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  1 / 183732 MEDLINE  
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[PMID]: 25735748
[Au] Autor:Yu Y; Chi B; Xia W; Gangopadhyay J; Yamazaki T; Winkelbauer-Hurt ME; Yin S; Eliasse Y; Adams E; Shaw CE; Reed R
[Ad] Address:Department of Cell Biology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115, USA....
[Ti] Title:U1 snRNP is mislocalized in ALS patient fibroblasts bearing NLS mutations in FUS and is required for motor neuron outgrowth in zebrafish.
[So] Source:Nucleic Acids Res;43(6):3208-18, 2015 Mar 31.
[Is] ISSN:1362-4962
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Mutations in FUS cause amyotrophic lateral sclerosis (ALS), but the molecular pathways leading to neurodegeneration remain obscure. We previously found that U1 snRNP is the most abundant FUS interactor. Here, we report that components of the U1 snRNP core particle (Sm proteins and U1 snRNA), but not the mature U1 snRNP-specific proteins (U1-70K, U1A and U1C), co-mislocalize with FUS to the cytoplasm in ALS patient fibroblasts harboring mutations in the FUS nuclear localization signal (NLS). Similar results were obtained in HeLa cells expressing the ALS-causing FUS R495X NLS mutation, and mislocalization of Sm proteins is RRM-dependent. Moreover, as observed with FUS, knockdown of any of the U1 snRNP-specific proteins results in a dramatic loss of SMN-containing Gems. Significantly, knockdown of U1 snRNP in zebrafish results in motor axon truncations, a phenotype also observed with FUS, SMN and TDP-43 knockdowns. Our observations linking U1 snRNP to ALS patient cells with FUS mutations, SMN-containing Gems, and motor neurons indicate that U1 snRNP is a component of a molecular pathway associated with motor neuron disease. Linking an essential canonical splicing factor (U1 snRNP) to this pathway provides strong new evidence that splicing defects may be involved in pathogenesis and that this pathway is a potential therapeutic target.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/nar/gkv157

  2 / 183732 MEDLINE  
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[PMID]: 25834301
[Au] Autor:Indo HP; Yen HC; Nakanishi I; Matsumoto K; Tamura M; Nagano Y; Matsui H; Gusev O; Cornette R; Okuda T; Minamiyama Y; Ichikawa H; Suenaga S; Oki M; Sato T; Ozawa T; Clair DK; Majima HJ
[Ad] Address:Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima 890-8544, Japan ; Department of Space Environmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima 890-8544, Japa...
[Ti] Title:A mitochondrial superoxide theory for oxidative stress diseases and aging.
[So] Source:J Clin Biochem Nutr;56(1):1-7, 2015 Jan.
[Is] ISSN:0912-0009
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Fridovich identified CuZnSOD in 1969 and manganese superoxide dismutase (MnSOD) in 1973, and proposed "the Superoxide Theory," which postulates that superoxide (O2 (•-)) is the origin of most reactive oxygen species (ROS) and that it undergoes a chain reaction in a cell, playing a central role in the ROS producing system. Increased oxidative stress on an organism causes damage to cells, the smallest constituent unit of an organism, which can lead to the onset of a variety of chronic diseases, such as Alzheimer's, Parkinson's, amyotrophic lateral sclerosis and other neurological diseases caused by abnormalities in biological defenses or increased intracellular reactive oxygen levels. Oxidative stress also plays a role in aging. Antioxidant systems, including non-enzyme low-molecular-weight antioxidants (such as, vitamins A, C and E, polyphenols, glutathione, and coenzyme Q10) and antioxidant enzymes, fight against oxidants in cells. Superoxide is considered to be a major factor in oxidant toxicity, and mitochondrial MnSOD enzymes constitute an essential defense against superoxide. Mitochondria are the major source of superoxide. The reaction of superoxide generated from mitochondria with nitric oxide is faster than SOD catalyzed reaction, and produces peroxynitrite. Thus, based on research conducted after Fridovich's seminal studies, we now propose a modified superoxide theory; i.e., superoxide is the origin of reactive oxygen and nitrogen species (RONS) and, as such, causes various redox related diseases and aging.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150402
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3164/jcbn.14-42

  3 / 183732 MEDLINE  
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[PMID]: 25834740
[Au] Autor:Abolhassani S; Yazdannik A; Taleghani F; Zamani A
[Ad] Address:Faculty of Nursing and Midwifery, Isfahan University of Medical Sciences, Isfahan, IR Iran....
[Ti] Title:Expectations of multiple sclerosis patients and their families: a qualitative study in iran.
[So] Source:Iran Red Crescent Med J;17(2):e18293, 2015 Feb.
[Is] ISSN:2074-1804
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:BACKGROUND: Multiple Sclerosis (MS) is a neurological disease that is most commonly observed among young people. Drug and non-drug treatments are used to prevent the progression of the disease and to control illness-related disorders. Patients with MS often have multiple and complicated needs that require a broad spectrum of health services. OBJECTIVES: This study was conducted to identify the expectations of individuals with MS and their families for healthcare services. PATIENTS AND METHODS: This article is part of a qualitative case study. The participants were selected by a purposive sampling method. In this study, semi-structured interviews of 20 individuals with MS and 8 family members were conducted to identify the expectations of MS patients and their families. In addition to the interviews, the documents related to the aim of the study, including weblogs, MS magazines, special websites of individuals with MS, and news agencies were gathered. Analysis of data was performed by a conventional content analysis method. RESULTS: The age of the participants ranged from 22-63 years. The data obtained from this study was classified into 5 main categories as follows: being cured, need for comfort, promoting knowledge, economic welfare, and social security. CONCLUSIONS: Individuals with MS and their families had different expectations pertaining to all dimensions of life, such that not meeting the needs related to any dimension could have affect the other dimensions. Therefore, it is necessary for healthcare providers to have a holistic assessment as well as try to meet all needs and expectations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150402
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5812/ircmj.18293

  4 / 183732 MEDLINE  
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[PMID]: 25834622
[Au] Autor:Cha MH; Kim MJ; Jung J; Kim JH; Lee MS; Kim MS
[Ad] Address:Medical Research Division, Korean Institute of Oriental Medicine, 1672 Yuseongdae-ro, Yuseong-gu, Daejeon 305-811, Republic of Korea....
[Ti] Title:Metabolomic analysis of clinical plasma from cerebral infarction patients presenting with blood stasis.
[So] Source:Evid Based Complement Alternat Med;2015:453423, 2015.
[Is] ISSN:1741-427X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Blood stasis (BS) is characterized as a disorder of blood circulation. In traditional Korean medicine (TKM), it is viewed as a cause factor of diseases such as multiple sclerosis and stroke. This study investigated differences in the plasma metabolites profiles of subjects displaying BS or non-BS patterns. Thirty-one patients with cerebral infarction diagnosed with BS and an equal number of sex- and age-matched non-BS patients were enrolled. Metabolic profiling was performed using UPLC-MS. The ratio of subjects with a rough pulse and purple coloration of the tongue was higher in patients presenting with BS pattern. Through metabolomics analysis, 82 metabolites that differed significantly between the BS and non-BS pattern were identified, and the two groups were significantly separated using an orthogonal partial least square-discriminant analysis model (P < 0.001). Of these 82 metabolites, acetyl carnitine, leucine, kynurenine, phosphocholine, hexanoyl carnitine, and decanoyl carnitine were present in significantly higher levels in patients with a BS pattern than those with a non-BS pattern. Our results also demonstrated that seven plasma metabolites, including acyl-carnitines and kynurenine, were associated with a BS pattern, suggesting that variant plasma metabolic profiles may serve as a biomarker for diagnosis of BS in patients with cerebral infarction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150402
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2015/453423

  5 / 183732 MEDLINE  
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[PMID]: 25708987
[Au] Autor:Barkauskas DS; Dixon Dorand R; Myers JT; Evans TA; Barkauskas KJ; Askew D; Purgert R; Huang AY
[Ad] Address:Division of Pediatric Hematology-Oncology, Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA....
[Ti] Title:Focal transient CNS vessel leak provides a tissue niche for sequential immune cell accumulation during the asymptomatic phase of EAE induction.
[So] Source:Exp Neurol;266:74-85, 2015 Apr.
[Is] ISSN:1090-2430
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Peripheral immune cells are critical to the pathogenesis of neurodegenerative diseases including multiple sclerosis (MS) (Hendriks et al., 2005; Kasper and Shoemaker, 2010). However, the precise sequence of tissue events during the early asymptomatic induction phase of experimental autoimmune encephalomyelitis (EAE) pathogenesis remains poorly defined. Due to the spatial-temporal constrains of traditional methods used to study this disease, most studies had been performed in the spine during peak clinical disease; thus the debate continues as to whether tissue changes such as vessel disruption represent a cause or a byproduct of EAE pathophysiology in the cortex. Here, we provide dynamic, high-resolution information on the evolving structural and cellular processes within the gray matter of the mouse cortex during the first 12 asymptomatic days of EAE induction. We observed that transient focal vessel disruptions precede microglia activation, followed by infiltration of and directed interaction between circulating dendritic cells and T cells. Histamine antagonist minimizes but not completely ameliorates blood vessel leaks. Histamine H1 receptor blockade prevents early microglia function, resulting in subsequent reduction in immune cell accumulation, disease incidence and clinical severity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 183732 MEDLINE  
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[PMID]: 25821548
[Au] Autor:El Amrani M; Azizi M
[Ad] Address:Service de Néphrologie, Dialyse et Transplantation Rénale, Hôpital Militaire d'Instruction Mohammed V, Rabat, Maroc.
[Ti] Title:Néphrectomie bilatérale de sauvetage compliquant une sclérose tubéreuse de Bourneville. [Lifesaving bilateral nephrectomy complicating Bourneville tuberous sclerosis].
[So] Source:Pan Afr Med J;19:205, 2014.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:fre
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.11604/pamj.2014.19.205.5483

  7 / 183732 MEDLINE  
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[PMID]: 25816143
[Au] Autor:El Mendili MM; Chen R; Tiret B; Villard N; Trunet S; Pélégrini-Issac M; Lehéricy S; Pradat PF; Benali H
[Ad] Address:Sorbonne Universités, UPMC Univ Paris 06, CNRS, INSERM, Laboratoire d'Imagerie Biomédicale, F-75013, Paris, Île de France, France....
[Ti] Title:Fast and Accurate Semi-Automated Segmentation Method of Spinal Cord MR Images at 3T Applied to the Construction of a Cervical Spinal Cord Template.
[So] Source:PLoS One;10(3):e0122224, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To design a fast and accurate semi-automated segmentation method for spinal cord 3T MR images and to construct a template of the cervical spinal cord. MATERIALS AND METHODS: A semi-automated double threshold-based method (DTbM) was proposed enabling both cross-sectional and volumetric measures from 3D T2-weighted turbo spin echo MR scans of the spinal cord at 3T. Eighty-two healthy subjects, 10 patients with amyotrophic lateral sclerosis, 10 with spinal muscular atrophy and 10 with spinal cord injuries were studied. DTbM was compared with active surface method (ASM), threshold-based method (TbM) and manual outlining (ground truth). Accuracy of segmentations was scored visually by a radiologist in cervical and thoracic cord regions. Accuracy was also quantified at the cervical and thoracic levels as well as at C2 vertebral level. To construct a cervical template from healthy subjects' images (n=59), a standardization pipeline was designed leading to well-centered straight spinal cord images and accurate probability tissue map. RESULTS: Visual scoring showed better performance for DTbM than for ASM. Mean Dice similarity coefficient (DSC) was 95.71% for DTbM and 90.78% for ASM at the cervical level and 94.27% for DTbM and 89.93% for ASM at the thoracic level. Finally, at C2 vertebral level, mean DSC was 97.98% for DTbM compared with 98.02% for TbM and 96.76% for ASM. DTbM showed similar accuracy compared with TbM, but with the advantage of limited manual interaction. CONCLUSION: A semi-automated segmentation method with limited manual intervention was introduced and validated on 3T images, enabling the construction of a cervical spinal cord template.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0122224

  8 / 183732 MEDLINE  
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[PMID]: 25726362
[Au] Autor:Chiò A; Mora G; Sabatelli M; Caponnetto C; Traynor BJ; Johnson JO; Nalls MA; Calvo A; Moglia C; Borghero G; Monsurrò MR; La Bella V; Volanti P; Simone I; Salvi F; Logullo FO; Nilo R; Battistini S; Mandrioli J; Tanel R; Murru MR; Mandich P; Zollino M; Conforti FL; Brunetti M; Barberis M; Restagno G; Penco S; Lunetta C; ITALSGEN Consortium
[Ad] Address:ALS Center, 'Rita Levi Montalcini' Department of Neuroscience, Neurology II, University of Torino, Torino, Italy; Azienda Ospedaliero-Universitaria Città della Salute e della Scienza, Torino, Italy. Electronic address: achio@usa.net....
[Ti] Title:CHCH10 mutations in an Italian cohort of familial and sporadic amyotrophic lateral sclerosis patients.
[So] Source:Neurobiol Aging;36(4):1767.e3-6, 2015 Apr.
[Is] ISSN:1558-1497
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mutations in CHCHD10 have recently been described as a cause of frontotemporal dementia (FTD) comorbid with amyotrophic lateral sclerosis (ALS). The aim of this study was to assess the frequency and clinical characteristics of CHCHD10 mutations in Italian patients diagnosed with familial (n = 64) and apparently sporadic ALS (n = 224). Three apparently sporadic patients were found to carry c.100C>T (p.Pro34Ser) heterozygous variant in the exon 2 of CHCHD10. This mutation had been previously described in 2 unrelated French patients with FTD-ALS. However, our patients had a typical ALS, without evidence of FTD, cerebellar or extrapyramidal signs, or sensorineural deficits. We confirm that CHCHD10 mutations account for ∼1% of Italian ALS patients and are a cause of disease in subjects without dementia or other atypical clinical signs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 183732 MEDLINE  
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[PMID]: 25810899
[Au] Autor:Fujimoto K; Kurokawa R
[Ad] Address:Division of Gene Structure and Function, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane, Hidaka-shi, Saitama, 350-1241 Japan.
[Ti] Title:Development of a mouse monoclonal antibody for the detection of asymmetric dimethylarginine of Translocated in LipoSarcoma/FUsed in Sarcoma and its application in analyzing methylated TLS.
[So] Source:Cell Biosci;4:77, 2014.
[Is] ISSN:2045-3701
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: RNA-binding protein Translocated in LipoSarcoma/FUsed Sarcoma (TLS/FUS) is one of causative genes for familial amyotrophic lateral sclerosis (ALS). We previously identified that TLS was associated with protein arginine methyltransferase 1 (PRMT1), and four arginine residues within TLS (R216, R218, R242 and R394) were consistently dimethylated. Protein arginine methylation is involved in various cellular events such as signal transduction, transcriptional regulation and protein-protein interactions. RESULTS: To understand the biological role of arginine methylation of RNA-binding protein, we prepared and characterized a mouse monoclonal antibody against asymmetric dimethylarginine of TLS. By cloning and screening, one stable hybridoma cell clone (2B12) producing anti-asymmetric dimethylated TLS on R216 and R218 antibody was established. The monoclonal antibody 2B12 is specific for the asymmetrically dimethylated arginine peptide and does not react with the same peptide sequence containing unmodified and symmetrically dimethylated arginine residues by dot-blot analysis. 2B12 was also validated GST tagged TLS with PRMT1 by in vitro arginine methylation assays. Since methylated TLS in HeLa cells and mouse and human brain protein extracts was immunoprecipitated with 2B12, we performed RNA-binding protein immunoprecipitation assays using HeLa cell lysate and this antibody. We demonstrated that the long noncoding RNA (lncRNA) transcribed from cyclin D1 promoter binds methylated TLS. CONCLUSIONS: A monoclonal antibody that is capable of detecting the methylarginine status of TLS will facilitate the molecular and cellular analysis of transcriptional regulation by lncRNA through methylated TLS, and can be used as a favorable tool for clinical diagnosis of ALS caused by TLS dysregulation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150326
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1186/2045-3701-4-77

  10 / 183732 MEDLINE  
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[PMID]: 25541297
[Au] Autor:Roddy KA; Boulter CA
[Ad] Address:School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, UK.
[Ti] Title:Targeted mutation of NOV/CCN3 in mice disrupts joint homeostasis and causes osteoarthritis-like disease.
[So] Source:Osteoarthritis Cartilage;23(4):607-15, 2015 Apr.
[Is] ISSN:1522-9653
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The matricellular protein NOV/CCN3, is implicated in osteoarthritis (OA) and targeted mutation of NOV in mice (Nov(del3)) leads to joint abnormalities. This investigation tested whether NOV is required for joint homeostasis and if its disruption causes joint degeneration. METHOD: NOV expression in the adult mouse joint was characterized by immunohistochemistry. A detailed comparison of the joints of Nov(del3)-/- and Nov(del3)+/+ (wild-type) males and females at 2, 6 and 12 months of age was determined by X-ray, histology and immunohistochemistry. RESULTS: NOV protein was found in specific cells in articular cartilage, meniscus, synovium and ligament attachment sites in adult knees. Nov(del3)-/- males exhibited severe OA-like pathology at 12 months (OARSI score 5.0 ± 0.5, P < 0.001), affecting all tissues of the joint: erosion of the articular cartilage, meniscal enlargement, osteophytic outgrowths, ligament degeneration and expansion of fibrocartilage. Subchondral sclerosis and changes in extracellular matrix composition consistent with OA, were also seen. The density of articular cartilage cells in Nov(del3)+/+ knee joints is maintained at a constant level from 2 to 12 months of age whereas this is not the case in Nov(del3)-/- mice. Compared with age and sex-matched Nov(del3)+/+ mice, a significant increase in articular cartilage density was seen in Nov(del3)-/- males at 2 months, whereas a significant decrease was seen at 6 and 12 months in both Nov(del3)-/- males and females. CONCLUSION: NOV is required for the maintenance of articular cartilage and for joint homeostasis, with disruption of NOV in ageing Nov(del3)-/- male mice causing OA-like disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review


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