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[PMID]: 25927543
[Au] Autor:Reyes S; Peirano P; Luna B; Lozoff B; Algarín C
[Ad] Address:Sleep and Functional Neurobiology Laboratory, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile....
[Ti] Title:Potential effects of reward and loss avoidance in overweight adolescents.
[So] Source:Pediatr Res;78(2):152-7, 2015 Aug.
[Is] ISSN:1530-0447
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Reward system and inhibitory control are brain functions that exert an influence on eating behavior regulation. We studied the differences in inhibitory control and sensitivity to reward and loss avoidance between overweight/obese and normal-weight adolescents. METHODS: We assessed 51 overweight/obese and 52 normal-weight 15-y-old Chilean adolescents. The groups were similar regarding sex and intelligence quotient. Using Antisaccade and Incentive tasks, we evaluated inhibitory control and the effect of incentive trials (neutral, loss avoidance, and reward) on generating correct and incorrect responses (latency and error rate). RESULTS: Compared to normal-weight group participants, overweight/obese adolescents showed shorter latency for incorrect antisaccade responses (186.0 (95% CI: 176.8-195.2) vs. 201.3 ms (95% CI: 191.2-211.5), P < 0.05) and better performance reflected by lower error rate in incentive trials (43.6 (95% CI: 37.8-49.4) vs. 53.4% (95% CI: 46.8-60.0), P < 0.05). Overweight/obese adolescents were more accurate on loss avoidance (40.9 (95% CI: 33.5-47.7) vs. 49.8% (95% CI: 43.0-55.1), P < 0.05) and reward (41.0 (95% CI: 34.5-47.5) vs. 49.8% (95% CI: 43.0-55.1), P < 0.05) compared to neutral trials. CONCLUSION: Overweight/obese adolescents showed shorter latency for incorrect responses and greater accuracy in reward and loss avoidance trials. These findings could suggest that an imbalance of inhibition and reward systems influence their eating behavior.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/pr.2015.82

  2 / 1290551 MEDLINE  
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[PMID]: 25682211
[Au] Autor:Petranovich CL; Wade SL; Taylor HG; Cassedy A; Stancin T; Kirkwood MW; Maines Brown T
[Ad] Address:Department of Psychology, University of Cincinnati, Division of Physical Medicine and Rehabilitation, Cincinnati Children's Hospital Medical Center, karvercl@mail.uc.edu....
[Ti] Title:Long-Term Caregiver Mental Health Outcomes Following a Predominately Online Intervention for Adolescents With Complicated Mild to Severe Traumatic Brain Injury.
[So] Source:J Pediatr Psychol;40(7):680-8, 2015 Aug.
[Is] ISSN:1465-735X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To examine the efficacy of counselor-assisted problem solving (CAPS) in improving long-term caregiver psychological functioning following traumatic brain injury (TBI) in adolescents. METHODS: This randomized clinical trial compared CAPS (n = 65), a predominantly online problem-solving intervention, with an Internet resource comparison (n = 67) program. Families of adolescents with TBI completed a baseline assessment and follow-up assessments 6, 12, and 18 months later. General linear mixed models were used to examine longitudinal changes in caregiver global psychological distress, depressive symptoms, and caregiving self-efficacy. Family income and injury severity were examined as moderators of treatment efficacy. RESULTS: Family income moderated long-term changes in caregiver psychological distress. For lower-income caregivers, the CAPS intervention was associated with lower levels of psychological distress at 6, 12, and 18 months post baseline. CONCLUSIONS: These findings support the utility of Web-based interventions in improving long-term caregiver psychological distress, particularly for lower-income families.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/jpepsy/jsv001

  3 / 1290551 MEDLINE  
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[PMID]: 26115192
[Au] Autor:Wüthrich C; Batson S; Koralnik IJ
[Ad] Address:From the Division of Neuro-Immunology, Department of Neurology, Center for Virology and Vaccine Research, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
[Ti] Title:Lack of Major Histocompatibility Complex Class I Upregulation and Restrictive Infection by JC Virus Hamper Detection of Neurons by T Lymphocytes in the Central Nervous System.
[So] Source:J Neuropathol Exp Neurol;74(8):791-803, 2015 Aug.
[Is] ISSN:1554-6578
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The human polyomavirus JC (JCV) infects glial cells in immunosuppressed individuals, leading to progressive multifocal leukoencephalopathy. Polyomavirus JC can also infect neurons in patients with JCV granule cell neuronopathy and JCV encephalopathy. CD8-positive T cells play a crucial role in viral containment and outcome in progressive multifocal leukoencephalopathy, but whether CD8-positive T cells can also recognize JCV-infected neurons is unclear. We used immunohistochemistry to determine the prevalence of T cells in neuron-rich areas of archival brain samples from 77 patients with JCV CNS infections and 94 control subjects. Neurons predominantly sustained a restrictive infection with expression of JCV regulatory protein T antigen (T Ag), whereas glial cells were productively infected and expressed both T Ag and the capsid protein VP1. T cells were more prevalent near JCV-infected cells with intact nuclei expressing both T Ag and VP1 compared with those expressing either protein alone. CD8-positive T cells also colocalized more with JCV-infected glial cells than with JCV-infected neurons. Major histocompatibility complex class I expression was upregulated in JCV-infected areas but could only be detected in rare neurons interspersed with infected glial cells. These results suggest that isolated neurons harboring restrictive JCV infection do not upregulate major histocompatibility complex class I and thus may escape recognition by CD8-positive T cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/NEN.0000000000000218

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[PMID]: 26091720
[Au] Autor:Sa Q; Ochiai E; Tiwari A; Perkins S; Mullins J; Gehman M; Huckle W; Eyestone WH; Saunders TL; Shelton BJ; Suzuki Y
[Ad] Address:Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536;...
[Ti] Title:Cutting Edge: IFN-γ Produced by Brain-Resident Cells Is Crucial To Control Cerebral Infection with Toxoplasma gondii.
[So] Source:J Immunol;195(3):796-800, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In vitro studies demonstrated that microglia and astrocytes produce IFN-γ in response to various stimulations, including LPS. However, the physiological role of IFN-γ production by brain-resident cells, including glial cells, in resistance against cerebral infections remains unknown. We analyzed the role of IFN-γ production by brain-resident cells in resistance to reactivation of cerebral infection with Toxoplasma gondii using a murine model. Our study using bone marrow chimeric mice revealed that IFN-γ production by brain-resident cells is essential for upregulating IFN-γ-mediated protective innate immune responses to restrict cerebral T. gondii growth. Studies using a transgenic strain that expresses IFN-γ only in CD11b(+) cells suggested that IFN-γ production by microglia, which is the only CD11b(+) cell population among brain-resident cells, is able to suppress the parasite growth. Furthermore, IFN-γ produced by brain-resident cells is pivotal for recruiting T cells into the brain to control the infection. These results indicate that IFN-γ produced by brain-resident cells is crucial for facilitating both the protective innate and T cell-mediated immune responses to control cerebral infection with T. gondii.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1500814

  5 / 1290551 MEDLINE  
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[PMID]: 25974698
[Au] Autor:Horning KJ; Caito SW; Tipps KG; Bowman AB; Aschner M
[Ad] Address:Department of Neurology, Vanderbilt University, Nashville, Tennessee 37232; email: kyle.j.horning@vanderbilt.edu , k.grace.tipps@vanderbilt.edu , aaron.bowman@vanderbilt.edu.
[Ti] Title:Manganese Is Essential for Neuronal Health.
[So] Source:Annu Rev Nutr;35:71-108, 2015 Jul 17.
[Is] ISSN:1545-4312
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The understanding of manganese (Mn) biology, in particular its cellular regulation and role in neurological disease, is an area of expanding interest. Mn is an essential micronutrient that is required for the activity of a diverse set of enzymatic proteins (e.g., arginase and glutamine synthase). Although necessary for life, Mn is toxic in excess. Thus, maintaining appropriate levels of intracellular Mn is critical. Unlike other essential metals, cell-level homeostatic mechanisms of Mn have not been identified. In this review, we discuss common forms of Mn exposure, absorption, and transport via regulated uptake/exchange at the gut and blood-brain barrier and via biliary excretion. We present the current understanding of cellular uptake and efflux as well as subcellular storage and transport of Mn. In addition, we highlight the Mn-dependent and Mn-responsive pathways implicated in the growing evidence of its role in Parkinson's disease and Huntington's disease. We conclude with suggestions for future focuses of Mn health-related research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1146/annurev-nutr-071714-034419

  6 / 1290551 MEDLINE  
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[PMID]: 25904410
[Au] Autor:Lu S; Seravalli J; Harrison-Findik D
[Ad] Address:Department of Internal Medicine, University of Nebraska Medical Center, 95820 UNMC, DRC I, Omaha, NE, 68198-5820, USA.
[Ti] Title:Inductively coupled mass spectrometry analysis of biometals in conditional Hamp1 and Hamp1 and Hamp2 transgenic mouse models.
[So] Source:Transgenic Res;24(4):765-73, 2015 Aug.
[Is] ISSN:1573-9368
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Hepcidin, a circulatory antimicrobial peptide, is involved in iron homeostasis, inflammation, infection and metabolic signals. Humans express one hepcidin gene, HAMP but mice express two hepcidin genes, Hamp1 and Hamp2. Consecutive gene targeting events were performed to produce transgenic mice expressing conditional alleles of either Hamp1 or both Hamp1 and Hamp2 (Hamp1/2). The deletion of Hamp1 alleles elevated Hamp2 expression, particularly in males, which was reduced by endotoxin treatment. The tissue levels of iron and other biometals were quantified by inductively coupled mass spectrometry. The ubiquitous or liver-specific deletion of Hamp1 alleles yielded similar quantitative changes in iron levels in the liver, duodenum, spleen, kidney, heart and brain. The introduction of Hamp2 null allele did not exacerbate the iron-related phenotype of Hamp1 null allele. Besides iron, Hamp1 null allele significantly elevated the levels of selenium in the liver, manganese in the liver and duodenum, and copper in the brain. Mice with conditional Hamp alleles will be useful to determine the tissue-specific regulation and functions of Hamp1 and Hamp2 in biometal homeostasis and other biological processes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s11248-015-9879-3

  7 / 1290551 MEDLINE  
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[PMID]: 25956761
[Au] Autor:Onnink AM; Zwiers MP; Hoogman M; Mostert JC; Dammers J; Kan CC; Vasquez AA; Schene AH; Buitelaar J; Franke B
[Ad] Address:Department of Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Human Genetics, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands....
[Ti] Title:Deviant white matter structure in adults with attention-deficit/hyperactivity disorder points to aberrant myelination and affects neuropsychological performance.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;63:14-22, 2015 Dec 3.
[Is] ISSN:1878-4216
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Attention-deficit/hyperactivity disorder (ADHD) in childhood is characterized by gray and white matter abnormalities in several brain areas. Considerably less is known about white matter microstructure in adults with ADHD and its relation with clinical symptoms and cognitive performance. In 107 adult ADHD patients and 109 gender-, age- and IQ-matched controls, we used diffusion tensor imaging (DTI) with tract-based spatial statistics (TBSS) to investigate whole-skeleton changes of fractional anisotropy (FA) and mean, axial, and radial diffusivity (MD, AD, RD). Additionally, we studied the relation of FA and MD values with symptom severity and cognitive performance on tasks measuring working memory, attention, inhibition, and delay discounting. In comparison to controls, participants with ADHD showed reduced FA in corpus callosum, bilateral corona radiata, and thalamic radiation. Higher MD and RD were found in overlapping and even more widespread areas in both hemispheres, also encompassing internal and external capsule, sagittal stratum, fornix, and superior lateral fasciculus. Values of FA and MD were not associated with symptom severity. However, within some white matter clusters that distinguished patients from controls, worse inhibition performance was associated with reduced FA and more impulsive decision making was associated with increased MD. This study shows widespread differences in white matter integrity between adults with persistent ADHD and healthy individuals. Changes in RD suggest aberrant myelination as a pathophysiological factor in persistent ADHD. The microstructural differences in adult ADHD may contribute to poor inhibition and greater impulsivity but appear to be independent of disease severity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 1290551 MEDLINE  
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[PMID]: 25856109
[Au] Autor:Lau SK; Zakeri K; Zhao X; Carmona R; Knipprath E; Simpson DR; Nath SK; Kim GY; Sanghvi P; Hattangadi-Gluth JA; Chen CC; Murphy KT
[Ad] Address:Departments of ‡Radiation Medicine and Applied Sciences and §Surgery, Division of Neurosurgery, Moores University of California San Diego Cancer Center, La Jolla, California; ¶Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut.
[Ti] Title:Single-Isocenter Frameless Volumetric Modulated Arc Radiosurgery for Multiple Intracranial Metastases.
[So] Source:Neurosurgery;77(2):233-40, 2015 Aug.
[Is] ISSN:1524-4040
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Stereotactic radiosurgery (SRS) is a well-accepted treatment for patients with intracranial metastases, but outcomes with volumetric modulated arc radiosurgery (VMAR) are poorly described. OBJECTIVE: To report our initial clinical experience applying a novel single-isocenter technique to frameless VMAR for simultaneous treatment of multiple intracranial metastases. METHODS: We performed a retrospective analysis of 15 patients undergoing frameless VMAR for multiple intracranial metastases using a single, centrally located isocenter in the period 2009 and 2011. Of these, 3 patients were treated for progressive or recurrent intracranial disease. A total of 62 metastases (median, 3 per patient; range, 2-13) were treated to a median dose of 20 Gy (range, 15-30 Gy). Three patients were treated with fractionated SRS. Follow-up including clinical examination and magnetic resonance imaging (MRI) occurred every 3 months. RESULTS: The median follow-up for all patients was 7.1 months (range, 1.1-24.3), with 11 patients (73.3%) followed until death. For the remaining 4 patients alive at the time of analysis, the median follow-up was 19.6 months (range, 9.2-24.3). Local control at 6 and 12 months was 91.7% (95% confidence interval [CI], 84.6%-100.0%) and 81.5% (95% CI, 67.9%-100.0%), respectively. Regional failure was observed in 9 patients (60.0%), and 7 patients (46.7%) received salvage therapy. Overall survival at 6 months was 60.0% (95% CI, 40.3%-88.2%). Grade 3 or higher treatment-related toxicity was not observed. The median total treatment time was 7.2 minutes (range, 2.8-13.2 minutes). CONCLUSION: Single-isocenter, frameless VMAR for multiple intracranial metastases is a promising technique that may provide similar clinical outcomes compared with conventional radiosurgery. ABBREVIATIONS: CI, confidence intervalFFF, flattening filter-freeIMRS, intensity-modulated linear accelerator-based radiosurgeryPTV, planning target volumeRTOG, Radiation Therapy Oncology GroupSIG, surface image guidanceSRS, stereotactic radiosurgeryVMAR, volumetric modulated arc radiosurgeryVMAT, volumetric-modulated arc therapyWBRT, whole-brain radiation therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1227/NEU.0000000000000763

  9 / 1290551 MEDLINE  
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[PMID]: 26003445
[Au] Autor:Duman JG; Mulherkar S; Tu YK; X Cheng J; Tolias KF
[Ad] Address:Department of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA....
[Ti] Title:Mechanisms for spatiotemporal regulation of Rho-GTPase signaling at synapses.
[So] Source:Neurosci Lett;601:4-10, 2015 Aug 5.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Synapses mediate information flow between neurons and undergo plastic changes in response to experience, which is critical for learning and memory. Conversely, synaptic defects impair information processing and underlie many brain pathologies. Rho-family GTPases control synaptogenesis by transducing signals from extracellular stimuli to the cytoskeleton and nucleus. The Rho-GTPases Rac1 and Cdc42 promote synapse development and the growth of axons and dendrites, while RhoA antagonizes these processes. Despite its importance, many aspects of Rho-GTPase signaling remain relatively unknown. Rho-GTPases are activated by guanine nucleotide exchange factors (GEFs) and inhibited by GTPase-activating proteins (GAPs). Though the number of both GEFs and GAPs greatly exceeds that of Rho-GTPases, loss of even a single GEF or GAP often has profound effects on cognition and behavior. Here, we explore how the actions of specific GEFs and GAPs give rise to the precise spatiotemporal activation patterns of Rho-GTPases in neurons. We consider the effects of coupling GEFs and GAPs targeting the same Rho-GTPase and the modular pathways that connect specific cellular stimuli with a given Rho-GTPase via different GEFs. We discuss how the creation of sharp borders between Rho-GTPase activation zones is achieved by pairing a GEF for one Rho-GTPase with a GAP for another and the extensive crosstalk between different Rho-GTPases. Given the importance of synapses for cognition and the fundamental roles that Rho-GTPases play in regulating them, a detailed understanding of Rho-GTPase signaling is essential to the progress of neuroscience.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review

  10 / 1290551 MEDLINE  
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[PMID]: 25623036
[Au] Autor:Kyzar EJ; Pandey SC
[Ad] Address:Department of Psychiatry, University of Illinois at Chicago, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA.
[Ti] Title:Molecular mechanisms of synaptic remodeling in alcoholism.
[So] Source:Neurosci Lett;601:11-9, 2015 Aug 5.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Alcohol use and alcohol addiction represent dysfunctional brain circuits resulting from neuroadaptive changes during protracted alcohol exposure and its withdrawal. Alcohol exerts a potent effect on synaptic plasticity and dendritic spine formation in specific brain regions, providing a neuroanatomical substrate for the pathophysiology of alcoholism. Epigenetics has recently emerged as a critical regulator of gene expression and synaptic plasticity-related events in the brain. Alcohol exposure and withdrawal induce changes in crucial epigenetic processes in the emotional brain circuitry (amygdala) that may be relevant to the negative affective state defined as the "dark side" of addiction. Here, we review the literature concerning synaptic plasticity and epigenetics, with a particular focus on molecular events related to dendritic remodeling during alcohol abuse and alcoholism. Targeting epigenetic processes that modulate synaptic plasticity may yield novel treatments for alcoholism.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review


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