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Search Results: 1 - 10 of 200738 matches for " Junie P. Warrington "
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Whole Brain Radiation-Induced Impairments in Learning and Memory Are Time-Sensitive and Reversible by Systemic Hypoxia
Junie P. Warrington,Anna Csiszar,Matthew Mitschelen,Yong Woo Lee,William E. Sonntag
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030444
Abstract: Whole brain radiation therapy (WBRT) is commonly used for treatment of primary and metastatic brain tumors; however, cognitive impairment occurs in 40–50% of brain tumor survivors. The etiology of the cognitive impairment following WBRT remains elusive. We recently reported that radiation-induced cerebrovascular rarefaction within hippocampal subregions could be completely reversed by systemic hypoxia. However, the effects of this intervention on learning and memory have not been reported. In this study, we assessed the time-course for WBRT-induced impairments in contextual and spatial learning and the capacity of systemic hypoxia to reverse WBRT-induced deficits in spatial memory. A clinical fractionated series of 4.5Gy WBRT was administered to mice twice weekly for 4 weeks, and after various periods of recovery, behavioral analyses were performed. To study the effects of systemic hypoxia, mice were subjected to 11% (hypoxia) or 21% oxygen (normoxia) for 28 days, initiated 1 month after the completion of WBRT. Our results indicate that WBRT induces a transient deficit in contextual learning, disruption of working memory, and progressive impairment of spatial learning. Additionally, systemic hypoxia completely reversed WBRT-induced impairments in learning and these behavioral effects as well as increased vessel density persisted for at least 2 months following hypoxia treatment. Our results provide critical support for the hypothesis that cerebrovascular rarefaction is a key component of cognitive impairment post-WBRT and indicate that processes of learning and memory, once thought to be permanently impaired after WBRT, can be restored.
Concurrent hippocampal induction of MHC II pathway components and glial activation with advanced aging is not correlated with cognitive impairment
Heather D VanGuilder, Georgina V Bixler, Robert M Brucklacher, Julie A Farley, Han Yan, Junie P Warrington, William E Sonntag, Willard M Freeman
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-138
Abstract: Three independent cohorts of adult (12-13 months) and aged (26-28 months) F344xBN rats were behaviorally characterized by Morris water maze testing. Expression of MHC II pathway-associated genes identified by transcriptomic analysis as upregulated with advanced aging was quantified by qPCR in synaptosomal fractions derived from whole hippocampus and in hippocampal subregion dissections (CA1, CA3, and DG). Activation of astrocytes and microglia was assessed by GFAP and Iba1 protein expression, and by immunohistochemical visualization of GFAP and both CD74 (Ox6) and Iba1.We report a marked age-related induction of neuroinflammatory signaling transcripts (i.e., MHC II components, toll-like receptors, complement, and downstream signaling factors) throughout the hippocampus in all aged rats regardless of cognitive status. Astrocyte and microglial activation was evident in CA1, CA3 and DG of intact and impaired aged rat groups, in the absence of differences in total numbers of GFAP+ astrocytes or Iba1+ microglia. Both mild and moderate microglial activation was significantly increased in all three hippocampal subregions in aged cognitively intact and cognitively impaired rats compared to adults. Neither induction of MHCII pathway gene expression nor glial activation correlated to cognitive performance.These data demonstrate a novel, coordinated age-related induction of the MHC II immune response pathway and glial activation in the hippocampus, indicating an allostatic shift toward a para-inflammatory phenotype with advancing age. Our findings demonstrate that age-related induction of these aspects of hippocampal neuroinflammation, while a potential contributing factor, is not sufficient by itself to elicit impairment of spatial learning and memory in models of normative aging. Future efforts are needed to understand how neuroinflammation may act synergistically with cognitive-decline specific alterations to cause cognitive impairment.Cognitive aging, characterized by a de
Aptian-Late Cenomanian Fluvio-Lacustrine Lithofacies and Palynomorphs from Mamfe Basin, Southwest Cameroon, West Africa  [PDF]
Olivier A. Njoh, Miriam B. Nforsi, Junie N. Datcheu
International Journal of Geosciences (IJG) , 2015, DOI: 10.4236/ijg.2015.67064
Abstract: The sedimentary sequences in the Mamfe Basin are generally thought of as continental (fluvio-lacustrine) in origin. But the wide spread occurrence of salt springs and salt accumulations and in places gypsum, often puts to question the exclusive continentality throughout this basin’s history. The sequences studied portray a wide range of complex lithologies and lithofacies relationships and include basal and intra-formational conglomerates, sandstones, shales, carbonaceous, carbonate and halite facies respectively. All these are well exposed at several outcrop sections distributed all over the basin with some measuring up to and above 30 m in height.Sedimentary structures include: parallel aligned imbricated prismatic pebbles, plannar to trough-cross stratifications, fining upward grain size distribution and thin frequently alternating sandstone-shale beds. Palynological data have been obtained for the first time from the shally and carbonate intervals and integrated with five lithofacies associations, permitting the determination of the ages and paleo environmental reconstruction. The palynomorphs are characterized by pteridophytic spores dominated byCicatricosisporitessp.,Cyathiditessp. andDeltoidsporasp., pollen grains include gymnosperms dominated byClassopollis annulatus
Lack of Correlation between Severity of Clinical Symptoms, Skin Test Reactivity, and Radioallergosorbent Test Results in Venom-Allergic Patients
RJ Warrington
Allergy, Asthma & Clinical Immunology , 2006, DOI: 10.1186/1710-1492-2-2-62
Abstract: Thirty-six patients (including 15 females) who presented with a history of allergic reactions to insect stings were assessed. The mean age at the time of the reactions was 33.4 ± 15.1 years (range, 4-76 years), and patients were evaluated 43.6 ± 90 months (range, 1-300 months) after the reactions. Clinical reactions were scored according to severity, from 1 (cutaneous manifestations only) to 3 (anaphylaxis with shock). These scores were compared to scores for skin test reactivity (0 to 5, indicating the log increase in sensitivity from 1 μg/mL to 0.0001 μg/mL) and radioallergosorbent test (RAST) levels (0 to 4, indicating venom-specific IgE levels, from undetectable to >17.5 kilounits of antigen per litre [kUA/L]).No correlation was found between skin test reactivity (Spearman's coefficient = 0.15, p = .377) or RAST level (Spearman's coefficient = 0.32, p = .061) and the severity of reaction. Skin test and RAST scores both differed significantly from clinical severity (p < .05), but there was a significant correlation between skin test reactivity and RAST score (p = .042). There was no correlation between skin test reactivity and time since reaction (Spearman's coefficient = 0.18, p = .294) nor between RAST and time since reaction (r = 0.1353, p = .438). Elimination of patients tested more than 12 months after their reaction still produced no correlation between skin test reactivity (p = .681) or RAST score (p = .183) and the severity of the clinical reaction.In venom-allergic patients (in contrast to reported findings in cases of inhalant IgE-mediated allergy), there appears to be no significant correlation between the degree of skin test reactivity or levels of venom-specific IgE (determined by RAST) and the severity of the clinical reaction.There is an understandable tendency on the part of patients (and probably also physicians) to assume that there is a clinical correlation between (1) the degree of skin test reactivity to an allergen on intradermal or epicutan
AACI is now an open access journal
Richard Warrington
Allergy, Asthma & Clinical Immunology , 2009, DOI: 10.1186/1710-1492-5-1
Abstract: I would like to welcome you to Allergy, Asthma & Clinical Immunology (AACI), as an open access journal published by BioMed Central, the pioneering open access publisher.AACI is the official Journal of the Canadian Society of Allergy & Clinical Immunology (CSACI), one of the oldest medical specialty societies in Canada and dedicated to the advancement of the knowledge and practice of allergy, clinical immunology, and asthma, and the provision of optimal patient care. AACI will publish both basic science manuscripts in allergy & immunology, as well as clinical research and review articles in these areas. We welcome manuscripts from anywhere in the World, for peer review.Our journal was founded in 1996, as the Canadian Journal of Allergy and Clinical Immunology, and in 2004 became Allergy, Asthma & Clinical Immunology. We, the Editors-in Chief of AACI and the Board of Directors of CSACI, have decided that our journal should become an open-access journal because we believe that medical knowledge should be freely available to all, not just those with access to libraries or the financial ability to subscribe to medical journals. We accept that "Only presidents, editors and people with tapeworms have the right to use the editorial we."- Mark TwainWe would ask all authors to remember the words of Francis Crick, that "There is no form of prose more difficult to understand and more tedious to read, than the average scientific paper." We appreciate your efforts not to make this true of your manuscripts, since "No passion in the world is equal to the passion to alter someone else's draft."- H.G. WellsIn reviewing the available journals for publication in this field, most still require subscription, and so we hope that our open-access format will be attractive to those authors who wish to have their work available to the greatest number of researchers, clinicians, and others, wherever they are, if they have access to the Internet. We are excited about the future success of AACI,
The longitudinal association of common susceptibility variants for type 2 diabetes and obesity with fasting glucose level and BMI
Rebecca J Webster, Nicole M Warrington, John P Beilby, Timothy M Frayling, Lyle J Palmer
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-140
Abstract: The study analysed data from the Busselton Health Study (n = 4,554). Cross-sectional association analyses included family data and used the total association test. Longitudinal association analyses of unrelated participant data (n = 2,864) used linear mixed-effects models.In cross-sectional analyses, we observed associations of the T allele at the IGF2BP2 single nucleotide polymorphism (SNP) rs4402960 with raised fasting glucose (p = 0.045), and the A allele at the FTO SNP rs9939609 with raised BMI (p = 0.003). Longitudinal analyses showed no significant associations between SNPs and changes in fasting glucose or BMI in the same individuals, either over mean follow-up times of 18.7 and 21.8 years respectively, or with age during adulthood.There was no indication that the effects of common type 2 diabetes variants on fasting glucose varied with age during adulthood or over time.Physiological traits are frequently dynamic, varying over time with changing or accumulating environmental and physiological factors. The influence of genotype on these traits may also vary over time through interaction with factors such as age, developmental stage or time-dependent environmental factors. Variation in the effects of genetic variants at different stages of life could significantly alter the trajectories of traits and potentially also the risks of certain diseases. Hence, studies that do not consider the possibility of longitudinal variation in genetic associations may lead to over-simplistic models of variant effects.Type 2 diabetes (T2D) is a complex disease with numerous risk factors, including a growing number of known genetic susceptibility variants [1-4]. The risk of T2D also rises with increasing age [5]. Some of the intermediate traits of T2D, such as obesity and raised fasting plasma glucose, similarly have complex determinants and indeed both BMI and fasting plasma glucose also tend to increase with age [6,7]. These observations raise the question of whether time- or a
Primary immunodeficiency
McCusker Christine,Warrington Richard
Allergy, Asthma & Clinical Immunology , 2011, DOI: 10.1186/1710-1492-7-s1-s11
Abstract: Primary immunodeficiency disorder (PID) refers to a heterogeneous group of over 130 disorders that result from defects in immune system development and/or function. PIDs are broadly classified as disorders of adaptive immunity (i.e., T-cell, B-cell or combined immunodeficiencies) or of innate immunity (e.g., phagocyte and complement disorders). Although the clinical manifestations of PIDs are highly variable, most disorders involve at least an increased susceptibility to infection. Early diagnosis and treatment are imperative for preventing significant disease-associated morbidity and, therefore, consultation with a clinical immunologist is essential. PIDs should be suspected in patients with: recurrent sinus or ear infections or pneumonias within a 1 year period; failure to thrive; poor response to prolonged use of antibiotics; persistent thrush or skin abscesses; or a family history of PID. Patients with multiple autoimmune diseases should also be evaluated. Diagnostic testing often involves lymphocyte proliferation assays, flow cytometry, measurement of serum immunoglobulin (Ig) levels, assessment of serum specific antibody titers in response to vaccine antigens, neutrophil function assays, stimulation assays for cytokine responses, and complement studies. The treatment of PIDs is complex and generally requires both supportive and definitive strategies. Ig replacement therapy is the mainstay of therapy for B-cell disorders, and is also an important supportive treatment for many patients with combined immunodeficiency disorders. The heterogeneous group of disorders involving the T-cell arm of the adaptive system, such as severe combined immunodeficiency (SCID), require immune reconstitution as soon as possible. The treatment of innate immunodeficiency disorders varies depending on the type of defect, but may involve antifungal and antibiotic prophylaxis, cytokine replacement, vaccinations and bone marrow transplantation. This article provides a detailed overview of the major categories of PIDs and strategies for the appropriate diagnosis and management of these rare disorders.
Equivalence classes for the mu-coefficient of Kazhdan-Lusztig polynomials in S_n
Gregory S. Warrington
Mathematics , 2010,
Abstract: We study equivalence classes relating to the Kazhdan-Lusztig mu(x,w) coefficients in order to help explain the scarcity of distinct values. Each class is conjectured to contain a "crosshatch" pair. We also compute the values attained by mu(x,w) for the permutation groups S_10 and S_11.
Two formulae for inverse Kazhdan-Lusztig polynomials in S_n
Gregory S. Warrington
Mathematics , 2002,
Abstract: Let w_0 denote the permutation [n,n-1,...,2,1]. We give two new explicit formulae for the Kazhdan-Lusztig polynomials P_{w_0w,w_0x} in S_n when x is a maximal element in the singular locus of the Schubert variety X_w. To do this, we utilize a standard identity that relates P_{x,w} and P_{w_0w,w_0x}.
Juggling probabilities
Gregory S. Warrington
Mathematics , 2003,
Abstract: The act of a person juggling can be viewed as a Markov process if we assume that the juggler throws to random heights. I make this association for the simplest reasonable model of random juggling and compute the steady state probabilities in terms of the Stirling numbers of the second kind. I also explore several alternate models of juggling.
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