bluuebunny/crossref_metadata_2025_split huggingface dataset:
Poly(vinylbenzylchloride) beads grafted with polymer brushes carrying hydrazine ligand for reversible enzyme immobilization
Authors: Yavuz Erdem , Bayramoğlu Gülay , Şenkal B. Filiz , Arıca M. Yakup 
Published: April 2009

AbstractPoly(glycidylmethacrylate), p(GMA), brush grafted poly(vinylbenzyl chloride/ethyleneglycol dimethacrylate), p(VBC/EGDMA), beads were prepared by suspension polymerization and the beads were grafted with poly(glycidyl methacrylate), p(GMA), via surface‐initiated atom transfer radical polymerization aiming to construct a material surface with fibrous polymer. The epoxy groups of the fibrous polymer were reacted with hydrazine (HDZ) to create affinity binding site on the support for adsorption of protein. The influence of pH, and initial invertase concentration on the immobilization capacity of the p(VBC/EGDMA‐g‐GMA)‐HDZ beads has been investigated. Maximum invertase immobilization onto hydrazine functionalized beads was found to be 86.7 mg/g at pH 4.0. The experimental equilibrium data obtained invertase adsorption onto p(VBC/EGDMA‐g‐GMA)‐HDZ affinity beads fitted well to the Langmuir isotherm model. It was shown that the relative activity of immobilized invertase was higher than that of the free enzyme over broader pH and temperature ranges. The Km and Vmax values of the immobilized invertase were larger than those of the free enzyme. After inactivation of enzyme, p(VBC/EGDMA‐g‐GMA)‐HDZ beads can be easily regenerated and reloaded with the enzyme for repeated use. © 2009 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Adsorption of a gold‐iodide complex (AuI2−) onto cellulose acetate‐polyaniline membranes: Equilibrium experiments
Authors: Rodríguez F. , Castillo‐Ortega M. M. , Encinas J. C. , Sánchez‐Corrales V. M. , Pérez‐Tello M. , Munive G. T. 
Published: April 2009

AbstractThe adsorption of AuI complex onto acetate cellulose‐polyaniline membranes was investigated. Kinetic experiments showed a rapid adsorption of this complex, which was attributed to an ion‐exchange mechanism. Equilibrium adsorption results were represented by the Langmuir model, showing a correlation coefficient of 0.9852. Langmuir parameters K and Qm were found to be 0.2937 L mg−1 and 1.2394 mg g−1, respectively. Approximately 94% of AuI was adsorbed when a solid/liquid ratio of 40 g L−1 (grams of membrane/ liter of solution) was used. © 2009 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Treatment of relapsing polychondritis with rituximab: A retrospective study of nine patients
Authors: Leroux Gaëlle , Costedoat‐Chalumeau Nathalie , Brihaye Benoît , Cohen‐Bittan Judith , Amoura Zahir , Haroche Julien , Limal Nicolas , Bletry Olivier , Piette Jean‐Charles 
Published: April 2009

AbstractObjectiveRituximab, a chimeric monoclonal antibody directed against the CD20 antigen expressed by B cells, is now considered an effective second‐line therapy in various systemic diseases. We describe here the effects of rituximab in patients with relapsing polychondritis.MethodsThis was a retrospective study of 9 patients with relapsing polychondritis who received different regimens of rituximab in addition to their ongoing therapies. Clinical, laboratory, physiologic, and radiologic indicators were used to assess disease activity. We also examined their corticosteroid doses and any change in immunosuppressive agents. We then compared disease activity in the 6 months preceding rituximab administration and at 6 and 12 months after.ResultsAt 6 months, 2 patients showed partial improvement, 4 were stable, and 3 had worsened disease; however, no patient had complete remission. At 12 months (after exclusion of the 3 patients whose disease had worsened at 6 months), 2 patients remained stable and 4 had worsened disease; however, there were no partial or complete remissions. B cells were counted in 8 patients during the first 6 months after treatment, and B cell depletion was observed in all of the patients.ConclusionAlthough we cannot rule out the possibility that rituximab had a small effect, our patients' clinical courses did not improve significantly with this treatment.
Epidemiology and clinical characteristics of behçet's disease in the US: A population‐based study
Authors: Calamia Kenneth T. , Wilson Floranne C. , Icen Murat , Crowson Cynthia S. , Gabriel Sherine E. , Kremers Hilal Maradit 
Published: April 2009

AbstractObjectiveBehçet's disease (BD) is a rare, multisystem inflammatory disorder of unknown cause. Although well‐documented in Eastern populations, epidemiologic data is scarce in North American countries. Here we describe the incidence and prevalence of BD in Olmsted County, Minnesota over 45 years.MethodsWe identified an incidence cohort of subjects age ≥18 years who had a clinical diagnosis of and/or fulfilled the International Study Group (ISG) criteria for BD from January 1, 1960 to January 1, 2005. Age‐ and sex‐specific incidence and prevalence were estimated and age‐ and sex‐adjusted to the 2000 US total population.ResultsThe study population was comprised of 13 subjects with BD; 11 fulfilled ISG criteria between 1960 and 2005. Mean ± SD age was 31 ± 9 years, and 69% were white. Point prevalence in 2000 was 5.2 per 100,000 population (95% confidence interval [95% CI] 0.64–9.84). The overall annual age‐ and sex‐adjusted incidence of BD was 0.38 per 100,000 population (95% CI 0.17–0.59), with a higher incidence in women (0.51 per 100,000; 95% CI 0.17–0.84) than in men (0.26 per 100,000; 95% CI 0.004–0.52). Dermatologic lesions included oral ulcers (100%), genital ulcers (62%), erythema nodosum (46%), and papulopustular lesions (54%). Ocular lesions, vascular complications, and central nervous system involvement were present in 8, 3, and 3 subjects, respectively.ConclusionOur study shows an overall incidence of 0.38 per 100,000 population, which is comparable with other Western populations. The prevalence of 5.2 per 100,000 population is similar to estimates reported in Western countries, but lower than that in countries along the Silk Road.
Chlamydiae as etiologic agents in chronic undifferentiated spondylarthritis
Authors: Carter John D. , Gérard Hervé C. , Espinoza Luis R. , Ricca Louis R. , Valeriano Joanne , Snelgrove Jessica , Oszust Cynthia , Vasey Frank B. , Hudson Alan P. 
Published: April 2009

AbstractObjectiveThe majority of patients with Chlamydia‐induced reactive arthritis do not present with the classic triad of arthritis, conjunctivitis/iritis, and urethritis. Moreover, acute chlamydial infections are often asymptomatic. The aim of the present study was to assess the prevalence of synovial Chlamydia trachomatis and Chlamydia pneumoniae infections in patients with chronic undifferentiated spondylarthritis (uSpA).MethodsStudy patients met the European Spondylarthropathy Study Group criteria for SpA, without evidence of ankylosing spondylitis, psoriasis, inflammatory bowel disease, or preceding dysentery. Symptoms were present for ≥6 months. Each patient underwent a synovial biopsy; tissue and concomitantly obtained peripheral blood mononuclear cells (PBMCs) were analyzed by polymerase chain reaction (PCR) for C trachomatis and C pneumoniae DNA. Other data collected on the day of the biopsy included standard demographic information and medical history, including any known history of C trachomatis or C pneumoniae. Physical examination (including joint count, evaluation for dactylitis and/or enthesitis, and skin examination) and HLA–B27 typing were performed. Synovial tissue (ST) samples from 167 patients with osteoarthritis (OA) were used as controls.ResultsTwenty‐six patients met the entry criteria and underwent synovial biopsy (25 knee, 1 wrist). Sixteen of them (62%) were positive for C trachomatis and/or C pneumoniae DNA (10 for C trachomatis, 4 for C pneumoniae, and 2 for both). PCR analysis of ST revealed the presence of Chlamydia significantly more frequently in patients with uSpA than in OA controls (P < 0.0001). No specific clinical characteristics differentiated Chlamydia‐positive from Chlamydia‐negative patients. PBMCs from 4 of the 26 uSpA patients (15%) were positive for Chlamydia, and Chlamydia was found in ST from 2 of these 4 patients. No significant correlation between PCR positivity and HLA–B27 positivity was found.ConclusionThe frequency of Chlamydia‐positive ST samples, as determined by PCR, was found to be significantly higher in patients with uSpA than in patients with OA. Our results suggest that in many patients with uSpA, chlamydial infection, which is often occult, may be the cause.
Important role of interleukin‐3 in the early phase of collagen‐induced arthritis
Authors: Brühl Hilke , Cihak Josef , Niedermeier Marianne , Denzel Andrea , Gomez Manuel Rodriguez , Talke Yvonne , Goebel Nicole , Plachý Jiří , Stangassinger Manfred , Mack Matthias 
Published: April 2009

AbstractObjectiveActivation of basophils contributes to memory immune responses and results in exacerbation of collagen‐induced arthritis (CIA). We undertook the present study to analyze the production and biologic effects of interleukin‐3 (IL‐3), a strong activator of basophils, in CIA.MethodsArthritis was induced by immunization with type II collagen. Mice were treated with blocking monoclonal antibodies against IL‐3 or with recombinant IL‐3. Clinical scoring, histologic analysis, fluorescence‐activated cell sorter analysis, enzyme‐linked immunosorbent assay, and cell culturing were performed to assess disease activity and IL‐3 production.ResultsIL‐3 was produced in large quantities by collagen‐specific CD4+ T cells in the spleen and was present in the synovial tissue during onset of arthritis, but was down‐regulated in paws with severe inflammation. Blockade of IL‐3 during the time of arthritis onset resulted in profound improvement of the disease, with reductions in synovial leukocyte and cytokine levels, peripheral blood basophil levels, and anticollagen antibody titers. Blockade of IL‐3 during the late phase of arthritis had no beneficial effect. Administration of recombinant IL‐3 during onset of arthritis induced a marked exacerbation of the disease, with increased peripheral blood basophil and plasma IL‐6 levels and increased titers of anticollagen antibody. In studies of the regulation of IL‐3 expression in CD4+ T cells, IL‐6 and IL‐4 suppressed the release of IL‐3 by activated CD4+ T cells, whereas lipopolysaccharide and CpG DNA up‐regulated IL‐3 secretion in activated CD4+ T cells by acting on costimulatory cells.ConclusionTaken together, the present results demonstrate for the first time that IL‐3 has an important role in the early phase of CIA.
Coexpression of CD177 and membrane proteinase 3 on neutrophils in antineutrophil cytoplasmic autoantibody–associated systemic vasculitis: Anti–proteinase 3–mediated neutrophil activation is independent of the role of CD177‐expressing neutrophils
Authors: Hu N. , Westra J. , Huitema M. G. , Bijl M. , Brouwer E. , Stegeman C. A. , Heeringa P. , Limburg P. C. , Kallenberg C. G. M. 
Published: April 2009

AbstractObjectiveWegener's granulomatosis (WG) is strongly associated with antineutrophil cytoplasmic autoantibodies (ANCAs) directed against proteinase 3 (PR3). Recent studies have shown that membrane‐bound PR3 (mPR3) is differentially expressed and colocalizes with CD177/NB1 on circulating neutrophils. We undertook this study to assess the differential expression of CD177 on neutrophils from patients with ANCA‐associated systemic vasculitis (ASV) in comparison with patients with systemic lupus erythematosus (SLE), patients with rheumatoid arthritis (RA), and healthy individuals, and to investigate whether colocalization of mPR3 and CD177 affects anti‐PR3–mediated neutrophil activation.MethodsExpression of CD177 and mPR3 was analyzed by flow cytometry on isolated neutrophils from patients with ASV (n = 53), those with SLE (n = 30), those with RA (n = 26), and healthy controls (n = 31). Neutrophil activation mediated by anti‐PR3 antibodies was assessed by measuring the oxidative burst with a dihydrorhodamine assay.ResultsPercentages of CD177‐expressing neutrophils were significantly higher in patients with ASV and those with SLE than in healthy controls. In 3 healthy donors, CD177 expression was not detected. After priming with tumor necrosis factor α, neutrophils remained negative for CD177 while mPR3 expression was induced. Neutrophils from CD177‐negative donors or CD177− neutrophils sorted from donors with bimodal expression were susceptible to anti‐PR3–mediated oxidative burst. Variation in the extent of anti‐PR3–mediated neutrophil activation among different donors occurred independent of the percentage of CD177‐expressing neutrophils.ConclusionMembrane expression of CD177 on circulating neutrophils is increased in patients with ASV and in those with SLE, but not in RA patients. However, primed neutrophils from CD177‐negative individuals also express mPR3 and are susceptible to anti‐PR3–mediated oxidative burst, suggesting that recruitment of CD177‐independent mPR3 is involved in anti‐PR3–induced neutrophil activation.
Cartilage repair in a rat model of osteoarthritis through intraarticular transplantation of muscle‐derived stem cells expressing bone morphogenetic protein 4 and soluble flt‐1
Authors: Matsumoto Tomoyuki , Cooper Gregory M. , Gharaibeh Burhan , Meszaros Laura B. , Li Guangheng , Usas Arvydas , Fu Freddie H. , Huard Johnny 
Published: April 2009

AbstractObjectiveThe control of angiogenesis during chondrogenic differentiation is an important issue affecting the use of stem cells in cartilage repair, especially with regard to the persistence of regenerated cartilage. This study was undertaken to investigate the effect of vascular endothelial growth factor (VEGF) stimulation and the blocking of VEGF with its antagonist, soluble Flt‐1 (sFlt‐1), on the chondrogenesis of skeletal muscle‐derived stem cells (MDSCs) in a rat model of osteoarthritis (OA).MethodsWe investigated the effect of VEGF on cartilage repair in an immunodeficiency rat model of OA after intraarticular injection of murine MDSCs expressing bone morphogenetic protein 4 (BMP‐4) in combination with MDSCs expressing VEGF or sFlt‐1.ResultsIn vivo, a combination of sFlt‐1– and BMP‐4–transduced MDSCs demonstrated better repair without osteophyte formation macroscopically and histologically following OA induction, when compared with the other groups. Higher differentiation/proliferation and lower levels of chondrocyte apoptosis were also observed in sFlt‐1– and BMP‐4–transduced MDSCs compared with a combination of VEGF‐ and BMP‐4–transduced MDSCs or with BMP‐4–transduced MDSCs alone. In vitro experiments with mixed pellet coculture of MDSCs and OA chondrocytes revealed that BMP‐4–transduced MDSCs produced the largest pellets, which had the highest gene expression of not only type II collagen and SOX9 but also type X collagen, suggesting formation of hypertrophic chondrocytes.ConclusionOur results demonstrate that MDSC‐based therapy involving sFlt‐1 and BMP‐4 repairs articular cartilage in OA mainly by having a beneficial effect on chondrogenesis by the donor and host cells as well as by preventing angiogenesis, which eventually prevents cartilage resorption, resulting in persistent cartilage regeneration and repair.
Prevention of glucocorticoid‐induced bone loss in mice by inhibition of RANKL
Authors: Hofbauer Lorenz C. , Zeitz Ute , Schoppet Michael , Skalicky Monika , Schüler Christiane , Stolina Marina , Kostenuik Paul J. , Erben Reinhold G. 
Published: April 2009

AbstractObjectiveRANKL has been implicated in the pathogenesis of glucocorticoid‐induced osteoporosis. This study was undertaken to evaluate the efficacy of denosumab, a neutralizing monoclonal antibody against human RANKL (hRANKL), in a murine model of glucocorticoid‐induced osteoporosis.MethodsEight‐month‐old male homozygous hRANKL‐knockin mice expressing a chimeric RANKL protein with a humanized exon 5 received 2.1 mg/kg of prednisolone or placebo daily over 4 weeks via subcutaneous slow‐release pellets and were additionally treated with phosphate buffered saline or denosumab (10 mg/kg subcutaneously twice weekly). Two groups of wild‐type mice were also treated with either prednisolone or vehicle.ResultsThe 4‐week prednisolone treatment induced loss of vertebral and femoral volumetric bone mineral density in the hRANKL‐knockin mice. Glucocorticoid‐induced bone loss was associated with suppressed vertebral bone formation and increased bone resorption, as evidenced by increases in the number of tartrate‐resistant acid phosphatase (TRAP)–positive osteoclasts, TRAP‐5b protein in bone extracts, serum levels of TRAP‐5b, and urinary excretion of deoxypyridinoline. Denosumab prevented prednisolone‐induced bone loss by a pronounced antiresorptive effect. Biomechanical compression tests of lumbar vertebrae revealed a detrimental effect of prednisolone on bone strength that was prevented by denosumab.ConclusionOur findings indicate that RANKL inhibition by denosumab prevents glucocorticoid‐induced loss of bone mass and strength in hRANKL‐knockin mice.
The good initial response to therapy with a combination of traditional disease‐modifying antirheumatic drugs is sustained over time: The eleven‐year results of the Finnish rheumatoid arthritis combination therapy trial
Authors: Rantalaiho Vappu , Korpela Markku , Hannonen Pekka , Kautiainen Hannu , Järvenpää Salme , Leirisalo‐Repo Marjatta , Hakala Markku , Puolakka Kari , Julkunen Heikki , Luosujärvi Riitta , Möttönen Timo ,   FIN‐RACo Trial Group
Published: April 2009

AbstractObjectiveTo evaluate the evolution of functional and clinical outcomes over 11 years in patients with early rheumatoid arthritis (RA) initially treated with a combination of 3 disease‐modifying antirheumatic drugs (DMARDs) or with a single DMARD.MethodsA cohort of 199 patients with early active RA were initially randomized to receive treatment with a combination of methotrexate, sulfasalazine, and hydroxychloroquine with prednisolone or treatment with a single DMARD (initially, sulfasalazine) with or without prednisolone. After 2 years, the drug treatment strategy became unrestricted, but still targeted remission. At 11 years, function was assessed with the Health Assessment Questionnaire (HAQ), and clinical outcomes were assessed with the modified Minimal Disease Activity (MDA) measure and the American College of Rheumatology (ACR) criteria for remission.ResultsAt 11 years, 138 patients were assessed (68 in the combination‐DMARD group and 70 in the single‐DMARD group). The mean ± SD HAQ scores were 0.34 ± 0.54 in the combination‐DMARD group and 0.38 ± 0.58 in the single‐DMARD group (P = 0.88). Modified MDA was achieved by 63% (95% confidence interval [95% CI] 51, 77) and by 43% (95% CI 32, 55) (P = 0.016) of the combination‐DMARD group and the single‐DMARD group, respectively, and ACR remission by 37% (95% CI 26, 49) and by 19% (95% CI 11, 29) (P = 0.017), respectively.ConclusionInitial therapy with a combination of DMARDs in early RA results in higher rates of patients achieving modified MDA and strict ACR remission even over the long term than initial single‐DMARD therapy. Targeting remission with tight clinical controls results in good functional and clinical outcomes in most RA patients.
Induction of CCR2‐dependent macrophage accumulation by oxidized phospholipids in the air‐pouch model of inflammation
Authors: Kadl Alexandra , Galkina Elena , Leitinger Norbert 
Published: April 2009

AbstractObjectiveMacrophages are key players in the pathogenesis of rheumatoid synovitis as well as in atherosclerosis. To determine whether atherogenic oxidized phospholipids potentially contribute to synovial inflammation and subsequent monocyte/macrophage recruitment, we examined the effects of oxidized 1‐ palmitoyl‐2‐arachidonoyl‐sn‐3‐glycero‐phosphorylcholine (OxPAPC) on chemokine expression and leukocyte recruitment in a facsimile synovium in vivo using the murine air‐pouch model.MethodsAir pouches were raised by 2 injections of sterile air, and inflammation was induced by injecting either lipopolysaccharide (LPS) or OxPAPC into the pouch lumen. Inflammation was assessed by analysis of inflammatory gene expression using reverse transcription–polymerase chain reaction or immunohistochemical analysis, and leukocytes were quantified in the lavage fluid and in the pouch wall after staining with Giemsa or after enzymatic digestion followed by fluorescence‐activated cell sorter analysis.ResultsApplication of OxPAPC resulted in selective recruitment of monocyte/macrophages into the air‐pouch wall, but not in the lumen. In contrast, LPS induced both monocyte and neutrophil accumulation in the pouch lumen as well as in the wall. LPS, but not OxPAPC, induced the expression of adhesion molecules E‐selectin, P‐selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1. OxPAPC increased the expression of the CCR2 ligands monocyte chemotactic protein 1 (MCP‐1), MCP‐3, and MCP‐5, as well as RANTES and growth‐related oncogene α (GROα), while it down‐regulated the expression of CCR2 on macrophages. Moreover, oxidized phospholipid–induced macrophage accumulation was abrogated in CCR2−/− mice.ConclusionThese data demonstrate that oxidized phospholipids trigger a type of inflammatory response that leads to selective macrophage accumulation in vivo, a process relevant for the pathogenesis of chronic inflammatory rheumatic diseases.
Activation of the interferon‐γ signaling pathway in systemic lupus erythematosus peripheral blood mononuclear cells
Authors: Karonitsch Thomas , Feierl Eva , Steiner Carl Walter , Dalwigk Karolina , Korb Adelheid , Binder Nikolaus , Rapp Alfred , Steiner Günter , Scheinecker Clemens , Smolen Josef , Aringer Martin 
Published: April 2009

AbstractObjectiveTo investigate interferon‐γ (IFNγ) signaling in peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE) by analyzing IFNγ receptor (IFNγR) expression, STAT‐1 expression and phosphorylation, and the regulation of IFNγ‐inducible genes.MethodsFluorocytometry was used to investigate expression of STAT‐1, pSTAT‐1, CD95, HLA–DR, class I major histocompatibility complex (MHC), IFNγ‐inducible 10‐kd protein (IP‐10), monokine induced by IFNγ (Mig), and IFNγR in PBMCs from SLE patients and healthy individuals. STAT‐1 phosphorylation was determined by fluorocytometry and Western blotting after stimulation with IFNα or IFNγ. Quantitative polymerase chain reaction was used to assess messenger RNA (mRNA) expression of the IFNγ‐inducible genes IP‐10 and Mig shortly after preparation or after stimulation with IFNγ in monocytes.ResultsSTAT‐1 expression was increased in PBMCs from SLE patients and correlated significantly with disease activity and with the IFN‐inducible expression of CD95 and HLA–DR. STAT‐1 expression also showed a trend toward association with class I MHC expression. In addition, the expression of other IFNγ‐inducible genes, such as IP‐10 or Mig, was increased in SLE monocytes. While STAT‐1 phosphorylation in SLE PBMCs and PBMCs from healthy individuals was similar after IFNα stimulation, incubation with IFNγ induced STAT‐1 phosphorylation only in SLE lymphocytes. Moreover, SLE monocytes showed a considerably higher increase in pSTAT‐1 expression upon IFNγ stimulation than monocytes from healthy individuals. Increased responsiveness of SLE monocytes to IFNγ was also confirmed on the mRNA level, where expression of the IFN‐inducible, STAT‐1–dependent genes IP‐10 and Mig was more efficiently increased in SLE cells. However, IFNγR was similarly expressed on SLE lymphocytes and monocytes and those from healthy individuals.ConclusionIn addition to supporting the role of IFNs in SLE immunopathogenesis in general, the findings of the present study support a role of IFNγ in this disease.