bluuebunny/crossref_metadata_2025_split huggingface dataset:
Eudragit S (methyl methacrylate methacrylic acid copolymer)/fatty acid blends as form‐stable phase change material for latent heat thermal energy storage
Authors: Sari Ahmet , Alkan Cemil , Kolemen Ugur , Uzun Orhan 
Published: April 2006

AbstractBy composing (Eudragit S) with fatty acids (stearic acid (SA), palmitic acid (PA), and myristic acid (MA)), form‐stable phase change materials (PCMs), which can retain the same shape in a solid state even when the temperature of the PCMs is over the melting points of the fatty acids, are prepared. The compatibility of fatty acids with the Eudragit S is proved by microscopic investigation and infrared (FTIR) spectroscopy. The melting and crystallization temperatures and the latent heats of melting and crystallization of the form‐stable PCMs are measured by Differential Scanning Calorimetry (DSC) method. The maximum mass percentage of all fatty acids in the form‐stable PCMs is found as 70%, and no leakage of fatty acid is observed at the temperature range of 50–70°C for several heating cycles. Thermal properties obtained from the DSC analysis indicate that the Eudragit S/fatty acid blends as form‐stable PCM have great potential for passive solar latent heat thermal energy storage (LHTES) applications in terms of their satisfactory thermal properties and utility advantage. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 101: 1402–1406, 2006
The effect of therapeutic glucocorticoids on the adrenal response in a randomized controlled trial in patients with rheumatoid arthritis
Authors: Kirwan John R. , Hickey Sarah H. , Hällgren Roger , Mielants Herman , Björck Ewa , Persson Tore , Wollheim Frank A. 
Published: April 2006

AbstractObjectiveTo measure the effect of low‐dose systemic glucocorticoid treatment on the adrenal response to adrenocorticotropic hormone (ACTH) in patients with rheumatoid arthritis (RA).MethodsPatients with RA who took part in a randomized double‐blind placebo‐controlled trial of budesonide (3 mg/day and 9 mg/day) and prednisolone (7.5 mg/day) underwent a short (60‐minute) test with injection of ACTH (tetracosactide hexaacetate) at baseline and the day after completing the 3‐month treatment program. Plasma cortisol measurements at baseline and 3 months were compared within and between the treatment groups. Individual patients were classified as normal responders to ACTH or as abnormal responders if changes were >2 SD below the pretreatment value in the entire group of study patients.ResultsShort tests with ACTH injection were performed on 139 patients before beginning the study medication and on 134 patients after cessation of the medication. There were no changes in the placebo group. Mean plasma cortisol levels following treatment were reduced in all active treatment groups. In addition, mean values were significantly reduced for the 30‐minute and 60‐minute responses to ACTH. The maximum reduction (35%) occurred in the prednisolone group at 60 minutes. Following treatment, 34% of patients taking budesonide 9 mg and 46% of those taking prednisolone 7.5 mg failed to reach the normal maximum cortisol response to ACTH. Four patients failed to achieve the normal percentage increase in cortisol levels, but only 1 patient failed to meet both criteria.ConclusionLow doses of a glucocorticoid resulted in depression of baseline and ACTH‐stimulated cortisol levels after 12 weeks of therapy. Although the responsiveness of the hypothalamic–pituitary–adrenal axis in individual patients generally remained within the normal range, these changes should be investigated further.
A novel role for suppressor of cytokine signaling 3 in cartilage destruction via induction of chondrocyte desensitization toward insulin‐like growth factor
Authors: Smeets R. L. , Veenbergen S. , Arntz O. J. , Bennink M. B. , Joosten L. A. B. , van den Berg W. B. , van de Loo F. A. J. 
Published: April 2006

AbstractObjectiveAn important mechanism contributing to cartilage destruction in arthritis is chondrocyte desensitization toward its main anabolic factor, insulin‐like growth factor 1 (IGF‐1). In this study, we sought to determine the role of suppressor of cytokine signaling 3 (SOCS‐3) in the induction of IGF‐1 desensitization of murine chondrocytes.MethodsChondrocyte responsiveness to IGF‐1 was assessed by 35S‐sulfate incorporation into proteoglycans (PGs), via aggrecan messenger RNA expression, using quantitative real‐time polymerase chain reaction or insulin receptor substrate 1 (IRS‐1) tyrosine phosphorylation (Western blot analysis). IGF‐1 desensitization of patellar chondrocytes was studied in zymosan‐induced arthritis. IGF‐1 desensitization was induced in patellar cartilage explants or the H4 chondrocyte cell line, exposed to interleukin‐1α (IL‐1α). SOCS‐3 protein expression was assessed by immunohistochemistry or by Western blot analysis of protein extracts. The role of SOCS‐3 in IGF‐1 signaling was elucidated by adenoviral overexpression.ResultsExposure of murine articular cartilage to IL‐1 caused a significant decrease in IGF‐1–induced PG synthesis. This effect also occurred in inducible nitric oxide synthase–knockout mice, revealing the involvement of a secondary IL‐1–induced factor other than nitric oxide. We showed that IL‐1 significantly up‐regulated SOCS‐3 transcription and protein synthesis in H4 chondrocytes. In contrast, IL‐18 was unable to induce SOCS‐3 expression and failed to induce chondrocyte IGF‐1 desensitization. Histologic analysis of samples from arthritic knee joints revealed high expression of SOCS‐3 in chondrocytes. Through adenoviral overexpression of SOCS‐3, we obtained direct evidence that SOCS‐3 inhibits IGF‐1–mediated cell signaling, since IRS‐1 phosphorylation was reduced.ConclusionThis study demonstrates that IL‐1–induced SOCS‐3 expression is a novel mechanism of IGF‐1 desensitization in chondrocytes; in conjunction with nitric oxide it can contribute to cartilage damage during arthritis.
Intraarticular corticosteroids decrease synovial RANKL expression in inflammatory arthritis
Authors: Makrygiannakis Dimitrios , af Klint Erik , Catrina Sergiu‐Bogdan , Botusan Ileana Ruxandra , Klareskog Elin , Klareskog Lars , Ulfgren Ann‐Kristin , Catrina Anca Irinel 
Published: April 2006

AbstractObjectiveIntraarticular corticosteroids are frequently used as successful adjuvant therapy for inflammatory arthritides, but little is known about their effects on molecules that regulate bone biology. We undertook this study to investigate the effect of intraarticular corticosteroids on the synovial expression of RANKL and osteoprotegerin (OPG).MethodsWe evaluated RANKL, OPG, and surface marker expression by immunohistochemical methods in synovial knee biopsy samples obtained from 13 patients with inflammatory arthritis before and 2 weeks following intraarticular injection of triamcinolone hexacetonide. We further investigated the effect of dexamethasone (DEX) on RANKL expression by lymphocytes from rheumatoid arthritis synovial fluids (RA SF), using flow cytometric analysis. Finally, we evaluated the in vitro effect of DEX on RANKL and OPG expression in osteoblast‐like cells, by Western blotting.ResultsIntraarticular corticosteroids induced a decrease in the number of synovial T cells without influencing the number of macrophages, evaluated as both CD68+ and CD163+ cells. This change was paralleled by a decrease of synovial RANKL expression with a concomitant reduction of the RANKL:OPG ratio. DEX down‐regulated RANKL expression on lymphocytes derived from RA SF. Moreover, in vitro pretreatment of osteoblast‐like cells with tumor necrosis factor favored an antiresorptive effect of DEX treatment through a similar down‐regulation of RANKL expression.ConclusionThe decrease in inflammation attributed to intraarticular corticosteroids is accompanied by down‐modulation of bone destruction markers. These findings offer a rationale for the beneficial effect of corticosteroids on joint erosion in arthritis.
Fas activation of a proinflammatory program in rheumatoid synoviocytes and its regulation by FLIP and caspase 8 signaling
Authors: Palao Guillermo , Santiago Begoña , Galindo Marı´a , Rullas Joaquı´n , Alcamı´ José , Ramirez Juan C. , Pablos José L. 
Published: April 2006

AbstractObjectiveThe expansion of an aggressive population of fibroblast‐like synoviocytes (FLS) in rheumatoid arthritis (RA) synovium occurs despite their expression of functional death receptors and exposure to death receptor ligands. FLS can survive Fas challenge because of the constitutive expression of FLIP apoptosis inhibitor. We investigated whether Fas signaling plays a pathogenetic role by activating a nonapoptotic proinflammatory program in RA FLS.MethodsCultured RA FLS were stimulated with an agonistic anti‐Fas antibody in the presence or absence of the caspase inhibitor Z‐VAD‐FMK or after RNA interference with a short hairpin RNA expression plasmid directed against FLIP. NF‐κB and activator protein 1 (AP‐1) activation was studied by electrophoretic mobility shift assays and p65 immunofluorescence analysis, and expression of messenger RNA (mRNA) for monocyte chemoattractant protein 1, interleukin‐8, IκBα, and matrix metalloproteinases (MMPs) 1, 9, and 13 was examined by reverse transcription–polymerase chain reaction. Chemotactic activity of Fas‐activated FLS–conditioned media was studied in Transwell migration assays.ResultsFas stimulation activated NF‐κB and AP‐1, and this response required caspase activity, since Z‐VAD‐FMK inhibitor precluded it. FLIP was processed to p43 protein after Fas stimulation in a caspase‐dependent manner, and inhibition of FLIP expression resulted in reduced Fas‐triggered NF‐κB activation. Fas stimulation increased expression of mRNA for IκBα, MMPs, and chemokines, and Fas‐activated RA FLS displayed increased chemotactic activity for monocytic cells.ConclusionFas triggering may contribute to the proinflammatory features of RA FLS by activating NF‐κB and AP‐1 and by expression of relevant target genes, such as MMPs and chemokines. Fas proinflammatory signaling is dependent upon caspase activity and FLIP expression. These data implicate FLIP as a potentially important molecular switch that turns the Fas signaling away from apoptosis and toward induction of a proinflammatory phenotype in RA FLS.
Development of a preliminary index that predicts adverse events after total knee replacement
Authors: Solomon Daniel H. , Chibnik Lori B. , Losina Elena , Huang Jenny , Fossel Anne H. , Husni Elaine , Katz Jeffrey N. 
Published: April 2006

AbstractObjectiveWe undertook this study to assess the relationships between hospital characteristics, volume of procedures, and perioperative outcomes after total knee replacement (TKR), and to use this information to construct a simple predictive index for perioperative outcomes that incorporates hospital‐ and patient‐level characteristics.MethodsWe studied Medicare beneficiaries who underwent TKR in 4 US states in 2000. Orthopedic surgery administrators from hospitals caring for patients in this sample were surveyed about a range of hospital characteristics. The relationships between these hospital characteristics, patient variables, and 90‐day postoperative adverse events (including death, pulmonary embolus, pneumonia, deep wound infection, and acute myocardial infarction) were assessed using generalized estimating equations adjusting for hospital volume. These relationships were assessed in low‐ and high‐risk patient groups. Variables from the final multivariate model were used to create an index that was tested against 90‐day adverse event rates.ResultsThree hundred twenty‐seven (3.6%) of the patients undergoing TKR in our sample experienced an adverse event. In the final multivariate regression models, variables that predicted adverse perioperative events included low hospital volume (fewer than 23 TKRs in the Medicare population per year), absence of a preoperative teaching program, fewer TKRs conducted in a dedicated orthopedic surgery operating room, patient age >70 years, male sex, and at least 1 comorbid condition. The effect of volume on perioperative adverse events was evident both in patients with few risk factors and in patients with several risk factors. An index including the 6 patient and hospital variables discriminated well, with adverse events occurring in 2.0% (95% confidence interval [95% CI] 1.4–2.7%) of patients in the lowest risk category and in 7.4% (95% CI 4.5–12.3%) of patients in the highest risk category (P for trend < 0.001). The index predicted adverse event rates both in hospitals with a low volume of TKRs and in those with a high volume of TKRs.ConclusionCharacteristics of hospital care, procedure volume, and patient‐level factors are all associated with perioperative outcomes of TKR. A preliminary index combining hospital characteristics and volume is moderately predictive of adverse perioperative outcomes. The index is predictive of outcome in low‐ and high‐volume hospitals.
Mediation of endothelial cell damage by serine proteases, but not superoxide, released from antineutrophil cytoplasmic antibody–stimulated neutrophils
Authors: Lu X. , Garfield A. , Rainger G. E. , Savage C. O. S. , Nash G. B. 
Published: April 2006

AbstractObjectiveTo evaluate potential mediators of endothelial cell injury in systemic vasculitis associated with antineutrophil cytoplasmic antibodies (ANCAs), we investigated the factors controlling the neutrophil respiratory burst and endothelial release of von Willebrand factor (vWF) during neutrophil–endothelial cell interactions.MethodsSuperoxide release from neutrophils binding to purified P‐selectin or to tumor necrosis factor–activated endothelial cells was measured under flow or static conditions using the superoxide dismutase (SOD)–inhibitable reduction of ferricytochrome c. Neutrophils were activated with fMLP, normal IgG, or ANCA IgG. Enzyme‐linked immunosorbent assay was used to measure vWF. Serine protease activity was measured enzymatically.ResultsANCA IgG or fMLP induced superoxide release when perfused over neutrophils that were rolling over P‐selectin, but not those that were binding to endothelial cells. In static assays, endothelial cells inhibited superoxide production by neutrophils. Adenosine inhibited the respiratory burst, and, in cocultures, adenosine deaminase overcame the inhibitory effects of endothelial cells. Serine proteases were released during activated neutrophil–endothelial cell coculture. There was enhanced release of vWF during activated neutrophil–endothelial cell coculture; this was not inhibited by diphenyleneiodonium or by SOD plus catalase, but was inhibited by diisopropylfluorophosphate.ConclusionEndothelial cells inhibit superoxide generation by fMLP and ANCA‐activated neutrophils. The release of vWF occurs during coculture and is sensitive to serine protease, but not NADPH oxidase inhibition. Serine proteases may play a more important role than reactive oxygen species as mediators of endothelial injury during ANCA‐associated systemic vasculitis.
Tissue‐specific up‐regulation of the proteasome subunit β5i (LMP7) in Sjögren's syndrome
Authors: Egerer Thomas , Martinez‐Gamboa Lorena , Dankof Anja , Stuhlmüller Bruno , Dörner Thomas , Krenn Veit , Egerer Karl , Rudolph Paul E. , Burmester Gerd‐R. , Feist Eugen 
Published: April 2006

AbstractObjectiveSjögren's syndrome (SS) is characterized by autoimmune infiltration and focal accumulation of lymphocytes in the exocrine glands, with a predominance of CD4‐positive T cells. Since these histologic findings are nonspecific, determination of clinical and serologic abnormalities contribute to the diagnosis. The aim of this study was to identify a novel, disease‐specific, immunologically relevant marker for SS.MethodsTo analyze disease‐related and tissue‐specific expression of candidate markers, we examined biopsied minor salivary glands and peripheral blood mononuclear cells from patients with primary and secondary SS (n = 26) as well as from patients with sicca symptoms without autoimmune sialadenitis (n = 15). Expression of the Th1/Th2‐related chemokines CCL3 (macrophage inflammatory protein 1α) and CCL2 (monocyte chemoattractant protein 1), CXCL7 (neutrophil‐activating peptide 2 [NAP‐2]), interleukin‐1β, inducible costimulator, and the proteasome subunits α3 (C9) and β5i (LMP7) was analyzed at the messenger RNA (mRNA) level using real‐time polymerase chain reaction techniques. Immunohistochemical analysis was used to identify the β5i (LMP7)–expressing cell populations in minor salivary glands.ResultsThe expression profiles revealed a significant up‐regulation of β5i (LMP7) exclusively in the salivary glands of SS patients. Immunohistochemistry confirmed expression of the immunoproteasome subunit β5i (LMP7) within the acinar and ductal epithelial cells. No significant difference in the distinct histologic focus scores was evident for the expression of the markers investigated. In the peripheral blood compartment, the expression of CXCL7 was up‐regulated both in primary and in secondary SS.ConclusionTissue‐specific up‐regulation of β5i (LMP7) mRNA was shown to be characteristic of SS, indicating a disease‐specific modulation of the proteasome system. Expression of β5i (LMP7) represents an independent parameter that can be used in addition to the focus score to distinguish SS in biopsied labial salivary glands.
A comparison of response criteria to evaluate therapeutic response in patients with juvenile idiopathic arthritis treated with methotrexate and/or anti–tumor necrosis factor α agents
Authors: Lurati A. , Pontikaki I. , Teruzzi B. , Desiati F. , Gerloni V. , Gattinara M. , Cimaz R. , Fantini F. 
Published: April 2006

AbstractObjectiveThere are no validated criteria to evaluate clinical response in juvenile idiopathic arthritis (JIA). The purpose of this study was to compare 4 sets of criteria (2 from the American College of Rheumatology [ACR] and 2 from the European League Against Rheumatism [EULAR]) for clinical response evaluation in JIA patients treated with methotrexate and/or anti–tumor necrosis factor α drugs.MethodsSeventy‐five patients with JIA were evaluated at baseline and after 6 months of therapy with second‐line drugs. Mean age at study onset was 12.8 years (range 2–32.9 years). Diagnoses were systemic JIA (n = 16), rheumatoid factor–positive JIA (n = 5), rheumatoid factor–negative JIA (n = 9), persistent oligoarticular JIA (n = 10), extended oligoarticular JIA (n = 33), and psoriatic arthritis (n = 2). Clinical response was evaluated with the ACR Pediatric 30 criteria and the ACR 20% response criteria (ACR20), and with the EULAR Disease Activity Score (DAS) and 28‐joint DAS (DAS28). Patients with EULAR criteria responses of “good” or “moderate” were classified as responders. Responders and nonresponders according to the different criteria were then compared.ResultsFor patients younger than 16 years, Cohen's kappa varied between 0.51 and 0.72, with a good‐to‐excellent reproducibility index for all comparisons, except for the DAS28/ACR20 comparison. The best agreement was obtained by comparing the DAS and the ACR Pediatric 30. For patients older than 16 years, the reproducibility index was good or excellent in only 2 cases, i.e., comparing the DAS and the ACR Pediatric 30 and comparing the DAS and the DAS28 (as expected).ConclusionOur study shows a good agreement overall for the different criteria tested. The highest concordance was observed between the DAS and the ACR Pediatric 30, the lowest between the DAS28 and the ACR20. Our data suggest that the ACR Pediatric 30 criteria can be used also in adult patients affected by JIA, and that the original DAS can be an alternative to the ACR Pediatric 30 in both children and young adults with JIA.
Major reduction in spinal inflammation in patients with ankylosing spondylitis after treatment with infliximab: Results of a multicenter, randomized, double‐blind, placebo‐controlled magnetic resonance imaging study
Authors: Braun Jürgen , Landewé Robert , Hermann Kay‐Geert A. , Han John , Yan Songkai , Williamson Paul , van der Heijde Désirée 
Published: April 2006

AbstractObjectiveTo determine whether the effects of anti–tumor necrosis factor α (TNFα) in reducing the signs and symptoms of ankylosing spondylitis (AS) coincide with a reduction in spinal inflammation as detected by magnetic resonance imaging (MRI).MethodsPre‐ and postgadolinium T1 and STIR MR images of the spine were acquired at baseline and at week 24 in patients with AS who participated in a multicenter, randomized, double‐blind, placebo‐controlled study. Patients were randomly assigned at an 8:3 ratio to receive infusions of infliximab (5 mg/kg) or placebo at weeks 0, 2, and 6 and then every 6 weeks thereafter. MR images were obtained and evaluated independently by 2 readers who were blinded to the treatment allocation and time sequence of the images.ResultsA total of 194 patients in the infliximab group and 72 patients in the placebo group had evaluable images at baseline and week 24. About 80% of the patients had at least 1 active spinal lesion at baseline, as assessed by MRI. The improvement in the MRI Activity Score after 6 months was significantly greater in the patients who received infliximab (mean 5.02, median 2.72) than in those who received placebo (mean 0.60, median 0.0) (P < 0.001). Almost complete resolution of spinal inflammation was seen in most patients who received infliximab, irrespective of baseline activity.ConclusionPatients with AS who received infliximab therapy showed a decrease in spinal inflammation as detected by MRI, whereas those who received placebo showed persistent inflammatory spondylitis.
Linkage analysis of rheumatoid arthritis in US and UK families reveals interactions between HLA–DRB1 and loci on chromosomes 6q and 16p
Authors: John Sally , Amos Christopher , Shephard Neil , Chen Wei , Butterworth Adam , Etzel Carol , Jawaheer Damini , Seldin Michael , Silman Alan , Gregersen Peter , Worthington Jane 
Published: April 2006

AbstractObjectiveHLA is the most strongly associated locus in rheumatoid arthritis (RA), accounting for up to one‐third of the genetic contribution. Conditioning on the effect of true disease loci such as HLA can lead to increased power to detect effects at other loci and, in addition, allows investigation of the underlying disease models, including interactions. The aim of this study was to detect susceptibility loci for RA by conditioning on HLA in a large sample of affected sibling pairs (ASPs) and to test for evidence of interaction between novel loci and HLA.MethodsGenotype data from 3 whole‐genome linkage scans for RA in a US population and a UK population were pooled, resulting in a combined data set of 886 ASPs. This pooling of data increased the power to detect loci showing low levels of heterogeneity. Nonparametric linkage analysis was performed to identify regions of interest. Joint 2‐locus analysis was then performed for HLA and each of the loci that demonstrated evidence of linkage in the 886 ASPs.ResultsEvidence for linkage was most significant at HLA (P = 4 × 10−16), with 7 non‐HLA loci showing some evidence for linkage (P = 0.05–0.003). Joint modeling of these loci with HLA provided evidence for linkage at a genome‐wide significance level for loci on 6q (P = 2.7 × 10−6) and 16p (P = 2 × 10−4).ConclusionThese data provide the most convincing evidence to date that 6q and 16p harbor susceptibility genes. In addition, these loci may interact with HLA, facilitating the search for candidate genes within this region.