErbB2. A crosslinking assay ascertained the presence of neuregulin-1 immunoreactivity in the ErbB2 immune complexes of L929 expressing ErbB2 alone. These results suggest that the higher concentrations of neuregulin-1 exert an anti-oncogenic activity to attenuate ErbB2 auto-phosphorylation potentially through its low-affinity interaction with ErbB2.