Database : MEDLINE
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[PMID]: 25005000
[Au] Autor:Kearse MG; Todd PK
[Ad] Address:Department of Neurology, University of Michigan Medical School, 4005 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA.
[Ti] Title:Repeat-Associated Non-AUG Translation and Its Impact in Neurodegenerative Disease.
[So] Source:Neurotherapeutics;11(4):721-31, 2014 Oct.
[Is] ISSN:1878-7479
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nucleotide repeat expansions underlie numerous human neurological disorders. Repeats can trigger toxicity through multiple pathogenic mechanisms, including RNA gain-of-function, protein gain-of-function, and protein loss-of-function pathways. Traditionally, inference of the underlying pathogenic mechanism derives from the repeat location, with dominantly inherited repeats within transcribed noncoding sequences eliciting toxicity predominantly as RNA via sequestration of specific RNA binding proteins. However, recent findings question this assumption and suggest that repeats outside of annotated open reading frames may also trigger toxicity through a novel form of protein translational initiation known as repeat-associated non-AUG (RAN) translation. To date, RAN translation has been implicated in 4 nucleotide repeat expansion disorders: spinocerebellar ataxia type 8; myotonic dystrophy type 1 with CTG•CAG repeats; C9orf72 amyotrophic lateral sclerosis/frontotemporal dementia with GGGGCC•GGCCCC repeats; and fragile X-associated tremor/ataxia syndrome with CGG repeats. RAN translation contributes to hallmark pathological characteristics in these disorders by producing homopolymeric or dipeptide repeat proteins. Here, we review what is known about RAN translation, with an emphasis on how differences in both repeat sequence and context may confer different requirements for unconventional initiation. We then discuss how this new mechanism of translational initiation might function in normal physiology and lay out a roadmap for addressing the numerous questions that remain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s13311-014-0292-z

  2 / 178927 MEDLINE  
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[PMID]: 25193661
[Au] Autor:Harari D; Kuhn N; Abramovich R; Sasson K; Zozulya AL; Smith P; Schlapschy M; Aharoni R; Kster M; Eilam R; Skerra A; Schreiber G
[Ad] Address:From the Departments of Biological Chemistry, daniel.harari@weizmann.ac.il....
[Ti] Title:Enhanced in Vivo Efficacy of a Type I Interferon Superagonist with Extended Plasma Half-life in a Mouse Model of Multiple Sclerosis.
[So] Source:J Biol Chem;289(42):29014-29, 2014 Oct 17.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:IFN is a common therapeutic option to treat multiple sclerosis. It is unique among the family of type I IFNs in that it binds to the interferon receptors with high affinity, conferring exceptional biological properties. We have previously reported the generation of an interferon superagonist (dubbed YNSα8) that is built on the backbone of a low affinity IFNα but modified to exhibit higher receptor affinity than even for IFN. Here, YNSα8 was fused with a 600-residue hydrophilic, unstructured N-terminal polypeptide chain comprising proline, alanine, and serine (PAS) to prolong its plasma half-life via "PASylation." PAS-YNSα8 exhibited a 10-fold increased half-life in both pharmacodynamic and pharmacokinetic assays in a transgenic mouse model harboring the human receptors, notably without any detectable loss in biological potency or bioavailability. This long-lived superagonist conferred significantly improved protection from MOG35-55-induced experimental autoimmune encephalomyelitis compared with IFN, despite being injected with a 4-fold less frequency and at an overall 16-fold lower dosage. These data were corroborated by FACS measurements showing a decrease of CD11b(+)/CD45(hi) myeloid lineage cells detectable in the CNS, as well as a decrease in IBA(+) cells in spinal cord sections determined by immunohistochemistry for PAS-YNSα8-treated animals. Importantly, PAS-YNSα8 did not induce antibodies upon repeated administration, and its biological efficacy remained unchanged after 21 days of treatment. A striking correlation between increased levels of CD274 (PD-L1) transcripts from spleen-derived CD4(+) cells and improved clinical response to autoimmune encephalomyelitis was observed, indicating that, at least in this mouse model of multiple sclerosis, CD274 may serve as a biomarker to predict the effectiveness of IFN therapy to treat this complex disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M114.602474

  3 / 178927 MEDLINE  
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[PMID]: 25183005
[Au] Autor:Liu X; He F; Pang R; Zhao D; Qiu W; Shan K; Zhang J; Lu Y; Li Y; Wang Y
[Ad] Address:From the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China....
[Ti] Title:Interleukin-17 (IL-17)-induced MicroRNA 873 (miR-873) Contributes to the Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting A20 Ubiquitin-editing Enzyme.
[So] Source:J Biol Chem;289(42):28971-86, 2014 Oct 17.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interleukin 17 (IL-17), produced mainly by T helper 17 (Th17) cells, is increasingly recognized as a key regulator in various autoimmune diseases, including human multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Although several microRNAs (miRNAs) with aberrant expression have been shown to contribute to the pathogenesis of MS and EAE, the mechanisms underlying the regulation of abnormal miRNA expression in astrocytes upon IL-17 stimulation remain unclear. In the present study, we detected the changes of miRNA expression profiles both in the brain tissue of EAE mice and in cultured mouse primary astrocytes stimulated with IL-17 and identified miR-873 as one of the co-up-regulated miRNAs in vivo and in vitro. The overexpression of miR-873, demonstrated by targeting A20 (TNFα-induced protein 3, TNFAIP3), remarkably reduced the A20 level and promoted NF-κB activation in vivo and in vitro as well as increasing the production of inflammatory cytokines and chemokines (i.e. IL-6, TNF-α, MIP-2, and MCP-1/5). More importantly, silencing the endogenous miR-873 or A20 gene with lentiviral vector of miR-873 sponge (LV-miR-873 sponge) or short hairpin RNA (shRNA) of A20 (LV-A20 shRNA) in vivo significantly lessened or aggravated inflammation and demyelination in the central nervous system (CNS) of EAE mice, respectively. Taken together, these findings indicate that miR-873 induced by IL-17 stimulation promotes the production of inflammatory cytokines and aggravates the pathological process of EAE mice through the A20/NF-κB pathway, which provides a new insight into the mechanism of inflammatory damage in MS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.M114.577429

  4 / 178927 MEDLINE  
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[PMID]: 24417588
[Au] Autor:Martinez NE; Karlsson F; Sato F; Kawai E; Omura S; Minagar A; Grisham MB; Tsunoda I
[Ad] Address:Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, LA.
[Ti] Title:Protective and detrimental roles for regulatory T cells in a viral model for multiple sclerosis.
[So] Source:Brain Pathol;24(5):436-51, 2014 Sep.
[Is] ISSN:1750-3639
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) has been proposed to be an immune-mediated disease in the central nervous system (CNS) that can be triggered by virus infections. In Theiler's murine encephalomyelitis virus (TMEV) infection, during the first week (acute stage), mice develop polioencephalomyelitis. After 3 weeks (chronic stage), mice develop immune-mediated demyelination with virus persistence, which has been used as a viral model for MS. Regulatory T cells (Tregs) can suppress inflammation, and have been suggested to be protective in immune-mediated diseases, including MS. However, in virus-induced inflammatory demyelination, although Tregs can suppress inflammation, preventing immune-mediated pathology, Tregs may also suppress antiviral immune responses, leading to more active viral replication and/or persistence. To determine the role and potential translational usage of Tregs in MS, we treated TMEV-infected mice with ex vivo generated induced Tregs (iTregs) on day 0 (early) or during the chronic stage (therapeutic). Early treatment worsened clinical signs during acute disease. The exacerbation of acute disease was associated with increased virus titers and decreased immune cell recruitment in the CNS. Therapeutic iTreg treatment reduced inflammatory demyelination during chronic disease. Immunologically, iTreg treatment increased interleukin-10 production from B cells, CD4(+) T cells and dendritic cells, which may contribute to the decreased CNS inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/bpa.12119

  5 / 178927 MEDLINE  
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[PMID]: 24286167
[Au] Autor:Manetti M; Guiducci S; Romano E; Avouac J; Rosa I; Ruiz B; Lepri G; Bellando-Randone S; Ibba-Manneschi L; Allanore Y; Matucci-Cerinic M
[Ti] Title:Decreased expression of the endothelial cell-derived factor EGFL7 in systemic sclerosis: potential contribution to impaired angiogenesis and vasculogenesis.
[So] Source:Arthritis Res Ther;15(5):R165, 2013.
[Is] ISSN:1478-6362
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Microvascular damage and defective angiogenesis and vasculogenesis have a major role in the pathogenesis of systemic sclerosis (SSc). Epidermal growth factor-like domain 7 (EGFL7) is a proangiogenic molecule which is predominantly expressed and secreted by endothelial cells and their progenitors and controls vascular development and integrity. In this study, we investigated the possible involvement of EGFL7 in SSc. METHODS: Serum EGFL7 levels from 60 patients with SSc and 35 age- and sex-matched healthy controls were examined by colorimetric sandwich enzyme-linked immunosorbent assay. The expression of EGFL7 in forearm skin biopsies (n = 16 SSc, n = 10 controls), cultured dermal microvascular endothelial cells (MVECs) (n = 3 SSc, n = 3 controls) and late-outgrowth peripheral blood endothelial progenitor cell (EPC)-derived endothelial cells (n = 15 SSc, n = 8 controls) was investigated by immunofluorescence and Western blotting. RESULTS: Serum EGFL7 levels were detectable in 68.6% of healthy controls and 45% of SSc cases (P < 0.05). Circulating levels of EGFL7 were significantly decreased in SSc patients compared with healthy controls (P = 0.01). Serum levels of EGFL7 were significantly lower in both limited cutaneous SSc and diffuse cutaneous SSc patients than in controls (P = 0.02 and P = 0.04, respectively). In SSc, decreased serum EGFL7 levels were significantly correlated with the severity of nailfold capillary abnormalities. Patients with the most severe capillary changes and digital ulcers had serum EGFL7 levels significantly lower than healthy controls, while the EGFL7 levels did not differ significantly between controls and SSc patients with less capillary damage and lack of digital ulcers. Endothelial EGFL7 expression was strongly downregulated or even almost completely undetectable in SSc-affected dermis compared with controls (P < 0.001). In cultured SSc dermal MVECs and late-outgrowth peripheral blood EPC-derived endothelial cells, EGFL7 was significantly downregulated compared with cells obtained from healthy subjects (P < 0.01 and P < 0.001, respectively). CONCLUSIONS: Our findings suggest that the loss of EGFL7 expression in endothelial cells and their progenitors might play a role in the development and progression of peripheral microvascular damage and the defective vascular repair process characteristic of SSc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/ar4349

  6 / 178927 MEDLINE  
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[PMID]: 25318088
[Au] Autor:Silva PG; Jones A; Araujo PM; Natour J
[Ad] Address:Disciplina de Reumatologia, Universidade Federal de So Paulo (UNIFESP), So Paulo, SP, Brazil....
[Ti] Title:Assessment of light touch sensation in the hands of systemic sclerosis patients.
[So] Source:Clinics (Sao Paulo);69(9):585-8, 2014 Sep.
[Is] ISSN:1980-5322
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Systemic sclerosis is a relatively rare connective tissue disorder characterized by severe and progressive fibrosis of the skin. Due to the current lack of available information on this subject, the aim of the present study was to assess light touch sensations in the hands of patients with systemic sclerosis. METHODS: We completed a cross-sectional comparative study. Light touch sensations were evaluated in 30 individuals, including 15 patients with systemic sclerosis who exhibited changes in the dermis of their hands without loss of the distal phalanx and 15 subjects who did not exhibit changes in the upper limbs (control group). The groups were age- and sex-matched. Tactile sensory evaluations were performed using the Semmes-Weinstein monofilament test and the two-point discrimination test. RESULTS: Statistically significant differences were found between groups in the monofilament test. The study group had lower scores across all points of the hand when compared with the control group. Differences were also found when dominant and non-dominant hands were compared (p<0.05). Statistically significant differences were found between groups for a subset of the assessed points in the two-point discrimination test. CONCLUSIONS: The results of a monofilament test showed that tactile sensation, specifically light touch and deep pressure sensations, is altered in the hands of systemic sclerosis patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 178927 MEDLINE  
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[PMID]: 25320567
[Au] Autor:Lee D; Arora G
[Ad] Address:Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
[Ti] Title:Medical management of fecal incontinence in challenging populations: a review.
[So] Source:Clin Colon Rectal Surg;27(3):91-8, 2014 Sep.
[Is] ISSN:1531-0043
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Fecal incontinence (FI) is a common and growing problem in the United States. Although there are multiple emerging novel interventions for the treatment of FI, the mainstay of initial therapy remains medical management. In this article, we review the available literature on the medical management of FI, with a special focus on patients with multiple sclerosis, diabetes mellitus, and the elderly.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1410
[Cu] Class update date: 141018
[Lr] Last revision date:141018
[Da] Date of entry for processing:141016
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1055/s-0034-1384661

  8 / 178927 MEDLINE  
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[PMID]: 25313834
[Au] Autor:Wang Y; Jin S; Sonobe Y; Cheng Y; Horiuchi H; Parajuli B; Kawanokuchi J; Mizuno T; Takeuchi H; Suzumura A
[Ad] Address:Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan....
[Ti] Title:Interleukin-1 induces blood-brain barrier disruption by downregulating sonic hedgehog in astrocytes.
[So] Source:PLoS One;9(10):e110024, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The blood-brain barrier (BBB) is composed of capillary endothelial cells, pericytes, and perivascular astrocytes, which regulate central nervous system homeostasis. Sonic hedgehog (SHH) released from astrocytes plays an important role in the maintenance of BBB integrity. BBB disruption and microglial activation are common pathological features of various neurologic diseases such as multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. Interleukin-1 (IL-1), a major pro-inflammatory cytokine released from activated microglia, increases BBB permeability. Here we show that IL-1 abolishes the protective effect of astrocytes on BBB integrity by suppressing astrocytic SHH production. Astrocyte conditioned media, SHH, or SHH signal agonist strengthened BBB integrity by upregulating tight junction proteins, whereas SHH signal inhibitor abrogated these effects. Moreover, IL-1 increased astrocytic production of pro-inflammatory chemokines such as CCL2, CCL20, and CXCL2, which induce immune cell migration and exacerbate BBB disruption and neuroinflammation. Our findings suggest that astrocytic SHH is a potential therapeutic target that could be used to restore disrupted BBB in patients with neurologic diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0110024

  9 / 178927 MEDLINE  
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[PMID]: 25317213
[Au] Autor:Wang J; Yi L; Guo X; He D; Li H; Guo G; Wang Y; Zou H; Gu Y; Tu W; Wu W; Yang L; Xiao R; Lai S; Assassi S; Mayes MD; Zhou X
[Ad] Address:Ministry of Education Key Laboratory of Contemporary Anthropology and State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, China ; Institute of Rheumatology, Immunology, and Allergy, Fudan University, China....
[Ti] Title:Lack of Association of the CD247 SNP rs2056626 with Systemic Sclerosis in Han Chinese.
[So] Source:Open Rheumatol J;8:43-5, 2014.
[Is] ISSN:1874-3129
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Systemic sclerosis (SSc) is a complex disease involving multiple genetic factors. A recent genome-wide association study (GWAS) indicated that CD247 was strongly associated with SSc, which was subsequently confirmed in a SSc cohort of European population. However, genetic heterogeneity in different ethnic populations may significantly impact the complex trait of SSc. The studies herein aimed to examine whether the SSc-associated SNP rs2056626 of CD247 identified in Caucasian is also associated with Han Chinese SSc. A Han Chinese cohort consisting of 387 SSc patients and 523 healthy controls were examined in the studies. TaqMan assays were performed to examine the SNP. Exact p-values were obtained (Fisher's test) from 2x2 tables of allele counts and disease status. The results showed that there was no association between rs2056626 of CD247 and SSc or any SSc subtypes of Han Chinese. The negative results are important in understanding genetics of SSc in different ethnic populations, which further suggest complex nature of genetics of SSc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Cu] Class update date: 141018
[Lr] Last revision date:141018
[Da] Date of entry for processing:141015
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.2174/1874312901408010043

  10 / 178927 MEDLINE  
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[PMID]: 25317296
[Au] Autor:Torabipour A; Asl ZA; Majdinasab N; Ghasemzadeh R; Tabesh H; Arab M
[Ad] Address:Department of Health Economic and Management, School of Public Health, Tehran University of Medical Sciences Tehran, Iran....
[Ti] Title:A study on the direct and indirect costs of multiple sclerosis based on expanded disability status scale score in khuzestan, iran.
[So] Source:Int J Prev Med;5(9):1131-8, 2014 Sep.
[Is] ISSN:2008-7802
[Cp] Country of publication:Iran
[La] Language:eng
[Ab] Abstract:BACKGROUND: Multiple sclerosis is a common and chronic neurologic disorder. This disorder imposes physical, economic, and psychosocial burden on individuals, their families and society. This study aims to analyze the costs of multiple sclerosis disease based on the severity of disability. METHODS: We performed a cross-sectional cost of illness study. This study was conducted in 332 patients of Khuzestan province of Iran. Data were included: Patient's characteristics, disability status, medical, and nonmedical costs and were gathered by using the questionnaire during 3 months period. Costs analysis was performed in the basis of expanded disability status scale (EDSS). Data were analyzed by using SPSS 18 software. RESULTS: Mean age of the patients was 33.5 (standard deviation [SD]: 9.1) and 70.5% of patients were female. Mean EDSS score of the patients was 2.2 (SD: 1.6). Most patients (92.1%) had relapsing remitting multiple sclerosis (MS) form of the disease. Costs mean per patients was 8.6 7.9 million Rial. The direct and indirect costs were 93.1% and 6.9% of total costs, respectively. The major cost of the disease belongs to the pharmaceutical treatment (22% of costs). The majority costs (approximately 62%) attributed to EDSS of 6-7 and >7. Furthermore, there was strong significant relationship between cost of illness and disability severity of patients (P < 0.05). CONCLUSIONS: Cost mean per MS patients was relatively high. Furthermore, the results showed that cost of disease had positive and significant relationships with EDSS score that is, progression of disability increase costs of patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Cu] Class update date: 141018
[Lr] Last revision date:141018
[Da] Date of entry for processing:141015
[St] Status:PubMed-not-MEDLINE


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