Signs of enhanced formation of gist memory in children with autism spectrum disorder - a study of memory functions of sleep.

BACKGROUND: Autism spectrum disorder (ASD) is characterized by impaired cognitive and social skills, including emotional dysregulation, and symptoms have been suspected to partly arise from impaired formation of memory representations regulating these behaviours. Sleep, which is subjectively impaired in ASD, is critical for forming long-term memories and abstracted gist-based representations. We expected a generally reduced memory benefit from sleep in children with ASD, and a diminished enhancement of gist representations, in particular. METHODS: We compared effects of sleep on memory consolidation between boys (9-12 years) with ASD (n = 21) and typically developing (TD, n = 20) boys, matched for age and IQ, in a within-subjects crossover design. We employed an emotional picture recognition task and the Deese-Roediger-McDermott (DRM) word list task for assessing gist memory formation in the emotional and nonemotional domain, respectively. Learning took place before retention intervals of nocturnal sleep and daytime wakefulness, and retrieval was tested afterwards. RESULTS: Surprisingly, on the DRM task, children with ASD showed an enhanced sleep-dependent formation of gist-based memory (i.e. more recall of 'critical lure words' after sleep compared to wakefulness) than TD children, with this effect occurring on top of a diminished veridical word memory. On the picture recognition task, children with ASD also showed a stronger emotional enhancement in memory (i.e. relatively better memory for negative than neutral pictures) than TD children, with this enhancement occurring independent of sleep. Sleep polysomnography was remarkably comparable between groups. CONCLUSIONS: Children with ASD show well-preserved sleep-dependent memory consolidation. Enhanced gist memory formation in these children might reflect a compensatory response for impairments at earlier stages of memory processing, that is during encoding.

Utility and cutoff value of hair nicotine as a biomarker of long-term tobacco smoke exposure, compared to salivary cotinine.

While hair samples are easier to collect and less expensive to store and transport than biological fluids, and hair nicotine characterizes tobacco exposure over a longer time period than blood or urine cotinine, information on its utility, compared with salivary cotinine, is still limited. We conducted a cross-sectional study with 289 participants (107 active smokers, 105 passive smokers with self-reported secondhand smoke (SHS) exposure, and 77 non-smokers with no SHS exposure) in Baltimore (Maryland, USA). A subset of the study participants (n = 52) were followed longitudinally over a two-month interval.  Median baseline hair nicotine concentrations for active, passive and non-smokers were 16.2, 0.36, and 0.23 ng/mg, respectively, while those for salivary cotinine were 181.0, 0.27, and 0.27 ng/mL, respectively. Hair nicotine concentrations for 10% of passive or non-smokers were higher than the 25th percentile value for active smokers while all corresponding salivary cotinine concentrations for them were lower than the value for active smokers. This study showed that hair nicotine concentration values could be used to distinguish active or heavy passive adult smokers from non-SHS exposed non-smokers. Our results indicate that hair nicotine is a useful biomarker for the assessment of long-term exposure to tobacco smoke.

Environmental monitoring of secondhand smoke exposure.

The complex composition of secondhand smoke (SHS) provides a range of constituents that can be measured in environmental samples (air, dust and on surfaces) and therefore used to assess non-smokers' exposure to tobacco smoke. Monitoring SHS exposure (SHSe) in indoor environments provides useful information on the extent and consequences of SHSe, implementing and evaluating tobacco control programmes and behavioural interventions, and estimating overall burden of disease caused by SHSe. The most widely used markers have been vapour-phase nicotine and respirable particulate matter (PM). Numerous other environmental analytes of SHS have been measured in the air including carbon monoxide, 3-ethenylpyridine, polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines, nitrogen oxides, aldehydes and volatile organic compounds, as well as nicotine in dust and on surfaces. The measurement of nicotine in the air has the advantage of reflecting the presence of tobacco smoke. While PM measurements are not as specific, they can be taken continuously, allowing for assessment of exposure and its variation over time. In general, when nicotine and PM are measured in the same setting using a common sampling period, an increase in nicotine concentration of 1 µg/m(3) corresponds to an average increase of 10 µg/m3 of PM. This topic assessment presents a comprehensive summary of SHSe monitoring approaches using environmental markers and discusses the strengths and weaknesses of these methods and approaches.

Racial differences in hair nicotine concentrations among smokers.

INTRODUCTION: In the United States, race/ethnicity is a strong determinant of tobacco use patterns, biomarkers of tobacco smoke components and metabolites, and likelihood of successful cessation. Although Black smokers tend to smoke fewer cigarettes than White smokers, they have higher cotinine levels and disease risk and lower cessation success. We examined racial differences in hair nicotine concentrations among daily tobacco smokers (n = 103) in Baltimore, Maryland. METHODS: Participants completed a survey, and hair samples were collected and analyzed for nicotine concentration using gas chromatography coupled with mass spectrometry. RESULTS: After adjustment, hair nicotine concentrations among Black smokers were more than 5 times higher than among White smokers (95% CI 3.0, 10.5). Smokers reporting hair treatments other than coloring (bleaching, permanent, or straightening) in the past 12 months had 66% lower (95% CI 32%, 83%) hair nicotine concentrations. Smokers reporting smoking their first cigarette within 30 min of waking had twice the hair nicotine concentrations of those whose time to first cigarette was greater than 30 min after waking (95% CI 1.1, 4.2). For every additional cigarette smoked per day up to 20, mean hair nicotine concentration among all smokers increased by 4% (95% CI -1%, 9%). CONCLUSIONS: This study demonstrates that Black smokers have substantially higher hair nicotine levels than White smokers, after controlling for cigarettes smoked per day and other exposure sources. Time to first cigarette, cigarettes smoked per day, and use of hair treatments other than coloring were also associated with hair nicotine concentrations among smokers.