1,055 research outputs found

    The context dependence of network response properties in the primary visual cortex of the primate and cat

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    In the mammalian visual system, stimulus context was investigated with respect to the ways it influenced neuronal mean response magnitude (the average number of spikes fired per second), response temporal structure (the timing of spikes with respect to one another), and the extent to which distributed neurones fired spikes synchronous due to synaptic interaction between them. Neurones were presented with bipartite grating stimuli, in which the spatio-temporal relationship between the grating activating the excitatory receptive field and that presented to the surrounding visual space could be varied systematically. Simultaneous extracellular recordings were made of the responses of up to four single neurones separated by 750-1000µm, in the lateral geniculate nucleus (LGN) of the thalamus in the cat, or the primary visual cortex (V1) of non-human primates or cats. Changing context systematically influenced the activity of groups of cells. The responses of 83% of primate V1 cells to discontinuous stimuli, in which the centre/surround orientation difference was greater than 45°, contained stronger oscillations at frequencies below 80Hz, than responses to continuous stimuli. Many cat and primate V1 neurones exhibited elevated response magnitudes to such stimuli. In primate V1, the strength of a cell's oscillatory discharge was dependent on stimulus configuration rather than response magnitude. In the LGN and V1, cell pairs with different orientation preferences fired synchronised responses when stimulated by specific discontinuous grating configurations. Stimulus specific synchronised LGN input, and reciprocal excitatory and inhibitory cortico-cortical connections could generate these properties of cells, and the network in which they exist. A model is proposed to account for the function significance of contour discontinuities in generating coherent neural representations of objects in the visual world. It involves response synchronisation in horizontal, feedforward and feedback interactions, within and between the LGN, V1, V2 and V4

    The DEEP2 Galaxy Redshift Survey: Mean Ages and Metallicities of Red Field Galaxies at z ~ 0.9 from Stacked Keck/DEIMOS Spectra

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    As part of the DEEP2 galaxy redshift survey, we analyze absorption line strengths in stacked Keck/DEIMOS spectra of red field galaxies with weak to no emission lines, at redshifts 0.7 <= z <= 1. Comparison with models of stellar population synthesis shows that red galaxies at z ~ 0.9 have mean luminosity-weighted ages of the order of only 1 Gyr and at least solar metallicities. This result cannot be reconciled with a scenario where all stars evolved passively after forming at very high z. Rather, a significant fraction of stars can be no more than 1 Gyr old, which means that star formation continued to at least z ~ 1.2. Furthermore, a comparison of these distant galaxies with a local SDSS sample, using stellar populations synthesis models, shows that the drop in the equivalent width of Hdelta from z ~ 0.9 to 0.1 is less than predicted by passively evolving models. This admits of two interpretations: either each individual galaxy experiences continuing low-level star formation, or the red-sequence galaxy population from z ~ 0.9 to 0.1 is continually being added to by new galaxies with younger stars.Comment: A few typos were corrected and numbers in Table 1 were revise

    The Vehicle, Spring 2010

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    Table of Contents ForgettingRashelle McNairpage 34 MuseMary Lieskepage 35 My CompulsionAshton Tembypage 38 MemoryKate Vandermeerpage 41 Killmercialize MeGreg Petersonpage 42 PenJake Smithpage 46 GrassKate Vandermeerpage 48 Character CreationMary Lieskepage 52 Ring Around TheKim Hunter-Perkinspage 54 The Great Cursive ScareJake Smithpage 55 OpiateDoug Urbanskipage 61 What Happens to Little Girls...Jennifer O\u27Neilpage 63 Poetry Sunny DaysRyan Poolpage 2 AtlantisDoug Urbanskipage 4 Garbage CityKate Vandermeerpage 6 Fat Girl ThongsKim Hunter-Perkinspage 7 MercilessRosalia Pecorapage 19 ChemistryMary Lieskepage 20 He-Who-Stopped-TalkingJustin Sudkamppage 22 In Which Iris Contemplates a Barren EarthSean Slatterypage 24 At the Bottom of the WorldNick Canadaypage 27 Dogma: Mush!Scott Maypage 28 ThiefMary Lieskepage 29 Prose Coming HomeDoug Urbanskipage 8 DodoDan Davispage 31 The Poet in the PedestrianScott Maypage 37 Toxic RainJacob Swansonpage 40 What\u27s Your Greatest Fear?Justine Fittonpage 43 Soul VoiceHolly Thomaspage 49 Conversations with a SniperKim Hunter-Perkinspage 56 LettersDaniel Paquinpage 65 Art San Marcos, MexicoKate Vandermeercover Contemplation of the World\u27s EndNicholas Giffordpage 18 Little Lady SitsSarah Hadwigerpage 26 MoodAlycia Rockeypage 30 Four Ducks in a RowMegan Mathypage 36 The Daily EasternBen Tillerypage 39 BirdsAlycia Rockeypage 45 March of the BugsMegan Mathypage 47 Mexico Work ExperienceKate Vandermeerpage 53 Feather and JewelsAlycia Rockeypage 60 The ForgottenMegan Mathypage 64 Special Features Fall 2009-Spring 2010 Vehicle Award Winnerspage 1 James K. Johnson Creative Writing Awardpage 74 Kim Hunter-PerkinsWinning Entries (Poetry)page 75 Clint WalkerWinning Entry (Fiction)page 86 Faculty Spotlight: Professor Jason Brownpage 99 About the Contributorspage 106 About the Editorspage 110https://thekeep.eiu.edu/vehicle/1093/thumbnail.jp

    Loss of the nutrient sensor TAS1R3 leads to reduced bone resorption

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    The taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient status. TAS1R member 3 (TAS1R3) is a bi-functional protein that recognizes amino acids such as L-glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. It was recently reported that deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass but the underlying cellular mechanism leading to this phenotype remains unclear. Here, we independently corroborate the increased thickness of cortical bone in femurs of 20-week-old male Tas1R3 mutant mice and confirm that Tas1R3 is expressed in the bone environment. Tas1R3 is expressed in undifferentiated bone marrow stromal cells (BMSCs) in vitro and its expression is maintained during BMP2-induced osteogenic differentiation. However, levels of the bone formation marker procollagen type I N-terminal propeptide (PINP) are unchanged in the serum of 20-week-old Tas1R3 mutant mice as compared to controls. In contrast, levels of the bone resorption marker collagen type I C-telopeptide are reduced greater than 60% in Tas1R3 mutant mice. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and their expression levels positively correlate with differentiation status. Collectively, these findings suggest that high bone mass in Tas1R3 mutant mice is due to uncoupled bone remodeling with reduced osteoclast function and provide rationale for future experiments examining the cell-type-dependent role for TAS1R family members in nutrient sensing in postnatal bone remodeling

    Significance of Pelvic Fluid Observed during Ovarian Cancer Screening with Transvaginal Sonogram

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    The primary objective was to examine the role of pelvic fluid observed during transvaginal ultrasonography (TVS) in identifying ovarian malignancy. A single-institution, observational study was conducted within the University of Kentucky Ovarian Cancer Screening trial from January 1987 to September 2019. We analyzed true-positive (TP), false-positive (FP), true-negative (TN), and false-negative (FN) groups for the presence of pelvic fluid during screening encounters. Measured outcomes were the presence and duration of fluid over successive screening encounters. Of the 48,925 women surveyed, 2001 (4.1%) had pelvic fluid present during a TVS exam. The odds ratio (OR) of detecting fluid in the comparison group (TN screen; OR = 1) significantly differed from that of the FP cases (benign pathology; OR: 13.4; 95% confidence interval (CI): 9.1–19.8), the TP cases with a low malignant potential (LMP; OR: 28; 95% CI: 26.5–29.5), TP ovarian cancer cases (OR: 50.4; 95% CI: 27.2–93.2), and FN ovarian cancer cases (OR: 59.3; 95% CI: 19.7–178.1). The mean duration that pelvic fluid was present for women with TN screens was 2.2 ± 0.05 encounters, lasting 38.7 ± 1.3 months. In an asymptomatic screening population, free fluid identified in TVS exams was more associated with ovarian malignancy than in the control group or benign ovarian tumors. While pelvic free fluid may not solely discriminate malignancy from non-malignancy, it appears to be clinically relevant and warrants thoughtful consideration

    A proposed framework for the development and qualitative evaluation of West Nile virus models and their application to local public health decision-making

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    West Nile virus(WNV) is a globally distributed mosquito-borne virus of great public health concern. The number of WNV human cases and mosquito infection patterns vary in space and time. Many statistical models have been developed to understand and predict WNV geographic and temporal dynamics. However, these modeling efforts have been disjointed with little model comparison and inconsistent validation. In this paper, we describe a framework to unify and standardize WNV modeling efforts nationwide. WNV risk, detection, or warning models for this review were solicited from active research groups working in different regions of the United States. A total of 13 models were selected and described. The spatial and temporal scales of each model were compared to guide the timing and the locations for mosquito and virus surveillance, to support mosquito vector control decisions, and to assist in conducting public health outreach campaigns at multiple scales of decision-making. Our overarching goal is to bridge the existing gap between model development, which is usually conducted as an academic exercise, and practical model applications, which occur at state, tribal, local, or territorial public health and mosquito control agency levels. The proposed model assessment and comparison framework helps clarify the value of individual models for decision-making and identifies the appropriate temporal and spatial scope of each model. This qualitative evaluation clearly identifies gaps in linking models to applied decisions and sets the stage for a quantitative comparison of models. Specifically, whereas many coarse-grained models (county resolution or greater) have been developed, the greatest need is for fine-grained, short-term planning models (m–km, days–weeks) that remain scarce. We further recommend quantifying the value of information for each decision to identify decisions that would benefit most from model input

    Functional genomic screening identifies dual leucine zipper kinase as a key mediator of retinal ganglion cell death

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    Glaucoma, a major cause of blindness worldwide, is a neurodegenerative optic neuropathy in which vision loss is caused by loss of retinal ganglion cells (RGCs). To better define the pathways mediating RGC death and identify targets for the development of neuroprotective drugs, we developed a high-throughput RNA interference screen with primary RGCs and used it to screen the full mouse kinome. The screen identified dual leucine zipper kinase (DLK) as a key neuroprotective target in RGCs. In cultured RGCs, DLK signaling is both necessary and sufficient for cell death. DLK undergoes robust posttranscriptional up-regulation in response to axonal injury in vitro and in vivo. Using a conditional knockout approach, we confirmed that DLK is required for RGC JNK activation and cell death in a rodent model of optic neuropathy. In addition, tozasertib, a small molecule protein kinase inhibitor with activity against DLK, protects RGCs from cell death in rodent glaucoma and traumatic optic neuropathy models. Together, our results establish a previously undescribed drug/drug target combination in glaucoma, identify an early marker of RGC injury, and provide a starting point for the development of more specific neuroprotective DLK inhibitors for the treatment of glaucoma, nonglaucomatous forms of optic neuropathy, and perhaps other CNS neurodegenerations

    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

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    Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis
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