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    ABSTRACT: A dessert matrix previously used for diagnosis of food allergies was incurred with pasteurised egg white or skimmed milk powder at 3, 6, 15 and 30mg allergen protein per kg of dessert matrix and evaluated as a quality control material for allergen analysis in a multi-laboratory trial. Analysis was performed by immunoassay using five kits each for egg and milk (based on casein) and six 'other' milk kits (five based on β-lactoglobulin and one total milk). All kits detected allergen protein at the 3mgkg(-1) level. Based on ISO criteria only one egg kit accurately determined egg protein at 3mgkg(-1) (p=0.62) and one milk (casein) kit accurately determined milk at 6 (p=0.54) and 15mgkg(-1) (p=0.83), against the target value. The milk "other" kits performed least well of all the kits assessed, giving the least precise analyses. The incurred dessert material had the characteristics required for a quality control material for allergen analysis.
    Food Chemistry 04/2014; 148C:30-36. DOI:10.1016/j.foodchem.2013.09.115
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    Annals of the Rheumatic Diseases 12/2013;
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    ABSTRACT: Cachexia, a condition that kills about one-fifth of cancer patients, may be linked to Rb-a protein that is already linked to various cancers-moving from the cell nucleus to the cytoplasm.
    eLife Sciences 12/2013; 2:e01779. DOI:10.7554/eLife.01779
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    ABSTRACT: Transcription factor PAX3/Pax3 contributes to diverse cell lineages during embryonic development and is important in tumourigenesis. We found that PAX3 is re-expressed in neuroblastoma and malignant neuroblastic (N-type) neuroblastoma cells had significantly higher PAX3 protein expression than their benign substrate-adherent (S-type) counterparts. Knock-down of PAX3 expression by siRNA transfection resulted in persistent cell growth inhibition in both types of neuroblastoma cell, owing to G1 cell cycle arrest and progressive apoptosis. Inhibition of PAX3 expression significantly decreased the attachment of S-type SH-EP1 cells to extra-cellular matrix proteins, fibronectin, laminin and collagen IV. Migration and invasion of both neuroblastoma cell types were markedly reduced after PAX3 down-regulation. PAX3 knock-down significantly augmented the cytotoxic effect of chemotherapeutic agents, etoposide, vincristine and cisplatin, commonly used to treat neuroblastoma. Microarray analyses revealed that particularly signalling pathways involving cell cycle, apoptosis, cell adhesion, cytoskeletal remodelling and development were altered by PAX3 down-regulation. Changes in PAX3 downstream genes identified by microarray analyses were validated in 47 genes by quantitative PCR. These novel findings lead us to propose that PAX3 might contribute to oncogenic characteristics of neuroblastoma cells by regulating a variety of crucial signalling pathways.
    Journal of Cellular and Molecular Medicine 11/2013; 18(1). DOI:10.1111/jcmm.12155
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    ABSTRACT: In this study, real-time PCR was used to quantify adenovirus DNA in cell suspensions prepared from 106 right and left tonsils and 10 adenoids obtained from 57 patients who underwent routine tonsillectomies and/or adenoidectomies. Eighty-four (72.4%) tonsils and adenoids samples were positive for HAdV by real-time PCR. The viral load ranged from 2.8 × 10(2) to 2.6 × 10(6) copies/10(7) cells and varied up to sixfold between the right and left tonsils. In some cases, only one tonsil was positive and the viral load was lower in older children. Seventy-eight of 84 positive samples could be typed by sequencing of the hexon L1 region. Species C (types 1, 2, and 5) were detected in 84.1% of the patients followed by types 3 and 7 of species B (6.8%), HAdV-E4 (6.8%), and HAdV-F41 (2.3%). In one patient adenovirus C2 was found in the left tonsil and adenovirus C5 in the right tonsil. No DNA methylation was detected in either the E1A promoter or the major late promoter region of adenovirus DNA from six tonsils and adenoids samples and two clinical isolates. J. Med. Virol. © 2013 Wiley Periodicals, Inc.
    Journal of Medical Virology 11/2013; 85(11). DOI:10.1002/jmv.23678
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    ABSTRACT: To review the progress that has been made in understanding the genetics of the idiopathic inflammatory myopathies (IIMs) in the past 2 years, with particular focus on polymyositis, dermatomyositis and inclusion body myositis. Candidate gene studies in the Japanese population have implicated signal transducer and activator of transcription 4 as a risk locus for IIM, and HLA-DRB1 as a risk locus for anti-melanoma differentiation-associated gene 5-positive dermatomyositis. Evidence for gene-environment interactions has been found between HLA-DRB1*03 and smoking as a risk factor for the development of anti-histidyl tRNA synthetase antibodies, and HLA-DRB1*11:01 and statins for the development of anti-hydroxymethyl glutaryl-coenzyme A reductase-positive statin-induced myopathy. The HLA-DRB1*03:01/*01:01 genotype confers the highest disease risk in inclusion body myositis. A recent genome-wide association study has been performed in dermatomyositis. The most significant signals were in the major histocompatibility complex region, with other loci suggesting evidence of genetic overlap with different autoimmune diseases. Recent association and gene-environment interaction studies have increased our knowledge of genetic risk factors for the IIMs. Ongoing international collaborations will facilitate larger and more meaningful genetic studies revealing much about the genetic architecture of these complex diseases.
    Current opinion in rheumatology 11/2013; 25(6):735-41. DOI:10.1097/01.bor.0000434676.70268.66
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    ABSTRACT: Enteroendocrine cells in the gastrointestinal tract play an important role in the regulation of appetite and digestive responses through the secretion of peptides. Their involvement in gastrointestinal diseases has been acknowledged, but relatively few studies have sought to clearly define their role in the pathogenesis or as therapeutic targets. Recent, but still limited, work has identified new roles for EEC in GI diseases.
    Current Opinion in Pharmacology 10/2013; 13(6). DOI:10.1016/j.coph.2013.09.012
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    ABSTRACT: Significance: Chronic exposure to environmental ultraviolet radiation (UVR) plays a key role in both photocarcinogenesis and induction of accelerated skin ageing. Although the temporal and spatial consequences of UVR exposure for the composition and architecture of the dermal extracellular matrix (ECM) are well characterised, the pathogenesis of photoageing remains poorly defined. Given the compelling evidence for the role of reactive oxygen species (ROS) as mediators of photoageing, UVR exposed human skin may be an accessible model system in which to characterise the role of oxidative damage in both external and internal tissues. Recent advances: Although the cell-mediated degradation of dermal components via UVR-induced expression of ECM proteases has long been identified as an integral part of the photoageing pathway, the relative importance and identity of cellular and extracellular photosensitisers (direct hit and bystanders models respectively) in initiating this enzymatic activity is unclear. Recently, both age-related protein glycation and relative amino acid composition have been identified as potential risk factors for photo-ionization and/or photo-sensitisation. Here we propose a selective multi-hit model of photoageing. Critical issues: Bioinformatic analyses can be employed to identify candidate UVR targets/photosensitisers but the action of UVR on protein structure and/or ROS production must be verified experimentally. Crucially, in the case of biochemically active ECM components such as fibronectin and fibrillin, the downstream effects of photo-degradation on tissue homeostasis remain to be confirmed. Future directions: Both topical antioxidants and inhibitors of detrimental cell-signalling may be effective in abrogating the effects of specific UVR-mediated protein degradation in the dermis.
    Antioxidants & Redox Signaling 10/2013; DOI:10.1089/ars.2013.5653
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    ABSTRACT: Metabolic syndrome (MetS) is a recently defined clustering of cardiovascular risk factors associated with insulin resistance and an increased risk of future type II diabetes mellitus and cardiovascular disease (CVD). Systemic lupus erythematosus (SLE) patients have an increased prevalence of MetS and an increased prevalence of insulin resistance. Chronic inflammation may predispose to these complications in SLE and there is also evidence that corticosteroid therapy also contributes, although this finding has not been as consistent as would be predicted from the known metabolic effects of corticosteroids. MetS may represent a good model in which to begin to understand how SLE drives an increased risk of CVD. For now, the utility of identifying MetS in patients is to identify a subset in which more focused lifestyle interventions should be targeted and in whom medication review and adjustment (especially corticosteroid doses) should be considered to help modify future CVD risk.
    Lupus 10/2013; 22(12):1259-1266. DOI:10.1177/0961203313502570
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    ABSTRACT: There is currently great interest in the incorporation of genetic susceptibility loci into screening models to identify individuals at high risk of disease. Here, we present the first risk prediction model including all 46 known genetic loci associated with rheumatoid arthritis (RA). A weighted genetic risk score (wGRS) was created using 45 RA non-human leucocyte antigen (HLA) susceptibility loci, imputed amino acids at HLA-DRB1 (11, 71 and 74), HLA-DPB1 (position 9) HLA-B (position 9) and gender. The wGRS was tested in 11 366 RA cases and 15 489 healthy controls. The risk of developing RA was estimated using logistic regression by dividing the wGRS into quintiles. The ability of the wGRS to discriminate between cases and controls was assessed by receiver operator characteristic analysis and discrimination improvement tests. Individuals in the highest risk group showed significantly increased odds of developing anti-cyclic citrullinated peptide-positive RA compared to the lowest risk group (OR 27.13, 95% CI 23.70 to 31.05). The wGRS was validated in an independent cohort that showed similar results (area under the curve 0.78, OR 18.00, 95% CI 13.67 to 23.71). Comparison of the full wGRS with a wGRS in which HLA amino acids were replaced by a HLA tag single-nucleotide polymorphism showed a significant loss of sensitivity and specificity. Our study suggests that in RA, even when using all known genetic susceptibility variants, prediction performance remains modest; while this is insufficiently accurate for general population screening, it may prove of more use in targeted studies. Our study has also highlighted the importance of including HLA variation in risk prediction models.
    Annals of the Rheumatic Diseases 10/2013; DOI:10.1136/annrheumdis-2013-204133
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