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How working memory supports dual-task performance is the focus of a long-standing debate. Most previous research on this topic has focused on participant performance data. In three experiments, we investigated whether changes in participant-reported strategies across single- and dual-task conditions might help resolve this debate by offering new insights that lead to fruitful integration of theories rather than perpetuating debate by attempting to identify which theory best fits the data. Results indicated that articulatory suppression was associated with reduced reports of the use of rehearsal and clustering strategies but to an increase of the reported use of a visual strategy. Elaboration and clustering strategies were reported less for memory under dual task compared with single task. Under both dual task and articulatory suppression, more participants reported attempting to remember fewer memory items than were presented (memory reduction strategy). For arithmetic verification, articulatory suppression and dual task resulted in a reduction in reports of a counting strategy and an increase in reports of a retrieval strategy for arithmetic knowledge. It is argued that experimenters should not assume that participants perform the same task in the same way under different experimental conditions and that carefulty investigation of how participants change their strategies in response to changes in experimental conditions has considerable potential for resolving theoretical challenges. It is argued further that this approach points toward the value of attempting to integrate rather than proliferate theories of working memory.

Theories of working memory often disagree on the relationships between processing and storage, particularly on how heavily they rely on an attention-based limited resource. Some posit separation and specialization of resources resulting in minimal interference to memory when completing an ongoing processing task, while others argue for a greater overlap in the resources involved in concurrent tasks. Here, we present four experiments that investigated the presence or absence of dual-task costs for memory and processing. The experiments were carried in an adversarial collaboration in which researchers from three opposing theories collaboratively designed a set of experiments and provided differential predictions in line with each of their models. Participants performed delayed recall of aurally and visually presented letters and an arithmetic verification task either as single tasks or with the arithmetic verification task between presentation and recall of letter sequences. Single- and dual-task conditions were completed with and without concurrent articulatory suppression. A consistent pattern of dual-task and suppression costs was observed for memory, with smaller or null effects on processing. The observed data did not fit perfectly with any one framework, with each model having partial success in predicting data patterns. Implications for each of the models are discussed, with an aim for future research to investigate whether some combination of the models and their assumptions can provide a more comprehensive interpretation of the pattern of effects observed here and in relevant previous studies associated with each theoretical framework.

Introduction: We investigated the relationship between preclinical Alzheimer's disease (AD) biomarkers and adverse driving behaviors in a longitudinal analysis of naturalistic driving data. Methods: Naturalistic driving data collected using in‐vehicle dataloggers from 137 community‐dwelling older adults (65+) were used to model driving behavior over time. Cerebrospinal fluid (CSF) biomarkers were used to identify individuals with preclinical AD. Additionally, hippocampal volume and cognitive biomarkers for AD were investigated in exploratory analyses. Results: CSF biomarkers predicted the longitudinal trajectory of the incidence of adverse driving behavior. Abnormal amyloid beta (Aβ42/Aβ40) ratio was associated with an increase in adverse driving behaviors over time compared to ratios in the normal/lower range. Discussion: Preclinical AD is associated with increased adverse driving behavior over time that cannot be explained by cognitive changes. Driving behavior as a functional, neurobehavioral marker may serve as an early detection for decline in preclinical AD. Screening may also help prolong safe driving as older drivers age. [ABSTRACT FROM AUTHOR]

How working memory supports dual-task performance is the focus of a long-standing debate. Most previous research on this topic has focused on participant performance data. In three experiments, we investigated whether changes in participant-reported strategies across single- and dual-task conditions might help resolve this debate by offering new insights that lead to fruitful integration of theories rather than perpetuating debate by attempting to identify which theory best fits the data. Results indicated that articulatory suppression was associated with reduced reports of the use of rehearsal and clustering strategies but to an increase of the reported use of a visual strategy. Elaboration and clustering strategies were reported less for memory under dual task compared with single task. Under both dual task and articulatory suppression, more participants reported attempting to remember fewer memory items than were presented (memory reduction strategy). For arithmetic verification, articulatory suppression and dual task resulted in a reduction in reports of a counting strategy and an increase in reports of a retrieval strategy for arithmetic knowledge. It is argued that experimenters should not assume that participants perform the same task in the same way under different experimental conditions and that carefulty investigation of how participants change their strategies in response to changes in experimental conditions has considerable potential for resolving theoretical challenges. It is argued further that this approach points toward the value of attempting to integrate rather than proliferate theories of working memory. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.02.001 Byline: Mijeong Kim (a)(c), Ayman Habiba (a), Jason M. Doherty (b), Jason C. Mills (b), Robert W. Mercer (a), James E. Huettner (a) Keywords: Telencephalon; Spinal cord; Serum-free; Transcriptional profile Abstract: Pluripotent mouse embryonic stem cells (ESCs) derived from the early blastocyst can differentiate in vitro into a variety of somatic cell types including lineages from all three embryonic germ layers. Protocols for ES cell neural differentiation typically involve induction by retinoic acid (RA), or by exposure to growth factors or medium conditioned by other cell types. A serum-free differentiation (SFD) medium completely lacking exogenous retinoids was devised that allows for efficient conversion of aggregated mouse ESCs into neural precursors and immature neurons. Neural cells produced in this medium express neuronal ion channels, establish polarity, and form functional excitatory and inhibitory synapses. Brief exposure to RA during the period of cell aggregation speeds neuronal maturation and suppresses cell proliferation. Differentiation without RA yields neurons and neural progenitors with apparent telencephalic identity, whereas cells differentiated with exposure to RA express markers of hindbrain and spinal cord. Transcriptional profiling indicates a substantial representation of transit amplifying neuroblasts in SFD cultures not exposed to RA. Author Affiliation: (a) Department of Cell Biology and Physiology, Washington University Medical School, 660 South Euclid Avenue, St. Louis, MO 63110, USA (b) Department of Pathology and Immunology, Washington University Medical School, 660 South Euclid Avenue, St. Louis, MO 63110, USA (c) Program in Developmental Biology, Washington University Medical School, 660 South Euclid Avenue, St. Louis, MO 63110, USA Article History: Received 9 December 2008; Revised 20 January 2009; Accepted 3 February 2009

Natural killer (NK) cells are classically viewed as lymphocytes that provide innate surveillance against virally infected cells and[ tumour cells through the release of cytolytic mediators and interferon (IFN)-γ. In humans, blood [CD56.sup.dim] NK cells specialize in the lysis of cell targets (1). In the lymph nodes, [CD56.sup.bright] NK cells secrete IFN-γ cooperating with dendritic cells and T cells in the generation of adaptive responses (1, 2). Here we report the characterization of a human NK cell subset located in mucosa-associated lymphoid tissues, such as tonsils and Peyer's patches, which is hard-wired to secrete interleukin (IL)-22, IL-26 and leukaemia inhibitory factor. These NK cells, which we refer to as NK-22 cells, are triggered by acute exposure to IL-23. In vitro, NK-22-secreted cytokines stimulate epithelial cells to secrete IL-10, proliferate and express a variety of mitogenic and anti-apoptotic molecules. NK-22 cells are also found in mouse mucosa-associated lymphoid tissues and appear in the small intestine lamina propria during bacterial infection, suggesting that NK-22 cells provide an innate source of IL-22 that may help constrain inflammation and protect mucosal sites. Human NK cells have been dissected into [CD56.sup.dim] and [CD56.sup.bright] subsets possessing either lytic or IFN-γ secretory functions (1). Recently, a subset of tonsil NK cells was shown to express the receptor NKp44 (ref. 2), which is not present on blood NK cells unless they are activated in vitro with IL-2 or IL-15 (ref. 3). We noticed that [NKp44.sup.+] NK cells are present in tonsils, but not in lymph nodes (Supplementary Fig. 1). Immunohistochemical and immunofluorescent analyses showed that [NKp44.sup.+] NK cells are predominantly located in the mucosa surrounding the lymphoid follicles (Fig. 1a-c), with only a small number in the interfollicular area (data not shown). Because tonsils are associated with the oral mucosa, we conceived that NKp44 identifies a subset of NK cells preferentially situated in mucosa-associated lymphoid tissues (MALT). Indeed, we also found [NKp44.sup.+] cells in the Peyer's patches of the ileum and the appendix (Fig. 1d, e)., Gene expression profiles of tonsil [NKp44.sup.+] and [NKp44.sup.-] NK cells (Supplementary Fig. 2 and Supplementary Table 1) showed that [NKp44.sup.+] NK cells preferentially express the chemokine receptor CCR6 and its [...]

We identified cellular and molecular mechanisms within the stem cell niche that control the activity of colonic epithelial progenitors (ColEPs) during injury. Here, we show that while WT mice maintained [...]

Although there is evidence that the effect of including a concurrent processing demand on the storage of information in working memory is disproportionately larger for older than younger adults, not all studies show this age-related impairment, and the critical factors responsible for any such impairment remain elusive. Here we assess whether domain overlap between storage and processing activities, and access to semantic representations, are important determinants of performance in a sample of younger and older adults (N = 119). We developed four versions of a processing task by manipulating the type of stimuli involved (either verbal or non-verbal) and the decision that participants had to make about the stimuli presented on the screen. Participants either had to perform a spatial judgement, in deciding whether the verbal or non-verbal item was presented above or below the centre of the screen, or a semantic judgement, in deciding whether the stimulus refers to something living or not living. The memory task was serial-ordered recall of visually presented letters. The study revealed a large increase in age-related memory differences when concurrent processing was required. These differences were smaller when storage and processing activities both used verbal materials. Dual-task effects on processing were also disproportionate for older adults. Age differences in processing performance appeared larger for tasks requiring spatial decisions rather than semantic decisions. We discuss these findings in relation to three competing frameworks of working memory and the extant literature on cognitive ageing. [ABSTRACT FROM AUTHOR]

Abstract Background The ever-expanding population of gene expression profiles (EPs) from specified cells and tissues under a variety of experimental conditions is an important but difficult resource for investigators to utilize effectively. Software tools have been recently developed to use the distribution of gene ontology (GO) terms associated with the genes in an EP to identify specific biological functions or processes that are over- or under-represented in that EP relative to other EPs. Additionally, it is possible to use the distribution of GO terms inherent to each EP to relate that EP as a whole to other EPs. Because GO term annotation is organized in a tree-like cascade of variable granularity, this approach allows the user to relate (e.g., by hierarchical clustering) EPs of varying length and from different platforms (e.g., GeneChip, SAGE, EST library). Results Here we present GOurmet, a software package that calculates the distribution of GO terms represented by the genes in an individual expression profile (EP), clusters multiple EPs based on these integrated GO term distributions, and provides users several tools to visualize and compare EPs. GOurmet is particularly useful in meta-analysis to examine EPs of specified cell types (e.g., tissue-specific stem cells) that are obtained through different experimental procedures. GOurmet also introduces a new tool, the Targetoid plot, which allows users to dynamically render the multi-dimensional relationships among individual elements in any clustering analysis. The Targetoid plotting tool allows users to select any element as the center of the plot, and the program will then represent all other elements in the cluster as a function of similarity to the selected central element. Conclusion GOurmet is a user-friendly, GUI-based software package that greatly facilitates analysis of results generated by multiple EPs. The clustering analysis features a dynamic targetoid plot that is generalizable for use with any clustering application.

Introduction: We investigated the relationship between preclinical Alzheimer's disease (AD) biomarkers and adverse driving behaviors in a longitudinal analysis of naturalistic driving data., Methods: Naturalistic driving data collected using in-vehicle dataloggers from 137 community-dwelling older adults (65+) were used to model driving behavior over time. Cerebrospinal fluid (CSF) biomarkers were used to identify individuals with preclinical AD. Additionally, hippocampal volume and cognitive biomarkers for AD were investigated in exploratory analyses., Results: CSF biomarkers predicted the longitudinal trajectory of the incidence of adverse driving behavior. Abnormal amyloid beta (Aβ 42 /Aβ 40 ) ratio was associated with an increase in adverse driving behaviors over time compared to ratios in the normal/lower range., Discussion: Preclinical AD is associated with increased adverse driving behavior over time that cannot be explained by cognitive changes. Driving behavior as a functional, neurobehavioral marker may serve as an early detection for decline in preclinical AD. Screening may also help prolong safe driving as older drivers age., (© 2022 the Alzheimer's Association.)

Low-carbohydrate diets are used to manage obesity, seizure disorders, and malignancies of the central nervous system. These diets create a distinctive, but incompletely defined, cellular, molecular, and integrated metabolic state. Here, we determine the systemic and hepatic effects of long-term administration of a very low-carbohydrate, low-protein, and high-fat ketogenic diet, serially comparing these effects to a high-simple-carbohydrate, high-fat Western diet and a low-fat, polysaccharide-rich control chow diet in C57BL/6J mice. Longitudinal measurement of body composition, serum metabolites, and intrahepatic fat content, using in vivo magnetic resonance spectroscopy, reveals that mice fed the ketogenic diet over 12 wk remain lean, euglycemic, and hypoinsulinemic but accumulate hepatic lipid in a temporal pattern very distinct from animals fed the Western diet. Ketogenic diet-fed mice ultimately develop systemic glucose intolerance, hepatic endoplasmic reticulum stress, steatosis, cellular injury, and macrophage accumulation, but surprisingly insulin-induced hepatic Akt phosphorylation and whole-body insulin responsiveness are not impaired. Moreover, whereas hepatic Pparg mRNA abundance is augmented by both high-fat diets, each diet confers splice variant specificity. The distinctive nutrient milieu created by long-term administration of this low-carbohydrate, low-protein ketogenic diet in mice evokes unique signatures of nonalcoholic fatty liver disease and whole-body glucose homeostasis.