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Background The tumor necrosis factor (TNF) superfamily cytokine TNF-like protein 1A (TL1A) and its receptor DR3 are essential for diverse animal models of autoimmune disease and may be pathogenic in rheumatoid arthritis (RA). However, the relationship of TL1A to disease duration, activity, and response to anti-TNF and other therapies in RA is not clear. Methods We measured soluble TL1A in synovial fluid (SF), serum, or plasma from RA first-degree relatives (FDRs) and in early RA and established disease. We measured the effects of anti-TNF and methotrexate (MTX) therapy on circulating TL1A from multiple independent RA treatment trials. We also determined the ability of a blocking anti-TL1A antibody to inhibit clinical disease and articular bone destruction in the murine collagen-induced arthritis (CIA) model of human RA. Results Soluble TL1A was specifically elevated in the blood and SF of patients with RA compared to patients with other diseases and was elevated early in disease and in at-risk anti-cyclic citrullinated peptide (CCP) (+) first-degree relatives (FDRs). Therapeutic TNF inhibition reduced serum TL1A in both responders and non-responders, whereas TL1A declined following MTX treatment only in responders. In murine CIA, TL1A blockade was clinically efficacious and reduced bone erosions. Conclusions TL1A is specifically elevated in RA from early in the disease course and in at-risk FDRs. The decline in TL1A after TNF blockade suggests that TL1A levels may be a useful biomarker for TNF activity in RA. These results support the further investigation of the relationship between TL1A and TNF and TL1A blockade as a potential therapeutic strategy in RA.

ObjectiveThis report aims to determine the safety, pharmacokinetics (PK) and efficacy of subcutaneous golimumab in active polyarticular-course juvenile idiopathic arthritis (polyJIA).MethodsIn this three-part randomised double-blinded placebo-controlled withdrawal trial, all patients received open-label golimumab (30 mg/m2 of body surface area; maximum: 50 mg/dose) every 4 weeks together with weekly methotrexate during Part 1 (weeks 0–16). Patients with at least 30% improvement per American College of Rheumatology Criteria for JIA (JIA ACR30) in Part 1 entered the double-blinded Part 2 (weeks 16–48) after 1:1 randomisation to continue golimumab or start placebo. In Part 3, golimumab was continued or could be restarted as in Part 1. The primary outcome was JIA flares in Part 2; secondary outcomes included JIA ACR50/70/90 responses, clinical remission, PK and safety.ResultsAmong 173 patients with polyJIA enrolled, 89.0% (154/173) had a JIA ACR30 response and 79.2%/65.9%/36.4% demonstrated JIA ACR50/70/90 responses in Part 1. At week 48, the primary endpoint was not met as treatment groups had comparable JIA flare rates (golimumab vs placebo: 32/78=41% vs 36/76=47%; p=0.41), and rates of clinical remission were comparable (golimumab vs placebo: 10/78=12.8% vs 9/76=11.8%). Adverse event and serious adverse event rates were similar in the treatment groups during Part 2. Injection site reactions occurred with ConclusionAlthough the primary endpoint was not met, golimumab resulted in rapid, clinically meaningful, improvement in children with active polyJIA. Golimumab was well tolerated, and no unexpected safety events occurred.Clinical Trial RegistrationNCT01230827; Results.

Objective To establish whether the analysis of whole blood gene expression can be useful in predicting or monitoring response to anti-TNF therapy in RA.

Background Although genome-wide association studies (GWAS) have identified over 100 genetic loci associated with rheumatoid arthritis (RA), our ability to translate these results into disease understanding and novel therapeutics is limited. Most RA GWAS loci reside outside of protein-coding regions and likely affect distal transcriptional enhancers. Furthermore, GWAS do not identify the cell types where the associated causal gene functions. Thus, mapping the transcriptional regulatory roles of GWAS hits and the relevant cell types will lead to better understanding of RA pathogenesis. Results We combine the whole-genome sequences and blood transcription profiles of 377 RA patients and identify over 6000 unique genes with expression quantitative trait loci (eQTLs). We demonstrate the quality of the identified eQTLs through comparison to non-RA individuals. We integrate the eQTLs with immune cell epigenome maps, RA GWAS risk loci, and adjustment for linkage disequilibrium to propose target genes of immune cell enhancers that overlap RA risk loci. We examine 20 immune cell epigenomes and perform a focused analysis on primary monocytes, B cells, and T cells. Conclusions We highlight cell-specific gene associations with relevance to RA pathogenesis including the identification of FCGR2B in B cells as possessing both intragenic and enhancer regulatory GWAS hits. We show that our RA patient cohort derived eQTL network is more informative for studying RA than that from a healthy cohort. While not experimentally validated here, the reported eQTLs and cell type-specific RA risk associations can prioritize future experiments with the goal of elucidating the regulatory mechanisms behind genetic risk associations. Electronic supplementary material The online version of this article (doi:10.1186/s13059-016-0948-6) contains supplementary material, which is available to authorized users.

Motivation Next-generation sequencing (NGS) technologies have become much more efficient, allowing whole human genomes to be sequenced faster and cheaper than ever before. However, processing the raw sequence reads associated with NGS technologies requires care and sophistication in order to draw compelling inferences about phenotypic consequences of variation in human genomes. It has been shown that different approaches to variant calling from NGS data can lead to different conclusions. Ensuring appropriate accuracy and quality in variant calling can come at a computational cost. Results We describe our experience implementing and evaluating a group-based approach to calling variants on large numbers of whole human genomes. We explore the influence of many factors that may impact the accuracy and efficiency of group-based variant calling, including group size, the biogeographical backgrounds of the individuals who have been sequenced, and the computing environment used. We make efficient use of the Gordon supercomputer cluster at the San Diego Supercomputer Center by incorporating job-packing and parallelization considerations into our workflow while calling variants on 437 whole human genomes generated as part of large association study. Conclusions We ultimately find that our workflow resulted in high-quality variant calls in a computationally efficient manner. We argue that studies like ours should motivate further investigations combining hardware-oriented advances in computing systems with algorithmic developments to tackle emerging ‘big data’ problems in biomedical research brought on by the expansion of NGS technologies. Electronic supplementary material The online version of this article (doi:10.1186/s12859-015-0736-4) contains supplementary material, which is available to authorized users.

Arabidopsis thaliana has a relatively small genome of approximately 130 Mb containing about 10% repetitive DNA. Genome sequencing studies reveal a gene-rich genome, predicted to contain approximately 25 000 genes spaced on average every 4.5 kb. Between 10 to 20% of the predicted genes occur as clusters of related genes, indicating that local sequence duplication and subsequent divergence generates a significant proportion of gene families. In addition to gene families, repetitive sequences comprise individual and small clusters of two to three retroelements and other classes of smaller repeats. The clustering of highly repetitive elements is a striking feature of the A. thaliana genome emerging from sequence and other analyses.

The higher plant Arabidopsis thaliana (Arabidopsis) is an important model for identifying plant genes and determining their function. To assist biological investigations and to define chromosome structure, a coordinated effort to sequence the Arabidopsis genome was initiated in late 1996. Here we report one of the first milestones of this project, the sequence of chromosome 4. Analysis of 17.38 megabases of unique sequence, representing about 17% of the genome, reveals 3,744 protein coding genes, 81 transfer RNAs and numerous repeat elements. Heterochromatic regions surrounding the putative centromere, which has not yet been completely sequenced, are characterized by an increased frequency of a variety of repeats, new repeats, reduced recombination, lowered gene density and lowered gene expression. Roughly 60% of the predicted protein-coding genes have been functionally characterized on the basis of their homology to known genes. Many genes encode predicted proteins that are homologous to human and Caenorhabditis elegans proteins.

Background 14–3-3η is an emerging soluble Rheumatoid Arthritis (RA) biomarker that activates intracellular pathways that lead to the upregulation of inflammatory and joint damage factors. It is reported to be highly specific and sensitive for RA as a diagnostic marker, higher levels are associated with greater joint damage progression risk and 14–3-3η9s modulation with treatment suggests a role in disease monitoring. Objectives In this study, we examine the specificity of 14–3-3η in an independent, clinically well-characterized cohort of moderate to severe RA and disease control subjects. Methods Serum 14–3-3η levels were measured in a total of 147 patients using the Augurex 14–3-3η ELISA. The patient set comprised 36 with RA and 111 controls consisting of 20 with asthma (A), 20 with Crohn9s Disease (CD), 12 presumed healthy (H), 16 with psoriasis (PsO), 20 with sarcoid arthritis (S), and 23 with spondylarthropathies (SpA). Sample testing was done independently of Augurex. Mann-Whitney testing together with Kruskal-Wallis analysis with the post-hoc Dunn9s multiple comparison test was performed to assess group differences. Receiver operator characteristic curve (ROC) analysis was performed to assess the specificity of 14–3-3η for RA. Results Median (IQR) serum 14–3-3η levels were significantly higher in RA [2.35ng/ml (0.28–19.41)] than all controls [0 (0–0)], p Conclusions Serum 14–3-3η is a highly specific RA biomarker. As a novel mechanistic disease factor, 14–3-3η is expected to provide new insights and approaches to RA management and clinical studies. References Arthritis Res Ther 2014; 16(2):R99; J Rheumatol 2014; 41(11):2104. Disclosure of Interest B. Dasgupta Employee of: Janssen R & D, LLC, Y. Cherkas Employee of: Janssen R & D, LLC, S. Lamberth Employee of: Janssen R & D, LLC, K. Hayden Employee of: Janssen R & D, LLC, C. Brodmerkel Employee of: Janssen R & D, LLC, A. Marotta Grant/research support from: Janssen R & D, LLC, M. Curran Employee of: Janssen R & D, LLC

Background Genome wide association studies (GWAS) have yielded over 100 genetic loci associated with rheumatoid arthritis (RA). However, the utility of GWAS studies for drug discovery is limited because most GWAS hits do not reside in coding regions and have no known function. Elucidating potential transcriptional regulatory roles of GWAS hits will allow functional annotation of disease-related GWAS loci and lead to better understanding of RA etiology. Objectives To identify potential molecular drivers of RA by mapping expression quantitative trait loci (eQTLs) from gene expression and genotype data from a cohort of RA patients. Methods eQTLs were mapped using whole blood transcriptome data (Affymetrix microarray) from 377 RA patients with inadequate response to methotrexate enrolled in a clinical trial at baseline. Genotypes were generated from whole genome sequencing of DNA from the same subjects. eQTL mapping was performed by linear regression on adjusted data and FDR was estimated with a permutation method separately for local and distant associations. Results We report over 6,000 unique genes with significant eQTLs that represent potential molecular drivers. These eQTLs are enriched for genetic variants associated with RA. Additionally, the genes associated with these RA GWAS loci represent several disease-relevant biological pathways, including antigen presentation and B cell signaling. While there are multiple published eQTL datasets from non-RA cohorts, our analysis suggests that there is utility in detecting eQTLs from disease-relevant cohorts. Indeed, we identified several eQTLs overlapping with RA GWAS loci that have not been reported previously. We also demonstrate that integration with publicly available epigenomics datasets enables elucidation of cell-type-specific relationships. In particular, genes with expression driven by active enhancers in specific immune cell types (e.g., B cells and T helper cells) were identified, generating hypotheses that can be validated experimentally. Conclusions As one of the first studies to detect eQTLs from RA patients, this work provides a valuable resource to better understand the genetic basis for RA and aid in translating genetics research into therapeutic interventions. Overall, this analysis highlights the value of studying peripheral blood given the challenge of obtaining large numbers of synovial tissue biopsies from RA patients. Disclosure of Interest A. Walsh Employee of: Johnson & Johnson, J. Whitaker Employee of: Johnson & Johnson, C. Huang Employee of: Johnson & Johnson, Y. Cherkas Employee of: Johnson & Johnson, S. Lamberth Employee of: Johnson & Johnson, C. Brodmerkel Employee of: Johnson & Johnson, M. Curran Employee of: Johnson & Johnson, R. Dobrin Shareholder of: Johnson & Johnson, Employee of: Johnson & Johnson

Requirements of AM LCDs for avionics applications are discussed. Performance characteristics are discussed for two avionics grade AM LCDs we developed using the IPS, and MVA modes for use in both landscape and portrait orientation.

For the first time, an avionic grade MVA AM LCD with wide viewing angle has been developed for use in either landscape or portrait mode. The development of a high resolution Multi-domain Vertical Alignment (MVA) Active Matrix Liquid Crystal Display (AM LCD) is described. Challenges met in this development include achieving the required performance with high luminance and sunlight readability while meeting stringent optical (image quality) and environmental performance requirements of avionics displays. In this paper the optical and environmental performance of this high resolution 14.1” MVA-AM-LCD are discussed and some performance comparisons to conventional AM-LCDs are documented. This AM LCD has found multiple Business Aviation and Military display applications and cockpit pictures are presented.

Background Rheumatoid Arthritis (RA) is a chronic systemic autoimmune disease resulting in joint inflammation and damage. Despite the current therapies available, only a small percentage of RA pts achieve remission. To improve care and treatment for RA pts, a deeper understanding of the mechanisms that drive disease and response to therapy are desirable. The molecular understanding of disease and treatment mechanisms of RA continues to evolve. Objectives To explore the utility of peripheral blood expression profiling for informing disease and treatment mechanisms, samples derived from the GO-FURTHER golimumab study in RA were evaluated. This study examines if whole blood (WB) gene expression profiles can be utilized to: identify a baseline disease profile (DP) for pts with moderate-to-severe RA elucidate the pharmacodynamic (PD) and response profile of golimumab IV treatment, and delineate the peripheral biological processes dysregulated in RA and modulated by golimumab IV. Methods mRNA from 487 WB samples collected in a Phase III study of golimumab IV (GO-FURTHER) in pts with active RA despite methotrexate (MTX) therapy was isolated and profiled using the Affymetrix HT HG-U133+ PM Array (Santa Clara, CA). Samples were collected at Wks 0 and 14 from pts treated with IV placebo + MTX (PBO; n=161) or IV golimumab 2mg/kg + MTX (GLM; n=326) administered at Wks 0, 4, and every 8 wks thereafter. Non-RA WB samples (healthy controls; n=22) were obtained from Bioreclamation (Hicksville, NY). Results A disease profile comparing baseline gene expression profiles of RA to healthy controls yielded about 2000 differentially expressed genes (DEGs), while comparison of post-treatment to pre-treatment samples generated a PD profile of about 3000 DEGs. Over 70% of genes in the DP are downregulated as well as humoral immune response and B and T cell receptor signaling pathways. Pathways upregulated in the DP include innate immune response, Toll-like receptor (TLR), and cell activation. Treatment with golimumab modulates more than 30% of the disease profile, while just over 25% of PD effect is shared with the DP. The above mentioned pathways are common between the DP and PD profiles and are reversed, in part, through changes in peripheral cell populations post-golimumab treatment. A significant decrease in neutrophils and increase in lymphocytes was observed in the periphery at Wk 12 and in gene expression profiles representative of these cells at Wk 14 post-treatment. In addition, response to golimumab at Wk 14 was associated with more gene changes in B and T cell receptor signaling pathways in comparison to nonresponders. Conclusions Gene expression from the periphery of RA pts can be used for identification of a DP as well as the PD effect and response profile to golimumab IV. The most significant biological pathways and functions associated with the DP or PD effect are related to immune response and function. At baseline, RA pts had an increased innate and decreased adaptive immune profile in the periphery and majority of these processes were reversed by treatment with golimumab IV. Defining the pathways dysregulated in RA and modified by effective treatment as well as those that remain dysregulated aids in defining novel areas for potential therapeutic intervention. Disclosure of Interest Y. Cherkas Employee of: Janssen Research & Development, LLC., C. Brodmerkel Employee of: Janssen Research & Development, LLC., M. Curran Employee of: Janssen Research & Development, LLC., S. Lamberth Employee of: Janssen Research & Development, LLC. DOI 10.1136/annrheumdis-2014-eular.2032

Background Although PsA is heterogeneous and shows signs of rheumatoid arthritis (RA) and psoriasis (PsO), genetic studies indicate that PsA is a distinct disease with a strong heritable component. PsA is categorized into 5 overlapping clinical patterns: polyarthritis (POLY), arthritis of distal interphalangeal joints (DIP), spondylitis (SPON), and asymmetric peripheral arthritis (ASYM). Objectives This study examines if whole blood (WB) gene expression profiles can be utilized to: identify a baseline disease profile (DP) for pts with PsA, differentiate among the clinical subtypes, and compare/contrast the disease mechanisms of PsA, RA and PsO. Methods mRNA from 270 WB samples collected at wk0 in a Ph3 study of ustekinumab (PSUMMIT I) from pts with active PsA were isolated and profiled using the Affymetrix HT HG-U133+ PM Array (Santa Clara, CA). 36 healthy control WB samples were obtained from Bioreclamation (Hicksville, NY). Baseline gene expression profiling data comparing disease to healthy control (mRNA isolated from WB and run on Affymetrix HT HG-U133+ PM Array) from 487 RA patients in a Ph3 study of golimumab (GO-FURTHER) and 186 PsO patients in a Ph4 study of ustekinumab (TRANSIT) were used to compare the PsA disease profile to RA and PsO. All data were analyzed by iReport® and Ingenuity Pathway Analysis® (Ingenuity Systems). Results We identified a disease profile for PsA (PsA vs Healthy); the majority of the differentially expressed genes are upregulated and fall into diverse categories, such as cellular proliferation, inflammation and immune response. There were no differentially expressed genes that separated PsA subtypes. PsA showed a distinct gene expression profile from RA and PsO with moderate overlap at the gene level. The genes common to all 3 diseases are largely upregulated and the biology represented by these shared genes comprise immune/inflammatory processes and connective tissue disorders. Although PsA shows greater similarity to RA than PsO at the functional pathway level, the PsA disease profile is significantly different in that a majority of the genes are upregulated in PsA. Pathways related to cell proliferation, inflammation, B and T cell signaling are increased in PsA (these pathways are largely downregulated or not significant in RA and PsO). The differentially expressed genes unique to PsA were enriched for the Protein Kinase A and Ephrin signaling pathways. There is emerging evidence that the Ephrin signaling pathway is implicated in bone remodeling and homeostasis and these data may suggest evidence for differential pathways related to structural damage in PsA than RA. Conclusions PsA has a distinct gene expression profile, although the PsA clinical subtypes could not be differentiated at a molecular level. Disease profile is best represented by activated pathways related to immune function and immune response; data showed a novel association of PsA with the Ephrin signaling pathway. Majority of the differentially expressed genes are unique to PsA and provide molecular support for PsA as a distinct disease entity. WB gene expression profile of PsA pts may help in the diagnosis of PsA, provide insight into disease pathogenesis, and identification of novel disease markers and therapeutic targets. Disclosure of Interest B. Dasgupta Employee of: Janssen Research & Development, LLC, Y. Cherkas Employee of: Janssen Research & Development, LLC, S. Lamberth Employee of: Janssen Research & Development, LLC, C. Brodmerkel Employee of: Janssen Research & Development, LLC. DOI 10.1136/annrheumdis-2014-eular.2043

Background The use of whole blood gene expression to predict and follow the response to TNF inhibition therapy in RA has been challenging due to the complex nature of the data. Objectives Here we employ an approach to gene expression analysis that is based on gene expression “modules” previously reported by Chaussabel, et al. (1) Methods Whole blood RNA (PAXgene) was obtained at baseline and 12 weeks on two cohorts of rheumatoid arthritis patients beginning anti-TNF therapy. The initial cohort was enrolled by the Autoimmune Biomarkers Collaborative Network (ABCoN) and contains 50 subjects stratified by EULAR Good Responders (N=14), Moderate Responders (N=21) and Non Responders (N=15) at 12 weeks after starting therapy. Results Good and Moderate Responders exhibited highly significant changes in multiple modules using a hypergeometric analysis. These included dramatic decreases in modules related to the myeloid lineage and inflammation, along with increases in B cell and plasma cell modules as well as in a number of modules related to the MHC and ribosomal proteins and other “undefined” module groups. Strikingly, Non Responders exhibited very little change in any modules. We have replicated these data in patients enrolled in a clinical trial of Simponi®, with full expression data available on 29 Good Responders, and 37 Moderate Responders. We observed nearly identical modular changes to those identified in the ABCoN Responders after 14 weeks of treatment. Only 6 Non Responders were available for study in this dataset, making convincing replication difficult for this subgroup. Several other replication datasets are currently being analyzed. Conclusions These data suggest that using gene expression modules related to inflammatory disease may provide a valuable method of characterizing the responder status of RA patients treated with TNF inhibitors. References Chaussabel D, Quinn C, Shen J, Patel P, Glaser C, Baldwin N, Stichweh D, Blankenship D, Li L, Munagala I, Bennett L, Allantaz F, Mejias A, Ardura M, Kaizer E, Monnet L, Allman W, Randall H, Johnson D, Lanier A, Punaro M, Wittkowski KM, White P, Fay J, Klintmalm G, Ramilo O, Palucka AK, Banchereau J, Pascual V. A modular analysis framework for blood genomics studies: application to systemic lupus erythematosus. Immunity. 2008 Jul 18;29(1):150-64. doi: 10.1016/j.immuni.2008.05.012. Disclosure of Interest M. Curran Employee of: Janssen Research & Development, LLC., M. Oswald Grant/research support: Janssen Research & Development, LLC., A. Lee Grant/research support: Janssen Research & Development, LLC., Y. Cherkas Employee of: Janssen Research & Development, LLC., C. Brodmerkel Employee of: Janssen Research & Development, LLC., S. Lamberth Employee of: Janssen Research & Development, LLC., P. Gregersen Grant/research support: Janssen Research & Development, LLC. DOI 10.1136/annrheumdis-2014-eular.3724

The genome of the model plant Arabidopsis thaliana has been sequenced by an international collaboration, The Arabidopsis Genome Initiative. Here we report the complete sequence of chromosome 5. This chromosome is 26 megabases long; it is the second largest Arabidopsis chromosome and represents 21% of the sequenced regions of the genome. The sequence of chromosomes 2 and 4 have been reported previously and that of chromosomes 1 and 3, together with an analysis of the complete genome sequence, are reported in this issue. Analysis of the sequence of chromosome 5 yields further insights into centromere structure and the sequence determinants of heterochromatin condensation. The 5,874 genes encoded on chromosome 5 reveal several new functions in plants, and the patterns of gene organization provide insights into the mechanisms and extent of genome evolution in plants.

Background Currently, disease activity in Rheumatoid Arthritis (RA) is measured using scoring systems that rely primarily on a collection of subjective measures from patients and clinicians. To improve care and treatment for RA patients, objective measurements of disease activity and response to treatment are desirable. Using a small cohort derived from an ongoing study of intravenously administered golimumab (GO-FURTHER), we evaluated the performance of Vectra-DA™ (Crescendo Biosciences), a multi-biomarker serum-based test designed to measure RA disease activity through correlation with DAS28-CRP and is sensitive to anti-TNF therapy 1 . Objectives This analysis examines if Vectra-DA™ correlates with disease activity and golimumab response in a clinical trial setting. Methods 137 serum samples collected in a Phase III study of intravenously administered golimumab in pts with active RA despite methotrexate (MTX) therapy were analyzed using Vectra-DA™ (Crescendo Bioscience © ; San Francisco, CA, USA). Samples were collected at wks 0, 2, 4, and 14 from patients (pts) treated with IV placebo + MTX (PBO; n= 42) or IV golimumab 2mg/kg + MTX (GLM; n=95) who received study medications at wks 0, 4, and every 8 weeks thereafter. Healthy control serum samples (n=21) were obtained from Bioreclamation (Hicksville, NY). Results A subset of pts from the GO-FURTHER study was chosen for analysis with Vectra-DA™. Among pts in the GO-FURTHER subset, the ACR50 response rates were 35.8% for GLM and 7.1% for PBO at week 14 and 48.4% for GLM and 16.7% for PBO at wk 24. Correlation of Vectra-DA™ and DAS28-CRP scores was r=0.51 (95% CI=0.45-0.57) using all four timepoints tested. Study pts had statistically higher mean Vectra-DA™ scores (64.2 at wk 0; 45.5 at wk 2; 50.2 at wk4; 44.9 at wk14) compared to healthy controls (35.2). At baseline, there were no significant differences in GLM and PBO-treated pts by Vectra-DA™ or DAS28-CRP scores. As early as week 2, GLM-treated subjects had a significant drop in Vectra-DA™ score of ∆= -18.7 (p= 16 ). The decrease in Vectra-DA™ score was maintained through wk 14, whereas PBO-treated subjects did not have a significant change in Vectra-DA™ scores from baseline to weeks 2, 4 and 14. Vectra-DA™ scores were statistically different between GLM-treated pts who achieved ACR50 at wk 14 versus nonresponders at wks 0 (p=0.024), 4 (p=0.013), and 14 (p=0.009). Vectra-DA™ scores were not statistically different between GLM-treated pts who achieved an ACR50 response at wk 24 versus nonresponders at all timepoints tested, although a trend was seen at wk 14 (p= 0.054). Conclusions Vectra-DA™ offers a molecular measurement of RA disease activity that can discriminate between normal subjects and RA pts, and also PBO and GLM-treated pts as early as wk 2 post-treatment. GLM treated wk14 responders had significantly lower Vectra-DA™ scores compared with nonresponders. The Vectra-DA™ score reflects a patient’s disease activity before and after the treatment with intravenous golimumab. References Weinblatt ME, Shadick NA, Manning W, et al. Use of a Multi-Biomarker Score for Rheumatoid Arthritis Disease Activity (Vectra™ DA) to Assess Response to Therapy.(Poster Session I: May 26, 2011, 11:45 BST). EULAR Congress 2011. Disclosure of Interest S. Lamberth Employee of: Janssen R & D, LLC, Y. Cherkas Employee of: Janssen R & D, LLC, C. Brodmerkel Employee of: Janssen R & D, LLC, M. Curran Employee of: Janssen R & D, LLC

SAE display standards are used as guidelines for certifying commercial airborne electronic displays. The SAE document generation structure and approval process is described. The SAE committees that generate display standards are described. Three SAE documents covering flat panel displays (AS-8034, ARP-4256, and ARP-4260) are discussed with their current status. Head-Up Display documents are also in work.© (1994) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

We have succeeded in developing an IPS mode 10.4″ TFT-LCD with a wide-viewing angle of ±70°, high brightness of 400 nits and a wide operating temperature range (from −30° to 70 °C) for aircraft application. This performance is realized by using a new LC material and a new IPS-TFT array structure with top-level pixel/common electrodes and a new BM structure.

An equal volume, dual-frequency radar system is used to obtain a quantitative characterization of a precipitation volume. The power back-scattered is related to the rainfall rate through the use of an assumed exponential drop-size distribution and the Mie radar cross section. A method is given whereby the relative consistency of a dual-frequency radar system is aided by calibration in the Rayleigh scattering region of a light rainshower. Discrepancies that occur in the observed rainfall rate are attributed to: 1) errors in the form of the assumed drop-size distribution, and 2) local vertical velocity and velocity divergence. Simultaneous observations of precipitation by the dual-frequency radar and raingages are shown for two rain situations.