Database : MEDLINE
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[PMID]: 25079499
[Au] Autor:Thannhauser JE
[Ad] Address:University of Calgary, Calgary, Alberta, Canada jthannha@ucalgary.ca.
[Ti] Title:Navigating life and loss in pediatric multiple sclerosis.
[So] Source:Qual Health Res;24(9):1198-211, 2014 Sep.
[Is] ISSN:1049-7323
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a chronic disease of the central nervous system that can cause unpredictable disability. Over the past 10 to 15 years, practitioners and researchers have come to recognize that children and adolescents are at risk for this disease. Drawing on the experiences of pediatric MS patients and their parents, I designed this study to explicate the process of adjustment to the disease. Using Charmaz's constructivist grounded theory methodology, I developed a preliminary theory that captures the experience of grief in the adjustment process of young people with MS. The core of the theoretical model focuses on two separate, yet overlapping processes: recurring loss and carrying on. Significant turning points influenced the oscillation between these two processes, highlighting the interconnection of intrapersonal and interpersonal dynamics in adjustment to the disease. Results reinforce and extend current grief literature and provide an alternative perspective on adjustment to pediatric chronic illness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:T
[St] Status:In-Data-Review
[do] DOI:10.1177/1049732314544966

  2 / 176979 MEDLINE  
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[PMID]: 24693960
[Au] Autor:Gupta PK; Sayed N; Ding K; Agostini MA; Van Ness PC; Yablon S; Madden C; Mickey B; D'Ambrosio R; Diaz-Arrastia R
[Ad] Address:1 Department of Neurology and Neurotherapeutics, The University of Texas Southwestern Medical Center , Dallas, Texas.
[Ti] Title:Subtypes of post-traumatic epilepsy: clinical, electrophysiological, and imaging features.
[So] Source:J Neurotrauma;31(16):1439-43, 2014 Aug 15.
[Is] ISSN:1557-9042
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Abstract Post-traumatic epilepsy (PTE) is a consequence of traumatic brain injury (TBI), occurring in 10-25% of patients with moderate to severe injuries. The development of animal models for testing antiepileptogenic therapies and validation of biomarkers to follow epileptogenesis in humans necessitates sophisticated understanding of the subtypes of PTE, which is the objective of this study. In this study, retrospective review was performed of patients with moderate to severe TBI with subsequent development of medically refractory epilepsy referred for video-electroencephalography (EEG) monitoring at a single center over a 10-year period. Information regarding details of injury, neuroimaging studies, seizures, video-EEG, and surgery outcomes were collected and analyzed. There were 123 patients with PTE identified, representing 4.3% of all patients evaluated in the epilepsy monitoring unit. Most of them had localization-related epilepsy, of which 57% had temporal lobe epilepsy (TLE), 35% had frontal lobe epilepsy (FLE), and 3% each had parietal and occipital lobe epilepsy. Of patients with TLE, 44% had mesial temporal sclerosis (MTS), 26% had temporal neocortical lesions, and 30% were nonlesional. There was no difference in age at injury between the different PTE subtypes. Twenty-two patients, 13 of whom had MTS, proceeded to surgical resection. At a mean follow-up of 2.5 years, Engel Class I outcomes were seen in 69% of those with TLE and 33% of those with FLE. Our findings suggest PTE is a heterogeneous condition, and careful evaluation with video-EEG monitoring and high resolution MRI can identify distinct syndromes. These results have implications for the design of clinical trials of antiepileptogenic therapies for PTE.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1089/neu.2013.3221

  3 / 176979 MEDLINE  
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[PMID]: 24899671
[Au] Autor:De Luca CJ; Kline JC; Contessa P
[Ad] Address:NeuroMuscular Research Center, Boston University, Boston, Massachusetts; Department of Electrical and Computer Engineering, Boston University, Boston, Massachusetts; Department of Biomedical Engineering, Boston University, Boston, Massachusetts; Department of Neurology, Boston University, Boston, Massachusetts; and Department of Physical Therapy and Athletic Training, Boston University, Boston, Massachusetts cjd@bu.edu.
[Ti] Title:Transposed firing activation of motor units.
[So] Source:J Neurophysiol;112(4):962-70, 2014 Aug 15.
[Is] ISSN:1522-1598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Muscles are composed of groups of muscle fibers, called motor units, each innervated by a single motoneuron originating in the spinal cord. During constant or linearly varying voluntary force contractions, motor units are activated in a hierarchical order, with the earlier-recruited motor units having greater firing rates than the later-recruited ones. We found that this normal pattern of firing activation can be altered during oscillatory contractions where the force oscillates at frequencies ≥2 Hz. During these high-frequency oscillations, the activation of the lower-threshold motor units effectively decreases and that of the higher-threshold motor units effectively increases. This transposition of firing activation provides means to activate higher-threshold motor units preferentially. Our results demonstrate that the hierarchical regulation of motor unit activation can be manipulated to activate specific motoneuron populations preferentially. This finding can be exploited to develop new forms of physical therapies and exercise programs that enhance muscle performance or that target the preferential atrophy of high-threshold motor units as a result of aging or motor disorders such as stroke and amyotrophic lateral sclerosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1152/jn.00619.2013

  4 / 176979 MEDLINE  
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[PMID]: 25086173
[Au] Autor:de Bock L; Somers K; Fraussen J; Hendriks JJ; van Horssen J; Rouwette M; Hellings N; Villar LM; Alvarez-Cermeño JC; Espiño M; Hupperts R; Jongen P; Damoiseaux J; Verbeek MM; De Deyn PP; D'hooghe M; Van Wijmeersch B; Stinissen P; Somers V
[Ad] Address:Biomedical Research Institute, Hasselt University and Transnationale Universiteit Limburg, 3590 Diepenbeek, Belgium;...
[Ti] Title:Sperm-associated antigen 16 is a novel target of the humoral autoimmune response in multiple sclerosis.
[So] Source:J Immunol;193(5):2147-56, 2014 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We have previously identified eight novel autoantibody targets in the cerebrospinal fluid of multiple sclerosis (MS) patients, including sperm-associated Ag 16 (SPAG16). In the current study, we further investigated the autoantibody response against SPAG16-a protein with unknown function in the CNS-and its expression in MS pathology. Using isoelectric focusing, we detected SPAG16-specific oligoclonal bands in the cerebrospinal fluid of 5 of 23 MS patients (22%). Analysis of the anti-SPAG16 Ab reactivity in the plasma of a total of 531 donors using ELISA demonstrated significantly elevated anti-SPAG16 Ab levels (p = 0.002) in 32 of 153 MS patients (21%) compared with all other control groups with 95% specificity for the disease. To investigate the pathologic relevance of anti-SPAG16 Abs in vivo, anti-SPAG16 Abs were injected in mice with experimental autoimmune encephalomyelitis, resulting in a significant disease exacerbation. Finally, we demonstrated a consistent upregulation of SPAG16 in MS brain and experimental autoimmune encephalomyelitis spinal cord lesions, more specifically in reactive astrocytes. We conclude that SPAG16 is a novel autoantibody target in a subgroup of MS patients and in combination with other diagnostic criteria, elevated levels of anti-SPAG16 Abs could be used as a biomarker for diagnosis. Furthermore, the pathologic relevance of anti-SPAG16 Abs was shown in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401166

  5 / 176979 MEDLINE  
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[PMID]: 25063874
[Au] Autor:Ji Z; Fan Z; Zhang Y; Yu R; Yang H; Zhou C; Luo J; Ke ZJ
[Ad] Address:Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;...
[Ti] Title:Thiamine Deficiency Promotes T Cell Infiltration in Experimental Autoimmune Encephalomyelitis: The Involvement of CCL2.
[So] Source:J Immunol;193(5):2157-67, 2014 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a complex multifactorial disease that results from the interplay between environmental factors and a susceptible genetic background. Experimental autoimmune encephalomyelitis (EAE) has been widely used to investigate the mechanisms underlying MS pathogenesis. Chemokines, such as CCL2, are involved in the development of EAE. We have previously shown that thiamine deficiency (TD) induced CCL2 in neurons. We hypothesized that TD may affect the pathogenesis of EAE. In this study, EAE was induced in C57BL/6J mice by the injection of myelin oligodendroglial glycoprotein (MOG) peptides 35-55 with or without TD. TD aggravated the development of EAE, which was indicated by clinical scores and pathologic alterations in the spinal cord. TD also accelerated the development of EAE in an adoptive transfer EAE model. TD caused microglial activation and a drastic increase (up 140%) in leukocyte infiltration in the spinal cord of the EAE mice; specifically, TD increased Th1 and Th17 cells. TD upregulated the expression of CCL2 and its receptor CCR2 in the spinal cord of EAE mice. Cells in peripheral lymph node and spleen isolated from MOG-primed TD mice showed much stronger proliferative responses to MOG. CCL2 stimulated the proliferation and migration of T lymphocytes in vitro. Our results suggested that TD exacerbated the development of EAE through activating CCL2 and inducing pathologic inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1302702

  6 / 176979 MEDLINE  
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[PMID]: 25049355
[Au] Autor:Aubé B; Lévesque SA; Paré A; Chamma E; Kébir H; Gorina R; Lécuyer MA; Alvarez JI; De Koninck Y; Engelhardt B; Prat A; Côté D; Lacroix S
[Ad] Address:Centre de Recherche du Centre Hospitalier Universitaire de Québec-Centre Hospitalier de l'Université Laval, Quebec, Quebec G1V 4G2, Canada; Département de Médecine Moléculaire, Faculté de Médecine, Université Laval, Quebec, Quebec G1V 0A6, Canada; Centre de Recherche de l'Institut Universitaire en S...
[Ti] Title:Neutrophils mediate blood-spinal cord barrier disruption in demyelinating neuroinflammatory diseases.
[So] Source:J Immunol;193(5):2438-54, 2014 Sep 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Disruption of the blood-brain and blood-spinal cord barriers (BBB and BSCB, respectively) and immune cell infiltration are early pathophysiological hallmarks of multiple sclerosis (MS), its animal model experimental autoimmune encephalomyelitis (EAE), and neuromyelitis optica (NMO). However, their contribution to disease initiation and development remains unclear. In this study, we induced EAE in lys-eGFP-ki mice and performed single, nonterminal intravital imaging to investigate BSCB permeability simultaneously with the kinetics of GFP(+) myeloid cell infiltration. We observed a loss in BSCB integrity within a day of disease onset, which paralleled the infiltration of GFP(+) cells into the CNS and lasted for ∼4 d. Neutrophils accounted for a significant proportion of the circulating and CNS-infiltrating myeloid cells during the preclinical phase of EAE, and their depletion delayed the onset and reduced the severity of EAE while maintaining BSCB integrity. We also show that neutrophils collected from the blood or bone marrow of EAE mice transmigrate more efficiently than do neutrophils of naive animals in a BBB cell culture model. Moreover, using intravital videomicroscopy, we demonstrate that the IL-1R type 1 governs the firm adhesion of neutrophils to the inflamed spinal cord vasculature. Finally, immunostaining of postmortem CNS material obtained from an acutely ill multiple sclerosis patient and two neuromyelitis optica patients revealed instances of infiltrated neutrophils associated with regions of BBB or BSCB leakage. Taken together, our data provide evidence that neutrophils are involved in the initial events that take place during EAE and that they are intimately linked with the status of the BBB/BSCB.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1400401

  7 / 176979 MEDLINE  
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[PMID]: 24977661
[Au] Autor:Ruffilli I; Ferrari SM; Colaci M; Ferri C; Fallahi P; Antonelli A
[Ad] Address:Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy....
[Ti] Title:IP-10 in Autoimmune Thyroiditis.
[So] Source:Horm Metab Res;46(9):597-602, 2014 Aug.
[Is] ISSN:1439-4286
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:The interferon-γ-inducible protein 10 (IP-10) was initially identified as a chemokine that is induced by interferon (IFN)-γ. IP-10 exerts its function through binding to chemokine (C-X-C motif) receptor 3 (CXCR3). IP-10 and its receptor, CXCR3, appear to contribute to the pathogenesis of many autoimmune diseases, organ specific (such as type 1 diabetes, Graves' disease and ophthalmopathy), or systemic (such as systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren syndrome, or systemic sclerosis). The secretion of IP-10 by (CD)4+, CD8+, and natural killer is dependent on IFN-γ. Under the influence of IFN-γ, IP-10 is secreted by thyrocytes. Determination of high level of IP-10 in peripheral fluids is therefore a marker of a T helper 1 orientated immune response. High levels of circulating IP-10, have been shown in patients with autoimmune thyroiditis (AT). Among patients with AT, IP-10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern, which is a sign of a more severe lympho-monocytic infiltration, and in those with hypothyroidism. For these reasons, it has been postulated that IP-10 could be a marker of a stronger and more aggressive inflammatory response in the thyroid, subsequently leading to thyroid destruction and hypothyroidism. Further studies are needed to investigate whether IP-10 is a novel therapeutic target in AT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1055/s-0034-1382053

  8 / 176979 MEDLINE  
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[PMID]: 25087081
[Au] Autor:Braun M; Brandt AU; Schulz S; Boeker M
[Ad] Address:Center for Medical Biometry and Medical Informatics, Medical Center - University of Freiburg, Stefan-Meier-Str, 26, 79104 Freiburg, Germany. michael.braun@uniklinik-freiburg.de.
[Ti] Title:Validating archetypes for the Multiple Sclerosis Functional Composite.
[So] Source:BMC Med Inform Decis Mak;14(1):64, 2014.
[Is] ISSN:1472-6947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Numerous information models for electronic health records, such as openEHR archetypes are available. The quality of such clinical models is important to guarantee standardised semantics and to facilitate their interoperability. However, validation aspects are not regarded sufficiently yet. The objective of this report is to investigate the feasibility of archetype development and its community-based validation process, presuming that this review process is a practical way to ensure high-quality information models amending the formal reference model definitions. METHODS: A standard archetype development approach was applied on a case set of three clinical tests for multiple sclerosis assessment: After an analysis of the tests, the obtained data elements were organised and structured. The appropriate archetype class was selected and the data elements were implemented in an iterative refinement process. Clinical and information modelling experts validated the models in a structured review process. RESULTS: Four new archetypes were developed and publicly deployed in the openEHR Clinical Knowledge Manager, an online platform provided by the openEHR Foundation. Afterwards, these four archetypes were validated by domain experts in a team review. The review was a formalised process, organised in the Clinical Knowledge Manager. Both, development and review process turned out to be time-consuming tasks, mostly due to difficult selection processes between alternative modelling approaches. The archetype review was a straightforward team process with the goal to validate archetypes pragmatically. CONCLUSIONS: The quality of medical information models is crucial to guarantee standardised semantic representation in order to improve interoperability. The validation process is a practical way to better harmonise models that diverge due to necessary flexibility left open by the underlying formal reference model definitions.This case study provides evidence that both community- and tool-enabled review processes, structured in the Clinical Knowledge Manager, ensure archetype quality. It offers a pragmatic but feasible way to reduce variation in the representation of clinical information models towards a more unified and interoperable model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/1472-6947-14-64

  9 / 176979 MEDLINE  
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[PMID]: 25120144
[Au] Autor:Davidson JM
[Ad] Address:1] Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA [2] Research Service, VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA.
[Ti] Title:Proteomic revelations.
[So] Source:J Invest Dermatol;134(9):2301-2, 2014 Sep.
[Is] ISSN:1523-1747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The power of proteomics in cultured skin fibroblasts from individuals with either systemic sclerosis or recessive dystrophic epidermolysis bullosa has led to the common finding of senescence and deficiencies in autophagy. Both of these disorders exert high demand on fibroblast activity, and without the protective action of autophagy cellular stress could have many adverse effects that are further amplified by the senescent phenotype.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/jid.2014.242

  10 / 176979 MEDLINE  
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[PMID]: 24496236
[Au] Autor:Dumit VI; Küttner V; Käppler J; Piera-Velazquez S; Jimenez SA; Bruckner-Tuderman L; Uitto J; Dengjel J
[Ad] Address:1] Freiburg Institute for Advanced Studies (FRIAS), School of Life Science (LifeNet), University of Freiburg, Freiburg, Germany [2] Center for Biological Systems Analysis (ZBSA), University Medical Center Freiburg, Freiburg, Germany....
[Ti] Title:Altered MCM Protein Levels and Autophagic Flux in Aged and Systemic Sclerosis Dermal Fibroblasts.
[So] Source:J Invest Dermatol;134(9):2321-30, 2014 Sep.
[Is] ISSN:1523-1747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aging is a common risk factor of many disorders. With age, the level of insoluble extracellular matrix increases leading to increased stiffness of a number of tissues. Matrix accumulation can also be observed in fibrotic disorders, such as systemic sclerosis (SSc). Although the intrinsic aging process in skin is phenotypically distinct from SSc, here we demonstrate similar behavior of aged and SSc skin fibroblasts in culture. We have used quantitative proteomics to characterize the phenotype of dermal fibroblasts from healthy subjects of various ages and from patients with SSc. Our results demonstrate that proteins involved in DNA and RNA processing decrease with age and in SSc, whereas those involved in mitochondrial and other metabolic processes behave the opposite. Specifically, minichromosome maintenance (MCM) helicase proteins are less abundant with age and SSc, and they exhibit an altered subcellular distribution. We observed that lower levels of MCM7 correlate with reduced cell proliferation, lower autophagic capacity, and higher intracellular protein abundance phenotypes of aged and SSc cells. In addition, we show that SSc fibroblasts exhibit higher levels of senescence compared with their healthy counterparts, suggesting further similarities between the fibrotic disorder and the aging process. Hence, at the molecular level, SSc fibroblasts exhibit intrinsic characteristics of fibroblasts from aged skin.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/jid.2014.69


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