15,990 research outputs found
Glucose modulates event-related potential components of recollection and familiarity in healthy adolescents.
No full textIntroduction Behavioural evidence supports the notion that oral glucose ingestion enhances recognition memory judgements based on recollection, but not familiarity. The present study sought to clarify and extend upon these behavioural findings by investigating the influence of glucose administration on event-related potential (ERP) components that are thought to be differentially mediated by recollection and familiarity processes in healthy adolescents. Methods In a within-subjects design, participants performed a recognition memory task, during which time electroencephalogram (EEG) was recorded, subsequent to ingestion of either (a) glucose or (b) placebo in a counterbalanced order. Results Response times during the recognition memory task were observed to be faster for the glucose condition, relative to a placebo control. Further, glucose ingestion was associated with an enhanced left parietal old/new ERP effect (a marker of recollection) and an enhanced mid-frontal old/new ERP effect (known to be mediated by familiarity). Discussion These findings (a) support the results of previous research that the ‘glucose memory facilitation effect’ can be extended to healthy adolescents, but (b) suggest that glucose enhances both the recollection and familiarity components of recognition memory. The observed ERP profile has important implications for the proposal that glucose specifically targets the hippocampus in modulating cognitive performance
Disparities in registration and use of an online patient portal among older adults: findings from the LitCog cohort
No full text(C) The Author 2015. Published by Oxford University Press on behalf of the American Medical Informatics Association. All rights reserved.Financial disclosure: This project was supported by the
National Institute on Aging (R01 AG030611), the National
Center for Research Resources (5UL1RR025741), and the
National Center for Advancing Translational Sciences (Grant
8UL1TR000150). The content is solely the responsibility of the
authors and does not necessarily represent the official views of
the National Institutes of Health. Smith is currently supported
by a Cancer Research UK Fellowship
Distinct Intracellular Compartments Involved in Invariant Chain Degradation and Antigenic Peptide Loading of Major Histocompatibility Complex (MHC) Class II Molecules
No full textMajor histocompatibility complex (MHC) class II molecules are transported to intracellular MHC class II compartments via a transient association with the invariant chain (Ii). After removal of the invariant chain, peptides can be loaded onto class II molecules, a process catalyzed by human leukocyte antigen-DM (HLA-DM) molecules. Here we show that MHC class II compartments consist of two physically and functionally distinct organelles. Newly synthesized MHC class II/Ii complexes were targeted to endocytic organelles lacking HLA-DM molecules, where Ii degradation occurred. From these organelles, class II molecules were transported to a distinct organelle containing HLADM, in which peptides were loaded onto class II molecules. This latter organelle was not directly accessible via fluid phase endocytosis, suggesting that it is not part of the endosomal pathway. Uptake via antigen-specific membrane immunoglobulin resulted however in small amounts of antigen in the HLA-DM positive organelles. From this peptide-loading compartment, class II–peptide complexes were transported to the plasma membrane, in part after transit through endocytic organelles. The existence of two separate compartments, one involved in Ii removal and the other functioning in HLA-DM–dependent peptide loading of class II molecules, may contribute to the efficiency of antigen presentation by the selective recruitment of peptide-receptive MHC class II molecules and HLA-DM to the same subcellular location
The Role of GPR37 in Glucose Metabolism
No full textDiabetes mellitus (DM) represents a global health challenge, affecting approximately 422 million individuals worldwide (Safiri et al., 2022). Type II Diabetes is the most prevalent form; it is characterized by elevated blood glucose levels due to insulin resistance or inadequate insulin production. Under normal physiological conditions, glucose metabolism is a complex series of processes that uses simple sugars, specifically glucose, to produce energy. Glucose metabolism involves intricate pathways regulated by insulin, including glycogenesis, gluconeogenesis, glycolysis, and glycogenolysis. Insulin, a peptide hormone secreted by pancreatic β-cells, plays a central role in facilitating glucose uptake into cells through the activation of glucose transporters, like GLUT4 (Satoh et al., 2014). Insulin resistance, a characterization of T2DM, disrupts normal glucose metabolism, leading to chronically elevated blood glucose levels. The brain and the periphery both require glucose metabolism. G protein-coupled receptors (GPCRs), a diverse family of seven transmembrane proteins, play pivotal roles in cellular signaling cascades. Among them, G protein-coupled receptor 37 (GPR37) is an orphan receptor that is predominantly expressed in the brain, particularly in oligodendrocytes. GPR37 has been shown to be expressed in the liver. To date, nothing is known about GPR37’s role in regulating glucose metabolism, however its expression in the liver may suggest that it modulates metabolic parameters. The goal of this thesis is to characterize the metabolic profile of wild type mice (GPR37+/+), heterozygous mice (GPR37+/-), and knockout mice (GPR37-/-) in young, old, female, and male mice. The present study demonstrates that the loss of GPR37 decreases weights in young (6 month) and old (8-12 month) male mice. The loss of GPR37 induces lower blood glucose levels after 6 hr fast compared to baseline blood glucose levels in female and male mice; this effect is consistent with age. Loss of GPR37 increases insulin sensitivity in young (6 month) male mice
Mike Smith shares the stage with Richie Havens tonight
No full textThis document can also be found in hy-dm-docs-havens-tour-1997-001This newspaper article discusses Richie Havens performance alongside Mike Smith at the ICC. It also provides some biographical information on Mike Smith
Cassettes of the Richie Havens tour
No full textThis document can also be found in hy-dm-docs-havens-tour-1997-004This letter discusses the Richie Havens tour and that Marks have included parts of the tour on a cassette sent to Smith
Synchrotron emission from dark matter in galactic subhalos. A look into the Smith cloud
No full textOne of the key predictions of the "WIMP" paradigm for Dark Matter (DM) is that DM particles can annihilate into charged particles. These annihilations will proceed in e.g. Galactic subhalos such as dwarf Galaxies or, as recently pointed out, high velocity clouds such as the "Smith Cloud". In this note, we focus on the radio emission associated with DM annihilations into electrons and positrons occurring in the Smith Cloud. The phenomenology of this emission is discussed in quite some detail. We argue that the uncertainties in the propagation can be captured by the typical diffusion-loss length parameter (Syrovatskii variable) but that the angle-integrated radio fluxes are independent of the propagation. We conclude that if the Smith Cloud is indeed dominated by DM, radio signals from DM annihilation stand out amongst other messengers. Furthermore, low frequencies such as the ones observed by e.g. the Low Frequency Array (LOFAR) and the next-generation Square Kilometre Array (SKA) are optimal for searches for DM in the Smith Cloud. As a practical application, we set conservative constraints on dark matter annihilation cross section using data of continuum radio emission from the Galaxy at 22 MHz and at 1.4 GHz. Stronger constraints could be reached by background subtraction, exploiting the profile and frequency dependence of the putative DM signal. We set stronger but tentative limits using the median noise in brightness temperature from the Green Bank Telescope and the LOFAR sensitivities.SCOPUS: ar.jinfo:eu-repo/semantics/publishe
Edenophorus knysna Smith
No full textEdenophorus knysna Smith (Figs 1, 4) Edenophorus knysna Smith, 1969: 309. Recognition: This species is distinguished by its yellow scape and pedicel, presence of cell dm, and proboscis shorter than height of head. Diagnosis: Scape and pedicel yellow, postpedicel and style brown (Fig. 1); proboscis slightly shorter than head; precoxal bridge with 1 stout seta above fore coxa; legs and halter yellow, apical leg segments becoming darker; cell dm present (Fig. 4); abdomen paler than thorax, sclerites thinly sclerotised. Material examined: SOUTH AFRICA: Western Cape: female holotype (NMSA), female paratype (BMNH), Garden of Eden Forest, Knysna District, 10.x.1959, B. & P. Stuckenberg. Eastern Cape: 1 female, Storms River Village, 33 o 55'S 23 o 55'E, 9.ix.1992, B. R. Stuckenberg (ZFMK alc. coll.). Remarks: The most recently collected specimen was swept from stream-bank ferns in a humid forest.Published as part of Sinclair, Bradley J., 2002, Revision of the South African endemic genus Edenophorus Smith (Diptera: Empididae), pp. 109-122 in African Invertebrates 43 on pages 116-117, DOI: 10.5281/zenodo.766603
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