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[PMID]: 26026061
[Au] Autor:Dey M; Chang AL; Miska J; Wainwright DA; Ahmed AU; Balyasnikova IV; Pytel P; Han Y; Tobias A; Zhang L; Qiao J; Lesniak MS
[Ad] Address:Brain Tumor Center, University of Chicago Pritzker School of Medicine, Chicago, IL 60637; and....
[Ti] Title:Dendritic Cell-Based Vaccines that Utilize Myeloid Rather than Plasmacytoid Cells Offer a Superior Survival Advantage in Malignant Glioma.
[So] Source:J Immunol;195(1):367-76, 2015 Jul 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dendritic cells (DCs) are professional APCs that are traditionally divided into two distinct subsets, myeloid DC (mDCs) and plasmacytoid DC (pDCs). pDCs are known for their ability to secrete large amounts of IFN-α. Apart from IFN-α production, pDCs can also process Ag and induce T cell immunity or tolerance. In several solid tumors, pDCs have been shown to play a critical role in promoting tumor immunosuppression. We investigated the role of pDCs in the process of glioma progression in the syngeneic murine model of glioma. We show that glioma-infiltrating pDCs are the major APC in glioma and are deficient in IFN-α secretion (p < 0.05). pDC depletion leads to increased survival of the mice bearing intracranial tumor by decreasing the number of regulatory T cells (Tregs) and by decreasing the suppressive capabilities of Tregs. We subsequently compared the ability of mDCs and pDCs to generate effective antiglioma immunity in a GL261-OVA mouse model of glioma. Our data suggest that mature pDCs and mDCs isolated from naive mice can be effectively activated and loaded with SIINFEKL Ag in vitro. Upon intradermal injection in the hindleg, a fraction of both types of DCs migrate to the brain and lymph nodes. Compared to mice vaccinated with pDC or control mice, mice vaccinated with mDCs generate a robust Th1 type immune response, characterized by high frequency of CD4(+)T-bet(+) T cells and CD8(+)SIINFEKEL(+) T cells. This robust antitumor T cell response results in tumor eradication and long-term survival in 60% of the animals (p < 0.001).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401607

  2 / 1285489 MEDLINE  
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[PMID]: 25948637
[Au] Autor:Kennedy A; Asahina K; Hoopfer E; Inagaki H; Jung Y; Lee H; Remedios R; Anderson DJ
[Ad] Address:Division of Biology, California Institute of Technology, Pasadena, California 91125....
[Ti] Title:Internal States and Behavioral Decision-Making: Toward an Integration of Emotion and Cognition.
[So] Source:Cold Spring Harb Symp Quant Biol;79:199-210, 2014.
[Is] ISSN:1943-4456
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Social interactions, such as an aggressive encounter between two conspecific males or a mating encounter between a male and a female, typically progress from an initial appetitive or motivational phase, to a final consummatory phase. This progression involves both changes in the intensity of the animals' internal state of arousal or motivation and sequential changes in their behavior. How are these internal states, and their escalating intensity, encoded in the brain? Does this escalation drive the progression from the appetitive/motivational to the consummatory phase of a social interaction and, if so, how are appropriate behaviors chosen during this progression? Recent work on social behaviors in flies and mice suggests possible ways in which changes in internal state intensity during a social encounter may be encoded and coupled to appropriate behavioral decisions at appropriate phases of the interaction. These studies may have relevance to understanding how emotion states influence cognitive behavioral decisions at higher levels of brain function.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1101/sqb.2014.79.024984

  3 / 1285489 MEDLINE  
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[PMID]: 25746062
[Au] Autor:Fernald RD
[Ad] Address:Biology Department, Stanford University, Stanford, California 94305 rfernald@stanford.edu.
[Ti] Title:Cognitive Skills Needed for Social Hierarchies.
[So] Source:Cold Spring Harb Symp Quant Biol;79:229-36, 2014.
[Is] ISSN:1943-4456
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dominance hierarchies are ubiquitous in social species that require social cognition to maintain. Status may be established initially through physical conflict but is maintained by social signals between individuals that depend critically on the relative social status of those interacting. How do individuals collect information they need to modulate their behavior? Using a particularly suitable fish model system living in a complex social environment, we describe how the social context of behavior shapes the brain and, in turn, alters the behavior of animals as they interact. These fish observe social interactions carefully to gather information vicariously that guides future behavior. Social opportunities produce rapid changes in gene expression in key brain nuclei, and both social success and failure produce changes in neuronal cell size and connectivity in reproductive centers of the brain. It remains unknown how social information is transduced into cellular and molecular changes. Understanding the cellular and molecular changes underlying animal cognition will yield unique insights into how the brain works.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1101/sqb.2014.79.024752

  4 / 1285489 MEDLINE  
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[PMID]: 25463024
[Au] Autor:Bilimoria PM; Stevens B
[Ad] Address:Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children׳s Hospital, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Title:Microglia function during brain development: New insights from animal models.
[So] Source:Brain Res;1617:7-17, 2015 Aug 18.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The role of microglia in healthy brains is just beginning to receive notice. Recent studies have revealed that these phagocytic cells control the patterning and wiring of the developing central nervous system (CNS) by regulating, amongst many other processes, programmed cell death, activity-dependent synaptic pruning and synapse maturation. Microglia also play important roles in the mature brain and have demonstrated effects on behavior. Converging evidence from human and mouse studies together raise questions as to the role of microglia in disorders of brain development such as autism and, schizophrenia. In this review, we summarize a number of major findings regarding the role of microglia in brain development and highlight some key questions and avenues for future study. This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 1285489 MEDLINE  
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[PMID]: 25218556
[Au] Autor:Doty KR; Guillot-Sestier MV; Town T
[Ad] Address:Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
[Ti] Title:The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?
[So] Source:Brain Res;1617:155-73, 2015 Aug 18.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Neurodegenerative diseases share common features, including catastrophic neuronal loss that leads to cognitive or motor dysfunction. Neuronal injury occurs in an inflammatory milieu that is populated by resident and sometimes, infiltrating, immune cells - all of which participate in a complex interplay between secreted inflammatory modulators and activated immune cell surface receptors. The importance of these immunomodulators is highlighted by the number of immune factors that have been associated with increased risk of neurodegeneration in recent genome-wide association studies. One of the more difficult tasks for designing therapeutic strategies for immune modulation against neurodegenerative diseases is teasing apart beneficial from harmful signals. In this regard, learning more about the immune components of these diseases has yielded common themes. These unifying concepts should eventually enable immune-based therapeutics for treatment of Alzheimer׳s and Parkinson׳s diseases and amyotrophic lateral sclerosis. Targeted immune modulation should be possible to temper maladaptive factors, enabling beneficial immune responses in the context of neurodegenerative diseases. This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 1285489 MEDLINE  
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[PMID]: 25110235
[Au] Autor:Filiano AJ; Gadani SP; Kipnis J
[Ad] Address:Center for Brain Immunology and Glia (BIG), Department of Neuroscience, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: ajf5v@virginia.edu.
[Ti] Title:Interactions of innate and adaptive immunity in brain development and function.
[So] Source:Brain Res;1617:18-27, 2015 Aug 18.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:It has been known for decades that the immune system has a tremendous impact on behavior. Most work has described the negative role of immune cells on the central nervous system. However, we and others have demonstrated over the last decade that a well-regulated immune system is needed for proper brain function. Here we discuss several neuro-immune interactions, using examples from brain homeostasis and disease states. We will highlight our understanding of the consequences of malfunctioning immunity on neurodevelopment and will discuss the roles of the innate and adaptive immune system in neurodevelopment and how T cells maintain a proper innate immune balance in the brain surroundings and within its parenchyma. Also, we describe how immune imbalance impairs higher order brain functioning, possibly leading to behavioral and cognitive impairment. Lastly, we propose our hypothesis that some behavioral deficits in neurodevelopmental disorders, such as in autism spectrum disorder, are the consequence of malfunctioning immunity. This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 1285489 MEDLINE  
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[PMID]: 25003554
[Au] Autor:Lotrich FE
[Ad] Address:University of Pittsburgh Medical Center, Western Psychiatric Institute and Clinics, 3811 Ohara Street, Pittsburgh, PA 15213, USA. Electronic address: lotrichfe@upmc.edu.
[Ti] Title:Inflammatory cytokine-associated depression.
[So] Source:Brain Res;1617:113-25, 2015 Aug 18.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Inflammatory cytokines can sometimes trigger depression in humans, are often associated with depression, and can elicit some behaviors in animals that are homologous to major depression. Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an overlapping pathoetiology with major depression. This suggests that there could be a specific major depression subtype, inflammatory cytokine-associated depression (ICAD), which may require different therapeutic approaches. However, most people do not develop depression, even when exposed to sustained elevations in inflammatory cytokines. Thus several vulnerabilities and sources of resilience to inflammation-associated depression have been identified. These range from genetic differences in neurotrophic and serotonergic systems to sleep quality and omega-3 fatty acid levels. Replicating these sources of resilience as treatments could be one approach for preventing "ICAD". This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 1285489 MEDLINE  
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[PMID]: 25555483
[Au] Autor:Schmitt JE; Vandekar S; Yi J; Calkins ME; Ruparel K; Roalf DR; Whinna D; Souders MC; Satterwaite TD; Prabhakaran K; McDonald-McGinn DM; Zackai EH; Gur RC; Emanuel BS; Gur RE
[Ad] Address:Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania; Department of Radiology, Hospital of the University of Pennsylvania....
[Ti] Title:Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome.
[So] Source:Biol Psychiatry;78(2):135-43, 2015 Jul 15.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: There is increased risk of developing psychosis in 22q11.2 deletion syndrome (22q11DS). Although this condition is associated with morphologic brain abnormalities, simultaneous examination of multiple high-resolution measures of cortical structure has not been performed. METHODS: Fifty-three patients with 22q11DS, 30 with psychotic symptoms, were compared with demographically matched nondeleted youths: 53 typically developing and 53 with psychotic symptoms. High-resolution magnetic resonance imaging measures of cerebral volume, cortical thickness, surface area, and an index of local gyrification were obtained and compared between groups. RESULTS: Patients with 22q11DS demonstrated global increases in cortical thickness associated with reductions in surface area, reduced index of local gyrification, and lower cerebral volumes relative to typically developing controls. Findings were principally in the frontal lobe, superior parietal lobes, and in the paramedian cerebral cortex. Focally decreased thickness was seen in the superior temporal gyrus and posterior cingulate cortex in 22q11DS relative to nondeleted groups. Patterns between nondeleted participants with psychotic symptoms and 22q11DS were similar but with important differences in several regions implicated in schizophrenia. Post hoc analysis suggested that like the 22q11DS group, cortical thickness in nondeleted individuals with psychotic symptoms differed from typically developing controls in the superior frontal gyrus and superior temporal gyrus, regions previously linked to schizophrenia. CONCLUSIONS: Simultaneous examination of multiple measures of cerebral architecture demonstrates that differences in 22q11DS localize to regions of the frontal, superior parietal, superior temporal, and paramidline cerebral cortex. The overlapping patterns between nondeleted participants with psychotic symptoms and 22q11DS suggest partially shared neuroanatomic substrates.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 1285489 MEDLINE  
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[PMID]: 25851457
[Au] Autor:Gerard E; Spengler RN; Bonoiu AC; Mahajan SD; Davidson BA; Ding H; Kumar R; Prasad PN; Knight PR; Ignatowski TA
[Ad] Address:aDepartment of Pathology and Anatomical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA bNanoAxis, LLC, Clarence, NY, USA cInstitute for Lasers, Photonics, and Biophotonics, University at Buffalo, The State University of New York, Buffalo, NY, USA dDepartment of Medicine, Division of Allergy, Immunology, and Rheumatology, University at Buffalo, The State University of New York, Buffalo, NY, USA eDepartment of Anesthesiology, University at Buffalo, The State University of New York, Buffalo, NY, USA fVeterans Administration Western New York Healthcare System Departments of gChemistry and hMicrobiology and Immunology, University at Buffalo, The State University of New York, Buffalo, NY, USA iProgram for Neuroscience, University at Buffalo, The State University of New York, Buffalo, NY, USA.
[Ti] Title:Chronic constriction injury-induced nociception is relieved by nanomedicine-mediated decrease of rat hippocampal tumor necrosis factor.
[So] Source:Pain;156(7):1320-33, 2015 Jul.
[Is] ISSN:1872-6623
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neuropathic pain is a chronic pain syndrome that arises from nerve injury. Current treatments only offer limited relief, clearly indicating the need for more effective therapeutic strategies. Previously, we demonstrated that proinflammatory tumor necrosis factor-alpha (TNF) is a key mediator of neuropathic pain pathogenesis; TNF is elevated at sites of neuronal injury, in the spinal cord, and supraspinally during the initial development of pain. The inhibition of TNF action along pain pathways outside higher brain centers results in transient decreases in pain perception. The objective of this study was to determine whether specific blockade of TNF in the hippocampus, a site of pain integration, could prove efficacious in reducing sciatic nerve chronic constriction injury (CCI)-induced pain behavior. Small inhibitory RNA directed against TNF mRNA was complexed to gold nanorods (GNR-TNF siRNA; TNF nanoplexes) and injected into the contralateral hippocampus of rats 4 days after unilateral CCI. Withdrawal latencies to a noxious thermal stimulus (hyperalgesia) and withdrawal to innocuous forces (allodynia) were recorded up to 10 days and compared with baseline values and sham-operated rats. Thermal hyperalgesia was dramatically decreased in CCI rats receiving hippocampal TNF nanoplexes; and mechanical allodynia was transiently relieved. TNF levels (bioactive protein, TNF immunoreactivity) in hippocampal tissue were decreased. The observation that TNF nanoplex injection into the hippocampus alleviated neuropathic pain-like behavior advances our previous findings that hippocampal TNF levels modulate pain perception. These data provide evidence that targeting TNF in the brain using nanoparticle-protected siRNA may be an effective strategy for treatment of neuropathic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/j.pain.0000000000000181

  10 / 1285489 MEDLINE  
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[PMID]: 25806605
[Au] Autor:Egorova N; Yu R; Kaur N; Vangel M; Gollub RL; Dougherty DD; Kong J; Camprodon JA
[Ad] Address:aDepartment of Psychiatry, Massachusetts General Hospital, Charlestown, MA, USA bDepartment of Psychiatry Harvard Medical School, Boston, MA, USA cDepartment of Psychology, National University of Singapore, Singapore, Singapore dMGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
[Ti] Title:Neuromodulation of conditioned placebo/nocebo in heat pain: anodal vs cathodal transcranial direct current stimulation to the right dorsolateral prefrontal cortex.
[So] Source:Pain;156(7):1342-7, 2015 Jul.
[Is] ISSN:1872-6623
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Placebo and nocebo play an important role in clinical practice and medical research. Modulating placebo/nocebo responses using noninvasive brain stimulation methods, such as transcranial direct current stimulation (tDCS), has the potential to harness these effects to therapeutic benefit in a clinical setting. In this study, we assessed the effect of anodal and cathodal tDCS over the right dorsolateral prefrontal cortex (rDLPFC) on conditioned placebo/nocebo cue response to heat pain. Two matched groups of healthy volunteers were subjected to an identical session of conditioning, during which low and high cues (abstract images) were associated with low and high pain levels, respectively. Twenty-minute 2-mA tDCS (either anodal or cathodal) over the rDLPFC was applied. The influence of tDCS current polarity (anodal vs cathodal) on placebo and nocebo was assessed, using subjects' pain ratings in response to identical pain preceded by the conditioned high or low cues. The duration of cue presentation varied to allow either fully conscious or subliminal processing. Significant placebo and nocebo effects in the anodal but not the cathodal group were elicited with the conditioning paradigm. This study provides evidence of a possibility to modulate the conditioned placebo and nocebo effect by changing the excitability of the rDLPFC using tDCS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 150620
[Lr] Last revision date:150620
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/j.pain.0000000000000163


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