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Find video protocols related to scientific articles indexed in Pubmed.
Anticyclic Citrullinated Peptide Antibodies in Rheumatoid and Nonrheumatoid Rheumatic Disorders: Experience with 1162 Patients.
J. Rheumatol.
PUBLISHED: 10-03-2014
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Anticyclic citrullinated peptide antibodies (anti-CCP) are considered specific markers of rheumatoid arthritis (RA) and have been included in the revised classification criteria for RA diagnosis. However, these antibodies have also been detected in patients with other types of chronic inflammatory rheumatism. Our objectives were to identify the prevalence of positive anti-CCP patients in non-RA diseases, to determine the diagnostic value of anti-CCP for the diagnosis of RA, to specify the clinical characteristics of non-RA patients positive for anti-CCP, and to determine the discriminatory value of the levels of anti-CCP in patients among the various diseases.
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Rheumatic and musculoskeletal features of whipple disease: a report of 29 cases.
J. Rheumatol.
PUBLISHED: 11-01-2013
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Whipple disease is a rare infection caused by Tropheryma whipplei. Although patients commonly complain of osteoarticular involvement, musculoskeletal manifestations have been poorly described. We report cases of Whipple disease with rheumatic symptoms and describe their clinical presentation, modes of diagnosis, and outcomes.
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Radiological peripheral involvement in a cohort of patients with polyarticular juvenile idiopathic arthritis at adulthood.
J. Rheumatol.
PUBLISHED: 02-15-2013
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Radiographic damage was recently identified as a feature of poor prognosis in polyarticular juvenile idiopathic arthritis (pJIA). However, most radiographic studies did not differentiate pJIA from other subtypes of JIA and little is known about pJIA persisting into adulthood. We describe radiological peripheral involvement in young adults with pJIA compared to patients with rheumatoid arthritis (RA).
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Association study of CRP gene in systemic sclerosis in European Caucasian population.
Rheumatol. Int.
PUBLISHED: 01-08-2013
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Opsonization and apoptotic cell elements are critical in systemic lupus erythematosus (SLE) and could act through the activation of the innate immunity. C-reactive protein (CRP) belongs to opsonins, and polymorphisms of CRP gene have been shown to be associated with SLE susceptibility. Accumulating evidences show that SLE and systemic sclerosis (SSc) share some genetic susceptibility factors. To determine whether polymorphisms of CRP confer susceptibility to SSc, four SNPs (rs1130864, rs1205, rs1800947 and rs1341665), chosen using Hapmap linkage disequilibrium data and published data, were genotyped in a cohort of 651 SSc patients (569 with antinuclear antibodies, 258 with anti-centromere and 153 with anti-topoisomerase I) and 442 controls. All individuals were of French Caucasian origin. The four polymorphisms were in Hardy-Weinberg equilibrium in the control population. Allelic and genotypic frequencies for these four polymorphisms were found to be similar in SSc patients and controls. Moreover, subphenotype analyses in particular for subgroups having antinuclear antibodies did not detect any difference between SSc patients and controls. These results obtained through a large cohort of European Caucasian SSc patients do not support the implication of CRP gene in the pathogenesis of SSc.
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Association study of B-cell marker gene polymorphisms in European Caucasian patients with systemic sclerosis.
Clin. Exp. Rheumatol.
PUBLISHED: 04-07-2011
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BANK1 and BLK B-cell genetic markers have been reproducibly and convincingly found to contribute to susceptibility to systemic sclerosis (SSc).
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Genome-wide scan identifies TNIP1, PSORS1C1, and RHOB as novel risk loci for systemic sclerosis.
PLoS Genet.
PUBLISHED: 04-05-2011
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Systemic sclerosis (SSc) is an orphan, complex, inflammatory disease affecting the immune system and connective tissue. SSc stands out as a severely incapacitating and life-threatening inflammatory rheumatic disease, with a largely unknown pathogenesis. We have designed a two-stage genome-wide association study of SSc using case-control samples from France, Italy, Germany, and Northern Europe. The initial genome-wide scan was conducted in a French post quality-control sample of 564 cases and 1,776 controls, using almost 500 K SNPs. Two SNPs from the MHC region, together with the 6 loci outside MHC having at least one SNP with a P<10(-5) were selected for follow-up analysis. These markers were genotyped in a post-QC replication sample of 1,682 SSc cases and 3,926 controls. The three top SNPs are in strong linkage disequilibrium and located on 6p21, in the HLA-DQB1 gene: rs9275224, P?=?9.18×10(-8), OR?=?0.69, 95% CI [0.60-0.79]; rs6457617, P?=?1.14×10(-7) and rs9275245, P?=?1.39×10(-7). Within the MHC region, the next most associated SNP (rs3130573, P?=?1.86×10(-5), OR?=?1.36 [1.18-1.56]) is located in the PSORS1C1 gene. Outside the MHC region, our GWAS analysis revealed 7 top SNPs (P<10(-5)) that spanned 6 independent genomic regions. Follow-up of the 17 top SNPs in an independent sample of 1,682 SSc and 3,926 controls showed associations at PSORS1C1 (overall P?=?5.70×10(-10), OR:1.25), TNIP1 (P?=?4.68×10(-9), OR:1.31), and RHOB loci (P?=?3.17×10(-6), OR:1.21). Because of its biological relevance, and previous reports of genetic association at this locus with connective tissue disorders, we investigated TNIP1 expression. A markedly reduced expression of the TNIP1 gene and also its protein product were observed both in lesional skin tissue and in cultured dermal fibroblasts from SSc patients. Furthermore, TNIP1 showed in vitro inhibitory effects on inflammatory cytokine-induced collagen production. The genetic signal of association with TNIP1 variants, together with tissular and cellular investigations, suggests that this pathway has a critical role in regulating autoimmunity and SSc pathogenesis.
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Outcomes of Barretts oesophagus related to systemic sclerosis: a 3-year EULAR Scleroderma Trials and Research prospective follow-up study.
Rheumatology (Oxford)
PUBLISHED: 03-16-2011
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Barretts oesophagus (BE) is the major risk factor for oesophageal adenocarcinoma (EAC). SSc is associated with an increased risk of BE related to chronic reflux. The aim of this study is to determine the outcomes of BE and estimate the EAC risk in SSc patients over a 3-year prospective study.
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Association study of ITGAM, ITGAX, and CD58 autoimmune risk loci in systemic sclerosis: results from 2 large European Caucasian cohorts.
J. Rheumatol.
PUBLISHED: 03-01-2011
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Accumulating evidence shows that shared autoimmunity is critical for the pathogenesis of many autoimmune diseases. Systemic sclerosis (SSc) belongs to the connective tissue disorders, and recent data have highlighted strong associations with autoimmunity genes shared with other autoimmune diseases. To determine whether novel risk loci associated with systemic lupus erythematosus or multiple sclerosis may confer susceptibility to SSc, we tested single-nucleotide polymorphisms (SNP) from ITGAM, ITGAX, and CD58 for associations.
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Chronic recurrent multifocal osteomyelitis.
Joint Bone Spine
PUBLISHED: 01-06-2011
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Chronic recurrent multifocal osteomyelitis (CRMO), also known as chronic nonbacterial osteomyelitis, is an orphan disease that manifests as recurrent flares of inflammatory bone pain with or without a fever. The pain is related to one or more foci of nonbacterial osteomyelitis. To distinguish unifocal CRMO from a tumor or an infection, a bone biopsy is required in nearly all patients and a trial of antibiotic therapy in many. CRMO is now considered the pediatric equivalent of SAPHO syndrome, and recent data suggest that CRMO should be classified among the autoinflammatory diseases. The treatment of CRMO is not standardized. Although no randomized placebo-controlled trials are available, there is general agreement that nonsteroidal antiinflammatory drugs constitute the best first-line treatment and that bisphosphonates and biotherapies such as TNF? antagonists are effective in the most severe forms. Although CRMO is considered a benign disease, recent data suggest an up to 50% rate of residual impairments despite optimal management.
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Association study of serotonin transporter gene (SLC6A4) in systemic sclerosis in European Caucasian populations.
J. Rheumatol.
PUBLISHED: 04-15-2010
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Serotonin is a key contributing factor in pulmonary arterial hypertension (PAH) by inducing pulmonary arterial smooth muscle cell (PA-SMC) proliferation. This relates specifically to the internalization process in PA-SMC of the serotonin transporter (SLC6A4 or 5-HTT). A long (L)/short (S) (44 base pair insertion) functional polymorphism within the promoter of the transporter SLC6A4 gene has been reported to be associated with familial and idiopathic PAH. Our objective was to determine whether polymorphisms of SLC6A4 confer susceptibility to SSc and its vascular phenotype.
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Phenotype-haplotype correlation of IRF5 in systemic sclerosis: role of 2 haplotypes in disease severity.
J. Rheumatol.
PUBLISHED: 03-15-2010
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Identification of an association between IRF5 rs2004640 and systemic sclerosis (SSc) has highlighted a key role for type 1 interferon (IFN). Additional functional IRF5 variants have been identified as autoimmune susceptibility factors. Our aim was to investigate whether IRF5 haplotypes confer susceptibility to SSc, and to perform genotype haplotype-phenotype correlation analyses.
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Coccidioidomycosis of the spine in an immunocompetent patient.
Joint Bone Spine
PUBLISHED: 02-24-2010
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Coccidioidomycosis is a fungal disease caused by inhalation of airborne particles of Coccidioides spp. Coccidioidomycosis is endemic in several parts of the South-western US and South America. There are no symptoms in 60% of cases and, when symptoms exist, they usually consist of mild flu-like manifestations or mild lung disease. Disseminated coccidioidomycosis accounts for only 5% of symptomatic cases but can be life-threatening. The main targets of disseminated coccidioidomycosis are the skin, lymphoid tissue, central nervous system, and musculoskeletal system. Prolonged antifungal therapy is required and some patients may need surgical debridement. We report a case of disseminated spinal coccidioidomycosis in an immunocompetent patient.
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Association of metalloproteinase gene polymorphisms with systemic sclerosis in the European Caucasian population.
J. Rheumatol.
PUBLISHED: 01-28-2010
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Systemic sclerosis (SSc) is classified among the complex genetic disorders and is characterized by massive extracellular matrix deposits. These may be due to overactivation of transforming growth factor ss that may be in part a result of abnormal remodeling of extracellular matrix and microfibrils. Metalloproteinases (MMP) are a family of proteolytic enzymes, and MMP 2, 9, and 14 contribute to the degradation of microfibrils. Our aim was to determine whether polymorphisms of the MMP2, MMP9, and MMP14 genes confer susceptibility to SSc in a large population.
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Pulmonary arterial hypertension occurrence after liver transplant in systemic sclerosis: a report of 2 cases sustainably treated by sildenafil.
Clin. Exp. Rheumatol.
PUBLISHED: 01-12-2010
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We present the unusual cases of 2 systemic sclerosis patients with a history of liver transplant, who developed pulmonary hypertension in the course of their diseases. Sildenafil was the preferred pulmonary arterial hypertension drug because of its safety within this context. Clinical and functional responses were good, with a follow-up of more than 2 years.
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[Interactions between fibrillin-1 and tgf-beta: consequences and human pathology].
Med Sci (Paris)
PUBLISHED: 02-26-2009
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Fibrillin-1 (FBN-1) is the main component of the 10-12 nm microfibrils found in the extracellular matrix (ECM). ECM displays a structural role in the tissue-specific organization and takes part in the regulation of various cytokines and growth factors. A growing body of evidences supports a narrow relationship between FBN-1 and TGF-beta. Homology between FBN-1 and latent TGF-beta (LTGF) allows microfibrills to be a reservoir for this cytokine. The Marfan syndrome (MFS), a prototypic fibrillinopathy, highlights these relationships as it relates to 2 major genes that are FBN1 and TGF-beta type II receptor (TGFBR2) genes. In a mouse model of MFS, an up-regulation of the TGF-beta pathway is partly responsible for the phenotype. This FBN-1/TGF-beta relationship may play also a role in systemic sclerosis (SSc), a multigenic disease characterized by excessive generalised ECM deposit. Indeed, two related animal models results from both gene mutations: the Tight Skin 1 mouse is due to a partial in-frame duplication of the Fbn1 gene and another model conditionally overexpresses TGF-beta type I receptor. A better understanding of FBN-1/TGF-beta relationship appears of great importance in fibrillinopathies: it may allow reconsidering the nosologic framework of these diseases including the TGF-beta signalopathies and could lead to innovative therapeutic strategies.
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Angiotensin-converting enzyme gene does not contribute to genetic susceptibility to systemic sclerosis in European Caucasians.
J. Rheumatol.
PUBLISHED: 01-10-2009
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To determine whether angiotensin-converting enzyme (ACE) polymorphisms including I/D and 2 single-nucleotide polymorphisms (SNP) affect susceptibility to systemic sclerosis (SSc) in a large French Caucasian population.
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Prostaglandin transporter mutations cause pachydermoperiostosis with myelofibrosis.
Hum. Mutat.
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Pachydermoperiostosis, or primary hypertrophic osteoarthropathy (PHO), is an inherited multisystem disorder, whose features closely mimic the reactive osteoarthropathy that commonly accompanies neoplastic and inflammatory pathologies. We previously described deficiency of the prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (HPGD) as a cause of this condition, implicating elevated circulating prostaglandin E(2) (PGE(2)) as causative of PHO, and perhaps also as the principal mediator of secondary HO. However, PHO is genetically heterogeneous. Here, we use whole-exome sequencing to identify recessive mutations of the prostaglandin transporter SLCO2A1, in individuals lacking HPGD mutations. We performed exome sequencing of four probands with severe PHO, followed by conventional mutation analysis of SLCO2A1 in nine others. Biallelic SLCO2A1 mutations were identified in 12 of the 13 families. Affected individuals had elevated urinary PGE(2), but unlike HPGD-deficient patients, also excreted considerable quantities of the PGE(2) metabolite, PGE-M. Clinical differences between the two groups were also identified, notably that SLCO2A1-deficient individuals have a high frequency of severe anemia due to myelofibrosis. These findings reinforce the key role of systemic or local prostaglandin excess as the stimulus to HO. They also suggest that the induction or maintenance of hematopoietic stem cells by prostaglandin may depend upon transporter activity.
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Radiological cervical spine involvement in young adults with polyarticular juvenile idiopathic arthritis.
Rheumatology (Oxford)
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Radiological cervical spine involvement in JIA has already been assessed with a large range of prevalence (5-80%), but most studies were performed a long time ago, in symptomatic JIA and without differentiating subsets of JIA. We set out to describe structural cervical spine involvement in young adults with polyarticular JIA (pJIA) regardless of the cervical symptoms and to compare lesions with those observed in adult RA.
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Safety of rituximab in rheumatoid arthritis: a long-term prospective single-center study of gammaglobulin concentrations and infections.
Joint Bone Spine
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Rituximab seems well tolerated in patients with rheumatoid arthritis (RA). However, variations in the gammaglobulin profile that might increase the infection risk have been reported. Here, our objective was to evaluate gammaglobulin concentrations and the infection risk in patients receiving rituximab therapy for RA in everyday practice.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.