bluuebunny/crossref_metadata_2025_split huggingface dataset:
Damage extent and predictors in adult and juvenile dermatomyositis and polymyositis as determined with the myositis damage index
Authors: Rider Lisa G. , Lachenbruch Peter A. , Monroe Jason B. , Ravelli Angelo , Cabalar Imelda , Feldman Brian M. , Villalba Maria L. , Myones Barry L. , Pachman Lauren M. , Rennebohm Robert M. , Reed Ann M. , Miller Frederick W. 
Published: October 2009

AbstractObjectiveWe undertook this study to validate the Myositis Damage Index (MDI) in juvenile and adult myositis, to describe the degree and types of damage and to develop predictors of damage.MethodsRetrospective MDI evaluations and prospective assessment of disease activity and illness features were conducted. Patients with juvenile‐onset disease (n = 143) were evaluated a median of 18 months after diagnosis; 135 patients were assessed 7–9 months later, and 121 were last assessed a median of 82 months after diagnosis. Ninety‐six patients with adult‐onset dermatomyositis or polymyositis had a baseline assessment a median of 30 months after diagnosis; 77 patients had a 6‐month followup evaluation, and 55 had a final assessment a median of 60 months after diagnosis.ResultsDamage was present in 79% of juvenile patients and in 97% of adult patients. In juveniles, scarring, contractures, persistent weakness, muscle dysfunction, and calcinosis were most frequent (23–30%) at the last evaluation. In adults, muscle atrophy, muscle dysfunction, and muscle weakness were most frequent (74–84%). MDI severity correlated with physician‐assessed global damage, serum creatinine, and muscle atrophy on magnetic resonance imaging, and in juveniles also with functional disability and weakness. MDI damage scores and frequency were highest in patients with a chronic illness course and in adult patients who died. Predictors of damage included functional disability, duration of active disease, disease severity at diagnosis, physician‐assessed global disease activity, and illness features, including ulcerations in children and pericarditis in adults.ConclusionDamage is common in myositis after a median duration of 5 years in patients with adult‐onset disease and 6.8 years in patients with juvenile‐onset disease. The MDI has good content, construct, and predictive validity in juvenile and adult myositis.
The 423Q polymorphism of the X‐linked inhibitor of apoptosis gene influences monocyte function and is associated with periodic fever
Authors: Ferretti Massimo , Gattorno Marco , Chiocchetti Annalisa , Mesturini Riccardo , Orilieri Elisabetta , Bensi Thea , Sormani Maria Pia , Cappellano Giuseppe , Cerutti Elisa , Nicola Stefania , Biava Alessandra , Bardelli Claudio , Federici Silvia , Ceccherini Isabella , Baldi Maurizia , Santoro Claudio , Dianzani Irma , Martini Alberto , Dianzani Umberto 
Published: October 2009

AbstractObjectiveHereditary periodic fever syndromes (HPFs) develop as a result of uncontrolled activation of the inflammatory response, with a substantial contribution from interleukin‐1β or tumor necrosis factor α (TNFα). The HPFs include familial Mediterranean fever (FMF), hyperimmunoglobulinemia D with periodic fever syndrome (HIDS), TNF receptor–associated syndrome (TRAPS), and cryopyrinopathies, which are attributable to mutations of the MEFV, MVK, TNFRSF1A, and CIAS1 genes, respectively. However, in many patients, the mutated gene has not been determined; therefore, the condition in these patients with an HPF‐like clinical picture is referred to as idiopathic periodic fever (IPF). The aim of this study was to assess involvement of X‐linked inhibitor of apoptosis (XIAP), which plays a role in caspase inhibition and NF‐κB signaling, both of which are processes that influence the development of inflammatory cells.MethodsThe XIAP gene (X‐linked) was sequenced in 87 patients with IPF, 46 patients with HPF (13 with HIDS, 17 with TRAPS, and 16 with FMF), and 182 healthy control subjects. The expression of different alleles was evaluated by sequencing XIAP‐specific complementary DNA mini‐libraries and by real‐time polymerase chain reaction and Western blot analyses. The functional effect of XIAP on caspase 9 activity was assessed by a fluorimetric assay, and cytokine secretion was evaluated by enzyme‐linked immunosorbent assay.ResultsSequencing disclosed a 1268A>C variation that caused a Q423P amino acid substitution. The frequency of 423Q‐homozygous female patients and 423Q‐hemizygous male patients was significantly higher in the IPF group than in the control group (69% versus 51%; odds ratio 2.17, 95% confidence interval 1.23–3.87, P = 0.007), whereas no significant difference was detected in the HPF group (59%) compared with controls. In primary lymphocytes and transfected cell lines, 423Q, as compared with 423P, was associated with higher XIAP protein and messenger RNA expression and lower caspase 9 activation. In lipopolysaccharide‐activated monocytes, 423Q was associated with higher secretion of TNFα.ConclusionThese results suggest that 423Q is a predisposing factor for IPF development, possibly through its influence on monocyte function.
Epitope‐specific immunotherapy of rheumatoid arthritis: Clinical responsiveness occurs with immune deviation and relies on the expression of a cluster of molecules associated with T cell tolerance in a double‐blind, placebo‐controlled, pilot phase II trial
Authors: Koffeman Eva C. , Genovese Mark , Amox Diane , Keogh Elissa , Santana Ernesto , Matteson Eric L. , Kavanaugh Arthur , Molitor Jerry A. , Schiff Michael H. , Posever James O. , Bathon Joan M. , Kivitz Alan J. , Samodal Rodrigo , Belardi Francis , Dennehey Carolyn , van den Broek Theo , van Wijk Femke , Zhang Xiao , Zieseniss Peter , Le Tho , Prakken Berent A. , Cutter Gary C. , Albani Salvatore 
Published: October 2009

AbstractObjectiveInduction of immune tolerance to maintain clinical control with a minimal drug regimen is a current research focus in rheumatoid arthritis (RA). Accordingly, we are developing a tolerization approach to dnaJP1, a peptide part of a pathogenic mechanism that contributes to autoimmune inflammation in RA. We undertook this study to test 2 hypotheses: 1) that mucosal induction of immune tolerance to dnaJP1 would lead to a qualitative change from a proinflammatory phenotype to a more tolerogenic functional phenotype, and 2) that immune deviation of responses to an inflammatory epitope might translate into clinical improvement.MethodsOne hundred sixty patients with active RA and with immunologic reactivity to dnaJP1 were enrolled in a pilot phase II trial. They received oral doses of 25 mg of dnaJP1 or placebo daily for 6 months.ResultsThe dnaJP1 peptide was safe and well‐tolerated. In response to treatment with dnaJP1, there was a significant reduction in the percentage of T cells producing tumor necrosis factor α and a corresponding trend toward an increased percentage of T cells producing interleukin‐10. Coexpression of a cluster of molecules (programmed death 1 and its ligands) associated with T cell regulation was also found to be a prerequisite for successful tolerization in clinical responders. Analysis of the primary efficacy end point (meeting the American College of Rheumatology 20% improvement criteria at least once on day 112, 140, or 168) showed a difference between treatment groups that became significant in post hoc analysis using generalized estimating equations. Differences in clinical responses were also found between treatment groups on day 140 and at followup. Post hoc analysis showed that the combination of dnaJP1 and hydroxychloroquine (HCQ) was superior to the combination of HCQ and placebo.ConclusionTolerization to dnaJP1 leads to immune deviation and a trend toward clinical efficacy. Susceptibility to treatment relies on the coexpression of molecules that can down‐regulate adaptive immunity.
Association of ERAP1, but not IL23R, with ankylosing spondylitis in a Han Chinese population
Authors: Davidson Stuart I. , Wu Xin , Liu Yu , Wei Meng , Danoy Patrick A. , Thomas Gethin , Cai Qing , Sun Linyun , Duncan Emma , Wang Niansong , Yu Qinghong , Xu Anlong , Fu Yonggui , Brown Matthew A. , Xu Huji 
Published: October 2009

AbstractObjectiveThe results of a recent genome‐wide association study have shown that ERAP1 and IL23R are associated with ankylosing spondylitis (AS) in Caucasian populations from North America and the UK. Based on these findings, we undertook the current study to investigate whether single‐nucleotide polymorphisms (SNPs) covering the genes ERAP1 and IL23R are associated with AS in a Han Chinese population.MethodsA case–control study was performed in Han Chinese patients with AS (n = 527) and controls (n = 945) from Shanghai and Nanjing. All patients met the modified New York criteria for AS. The Sequenom iPlex platform was used to genotype cases and controls for 21 tag SNPs covering IL23R and 38 tag SNPs covering ERAP1. Statistical analysis was performed using the Cochran‐Armitage test for trend.ResultsMultiple SNPs in ERAP1 were significantly associated with AS (for rs27980, P = 0.0048; for rs7711564, P = 0.0081). However, no association was observed between IL23R and AS (for all SNPs, P > 0.1). The nonsynonymous SNP in IL23R, rs11209026, widely thought to be the primary AS‐associated SNP in IL23R in Europeans, was found not to be polymorphic in Chinese.ConclusionOur results demonstrate that genetic polymorphisms in ERAP1 are associated with AS in Han Chinese, suggesting a common pathogenic mechanism for the disease in Chinese and Caucasian populations, and that IL23R is not associated with AS in Chinese, indicating a difference in the mechanism of disease pathogenesis between Chinese and Caucasian populations. This may result from the fact that rs11209026, the nonsynonymous SNP in IL23R, is not polymorphic in Chinese patients, providing further evidence that rs11209026 is the key polymorphism associated with AS (and likely inflammatory bowel disease and psoriasis) in this gene.
Interleukin‐6 and type I interferon–regulated genes and chemokines mark disease activity in dermatomyositis
Authors: Bilgic Hatice , Ytterberg Steven R. , Amin Shreyasee , McNallan Kelly T. , Wilson Joseph C. , Koeuth Thearith , Ellingson Sonja , Newman Brant , Bauer Jason W. , Peterson Erik J. , Baechler Emily C. , Reed Ann M. 
Published: October 2009

AbstractObjectiveUp‐regulation of whole blood type I interferon (IFN)–driven transcripts and chemokines has been described in a number of autoimmune diseases. An IFN gene expression “signature” is a candidate biomarker in patients with dermatomyositis (DM). This study was performed to evaluate the capacity of IFN‐dependent peripheral blood gene and chemokine signatures and levels of proinflammatory cytokines to serve as biomarkers for disease activity in adult and juvenile DM.MethodsPeripheral blood samples and clinical data were obtained from 56 patients with adult or juvenile DM. The type I IFN gene signature in the whole blood of patients with DM was defined by determining the expression levels of 3 IFN‐regulated genes (IFIT1, G1P2, and IRF7) using quantitative real‐time reverse transcription–polymerase chain reaction. Multiplexed immunoassays were used to quantify the serum levels of 4 type I IFN–regulated chemokines (IFN‐inducible T cell α chemoattractant, IFNγ‐inducible 10‐kd protein, monocyte chemotactic protein 1 [MCP‐1], and MCP‐2) and the serum levels of other proinflammatory cytokines, including interleukin‐6 (IL‐6).ResultsDM disease activity correlated significantly with the type I IFN gene signature (r = 0.41, P = 0.007) and with the type I IFN chemokine signature (r = 0.61, P < 0.0001). Furthermore, the serum levels of IL‐6 were significantly correlated with disease activity (r = 0.45, P = 0.001). In addition, correlations between the serum levels of IL‐6 and both the type I IFN gene signature (r = 0.47, P < 0.01) and the type I IFN chemokine signature (r = 0.71, P < 0.0001) were detected in patients with DM.ConclusionThese results suggest that serum IL‐6 production and the type I IFN gene signature are candidate biomarkers for disease activity in adult and juvenile DM. Coregulation of the expression of IFN‐driven chemokines and IL‐6 suggests a novel pathogenic linkage in DM.
Inflammatory mediators and premature coronary atherosclerosis in rheumatoid arthritis
Authors: Rho Young Hee , Chung Cecilia P. , Oeser Annette , Solus Joseph , Asanuma Yu , Sokka Tuulikki , Pincus Theodore , Raggi Paolo , Gebretsadik Tebeb , Shintani Ayumi , Stein C. Michael 
Published: October 2009

AbstractObjectiveRheumatoid arthritis (RA) is an inflammatory disease associated with premature atherosclerosis. We hypothesized that mediators of inflammation associated with atherosclerosis in other populations (interleukin‐6 [IL‐6], tumor necrosis factor α [TNFα], serum amyloid A [SAA], vascular endothelial growth factor, neutrophil count, IL‐1α, E‐selectin, intercellular adhesion molecule 1 [ICAM‐1], myeloperoxidase [MPO], matrix metalloproteinase 9, and vascular cell adhesion molecule 1) would be increased and associated with the severity of coronary atherosclerosis in patients with RA.MethodsClinical variables, concentrations of inflammatory mediators, and coronary artery calcification were measured in 169 patients with RA and 92 control subjects. Differences in concentrations of inflammatory mediators were compared using median quantile regression. The relationship of inflammatory mediators with the severity of coronary calcification in RA and control subjects was examined using proportional odds logistic regression, allowing for interaction with disease status. Models were adjusted for traditional cardiovascular risk factors.ResultsMedian serum concentrations of IL‐6, SAA, ICAM‐1, E‐selectin, TNFα, and MPO and peripheral blood neutrophil count were higher in patients with RA than controls (all P < 0.05), independent of Framingham risk score and diabetes mellitus (DM). IL‐6 (main effect odds ratio [OR] 1.72; 95% confidence interval [95% CI] 1.12, 2.66) and TNFα (main effect OR 1.49; 95% CI 1.16, 1.90) concentrations were significantly associated with higher amounts of coronary calcium, independent of Framingham risk score and DM, and such main effects significantly differed from controls (P = 0.001 and 0.03 for interaction, respectively).ConclusionTNFα and IL‐6 are significantly associated with the severity of subclinical atherosclerosis, independent of Framingham risk score, in RA.
Proximal point method for optimal control processes governed by ordinary differential equations
Authors: Azhmyakov Vadim , Noriega Morales Salvador 
Published: October 2009

AbstractThis paper is concerned with the proximal‐based approach to linear and finite‐difference approximations of constrained convex optimal control problems. We consider control systems governed by ordinary differential equations in the presence of additional terminal/state inequalities and propose a numerical method derived from the proximal point algorithm. The aim of the paper is to study the convergence properties of the obtained conceptual algorithm and to show that it can be used to compute approximate optimal controls. Copyright © 2009 John Wiley and Sons Asia Pte Ltd and Chinese Automatic Control Society
Design of robust non‐fragile H∞ filters for uncertain neutral stochastic systems with distributed delays
Authors: Song Bo , Xu Shengyuan , Xia Jianwei , Zou Yun , Chu Yuming 
Published: October 2009

AbstractThis paper deals with the problem of robust non‐fragile H∞ filtering for neutral stochastic systems with distributed delays and norm‐bounded parameter uncertainties. Attention is focused on the design of a filter which is subject to gain variations, such that the filtering error system is robustly stochastically stable with a prescribed H∞ performance level for all admissible uncertainties. A delay‐dependent sufficient condition for the solvability of this problem is obtained in terms of a linear matrix inequality. Copyright © 2009 John Wiley and Sons Asia Pte Ltd and Chinese Automatic Control Society
Delay distribution based robust H∞ control of networked control systems with uncertainties
Authors: Peng Chen , Yue Dong , Tian Yu‐Chu 
Published: October 2009

AbstractNetwork induced delay in networked control systems (NCS) is inherently non‐uniformly distributed and behaves with multifractal nature. However, such network characteristics have not been well considered in NCS analysis and synthesis. Making use of the information of the statistical distribution of NCS network induced delay, a delay distribution based stochastic model is adopted to link Quality‐of‐Control and network Quality‐of‐Service for NCS with uncertainties. From this model together with a tighter bounding technology for cross terms, H∞ NCS analysis is carried out with significantly improved stability results. Furthermore, a memoryless H∞ controller is designed to stabilize the NCS and to achieve the prescribed disturbance attenuation level. Numerical examples are given to demonstrate the effectiveness of the proposed method. Copyright © 2009 John Wiley and Sons Asia Pte Ltd and Chinese Automatic Control Society
Controller design based on similar skew‐symmetric structure for nonlinear plants
Authors: Liu Yicheng , Zhang Tao , Song Jingyan , Liang Bin 
Published: October 2009

AbstractThis paper proposes a novel controller design approach for nonlinear plants. A class of stable nonlinear systems with a similar skew‐symmetric structure is chosen as the objective closed loop system, and two design methods are proposed with backstepping and direct construction. Compared with the conventional backstepping method, the proposed backstepping method need not construct a Lyapunov function step by step, thus the design procedure is simplified. The direct construction method can be applied to some nonlinear plants for which the conventional backstepping is not feasible; and the design can be accomplished in only one step. Furthermore, for some nonlinear plants which have a lower triangular structure with two subsystems, simpler controllers can be derived by the proposed direct construction method than those derived by backstepping design. In addition, the proposed methods are both system structure oriented, therefore their designs are more intuitive than the conventional backstepping design. Two controllers are derived for satellite attitude control by employing the proposed methods; simulation results demonstrate their effectiveness. Copyright © 2009 John Wiley and Sons Asia Pte Ltd and Chinese Automatic Control Society
Identification of chromosome 7 inversion breakpoints in an autistic family narrows candidate region for autism susceptibility
Authors: Cukier Holly N. , Skaar David A. , Rayner‐Evans Melissa Y. , Konidari Ioanna , Whitehead Patrice L. , Jaworski James M. , Cuccaro Michael L. , Pericak‐Vance Margaret A. , Gilbert John R. 
Published: October 2009

AbstractChromosomal breaks and rearrangements have been observed in conjunction with autism and autistic spectrum disorders. A chromosomal inversion has been previously reported in autistic siblings, spanning the region from approximately 7q22.1 to 7q31. This family is distinguished by having multiple individuals with autism and associated disabilities. The region containing the inversion has been strongly implicated in autism by multiple linkage studies, and has been particularly associated with language defects in autism as well as in other disorders with language components. Mapping of the inversion breakpoints by FISH has localized the inversion to the region spanning approximately 99–108.75 Mb of chromosome 7. The proximal breakpoint has the potential to disrupt either the coding sequence or regulatory regions of a number of cytochrome P450 genes while the distal region falls in a relative gene desert. Copy number variant analysis of the breakpoint regions detected no duplication or deletion that could clearly be associated with disease status. Association analysis in our autism data set using single nucleotide polymorphisms located near the breakpoints showed no significant association with proximal breakpoint markers, but has identified markers near the distal breakpoint (∼108–110 Mb) with significant associations to autism. The chromosomal abnormality in this family strengthens the case for an autism susceptibility gene in the chromosome 7q22‐31 region and targets a candidate region for further investigation.
In vitro–in vivo correlation for nevirapine extended release tablets
Authors: Macha Sreeraj , Yong Chan‐Loi , Darrington Todd , Davis Mark S. , MacGregor Thomas R. , Castles Mark , Krill Steven L. 
Published: October 2009

AbstractAn in vitro–in vivo correlation (IVIVC) for four nevirapine extended release tablets with varying polymer contents was developed. The pharmacokinetics of extended release formulations were assessed in a parallel group study with healthy volunteers and compared with corresponding in vitro dissolution data obtained using a USP apparatus type 1. In vitro samples were analysed using HPLC with UV detection and in vivo samples were analysed using a HPLC‐MS/MS assay; the IVIVC analyses comparing the two results were performed using WinNonlin®. A Double Weibull model optimally fits the in vitro data. A unit impulse response (UIR) was assessed using the fastest ER formulation as a reference. The deconvolution of the in vivo concentration time data was performed using the UIR to estimate an in vivo drug release profile. A linear model with a time‐scaling factor clarified the relationship between in vitro and in vivo data. The predictability of the final model was consistent based on internal validation. Average percent prediction errors for pharmacokinetic parameters were <10% and individual values for all formulations were <15%. Therefore, a Level A IVIVC was developed and validated for nevirapine extended release formulations providing robust predictions of in vivo profiles based on in vitro dissolution profiles. Copyright © 2009 John Wiley & Sons, Ltd.
Biegeschubversuche an Stahlbetonbalken mit nachträglich eingemörtelter Querkraftbewehrung
Authors: Randl Norbert , Kunz Jakob 
Published: October 2009

AbstractIm vorliegenden Beitrag wird über Querkraftversuche an insgesamt zehn Stahlbetonbalken berichtet, von denen acht mit nachträglich eingemörtelten Bewehrungsstäben verstärkt wurden. Anzahl und Abstand der geneigten Bewehrungsstäbe sowie die verwendeten Verbundmörtel wurden variiert. Während am oberen Ende der Stäbe eine Verankerung im Bauteilinneren durch Verbund erfolgte, wurden für die Verankerung an der Tragwerksunterseite eigene Ankerkörper entwickelt. Die Versuche bestätigen die Wirksamkeit der Maßnahme, die keine Änderungen der Bauteilabmessungen erfordert und von der Tragwerksunterseite her durchgeführt werden kann. Im Zuge der Untersuchungen wurden auch grundlegende phänomenologische Erkenntnisse zur Querkraftabtragung von Stahlbetonbalken gewonnen, insbesondere was die Rissverzahnung entlang des Schubrisses, den Anteil der Dübelwirkung der Längsbewehrung sowie die Mitwirkung der Biegedruckzone betrifft.Bending Shear Tests on R/C‐Beams with Post‐Installed Shear ReinforcementA research project has been started to investigate a new method of strengthening beams with insufficient shear resistance by applying post‐installed reinforcement. 10 reinforced concrete beams have been tested in shear, number and location of the inclined rebars as well as type of injection mortar have been varied. The rebars were installed in mortar‐injected boreholes and anchored with metal plates at the accessible bar end. The test results confirmed that post‐installed rebars can significantly increase the beam shear resistance provided they are situated properly and adequate injection mortars used. Above that the evaluation of the different contributions to shear resistance like truss action, dowel action and shear strength of compression chord provides new findings on the general shear failure mechanism in RC structures.