4 rows where subject contains "General Biochemistry, Genetics and Molecular Biology"
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|2||2||["Efficacy of biological disease-modifying antirheumatic drugs: a systematic literature review informing the 2013 update of the EULAR recommendations for the management of rheumatoid arthritis"]||10.1136/annrheumdis-2013-204577||http://dx.doi.org/10.1136/annrheumdis-2013-204577||2014-01-08T03:37:11Z||["Immunology", "General Biochemistry, Genetics and Molecular Biology", "Immunology and Allergy", "Rheumatology"]||89||199||["0003-4967", "1468-2060"]||Annals of the Rheumatic Diseases||<jats:sec><jats:title>Objectives</jats:title><jats:p>To update the evidence for the efficacy of biological disease-modifying antirheumatic drugs (bDMARD) in patients with rheumatoid arthritis (RA) to inform the European League Against Rheumatism(EULAR) Task Force treatment recommendations.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Medline, Embase and Cochrane databases were searched for articles published between January 2009 and February 2013 on infliximab, etanercept, adalimumab, certolizumab-pegol, golimumab, anakinra, abatacept, rituximab, tocilizumab and biosimilar DMARDs (bsDMARDs) in phase 3 development. Abstracts from 2011 to 2012 American College of Rheumatology (ACR) and 2011–2013 EULAR conferences were obtained.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Fifty-one full papers, and 57 abstracts were identified. The randomised controlled trials (RCT) confirmed the efficacy of bDMARD+conventional synthetic DMARDs (csDMARDs) versus csDMARDs alone (level 1B evidence). There was some additional evidence for the use of bDMARD monotherapy, however bDMARD and MTX combination therapy for all bDMARD classes was more efficacious (1B). Clinical and radiographic responses were high with treat-to-target strategies. Earlier improvement in signs and symptoms were seen with more intensive initial treatment strategies, but outcomes were similar upon addition of bDMARDs in patients with insufficient response to MTX. In general, radiographic progression was lower with bDMARD use, mainly due to initial treatment effects. Although patients may achieve bDMARD- and drug-free remission, maintenance of clinical responses was higher with bDMARD continuation (1B), but bDMARD dose reduction could be applied (1B). There was still no RCT data for bDMARD switching.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>The systematic literature review confirms efficacy of biological DMARDs in RA. It addresses different treatment strategies with the potential for re…||10||||["Jackie L Nam", "Sofia Ramiro", "Cecile Gaujoux-Viala", "Kaoru Takase", "Mario Leon-Garcia", "Paul Emery", "Laure Gossec", "Robert Landewe", "Josef S Smolen", "Maya H Buch"]||[""]||[""]||[""]|
|4||4||["Gene profiling reveals specific molecular pathways in the pathogenesis of atherosclerosis and cardiovascular disease in antiphospholipid syndrome, systemic lupus erythematosus and antiphospholipid syndrome with lupus"]||10.1136/annrheumdis-2013-204600||http://dx.doi.org/10.1136/annrheumdis-2013-204600||2014-03-12T01:09:55Z||["Immunology", "General Biochemistry, Genetics and Molecular Biology", "Immunology and Allergy", "Rheumatology"]||47||31||["0003-4967", "1468-2060"]||Annals of the Rheumatic Diseases||<jats:sec><jats:title>Objective</jats:title><jats:p>To identify shared and differential molecular pathways involved in the pathogenesis of atherosclerosis (AT) and cardiovascular disease (CVD) in systemic lupus erythematosus (SLE), primary antiphospholipid syndrome (APS) and APS associated with SLE (APS plus SLE).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>129 patients (42 APS, 31 APS plus SLE and 56 SLE) and 61 healthy donors were included. Microarray expression profiling was performed in monocytes. RT-PCR of selected genes and western blot were used to validate microarray data. Clinical and inflammatory parameters were also analysed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Compared with controls, 555, 1224 and 518 genes were differentially expressed in monocytes from SLE, APS plus SLE and APS patients, respectively. Approximately 25–30% of differentially expressed genes were related to AT and CVD. Each disease displayed a specific AT/CVD/Inflammation-related gene signature. Compared with SLE, APS showed alterations in mitochondria biogenesis and function and oxidative stress. Besides the interferon signature, found in APS plus SLE and SLE patients, various genes mediating atherosclerotic/inflammatory signalling were also differentially expressed in APS plus SLE. IgG-anticardiolipin (aCL) titres independently predicted both atherosclerotic and thrombosis in APS plus SLE. Moreover, a significant correlation of IgG-aCL titres with mRNA levels of certain inflammatory molecules in monocytes was further noticed. In vitro treatment of monocytes with IgG-aCL promoted an increase in the expression of the genes most significantly changed in APS plus SLE versus healthy donors.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Gene expression profiling allows the segregation of APS, APS plus SLE and SLE, with specific signatures explaining the pro-atherosclerotic and pro-thrombotic alterations in these highly related autoimmune diseases.</jats:p>…||11||||["Carlos Perez-Sanchez", "Nuria Barbarroja", "Sebastiano Messineo", "Patricia Ruiz-Limon", "Antonio Rodriguez-Ariza", "Yolanda Jimenez-Gomez", "Munther A Khamashta", "Eduardo Collantes-Estevez", "M\u00aa Jose Cuadrado", "M\u00aa Angeles Aguirre", "Chary Lopez-Pedrera"]||[""]||[""]||[""]|
|16||16||["Development of a consensus core dataset in juvenile dermatomyositis for clinical use to inform research"]||10.1136/annrheumdis-2017-212141||http://dx.doi.org/10.1136/annrheumdis-2017-212141||2017-10-30T16:15:10Z||49||9||["0003-4967", "1468-2060"]||Annals of the Rheumatic Diseases||<jats:sec><jats:title>Objectives</jats:title><jats:p>This study aimed to develop consensus on an internationally agreed dataset for juvenile dermatomyositis (JDM), designed for clinical use, to enhance collaborative research and allow integration of data between centres.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>A prototype dataset was developed through a formal process that included analysing items within existing databases of patients with idiopathic inflammatory myopathies. This template was used to aid a structured multistage consensus process. Exploiting Delphi methodology, two web-based questionnaires were distributed to healthcare professionals caring for patients with JDM identified through email distribution lists of international paediatric rheumatology and myositis research groups. A separate questionnaire was sent to parents of children with JDM and patients with JDM, identified through established research networks and patient support groups. The results of these parallel processes informed a face-to-face nominal group consensus meeting of international myositis experts, tasked with defining the content of the dataset. This developed dataset was tested in routine clinical practice before review and finalisation.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>A dataset containing 123 items was formulated with an accompanying glossary. Demographic and diagnostic data are contained within form A collected at baseline visit only, disease activity measures are included within form B collected at every visit and disease damage items within form C collected at baseline and annual visits thereafter.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Through a robust international process, a consensus dataset for JDM has been formulated that can capture disease activity and damage over time. This dataset can be incorporated into national and international collaborative efforts, including existing clinical research databases.</jats:p></jats…||23||["http://orcid.org/0000-0002-5400-9911"]||["Liza J McCann", "Clarissa A Pilkington", "Adam M Huber", "Angelo Ravelli", "Duncan Appelbe", "Jamie J Kirkham", "Paula R Williamson", "Amita Aggarwal", "Lisa Christopher-Stine", "Tamas Constantin", "Brian M Feldman", "Ingrid Lundberg", "Sue Maillard", "Pernille Mathiesen", "Ruth Murphy", "Lauren M Pachman", "Ann M Reed", "Lisa G Rider", "Annet van Royen-Kerkof", "Ricardo Russo", "Stefan Spinty", "Lucy R Wedderburn", "Michael W Beresford"]||||["Arthritis Research UK"]||["10.13039/501100000341"]|
|77||77||["Metabolic and cardiovascular effects of chronic mild hyperuricemia in rodents"]||10.1136/jim-2018-000729||http://dx.doi.org/10.1136/jim-2018-000729||2018-07-24T17:51:06Z||["General Biochemistry, Genetics and Molecular Biology", "General Medicine"]||33||0||["1081-5589", "1708-8267"]||Journal of Investigative Medicine||<jats:p>Mildly elevated serum uric acid levels are common in people with metabolic syndrome and type 2 diabetes mellitus (T2DM), but whether elevated uric acid has a causal role in the pathogenesis of diabetes remains uncertain. We tested whether chronic mild hyperuricemia in rodents under controlled laboratory conditions can cause glucose intolerance in otherwise healthy animals, or whether it can worsen glucometabolic control in animals that are genetically predisposed to T2DM. We used an established model of experimental hyperuricemia in rodents with potassium oxonate dietary supplementation, which led to sustained, approximately two-fold elevation of uric acid compared with control animals. We also reversed the hyperuricemic effect of oxonate in some animals by treatment with a xanthine oxidase inhibitor. Manipulation of serum uric acid levels in Sprague-Dawley rats for up to 18 weeks did not affect fasting glucose and glucose tolerance. Blood pressure was also not affected by hyperuricemia in rats fed a Western-type diet. We next sought to determine whether uric acid may aggravate or accelerate the onset of glucometabolic abnormalities in rats already predisposed to T2DM. Chronic oxonate treatment in Zucker diabetic fatty (ZDF) and lean control rats for up to 6 weeks did not affect fasting glucose, insulin, and glucose tolerance in ZDF rats. Taken together, these findings indicate that elevated uric acid does not directly contribute to the pathogenesis of glucose intolerance and T2DM in rodents.</jats:p>||7||||["Sun K Park", "Tara R Rosenthal", "Jessica S Williams", "John M Shelton", "Masaya Takahashi", "Shanrong Zhang", "Ion Alexandru Bobulescu"]||||["National Institutes of Health", "Takeda Pharmaceuticals U.S.A."]||["10.13039/100000002", "10.13039/100007723"]|