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Find video protocols related to scientific articles indexed in Pubmed.
Distribution pattern of MRI abnormalities within the knee and wrist of juvenile idiopathic arthritis patients: signature of disease activity.
AJR Am J Roentgenol
PUBLISHED: 04-25-2014
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The aim of this study in clinically active juvenile idiopathic arthritis (JIA) was to assess the frequency and distribution pattern of synovitis as hallmark of disease and additional soft-tissue and bony abnormalities on MRI in the knee and wrist as two target joints.
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Pixel-by-pixel analysis of DCE-MRI curve shape patterns in knees of active and inactive juvenile idiopathic arthritis patients.
Eur Radiol
PUBLISHED: 01-22-2014
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To compare DCE-MRI parameters and the relative number of time-intensity curve (TIC) shapes as derived from pixel-by-pixel DCE-MRI TIC shape analysis between knees of clinically active and inactive juvenile idiopathic arthritis (JIA) patients.
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One-year Followup Study on Clinical Findings and Changes in Magnetic Resonance Imaging-based Disease Activity Scores in Juvenile Idiopathic Arthritis.
J. Rheumatol.
PUBLISHED: 12-01-2013
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To evaluate whether clinical disease activity findings during 1-year followup of patients with juvenile idiopathic arthritis (JIA) is associated with changes of magnetic resonance imaging (MRI)-based disease activity scores.
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[Juvenile idiopathic arthritis: from biomarker to treatment].
Ned Tijdschr Geneeskd
PUBLISHED: 11-07-2013
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Juvenile idiopathic arthritis (JIA) is the most common cause of chronic joint inflammation in childhood. The aetiology is unknown and the pathogenesis is multifactorial. JIA manifests itself in many various ways. It is a diagnosis of exclusion: other disorders need to be ruled out for a diagnosis to be made. MRI examination is playing an increasingly important role in making a correct early diagnosis and in assessing response to therapy. After 6 months JIA patients are classified, based on clinical characteristics and laboratory results, into one of the JIA categories according to the criteria of the International League of Associations for Rheumatology. Recent developments in therapy, such as starting biological treatment at an early stage, have led to an improvement in the prognosis of JIA and to structural joint damage occurring less often.
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Contrast-enhanced MRI compared with the physical examination in the evaluation of disease activity in juvenile idiopathic arthritis.
Eur Radiol
PUBLISHED: 07-29-2013
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To assess the value of magnetic resonance imaging (MRI) in discriminating between active and inactive juvenile idiopathic arthritis (JIA) patients and to compare physical examination outcomes with MRI outcomes in the assessment of disease status in JIA patients.
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Treatment choices of paediatric rheumatologists for juvenile idiopathic arthritis: etanercept or adalimumab?
Rheumatology (Oxford)
PUBLISHED: 06-04-2013
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To evaluate differences in baseline characteristics between etanercept- and adalimumab-treated JIA patients and to reveal factors that influence the choice between these TNF inhibitors, which are considered equally effective in the recent ACR recommendations for JIA treatment.
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The diagnostic accuracy of unenhanced MRI in the assessment of joint abnormalities in juvenile idiopathic arthritis.
Eur Radiol
PUBLISHED: 02-01-2013
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To assess the diagnostic accuracy and reliability of MRI without contrast enhancement in the evaluation of JIA knee joint abnormalities.
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Aberrant humoral immune reactivity in DOCK8 deficiency with follicular hyperplasia and nodal plasmacytosis.
Clin. Immunol.
PUBLISHED: 01-29-2013
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Mutations in the DOCK8 gene define the most common form of autosomal-recessive Hyper-IgE-syndrome (AR-HIES/OMIM#243700). In a patient with extensive molluscum contagiosum lesions, a homozygous DOCK8 gene deletion was demonstrated. In-vivo 18-FDG uptake showed multiple non-enlarged lymph nodes without uptake in the spleen. Lymph node biopsies for subsequent immunohistochemistry showed clear differences with the mouse model of DOCK8 deficiency in which these mice show no GCs. Unexpectedly, the patients lymph nodes demonstrated lymphocyte polyclonality, follicular hyperplasia and an unusual IgE(+) plasma cell expansion. In contrast, the proliferative capacity of circulating B-cells was almost absent with little in-vitro Ig production or plasmablast formation. Also the T-cell proliferation indicated a partial defect. Hematopoietic stem cell transplantation (HSCT) was performed resulting in the disappearance of the molluscum contagiosum lesions. In sum, DOCK8 deficiency results in defective antibody responses and undirected plasma cell expansion in the lymph nodes, as part of a combined immunodeficiency cured by HSCT.
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Effectiveness of a web-based application to monitor health-related quality of life.
Pediatrics
PUBLISHED: 01-06-2013
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Monitoring health-related quality of life (HRQoL) by using electronic patient-reported outcomes (ePROs) has been only minimally evaluated in pediatrics. Children with juvenile idiopathic arthritis (JIA) are at risk for HRQoL problems. The aim of this study was to investigate the effectiveness of ePROs in clinical pediatric rheumatology care.
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Factors associated with treatment response to etanercept in juvenile idiopathic arthritis.
JAMA
PUBLISHED: 11-06-2011
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Since the introduction of biologic therapies, the pharmacological treatment approach for juvenile idiopathic arthritis (JIA) has changed substantially, with achievement of inactive disease as a realistic goal.
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A twice daily posaconazole dosing algorithm for children with chronic granulomatous disease.
Pediatr. Infect. Dis. J.
PUBLISHED: 07-21-2011
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Posaconazole (PSZ) may be an attractive alternative for antifungal prophylaxis in children with chronic granulomatous disease. Experience with PSZ in pediatric patients is limited, and no specific dose recommendations exist. A twice daily dosing algorithm based on allometric scaling (body-weight based) for PSZ results in adequate exposure and appears to be safe in children with chronic granulomatous disease.
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Educational paper: Defects in number and function of neutrophilic granulocytes causing primary immunodeficiency.
Eur. J. Pediatr.
PUBLISHED: 06-21-2011
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The neutrophilic granulocyte (neutrophil) is the most important cellular component of the innate immune system. A total absence of neutrophils or a significant decrease in their number leads to severe immunodeficiency. A mature neutrophil, released from the bone marrow, should be able to migrate from the blood towards the tissues, following a chemotactic gradient to a pathogen. In order to be neutralized, this pathogen has to be recognized, phagocytosed, and destroyed by lytic enzymes contained in the neutrophils granules and reactive oxygen species formed by the enzyme complex NADPH oxidase. Rare genetic defects leading to the loss of each one of these biological properties of the neutrophil have been described and are associated with immunodeficiency. This review provides a summary of the normal development and biological functions of neutrophils and describes the diseases caused by defects in neutrophil number and function.
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Induction of regulatory T cells by macrophages is dependent on production of reactive oxygen species.
Proc. Natl. Acad. Sci. U.S.A.
PUBLISHED: 09-22-2010
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The phagocyte NAPDH-oxidase complex consists of several phagocyte oxidase (phox) proteins, generating reactive oxygen species (ROS) upon activation. ROS are involved in the defense against microorganisms and also in immune regulation. Defective ROS formation leads to chronic granulomatous disease (CGD) with increased incidence of autoimmunity and disturbed resolution of inflammation. Because regulatory T cells (Tregs) suppress autoimmune T-cell responses and are crucial in down-regulating immune responses, we hypothesized that ROS deficiency may lead to decreased Treg induction. Previously, we showed that in p47(phox)-mutated mice, reconstitution of macrophages (Mph) with ROS-producing capacity was sufficient to protect the mice from arthritis. Now, we present evidence that Mph-derived ROS induce Tregs. In vitro, we showed that Mph ROS-dependently induce Treg, using an NADPH-oxidase inhibitor. This finding was confirmed genetically: rat or human CGD Mph with mutated p47(phox) or gp91(phox) displayed hampered Treg induction and T-cell suppression. However, basal Treg numbers in these subjects were comparable to those in controls, indicating a role for ROS in induction of peripheral Tregs. Induction of allogeneic delayed-type hypersensitivity with p47(phox)-mutated Mph confirmed the importance of Mph-derived ROS in Treg induction in vivo. We conclude that NAPDH oxidase activity in Mph is important for the induction of Tregs to regulate T cell-mediated inflammation.
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Spectrum of clinical presentations in familial hemophagocytic lymphohistiocytosis type 5 patients with mutations in STXBP2.
Blood
PUBLISHED: 06-17-2010
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Hemophagocytic lymphohistiocytosis (HLH) is an often-fatal hyperinflammatory syndrome characterized by fever, hepatosplenomegaly, cytopenia, and in some cases hemophagocytosis. Here, we describe the mutation analysis, clinical presentation, and functional analysis of natural killer (NK) cells in patients with mutations in STXBP2 encoding Munc18-2, recently associated with familial HLH type 5. The disease severity among 11 persons studied here was highly variable and, accordingly, age at diagnosis ranged from 2 months to 17 years. Remarkably, in addition to typical manifestations of familial HLH (FHL), the clinical findings included colitis, bleeding disorders, and hypogammaglobulinemia in approximately one-third of the patients. Laboratory analysis revealed impairment of NK-cell degranulation and cytotoxic capacity. Interleukin-2 stimulation of lymphocytes in vitro rescued the NK cell-associated functional defects. In conclusion, familial HLH type 5 is associated with a spectrum of clinical symptoms, which may be a reflection of impaired expression and function of Munc18-2 also in cells other than cytotoxic lymphocytes. Mutations in STXBP2 should thus also be considered in patients with clinical manifestations other than those typically associated with HLH.
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Role of NADPH oxidase in endothelial ischemia/reperfusion injury in humans.
Circulation
PUBLISHED: 05-17-2010
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Reactive oxygen species have been implicated in the pathogenesis of ischemia/reperfusion (IR) injury. Recent studies suggest that NADPH oxidase may be a source of ROS during IR. Using an in vivo model of endothelial IR injury in the arm, we compared the response to IR in healthy volunteers with that in patients with chronic granulomatous disease. These patients have a molecular lesion in a subunit of NADPH oxidase that renders the enzyme inactive.
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Chronic granulomatous disease: the European experience.
PLoS ONE
PUBLISHED: 04-21-2009
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CGD is an immunodeficiency caused by deletions or mutations in genes that encode subunits of the leukocyte NADPH oxidase complex. Normally, assembly of the NADPH oxidase complex in phagosomes of certain phagocytic cells leads to a "respiratory burst", essential for the clearance of phagocytosed micro-organisms. CGD patients lack this mechanism, which leads to life-threatening infections and granuloma formation. However, a clear picture of the clinical course of CGD is hampered by its low prevalence (approximately 1:250,000). Therefore, extensive clinical data from 429 European patients were collected and analyzed. Of these patients 351 were males and 78 were females. X-linked (XL) CGD (gp91(phox) deficient) accounted for 67% of the cases, autosomal recessive (AR) inheritance for 33%. AR-CGD was diagnosed later in life, and the mean survival time was significantly better in AR patients (49.6 years) than in XL CGD (37.8 years), suggesting a milder disease course in AR patients. The disease manifested itself most frequently in the lungs (66% of patients), skin (53%), lymph nodes (50%), gastrointestinal tract (48%) and liver (32%). The most frequently cultured micro-organisms per episode were Staphylococcus aureus (30%), Aspergillus spp. (26%), and Salmonella spp. (16%). Surprisingly, Pseudomonas spp. (2%) and Burkholderia cepacia (<1%) were found only sporadically. Lesions induced by inoculation with BCG occurred in 8% of the patients. Only 71% of the patients received antibiotic maintenance therapy, and 53% antifungal prophylaxis. 33% were treated with gamma-interferon. 24 patients (6%) had received a stem cell transplantation. The most prominent reason of death was pneumonia and pulmonary abscess (18/84 cases), septicemia (16/84) and brain abscess (4/84). These data provide further insight in the clinical course of CGD in Europe and hopefully can help to increase awareness and optimize the treatment of these patients.
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Two-year outcome of juvenile idiopathic arthritis in current daily practice: what can we tell our patients?
Clin. Exp. Rheumatol.
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This paper aims to evaluate disease course and outcome of patients in the first 2 years after diagnosis of juvenile idiopathic arthritis (JIA) when treated according to local standard of clinical care, focusing on achievement of inactive disease, functional ability and radiological joint damage.
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Reliability and responsiveness of the Juvenile Arthritis MRI Scoring (JAMRIS) system for the knee.
Eur Radiol
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To assess the reliability and responsiveness of a new Juvenile Arthritis MRI Scoring (JAMRIS) system for evaluating disease activity of the knee.
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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.

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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.