Nanoparticles in a biological milieu are known to form a sufficiently long-lived and well-organized 'corona' of biomolecules to confer a biological identity to the particle. Because this nanoparticle-biomolecule complex interacts with cells and biological barriers, potentially engaging with different biological pathways, it is important to clarify the presentation of functional biomolecular motifs at its interface. Here, we demonstrate that by using antibody-labelled gold nanoparticles, differential centrifugal sedimentation and various imaging techniques it is possible to identify the spatial location of proteins, their functional motifs and their binding sites. We show that for transferrin-coated polystyrene nanoparticles only a minority of adsorbed proteins exhibit functional motifs and the spatial organization appears random, which is consistent, overall, with a stochastic and irreversible adsorption process. Our methods are applicable to a wide array of nanoparticles and can offer a microscopic molecular description of the biological identity of nanoparticles.

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Cognitive vitality is essential to quality of life and survival in old age. With normal aging, cognitive changes such as slowed speed of processing are common, but there is substantial interindividual variability, and cognitive decline is clearly not inevitable. In this review, we focus on recent research investigating the association of various lifestyle factors and medical comorbidities with cognitive aging. Most of these factors are potentially modifiable or manageable, and some are protective. For example, animal and human studies suggest that lifelong learning, mental and physical exercise, continuing social engagement, stress reduction, and proper nutrition may be important factors in promoting cognitive vitality in aging. Manageable medical comorbidities, such as diabetes, hypertension, and hyperlipidemia, also contribute to cognitive decline in older persons. Other comorbidities such as smoking and excess alcohol intake may contribute to cognitive decline, and avoiding these activities may promote cognitive vitality in aging. Various therapeutics, including cognitive enhancers and protective agents such as antioxidants and anti-inflammatories, may eventually prove useful as adjuncts for the prevention and treatment of cognitive decline with aging. The data presented in this review should interest physicians who provide preventive care management to middle-aged and older individuals who seek to maintain cognitive vitality with aging.

Using the first 4 waves of data from the Early Childhood Longitudinal Study-Kindergarten cohort (ECLS-K), this piecewise 3-level (time-student-school) growth-curve model provides a portrait of students' reading growth over the first 2 years of school. On average, students make much greater reading gains in 1st grade than they do in kindergarten. First-grade monthly reading growth averages 2.65 points per month, whereas kindergarteners make approximately 1.67 points of reading growth per month. Student-level variables (including socioeconomic status, ethnicity, kindergarten entry age, and gender) were better able to explain between-schools variability in students' initial reading scores and students' reading growth than school-level variables (percentage of minority students, percentage of free-lunch students, and sector). Although socioeconomic status had a minimal impact on reading growth while school was in session, it had a larger impact on summer reading growth. These results suggest that between-schools differences in achievement are largely explained by the differences in school clientele, rather than differences in instruction or resource allocation. These results also underscore the potential importance of preschool and summer programs for low-socioeconomic status children.

Animals trained in a passive avoidance task exhibit a transient time‐dependent increase in hippocampal neural cell adhesion molecule (NCAM) polysialylation at 12–24 h following the initial learning trial. Using immunocytochemical techniques with a monoclonal antibody that specifically recognises NCAM‐polysialic acid homopolymers, a distinct population of granule‐like cells, at the border of the granule cell layer and the hilus in the dentate gyrus of the adult rat hippocampus, has been demonstrated to exhibit time‐dependent change in frequency at 10–12 h following the initial learning of a one‐trial, step‐through, passive avoidance response. These changes were paradigm specific as they failed to occur in those animals rendered amnesic with scopolamine. These polysialylated dentate neurons are not de novo granule cell precursors as administration of 5‐bromo‐2′‐deoxyuridine every 2 h from the point of learning to the 12‐h posttraining time showed no significant difference between trained and passive animals in the small number of heterogeneously distributed, labelled cells. These findings directly identify a morphological substrate of memory, implied by previous correlative and interventive studies on NCAM function.