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Objective: To investigate the longitudinal association of sleep quality with incidence of neurocognitive disorders in 6 years. Methods: This was a 6‐year follow‐up study of community‐living older adults who scored a Clinical Dementia Rating (CDR) of 0 at baseline. Sleep quality was assessed by the self‐rated Pittsburgh Sleep Quality Index (PSQI) questionnaire, where higher scores indicated poorer sleep quality, and a cutoff score of 5 or above was suggestive of sleep disorder. The study outcome was incident neurocognitive disorders in 6 years, as identified by a CDR of 0.5 or above. Poisson regression analysis was conducted to test if baseline sleep quality was independently associated with risk of incident neurocognitive disorders in 6 years. Results: Of the 290 participants in this study, 166 (57.2%) developed neurocognitive disorders in 6 years. They had poorer sleep quality (mean [SD] total PSQI score: 6.2 [3.8] vs. 4.9 [3.2], p = 0.001) and higher prevalence of sleep disorder (100 [60.2%] vs. 56 [45.2%], p = 0.01) at baseline than those who remained free of neurocognitive disorder. After controlling for age, gender, education, and physical and psychiatric morbidities, the risk ratios (RRs) for incident neurocognitive disorders were 1.05 (95% confidence interval (CI) = 1.00–1.11, p < 0.05) for PSQI total score and 1.50 (95% CI = 1.05–2.14, p = 0.03) for sleep disorder at baseline. Conclusions: Sleep quality might predict the development of neurocognitive disorders. From a clinical perspective, enquiry of sleep quality and screening for sleep disorder should be promoted as part of the neurocognitive disorder risk assessment in older adults. Key points: Older adults with poor sleep quality are more likely to develop neurocognitive disorders.Examination of sleep quality and screening for sleep disorder should be included as part of neurocognitive disorder risk assessment. [ABSTRACT FROM AUTHOR]

Monosodium methanearsonate (MSMA), an arsenic-based pesticide, has been used for the past 10 years in attempts to suppress mountain pine beetle (Dendroctonus ponderosae) outbreaks in British Columbia, Canada. Previous studies have shown that cavity nesting forest birds such as woodpeckers forage and breed in MSMA treated pine stands. Here we examined the effects of MSMA in the laboratory using the zebra finch (Taeniopygia guttata), with the objective to examine tissue distribution and sublethal toxic effects in a model avian species. Zebra finches were exposed to this pesticide at doses similar to those found in bark beetle samples from MSMA stands of trees treated in the southern interior of British Columbia (8, 24, and 72 μg/g/d and a control group). Results showed high excretion (>90%) of arsenic in all dose groups, as well as dose-dependent trends in accumulation of arsenic in the blood (p < 0.001) and specific tissues. Monomethylarsonic acid, MMA (V), was the predominant form of arsenic in the blood plasma. Dimethylarsinic acid was the major form of arsenic found in the liver (83%) and kidney (61%) tissues. The brain tissue contained primarily the MMA (V) form (57%). Significant weight loss occurred in the two highest dose groups (p < 0.05). Birds in the highest dose group lost up to 15% of initial body mass. [ABSTRACT FROM AUTHOR]

Presents information on a study which examined interactions between potato starch and the salts of alkali-earth metals and lead. Methodology; Results of the study; Possible mechanisms involved in the interaction.

The 1- to 2-h illumination of xylanase with visible polarized light (PL) prior to the action of that enzyme upon beechwood xylan significantly increased its activity. The activity only negligibly decreased on 3 months storage. The hydrolysis of xylan proceeded in three well-distinguished stages. In the first and fastest stage the effect of illumination was only slightly positive. The effect of the stimulation was noted in the second, slower stage. Enzyme stimulated with PL, preferably by means of the 2-h illumination, performed better than enzyme stimulated with nonpolarized light and non-stimulated enzyme. In the last, the slowest stage, the rates of the reaction were nearly the same using either stimulated or non-stimulated enzyme.