Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a well-recognized clinical sleep disorder that results in chronically fragmented sleep and recurrent hypoxemia. The primary daytime sequelae of the disorder include patient reports of excessive daytime sleepiness, depression, and attention and concentration problems. It has been well established that OSAHS negatively impacts certain aspects of cognitive functioning. The primary goals of this article are to (1) clarify the pattern of cognitive deficits that are specific to OSAHS; (2) identify the specific cognitive domains that improve with treatment; and (3) elucidate the possible mechanisms of cognitive dysfunction in OSAHS. At the conclusion of the paper, we propose a potential neurofunctional theory to account for the etiology of cognitive deficits in OSAHS. Thirty-seven peer-reviewed articles were selected for this review. In general, findings were equivocal for most cognitive domains. Treatment, however, was noted to improve attention/vigilance in most studies and consistently did not improve constructional abilities or psychomotor functioning. The results are discussed in the context of a neurofunctional theory for the effects of OSAHS on the brain.

Objectives: xMany Africans were brought to Brazil as slaves. The runaway or abandoned slaves founded isolated communities named quilombos. There are many quilombo remnants in Vale do Ribeira region in the southern part of São Paulo State. The aim of our study was to contribute to understanding the origins of these populations, through admixture studies. Methods: We genotyped 307 unrelated DNA samples obtained from ten quilombo populations from Vale do Ribeira region, using a panel of 48 INDEL polymorphisms. We estimated genetic differentiation between populations (FST) and genomic ancestry from these populations. Our data were compared to a similar study performed in quilombo remnants from the Brazilian Amazon region. Results: Population admixture estimates showed high degree of miscegenation in the quilombo remnants from Vale do Ribeira (average admixture estimates at 39.7% of African, 39.0% of European and 21.3% of Amerindian contribution). The proportions of ancestral genes varied greatly among individuals, ranging from 7.3 to 69.5%, 12.9 to 68.3%, and 7.3 to 58.5% (African, European, and Amerindian, respectively). Genetic differentiation between these populations was low (all FST values <5%), indicating gene flow between them. Both groups of quilombos, from Vale do Ribeira and Amazon, presented similar patterns of admixture. Conclusions: INDEL markers were useful to evidence the triple interbreeding among African, European, and Amerindian in the formation of quilombo populations. The low FST values suggested gene flow among quilombos from Vale do Ribeira. Our data highlight the important role of Amerindians in the formation of quilombo populations. Am. J. Hum. Biol., 2013. © 2012 Wiley Periodicals, Inc.

A meta-analysis was conducted to evaluate possible neuropsychological effects of treatments for cancer in adults. A search revealed 30 studies, encompassing 29 eligible samples, and leading to inclusion of a total of 838 patients and control participants. A total of 173 effect sizes (Cohen's d) were extracted across 7 cognitive domains and as assessed in the literature via 3 methods of comparison (post-treatment compared with normative data, controls, or baseline performance). Statistically significant negative effect sizes were found consistently across both normative and control methods of comparison for executive function, verbal memory, and motor function. The largest effects were for executive function and verbal memory normative comparisons (-.93 and -.91, respectively). When limiting the sample of studies in the analyses to only those with relatively "less severe" diagnoses and treatments, the effects remained. While these results point toward some specific cognitive effects of systemic cancer therapies in general, no clear clinical implications can yet be drawn from these results. More research is needed to clarify which treatments may produce cognitive decrements, the size of those effects, and their duration, while ruling out a wide variety of possible mediating or moderating variables.