Database : MEDLINE
Search on : Sclerosis [Words]
References found : 177245 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 17725 go to page                         

  1 / 177245 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 25152817
[Au] Autor:Dimisianos N; Rodi M; Kalavrizioti D; Georgiou V; Papathanasopoulos P; Mouzaki A
[Ad] Address:Department of Neurology, Patras University Hospital, 26500 Patras, Greece....
[Ti] Title:Cytokines as Biomarkers of Treatment Response to IFN ß in Relapsing-Remitting Multiple Sclerosis.
[So] Source:Mult Scler Int;2014:436764, 2014.
[Is] ISSN:2090-2654
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:Background. MS patients show a remarkable heterogeneity in their response to disease modifying treatments. Given the need for early treatment initiation and the diversity of available options, a predictive marker that indicates good or poor response to treatment is highly desirable. Objective. To find a biomarker for treatment response to IFNß among pro- and anti-inflammatory cytokines. Materials and Methods. IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10, IL-17A, and TGF-ß1 levels were measured in serum and CSF of 43 patients with RR-MS who were followed up for a mean period of 5.3 years. Thirty-five patients received IFNß treatment and were divided into good responders (GR, n = 19) and poor responders (PR, n = 16). The remaining 8 patients showed a very favorable outcome and remained untreated (noRx). Results. GR had significantly higher serum baseline levels of IL-17A than PR and significantly higher serum levels of IL-17A, IFN-γ, TNF-α, and IL-2 than noRx. PR had significantly higher IFN-γ serum levels than noRx. No significant differences were observed in serum levels of IL-6, IL-4, IL-10, and TGF-ß1 or the levels of all cytokines measured in CSF between the 3 groups of patients. Conclusions. Baseline serum levels of IL-17A can be used as a biomarker of IFNß treatment response.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Da] Date of entry for processing:140825
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2014/436764

  2 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25151007
[Au] Autor:McPherson RC; Cambrook HE; O'Connor RA; Anderton SM
[Ad] Address:MRC Centre for Inflammation Research and Centre for Multiple Sclerosis Research, Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.
[Ti] Title:Induction of Passive EAE Using Myelin-Reactive CD4+ T Cells.
[So] Source:Methods Mol Biol;1193:187-98, 2014.
[Is] ISSN:1940-6029
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Experimental autoimmune encephalomyelitis (EAE) is an autoimmune disease of the central nervous system (CNS) often used as a model for the early inflammatory stages of multiple sclerosis and also as a model of organ-specific autoimmune disease.This protocol describes the induction of passive EAE in mice, either using T cells isolated from mice primed with myelin antigens, or through the use of naïve TCR transgenic T cells activated in vitro in the presence of myelin-derived antigens.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/978-1-4939-1212-4_17

  3 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 24184699
[Au] Autor:Sanseverino I; Rinaldi AO; Purificato C; Cortese A; Millefiorini E; Gessani S; Gauzzi MC
[Ad] Address:Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, 00161 Rome, Italy....
[Ti] Title:CCL2 induction by 1,25(OH)2D3 in dendritic cells from healthy donors and multiple sclerosis patients.
[So] Source:J Steroid Biochem Mol Biol;144:102-5, 2014 Oct.
[Is] ISSN:1879-1220
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:CCL2 plays a pivotal role in the recruitment of different immune cells to sites of inflammation and evidence indicates its involvement in multiple sclerosis (MS) pathogenesis. MS lesions are characterized by an inflammatory infiltrate, whose nature is controlled by chemokines and cytokines, and elevated expression of CCL2 has been found in acute and chronic MS plaques within the brain. Vitamin D deficiency is currently considered one of the main environmental MS risk factors. In this study we analyzed the role of 1,25(OH)2D3, the bioactive vitamin D metabolite, in the regulation of CCL2 expression by dendritic cells (DC) obtained from healthy donors and relapsing-remitting MS patients. We report that 1,25(OH)2D3, as well as 25OHD3, its main blood precursor, induce the secretion of high levels of CCL2. 1,25(OH)2D3-induced CCL2 levels are comparable to those secreted in response to a classical DC maturation stimulus. Moreover, we observed that 1,25(OH)2D3 is able to induce a significant CCL2 secretion in DC obtained from relapsing-remitting MS patients, although CCL2 levels in these latter are lower with respect to healthy controls. The cause(s) of this apparently defective response of DC from patients and its consequences in the context of MS remain to be elucidated. However, we propose CCL2 as a molecular player contributing to the immunomodulatory activity of 1,25(OH)2D3 on DC, and hypothesize a role for this chemokine in the response of MS patients to vitamin D therapy. This article is part of a Special Issue entitled '16th Vitamin D Workshop'.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 24642042
[Au] Autor:Wayman D; Carmody KA
[Ad] Address:Department of Emergency Medicine, Boston University School of Medicine, Boston, Massachusetts.
[Ti] Title:Optic neuritis diagnosed by bedside emergency physician-performed ultrasound: a case report.
[So] Source:J Emerg Med;47(3):301-5, 2014 Sep.
[Is] ISSN:0736-4679
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Optic neuritis is an inflammatory demyelinating condition of the optic nerve that causes subacute visual loss. It is often the result of an underlying systemic condition, such as multiple sclerosis. Due to the possible long-term morbidity associated with this condition, it is essential that the emergency physician recognizes the diagnosis and expedites treatment. OBJECTIVE: This case report describes optic neuritis diagnosed at the bedside by emergency physician-performed ultrasound. CASE REPORT: This is a case report of a young man presenting with unilateral painful vision loss. Optic neuritis must be considered in the differential diagnosis of any young patient who presents with visual complaints without any other neurologic findings. This report is unique because there are very few cases describing the findings of optic neuritis on emergency physician-performed bedside ultrasound in the literature. CONCLUSIONS: This article presents the case, describes diagnostic modalities, especially the use of ultrasound in its diagnosis, and the course of treatment for this particular condition.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25152710
[Au] Autor:Jansen AH; Reits EA; Hol EM
[Ad] Address:Department of Cell Biology and Histology, Academic Medical Center Amsterdam, Netherlands.
[Ti] Title:The ubiquitin proteasome system in glia and its role in neurodegenerative diseases.
[So] Source:Front Mol Neurosci;7:73, 2014.
[Is] ISSN:1662-5099
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The ubiquitin proteasome system (UPS) is crucial for intracellular protein homeostasis and for degradation of aberrant and damaged proteins. The accumulation of ubiquitinated proteins is a hallmark of many neurodegenerative diseases, including amyotrophic lateral sclerosis, Alzheimer's, Parkinson's, and Huntington's disease, leading to the hypothesis that proteasomal impairment is contributing to these diseases. So far, most research related to the UPS in neurodegenerative diseases has been focused on neurons, while glial cells have been largely disregarded in this respect. However, glial cells are essential for proper neuronal function and adopt a reactive phenotype in neurodegenerative diseases, thereby contributing to an inflammatory response. This process is called reactive gliosis, which in turn affects UPS function in glial cells. In many neurodegenerative diseases, mostly neurons show accumulation and aggregation of ubiquitinated proteins, suggesting that glial cells may be better equipped to maintain proper protein homeostasis. During an inflammatory reaction, the immunoproteasome is induced in glia, which may contribute to a more efficient degradation of disease-related proteins. Here we review the role of the UPS in glial cells in various neurodegenerative diseases, and we discuss how studying glial cell function might provide essential information in unraveling mechanisms of neurodegenerative diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1408
[Da] Date of entry for processing:140825
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.3389/fnmol.2014.00073

  6 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 24726090
[Au] Autor:Armstrong ZB; Boughner DR; Carruthers CP; Drangova M; Rogers KA
[Ad] Address:Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada....
[Ti] Title:Effects of an Angiotensin II Type 1 Receptor Blocker on Aortic Valve Sclerosis in a Preclinical Model.
[So] Source:Can J Cardiol;30(9):1096-103, 2014 Sep.
[Is] ISSN:1916-7075
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Aortic valve sclerosis (AVS) is a chronic progressive disease involving lipid infiltration, inflammation, and tissue calcification. Despite its high prevalence, there are currently no clinically approved pharmaceuticals for the management of AVS. The objective of the current study was to elucidate the effects of an angiotensin II type 1 receptor blocker, alone or in combination with statin therapy, on the progression of AVS. METHODS: Male New Zealand white rabbits were fed an atherogenic diet for a period of 12 months to induce AVS. Once disease was established, rabbits were randomly assigned to receive no treatment, olmesartan medoxomil, atorvastatin calcium, or a combination of both drugs for a period of 6 months. Disease progression was monitored in vivo using clinically relevant magnetic resonance imaging, and aortic valve cusps were examined ex vivo using histologic and immunohistochemical methods. RESULTS: Cusp thickness significantly increased (0.58 ± 0.03 vs 0.39 ± 0.03 mm for cholesterol and control animals, respectively; P < 0.0001) and all classic hallmarks of disease progression-including lipid infiltration, inflammation, and tissue calcification-were observed after 12 months. Unfortunately, neither olmesartan medoxomil nor atorvastatin calcium were able to reverse or delay disease progression during the 6-month treatment period. However, several histologic changes were observed in the valvular microenvironment. CONCLUSIONS: The current study suggests that angiotensin receptor blockers, alone or in combination with statin therapy, may not be suitable for management of clinical AVS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25151395
[Au] Autor:Chen HL; Liao F; Lin TN; Liu FT
[Ad] Address:Institute of Biomedical Sciences, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei, Taiwan.
[Ti] Title:Galectins and neuroinflammation.
[So] Source:Adv Neurobiol;9:517-42, 2014.
[Is] ISSN:2190-5215
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Galectins, ß-galactoside-binding lectins, play multiple roles in the regulation of immune and inflammatory responses. The major galectins expressed in the CNS are galectins 1, 3, 4, 8, and 9. Under normal physiological conditions, galectins maintain CNS homeostasis by participating in neuronal myelination, neuronal stem cell proliferation, and apical vesicle transport in neuronal cells. In neuronal diseases and different experimental neuroinflammatory disease models, galectins may serve as extracellular mediators or intracellular regulators in controlling the inflammatory response or conferring the remodeling capacity in damaged CNS tissues. In general, galectins 1 and 9 attenuate experimental autoimmune encephalomyelitis (a model of multiple sclerosis), while galectin-3 promotes inflammation in this model. In brain ischemic lesions, both galectins 1 and 3 are induced to help neuronal regeneration. The expression of galectin-1 is required for astrocyte-derived neurotrophic factor secretion, and recombinant galectin-1 promotes neuronal regeneration. Galectin-3 promotes microglial cell proliferation and attenuates ischemic damage and neuronal apoptosis after cerebral ischemia. In amyotrophic lateral sclerosis models, galectin-3 is deleterious to neuroregeneration, while intramuscular administration of oxidized galectin-1 can improve neuromuscular disorders. In axotomy and Wallerian degeneration, galectin-3 helps phagocytosis of macrophages to clear degenerate myelin in the injured PNS or CNS. Thus, galectins are important modulators participating in homeostasis of the CNS and neuroinflammation. Continued investigations of the roles of galectins in neuroinflammation promise to provide a better understanding of the mechanism of this process and lead to new therapeutic approaches.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/978-1-4939-1154-7_24

  8 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25148523
[Au] Autor:Wang MD; Gomes J; Cashman NR; Little J; Krewski D
[Ad] Address:Department of Epidemiology and Community Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada....
[Ti] Title:Intermediate CAG Repeat Expansion in the ATXN2 Gene Is a Unique Genetic Risk Factor for ALS-A Systematic Review and Meta-Analysis of Observational Studies.
[So] Source:PLoS One;9(8):e105534, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Amyotrophic lateral sclerosis (ALS) is a rare degenerative condition of the motor neurons. Over 10% of ALS cases are linked to monogenic mutations, with the remainder thought to be due to other risk factors, including environmental factors, genetic polymorphisms, and possibly gene-environmental interactions. We examined the association between ALS and an intermediate CAG repeat expansion in the ATXN2 gene using a meta-analytic approach. Observational studies were searched with relevant disease and gene terms from MEDLINE, EMBASE, and PsycINFO from January 2010 through to January 2014. All identified articles were screened using disease terms, gene terms, population information, and CAG repeat information according to PRISMA guidelines. The final list of 17 articles was further evaluated based on the study location, time period, and authors to exclude multiple usage of the same study populations: 13 relevant articles were retained for this study. The range 30-33 CAG repeats in the ATXN2 gene was most strongly associated with ALS. The meta-analysis revealed that the presence of an intermediate CAG repeat (30-33) in the ATXN2 gene was associated with an increased risk of ALS [odds ratio (OR) = 4.44, 95%CI: 2.91-6.76)] in Caucasian ALS patients. There was no significant difference in the association of this CAG intermediate repeat expansion in the ATXN2 gene between familial ALS cases (OR = 3.59, 1.58-8.17) and sporadic ALS cases (OR = 3.16, 1.88-5.32). These results indicate that the presence of intermediate CAG repeat expansion in the ATXN2 gene is a specific genetic risk factor for ALS, unlike monogenic mutations with an autosomal dominant transmission mode, which cause a more severe phenotype of ALS, with a higher prevalence in familial ALS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0105534

  9 / 177245 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25148387
[Au] Autor:Wuest SC; Mexhitaj I; Chai NR; Romm E; Scheffel J; Xu B; Lane K; Wu T; Bielekova B
[Ad] Address:Neuroimmunological Diseases Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America....
[Ti] Title:A complex role of herpes viruses in the disease process of multiple sclerosis.
[So] Source:PLoS One;9(8):e105434, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS). Neither the antigenic target(s) nor the cell population(s) responsible for CNS tissue destruction in MS have been fully defined. The objective of this study was to simultaneously determine the antigen (Ag)-specificity and phenotype of un-manipulated intrathecal CD4+ and CD8+ T cells of patients with relapsing-remitting and progressive MS compared to subjects with other inflammatory neurological diseases. We applied a novel Ag-recognition assay based on co-cultures of freshly obtained cerebrospinal fluid T cells and autologous dendritic cells pre-loaded with complex candidate Ag's. We observed comparably low T cell responses to complex auto-Ag's including human myelin, brain homogenate, and cell lysates of apoptotically modified oligodendroglial and neuronal cells in all cohorts and both compartments. Conversely, we detected a strong intrathecal enrichment of Epstein-Barr virus- and human herpes virus 6-specific (but not cytomegalovirus-specific) reactivities of the Th1-phenotype throughout all patients. Qualitatively, the intrathecal enrichment of herpes virus reactivities was more pronounced in MS patients. This enrichment was completely reversed by long-term treatment with the IL-2 modulating antibody daclizumab, which strongly inhibits MS disease activity. Finally, we observed a striking discrepancy between diminished intrathecal T cell proliferation and enhanced cytokine production of herpes virus-specific T cells among progressive MS patients, consistent with the phenotype of terminally differentiated cells. The data suggest that intrathecal administration of novel therapeutic agents targeting immune cells outside of the proliferation cycle may be necessary to effectively eliminate intrathecal inflammation in progressive MS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0105434

  10 / 177245 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 25148080
[Au] Autor:Zucchini S; Marucci G; Paradiso B; Lanza G; Roncon P; Cifelli P; Ferracin M; Giulioni M; Michelucci R; Rubboli G; Simonato M
[Ad] Address:Department of Medical Sciences, Section of Pharmacology and Neuroscience Center, University of Ferrara, Ferrara, Italy; National Institute of Neuroscience, Torino, Italy; Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy....
[Ti] Title:Identification of miRNAs Differentially Expressed in Human Epilepsy with or without Granule Cell Pathology.
[So] Source:PLoS One;9(8):e105521, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The microRNAs (miRNAs) are small size non-coding RNAs that regulate expression of target mRNAs at post-transcriptional level. miRNAs differentially expressed under pathological conditions may help identifying mechanisms underlying the disease and may represent biomarkers with prognostic value. However, this kind of studies are difficult in the brain because of the cellular heterogeneity of the tissue and of the limited access to fresh tissue. Here, we focused on a pathology affecting specific cells in a subpopulation of epileptic brains (hippocampal granule cells), an approach that bypasses the above problems. All patients underwent surgery for intractable temporal lobe epilepsy and had hippocampal sclerosis associated with no granule cell pathology in half of the cases and with type-2 granule cell pathology (granule cell layer dispersion or bilamination) in the other half. The expression of more than 1000 miRNAs was examined in the laser-microdissected dentate granule cell layer. Twelve miRNAs were differentially expressed in the two groups. One of these, miR487a, was confirmed to be expressed at highly differential levels in an extended cohort of patients, using RT-qPCR. Bioinformatics searches and RT-qPCR verification identified ANTXR1 as a possible target of miR487a. ANTXR1 may be directly implicated in granule cell dispersion because it is an adhesion molecule that favors cell spreading. Thus, miR487a could be the first identified element of a miRNA signature that may be useful for prognostic evaluation of post-surgical epilepsy and may drive mechanistic studies leading to the identification of therapeutic targets.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0105521


page 1 of 17725 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information