Publications by authors named "E Knights"

Functional compensation is a common notion in the neuroscience of healthy ageing, whereby older adults are proposed to recruit additional brain activity to compensate for reduced cognitive function. However, whether this additional brain activity in older participants actually helps their cognitive performance remains debated. We examined brain activity and cognitive performance in a human lifespan sample ( = 223) while they performed a problem-solving task (based on Cattell's test of fluid intelligence) during functional magnetic resonance imaging.

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Background: Bispecific T-cell engaging antibodies (BsAbs) are novel agents used to treat B-cell non-Hodgkin lymphoma (B-NHL); these agents demonstrate a different toxicity profile compared with standard chemoimmunotherapy.

Objective: To describe common adverse events (AEs) experienced by patients with B-NHL during BsAb treatment.

Methods: MEDLINE, EMCARE, and EMBASE were searched for relevant studies.

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Whether attentional deficits are accompanied by visuomotor impairments following posterior parietal lesions has been debated for quite some time. This single-case study investigated reaching in a stroke survivor (E.B.

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Healthy aging is typically accompanied by cognitive decline. Previous work has shown that engaging in multiple, non-work activities during midlife can have a protective effect on cognition several decades later, rendering it less dependent on brain structural health; the definition of "cognitive reserve". Other work has shown that increasing age is associated with reduced segregation of large-scale brain functional networks.

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It is well documented that some brain regions, such as association cortices, caudate, and hippocampus, are particularly prone to age-related atrophy, but it has been hypothesized that there are individual differences in atrophy profiles. Here, we document heterogeneity in regional-atrophy patterns using latent-profile analysis of 1,482 longitudinal magnetic resonance imaging observations. The results supported a 2-group solution reflecting differences in atrophy rates in cortical regions and hippocampus along with comparable caudate atrophy.

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