AS could adversely affect the HRQoL of patients. Measuring HRQoL should be considered as an essential part of the overall assessment of health status of AS patients, which would provide valuable clues for improving the management of disease and making decisions regarding treatment.

Neurite extension and branching are affected by activity-dependent modulation of intracellular Ca 2+ , such that an optimal window of [Ca 2+ ] i is required for outgrowth. Our understanding of the molecular mechanisms regulating this optimal [Ca 2+ ] i remains unclear. Taking advantage of the large growth cone size of cultured primary neurons from pond snail Lymnaea stagnalis combined with dsRNA knockdown, we show that neuronal calcium sensor-1 (NCS-1) regulates neurite extension and branching, and activitydependent Ca 2+ signals in growth cones. An NCS-1 C-terminal peptide enhances only neurite branching and moderately reduces the Ca 2+ signal in growth cones compared with dsRNA knockdown. Our findings suggest that at least two separate structural domains in NCS-1 independently regulate Ca 2+ influx and neurite outgrowth, with the C-terminus specifically affecting branching. We describe a model in which NCS-1 regulates cytosolic Ca 2+ around the optimal window level to differentially control neurite extension and branching.

BackgroundCognitive impairment has been found in chronic obstructive pulmonary disease (COPD) patients. However, the structural alteration of the brain and underlying mechanisms are poorly understood.MethodsThirty-seven mild-to-moderate COPD patients, forty-eight severe COPD patients, and thirty-one control subjects were recruited for cognitive test and neuroimaging studies. Serum levels of S100B,pulmonary function and arterial blood gas levels were also evaluated in each subject.ResultsThe hippocampal volume was significantly smaller in COPD patients compared to the control group. It is positively correlated with a mini mental state examination (MMSE) score, SaO2 in mild-to-moderate COPD patients, the levels of PaO2 in both mild-to-moderate and severe COPD patients. Higher S100B concentrations were observed in mild-to-moderate COPD patients, while the highest S100B level was found in severe COPD patients when compared to the control subjects. S100B levels are negatively associated with MMSE in both mild-to-moderate and severe COPD patients and also negatively associated with the hippocampal volume in the total COPD patients.ConclusionsHippocampal atrophy based on quantitative assessment by magnetic resonance imaging does occur in COPD patients, which may be associated with cognitive dysfunction and the most prevalent mechanism accountable for hippocampal atrophy is chronic hypoxemia in COPD. Higher serum S100B levels may be peripheral biochemical marker for cognitive impairment in COPD.

Background: Chronic obstructive pulmonary disease (COPD) is understood to be a complex multicomponent disorder. The impairment of cognition is lasting and profound. However, the pattern of the cognitive decline and potentially adverse factors are poorly understood. Objectives: To evaluate the cognitive performances and the relevant factors in COPD patients and to investigate the relationship between cognition deficits and the classification of severity of the disease. Methods: Twenty-seven mild-to-moderate COPD patients, 35 severe COPD patients and 27 control subjects were recruited. Cognitive states were investigated by the Mini-Mental State Examination (MMSE). Pulmonary function, arterial blood gas and serum clusterin level were evaluated in each subject. Results: Lower MMSE score and higher serum clusterin concentration were observed in mild-to-moderate COPD patients, while the lowest MMSE score and the highest serum clusterin level were found in severe COPD patients when compared with control subjects. MMSE score is positively correlated with arterial oxygen tension and is inversely associated with serum clusterin level in both mild-to-moderate and severe COPD patients. Furthermore, MMSE scores and serum clusterin concentrations were correlated with forced expiratory volume in 1 s in severe COPD patients. Conclusion: Cognitive impairment was found in COPD patients. It is associated with the classification of disease severity, hypoxemia and serum clusterin level. An increased serum clusterin level may be a relevant peripheral biomarker of cognitive dysfunction in COPD patients.

No abstract