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The role of relational binding in item memory: evidence from face recognition in a case of developmental amnesia. - The Journal of neuroscience : the official journal of the Society for Neuroscience
Current theories state that the hippocampus is responsible for the formation of memory representations regarding relations, whereas extrahippocampal cortical regions support representations for single items. However, findings of impaired item memory in hippocampal amnesics suggest a more nuanced role for the hippocampus in item memory. The hippocampus may be necessary when the item elements need to be bound within and across episodes to form a lasting representation that can be used flexibly. The current investigation was designed to test this hypothesis in face recognition. H.C., an individual who developed with a compromised hippocampal system, and control participants incidentally studied individual faces that either varied in presentation viewpoint across study repetitions or remained in a fixed viewpoint across the study repetitions. Eye movements were recorded during encoding and participants then completed a surprise recognition memory test. H.C. demonstrated altered face viewing during encoding. Although the overall number of fixations made by H.C. was not significantly different from that of controls, the distribution of her viewing was primarily directed to the eye region. Critically, H.C. was significantly impaired in her ability to subsequently recognize faces studied from variable viewpoints, but demonstrated spared performance in recognizing faces she encoded from a fixed viewpoint, implicating a relationship between eye movement behavior in the service of a hippocampal binding function. These findings suggest that a compromised hippocampal system disrupts the ability to bind item features within and across study repetitions, ultimately disrupting recognition when it requires access to flexible relational representations.Copyright Â© 2015 the authors 0270-6474/15/355342-09$15.00/0.
Blau syndrome-associated Nod2 mutation alters expression of full-length NOD2 and limits responses to muramyl dipeptide in knock-in mice. - Journal of immunology (Baltimore, Md. : 1950)
The biochemical mechanism by which mutations in nucleotide-binding oligomerization domain containing 2 (NOD2) cause Blau syndrome is unknown. Several studies have examined the effect of mutations associated with Blau syndrome in vitro, but none has looked at the implication of the mutations in vivo. To test the hypothesis that mutated NOD2 causes alterations in signaling pathways downstream of NOD2, we created a Nod2 knock-in mouse carrying the most common mutation seen in Blau syndrome, R314Q (corresponding to R334Q in humans). The endogenous regulatory elements of mouse Nod2 were unaltered. R314Q mice showed reduced cytokine production in response to i.p. and intravitreal muramyl dipeptide (MDP). Macrophages from R314Q mice showed reduced NF-ÎºB and IL-6 responses, blunted phosphorylation of MAPKs, and deficient ubiquitination of receptor-interacting protein 2 in response to MDP. R314Q mice expressed a truncated 80-kDa form of NOD2 that was most likely generated by a posttranslational event because there was no evidence for a stop codon or alternative splicing event. Human macrophages from two patients with Blau syndrome also showed a reduction of both cytokine production and phosphorylation of p38 in response to MDP, indicating that both R314Q mice and cells from patients with Blau syndrome show reduced responses to MDP. These data indicate that the R314Q mutation when studied with the Nod2 endogenous regulatory elements left intact is associated with marked structural and biochemical changes that are significantly different from those observed from studies of the mutation using overexpression, transient transfection systems.Copyright Â© 2014 by The American Association of Immunologists, Inc.
The contribution of de novo coding mutations to autism spectrum disorder. - Nature
Whole exome sequencing has proven to be a powerful tool for understanding the genetic architecture of human disease. Here we apply it to more than 2,500 simplex families, each having a child with an autistic spectrum disorder. By comparing affected to unaffected siblings, we show that 13% of de novo missense mutations and 43% of de novo likely gene-disrupting (LGD) mutations contribute to 12% and 9% of diagnoses, respectively. Including copy number variants, coding de novo mutations contribute to about 30% of all simplex and 45% of female diagnoses. Almost all LGD mutations occur opposite wild-type alleles. LGD targets in affected females significantly overlap the targets in males of lower intelligence quotient (IQ), but neither overlaps significantly with targets in males of higher IQ. We estimate that LGD mutation in about 400 genes can contribute to the joint class of affected females and males of lower IQ, with an overlapping and similar number of genes vulnerable to contributory missense mutation. LGD targets in the joint class overlap with published targets for intellectual disability and schizophrenia, and are enriched for chromatin modifiers, FMRP-associated genes and embryonically expressed genes. Most of the significance for the latter comes from affected females.
Transsacral screw safe zone size by sacral segmentation variations. - Journal of orthopaedic research : official publication of the Orthopaedic Research Society
Variations in sacral segmentation may preclude safe placement of transsacral screws for posterior pelvis fixation. We developed a novel automated 3D technique to determine the safe zone size for transsacral screws in the upper two sacral segments in 526 adult pelvis computed tomography scans. Safe zone sizes were then compared by gender and sacral segmentation variations (number of neuroforamen and the presence/absence of lumbosacral transitional vertebrae, Â± LSTV). Ten millimeters was used as the safety threshold for a large screw. 3 (0.6%), 366 (70%), and 157 (30%) sacra had 3, 4, or 5 neuroforamen, respectively. Eighty-eight (17%) were +LSTV. Safe zone size depended on gender, number of neuroforamen in -LSTV sacra and presence of LSTV (p < 0.001) but not on the uni- or bilateral nature of the LSTV. 17% of -LSTV sacra were below the safety threshold in S1, 27% in S2, whereas 3% of +LSTV sacra were below in S1, 74% in S2. Of -LSTV sacra that cannot take an S1 screw safely, 77% can do so in S2, leaving only 4% of sacra that cannot accommodate a screw safely in either upper segment. The results demonstrate a predictable pattern of safe zone size based on gender and sacral segmentation variations.Â© 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
HLA-B27 and human Î²2-microglobulin affect the gut microbiota of transgenic rats. - PloS one
The HLA-B27 gene is a major risk factor for clinical diseases including ankylosing spondylitis, acute anterior uveitis, reactive arthritis, and psoriatic arthritis, but its mechanism of risk enhancement is not completely understood. The gut microbiome has recently been shown to influence several HLA-linked diseases. However, the role of HLA-B27 in shaping the gut microbiome has not been previously investigated. In this study, we characterize the differences in the gut microbiota mediated by the presence of the HLA-B27 gene. We identified differences in the cecal microbiota of Lewis rats transgenic for HLA-B27 and human Î²2-microglobulin (hÎ²2m), compared with wild-type Lewis rats, using biome representational in situ karyotyping (BRISK) and 16S rRNA gene sequencing. 16S sequencing revealed significant differences between transgenic animals and wild type animals by principal coordinates analysis. Further analysis of the data set revealed an increase in Prevotella spp. and a decrease in Rikenellaceae relative abundance in the transgenic animals compared to the wild type animals. By BRISK analysis, species-specific differences included an increase in Bacteroides vulgatus abundance in HLA-B27/hÎ²2m and hÎ²2m compared to wild type rats. The finding that HLA-B27 is associated with altered cecal microbiota has not been shown before and can potentially provide a better understanding of the clinical diseases associated with this gene.
Rituximab therapy for refractory scleritis: results of a phase I/II dose-ranging, randomized, clinical trial. - Ophthalmology
To determine whether rituximab, a monoclonal antibody against the B-lymphocyte antigen CD20, is effective in the treatment of refractory noninfectious scleritis.Prospective, dose-ranging, randomized, double-masked phase I/II clinical trial.Twelve patients with noninfectious scleritis refractory to systemic corticosteroid and â‰¥1 other systemic immunosuppressive agent were enrolled from January 2007 to March 2010.Subjects were randomly assigned to 500 (n = 5) or 1000 mg (n = 7) dosing arms of rituximab intravenous infusions (500 or 1000 mg), given at study days 1 and 15. Initial responders with breakthrough inflammation after study week 24 were offered treatment with an additional cycle of 2 open-label rituximab 1000 mg infusions.Primary outcomes were reduction of inflammation, as measured with a validated scleritis disease grading scale (SGS) and reduction in corticosteroid dose by â‰¥50%. Patients were characterized as responders to study therapy if â‰¥1 of these endpoints showed improvement and neither showed evidence of worsening. Secondary outcomes were improvement in visual acuity, reduction in pain, and improvement in patient and physician-reported global health assessment.Of 12 enrolled patients, 9 met the SGS endpoint at or before week 24, and 4 additionally were able to reduce corticosteroid dose by â‰¥50%. With regard to secondary outcome measures, 11 and 9 patients showed improvement in patient and physician global health scores, respectively, and 7 patients had reduction in pain. Of 9 initial responders, 7 experienced breakthrough inflammation after 24 weeks and were treated with a second cycle of rituximab infusions. Four patients had significant objective or subjective worsening within 8 weeks of receiving rituximab; this event was averted in subsequent patients by treatment with peri-infusional oral corticosteroid. No other significant adverse events were noted. No differences in efficacy, toxicity, or likelihood of retreatment were noted between the dosing arms.Rituximab was effective treatment for 9 of 12 enrolled patients with refractory, noninfectious scleritis at 24 weeks, although 7 required reinfusion with rituximab to maintain inflammatory control. The treatment was well-tolerated, and peri-infusional inflammatory exacerbations were managed successfully with oral corticosteroids. Further long-term studies are warranted to determine the safety and efficacy of rituximab in treating noninfectious scleritis and other ocular inflammatory diseases.Copyright Â© 2014 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.
Rituximab therapy for refractory orbital inflammation: results of a phase 1/2, dose-ranging, randomized clinical trial. - JAMA ophthalmology
Orbital inflammation is a potentially blinding and disfiguring disease process that is often treated with systemic corticosteroids and immunosuppression; better treatments are needed.To determine whether rituximab, a monoclonal antibody against the B-lymphocyte antigen CD20, is effective in the treatment of refractory orbital inflammation.A dose-ranging, randomized, double-masked phase 1/2 clinical trial was conducted at a tertiary referral ophthalmology clinic. Ten individuals with orbital inflammation refractory to systemic corticosteroids and at least 1 other immunosuppressive agent were enrolled from January 2007 to March 2010.Rituximab infusions were administered on study days 1 and 15 at doses of either 500 mg or 1000 mg. Initial responders with recurrent inflammation after week 24 were permitted reinfusion with an additional cycle of 2 open-label 1000-mg rituximab infusions.The primary outcomes were reduction of inflammation measured with a validated orbital disease grading scale and corticosteroid dose reduction by at least 50%. The secondary outcomes were visual acuity, reduction in pain, and participant- and physician-reported global health assessment.Of 10 enrolled patients, 7 demonstrated improvement on the orbital disease grading scale at the 24-week end point with rituximab therapy. Of these 7 individuals, 4 were receiving corticosteroids at study inception and all achieved successful dose reduction. For the secondary outcome measures in the 10 participants, 7 patients and 8 patients improved in self-rated and physician global health scores, respectively, and 7 patients had reduction in pain by 25% or more at 24 weeks. Four patients who were positive responders at the week 24 end point experienced breakthrough inflammation after week 24 and received reinfusions between 24 and 48 weeks. Vision remained stable in all participants. Three of 10 patients had short-term objective or subjective worsening 2 to 8 weeks after receiving rituximab infusions, which was averted in subsequent patients with oral corticosteroids administered during the infusion and did not affect the eventual positive treatment outcome. No significant differences with regard to efficacy, toxicity, or likelihood of retreatment were noted between the dosing arms.Rituximab was safe and effective in 7 of 10 patients with noninfectious orbital disease, although 4 required reinfusion with rituximab to maintain control of orbital inflammation. Substantial toxicity was not noted. Rituximab should be considered in the treatment of refractory orbital inflammation.clinicaltrials.gov Identifier: NCT00415506.
Muon reconstruction efficiency and momentum resolution of the ATLAS experiment in proton-proton collisions at [Formula: see text]Â TeV in 2010. - The European physical journal. C, Particles and fields
This paper presents a study of the performance of the muon reconstruction in the analysis of proton-proton collisions at [Formula: see text]Â TeV at the LHC, recorded by the ATLAS detector in 2010. This performance is described in terms of reconstruction and isolation efficiencies and momentum resolutions for different classes of reconstructed muons. The results are obtained from an analysis of [Formula: see text] meson and [Formula: see text] boson decays to dimuons, reconstructed from a data sample corresponding to an integrated luminosity of 40Â pb[Formula: see text]. The measured performance is compared to Monte Carlo predictions and deviations from the predicted performance are discussed.
The differential production cross section of the [Formula: see text](1020) meson in [Formula: see text] = 7Â TeV [Formula: see text] collisions measured with the ATLAS detector. - The European physical journal. C, Particles and fields
A measurement is presented of the [Formula: see text] production cross section at [Formula: see text] = 7Â TeV using [Formula: see text] collision data corresponding to an integrated luminosity of 383Â [Formula: see text], collected with the ATLAS experiment at the LHC. Selection of [Formula: see text](1020) mesons is based on the identification of charged kaons by their energy loss in the pixel detector. The differential cross section is measured as a function of the transverse momentum, [Formula: see text], and rapidity, [Formula: see text], of the [Formula: see text](1020) meson in the fiducial region 500 [Formula: see text] 1200Â MeV, [Formula: see text] 0.8, kaon [Formula: see text] 230Â MeV and kaon momentum [Formula: see text] 800Â MeV. The integrated [Formula: see text]-meson production cross section in this fiducial range is measured to be [Formula: see text] = 570 [Formula: see text] 8 (stat) [Formula: see text] 66 (syst) [Formula: see text] 20 (lumi) [Formula: see text].
Effects of a novel MC4R agonist on maintenance of reduced body weight in diet-induced obese mice. - Obesity (Silver Spring, Md.)
The physiology of the weight-reduced (WR) state suggests that pharmacologic agents affecting energy homeostasis may have greater efficacy in WR individuals. Our aim was to establish a protocol that allows for evaluation of efficacy of weight maintenance agents and to assess the effectiveness of AZD2820, a novel melanocortin 4 receptor (MC4R) agonist in such a paradigm.MC4R agonist was administered in stratified doses to mice who were either fed high-fat diet ad libitum (AL) throughout the study; or stabilized at a 20% reduced body weight (BW), administered the drug for 4 weeks, and thereafter released from caloric restriction while continuing to receive the drug (WR).After release of WR mice to AL feeding, the high-dose group (53.4 nmol/day) regained 12.4% less BW than their vehicle-treated controls since the beginning of drug treatment. In WR mice, 10.8 nmol/day of the agonist was sufficient to maintain these animals at 95.1% of initial BW versus 53.4 nmol/day required to maintain the BW of AL animals (94.5%).In the WR state, the MC4R agonist was comparably efficacious to a five-fold higher dose in the AL state. This protocol provides a model for evaluating the mechanisms and quantitative efficacy of weight-maintenance strategies and agents.Copyright Â© 2013 The Obesity Society.
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