bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sorption of Trace Metals by Standard and Micro Suction Cups in the Absence and Presence of Dissolved Organic Carbon
Authors: Rais D. , Nowack B. , Schulin R. , Luster J. 
Published: January 2006

ABSTRACTBoth the bioavailability of a trace metal (TM) in a soil and the risk of leaching to the ground water are linked to the metals concentration in the soil solution. Sampling soil solution by tension lysimetry with suction cups is a simple and established technique that is increasingly used for monitoring dissolved TM in soils. Of major concern, however, is the sorption of TM by the walls of the samplers. Metal sorption by different materials used in suction cups can vary widely, depending also on the chemistry of the soil solution. We compared the sorption of Cu, Zn, Cd, and Pb by different standard‐size and micro suction cups in the laboratory at two pH values (4.5 and 7.5 or 8.0) in absence and presence of dissolved organic carbon (DOC). In addition, we investigated the sorption of DOC from different origins by the cup materials. At both pH values, the weakest sorption of all four TMs was exhibited by standard‐size suction cups based on nylon membranes and by hollow fibers made from polyvinyl alcohol (PVA). At alkaline pH, borosilicate glass, ceramic materials, and polytetrafluorethylene (PTFE) mixed with silicate were characterized by generally strong sorption of all investigated TMs. In addition, Cu and Pb were strongly sorbed at low pH by PTFE–silicate and a ceramic material used for the construction of standard‐size suction cups. On the other hand, sorption of Cu, Zn, and Cd by ceramic capillaries produced from pure aluminum oxide was negligible at low pH. Micro suction cups made of an unknown polymerous tube sorbed Cu strongly, but were well suited to monitor Zn, Cd, and Pb at low pH, and, in the presence of DOC, also at high pH. Major cations (Na+, Mg2+, K+, Ca2+) and anions (Cl−, NO3−, SO42−) were not or very weakly sorbed by all cup materials, except for Mg2+, K+, and Ca2+ by borosilicate glass at pH 7.5. Trace metal sorption by suction cups was generally greatly reduced in the presence of DOC, especially at alkaline pH. The sorption of DOC itself depended on its source. Dissolved organic carbon from leaf litter extracts with a probably large hydrophobic fraction was sorbed more strongly than mainly hydrophilic DOC from a mineral soil solution.
Capecitabine-Induced Severe Hypertriglyceridemia: Report of Two Cases
Authors: Kurt Mevlut , Babaoglu Melih O , Yasar Umit , Shorbagi Ali , Guler Nilufer 
Published: January 2006

Objective: To report 2 cases of severe hypertriglyceridemia associated with the use of oral capecitabine. Case Summaries: The first patient was a 73-year-old woman with metastatic breast carcinoma who received capecitabine 2500 mg/m2/day in 2 divided doses for 2 weeks followed by a one week rest period. The baseline triglyceride level was 324 mg/dL; after 2 cycles of capecitabine, levels increased to 916 mg/dL. Although lipid-lowering treatment was initiated, triglyceride levels peaked at 1782 mg/dL by the end of the seventh cycle. Eight weeks after capecitabine treatment was stopped, triglyceride levels decreased to 118 mg/dL. The second patient was a 59-year-old man with metastatic colorectal carcinoma who was placed on capecitabine treatment at a dosage of 2500 mg/m2/day in 2 divided doses for 2 weeks followed by a one week rest period. The baseline triglyceride level was 244 mg/dL; levels peaked at 1455 mg/dL at the end of the fifth cycle. Capecitabine treatment was discontinued due to disease progression, and triglyceride levels decreased to 154 mg/dL after 11 weeks. Discussion: The most frequently reported adverse effects of capecitabine are gastrointestinal and hematologic effects and palmar-plantar erythrodysesthesia. Drug-induced hyperlipidemia may appear more readily in individuals with hereditary lipoprotein lipase deficiency because decreased lipoprotein lipase activity might make these individuals more susceptible to a rise in triglyceride levels. The Naranjo probability scale indicated a probable relationship between capecitabine and severe hypertriglyceridemia. Conclusions: Capecitabine should be prescribed with care, especially in patients with preexisting hypertriglyceridemia. The question of whether capecitabine actually causes hypertriglyceridemia needs careful consideration, and the possible mechanism by which it may cause this adverse effect requires further investigation.
BAFF‐induced changes in B cell antigen receptor–containing lipid rafts in Sjögren's syndrome
Authors: d'Arbonneau Frédérique , Pers Jacques‐Olivier , Devauchelle Valérie , Pennec Yvon , Saraux Alain , Youinou Pierre 
Published: December 2005

AbstractObjectiveTo determine the effect of excessive production of BAFF on the distribution and function of B cell subsets in patients with primary Sjögren's syndrome (SS).MethodsThe phenotype of B lymphocytes was analyzed by flow cytometry. Differences in the expression level of membrane IgD and CD38 were used to identify B lymphocyte subsets evolving from naive Bm1 through memory Bm5 cells. Based on our finding of a low expression of CD45RA, we sorted Bm2/Bm2′ cells to determine the time course of translocation of the CD19 molecule and the B cell receptor into lipid rafts, by confocal microscopy. Serum levels of BAFF were measured by an enzyme‐linked immunosorbent assay developed in‐house.Results“Circulating” Bm2/Bm2′ cells were expanded in patients with primary SS compared with rheumatic disease controls and with normal controls. In addition, these B cell subsets were functionally abnormal. Prolonged residency of the B cell receptor in lipid rafts in these cells was associated with elevated CD19 expression in B cells, most notably, Bm2 and Bm2′ cells, obtained from the patients with primary SS. BAFF levels were higher in the patients than in the normal controls and correlated with the percentage of Bm2/Bm2′ cells and their expression of CD19 in primary SS patients. These correlations were confirmed by placing sorted Bm1 or Bm2 cells from normal controls in culture in the presence or absence of BAFF.ConclusionBm2/Bm2′ cells express more CD19 molecules in primary SS patients than in normal controls. BAFF might participate in this elevated expression of CD19. These patients might be suitable candidates for treatment with BAFF antagonists.
The effectiveness of anti–tumor necrosis factor therapy in preventing progressive radiographic joint damage in rheumatoid arthritis: A population‐based study
Authors: Finckh Axel , Simard Julia F. , Duryea Jeffrey , Liang Matthew H. , Huang Jie , Daneel Synove , Forster Adrian , Gabay Cem , Guerne Pierre‐André 
Published: December 2005

AbstractObjectiveTo compare the effectiveness of 3 therapeutic strategies in preventing progressive joint damage, in a population‐based cohort. The 3 strategies were infliximab with concomitant disease‐modifying antirheumatic drugs (DMARDs), etanercept with concomitant DMARDs, and etanercept alone.MethodsWe used sequential radiographs to assess all patients who were treated with infliximab or etanercept for >10 months. The rates of erosion progression and joint space narrowing (JSN) were analyzed using multivariate regression models for longitudinal data, with adjustment for potential confounders.ResultsA total of 372 patients treated with anti–tumor necrosis factor (TNF) therapies met the inclusion criteria. The baseline characteristics of the patients assigned to the 3 strategies were not significantly different, except that, as expected, more patients were receiving combination therapy with infliximab. The combination of infliximab plus DMARDs was significantly more effective than etanercept alone for controlling erosion progression (P< 0.001), but the effectiveness of the 2 combination‐treatment strategies was similar (P= 0.07). The combination of infliximab plus DMARDs was also more effective at controlling progressive JSN compared with etanercept alone (P= 0.04) or etanercept plus DMARDs (P= 0.02). Treatment with anti‐TNF agents (infliximab or etanercept) plus concomitant DMARDs was more effective than treatment with etanercept alone for controlling erosion progression (P= 0.045).ConclusionWhen combined with traditional DMARDs, both etanercept and infliximab appear to offer similar protection against progressive structural joint damage, and combination therapy with either of these agents appears to be more effective than treatment with etanercept alone.
Monocyte chemoattractant protein 1 released from glycosaminoglycans mediates its profibrotic effects in systemic sclerosis via the release of interleukin‐4 from T cells
Authors: Distler Jörg H. W. , Jüngel Astrid , Caretto David , Schulze‐Horsel Ursula , Kowal‐Bielecka Otylia , Gay Renate E. , Michel Beat A. , Müller‐Ladner Ulf , Kalden Joachim R. , Gay Steffen , Distler Oliver 
Published: December 2005

AbstractObjectiveMonocyte chemoattractant protein 1 (MCP‐1; CCL2) has been implicated in the pathogenesis of fibrotic diseases and is up‐regulated in patients with systemic sclerosis (SSc). The aim of the present study was to examine the mechanisms by which MCP‐1 mediates its profibrotic effects in the setting of SSc.MethodsThe expression of receptors for MCP‐1 on dermal fibroblasts was analyzed by real‐time polymerase chain reaction and fluorescence‐activated cell sorting. The ability of extracellular matrix proteins to bind and release MCP‐1 was quantified by enzyme‐linked immunosorbent assay. Th0 cells were isolated using a magnetic‐activated cell sorting system and were stimulated twice in the presence of MCP‐1. The synthesis of collagen was measured using the Sircol collagen assay kit.ResultsThe glycosaminoglycan chondroitin sulfate, but not fibronectin or collagens, bound and released MCP‐1 in a time‐dependent manner. MCP‐1 that was released from chondroitin sulfate induced the differentiation of interleukin‐4 (IL‐4)–producing T cells in a dose‐dependent manner. In turn, dermal fibroblasts from patients with SSc expressed IL‐4 receptor, and stimulation with IL‐4 significantly increased the production of collagen in dermal fibroblasts. In contrast, CCR2a and CCR2b, as well as D6 and US28 (other potential receptors of MCP‐1), were not detectable in SSc and normal fibroblasts, and their expression was not induced by platelet‐derived growth factor, IL‐1β, or IL‐4. In addition, MCP‐1 had no direct effects on collagen production by fibroblasts.ConclusionMCP‐1 has no direct effects on dermal fibroblasts but contributes to fibrosis in patients with SSc by inducing the differentiation of IL‐4–producing T cells. Because MCP‐1 has both proinflammatory and profibrotic effects, pharmacologic targeting of MCP‐1 could be a promising therapeutic approach in SSc.
Association between protein tyrosine phosphatase 22 variant R620W in conjunction with the HLA–DRB1 shared epitope and humoral autoimmunity to an immunodominant epitope of cartilage‐specific type II collagen in early rheumatoid arthritis
Authors: Burkhardt Harald , Hüffmeier Ulrike , Spriewald Bernd , Böhm Beate , Rau Rolf , Kallert Stefan , Engström Åke , Holmdahl Rikard , Reis André 
Published: December 2005

AbstractObjectiveTo analyze the genetic impact of allelic variants of the protein tyrosine phosphatase N22 (PTPN22) and HLA–DRB1 alleles on IgG autoantibody formation directed toward an immunodominant conformational epitope (C1III; amino acid residues 359–369) of type II collagen (CII) in early rheumatoid arthritis (RA).MethodsSera obtained at study inclusion from an inception cohort of RA patients (n = 221; mean symptom duration 6 months) were analyzed for circulating anti–C1III IgG autoantibodies. An enzyme‐linked immunosorbent assay based on solid‐phase–coupled synthetic triple‐helical collagen peptides was used to quantify humoral autoimmune responses. HLA–DRB1 genotypes were determined by allele‐specific polymerase chain reaction amplification of genomic DNA and sequence‐specific hybridization. PTPN22*620W genotyping was performed using an allelic discrimination TaqMan assay.ResultsAnti–C1III IgG autoantibody titers were significantly elevated in patients with early RA as compared with those in healthy controls (n = 70). The increased titers were more pronounced in RA patients harboring alleles of the RA‐associated HLA–DRB1 shared epitope (SE) consensus sequence than in those lacking the SE. In addition, the PTPN22*620W variant was strongly associated with a vigorous humoral autoimmune response to the cartilage‐specific CII determinant C1III.ConclusionAllelic variants encoding the binding pocket for peptide presentation (SE) to T cells and a functional domain of a negative regulator of T cell receptor signaling (PTPN22*620W), respectively, synergize in early RA to break self tolerance toward C1III, an evolutionarily conserved cartilage determinant that is also frequently targeted in arthritogenic humoral autoimmunity in mice.
The PREMIER study: A multicenter, randomized, double‐blind clinical trial of combination therapy with adalimumab plus methotrexate versus methotrexate alone or adalimumab alone in patients with early, aggressive rheumatoid arthritis who had not had previous methotrexate treatment
Authors: Breedveld Ferdinand C. , Weisman Michael H. , Kavanaugh Arthur F. , Cohen Stanley B. , Pavelka Karel , Vollenhoven Ronald van , Sharp John , Perez John L. , Spencer‐Green George T. 
Published: December 2005

AbstractObjectiveTo compare the efficacy and safety of adalimumab plus methotrexate (MTX) versus MTX monotherapy or adalimumab monotherapy in patients with early, aggressive rheumatoid arthritis (RA) who had not previously received MTX treatment.MethodsThis was a 2‐year, multicenter, double‐blind, active comparator–controlled study of 799 RA patients with active disease of <3 years' duration who had never been treated with MTX. Treatments included adalimumab 40 mg subcutaneously every other week plus oral MTX, adalimumab 40 mg subcutaneously every other week, or weekly oral MTX. Co‐primary end points at year 1 were American College of Rheumatology 50% improvement (ACR50) and mean change from baseline in the modified total Sharp score.ResultsCombination therapy was superior to both MTX and adalimumab monotherapy in all outcomes measured. At year 1, more patients receiving combination therapy exhibited an ACR50 response (62%) than did patients who received MTX or adalimumab monotherapy (46% and 41%, respectively; both P < 0.001). Similar superiority of combination therapy was seen in ACR20, ACR70, and ACR90 response rates at 1 and 2 years. There was significantly less radiographic progression (P ≤ 0.002) among patients in the combination treatment arm at both year 1 and year 2 (1.3 and 1.9 Sharp units, respectively) than in patients in the MTX arm (5.7 and 10.4 Sharp units) or the adalimumab arm (3.0 and 5.5 Sharp units). After 2 years of treatment, 49% of patients receiving combination therapy exhibited disease remission (28‐joint Disease Activity Score <2.6), and 49% exhibited a major clinical response (ACR70 response for at least 6 continuous months), rates approximately twice those found among patients receiving either monotherapy. The adverse event profiles were comparable in all 3 groups.ConclusionIn this population of patients with early, aggressive RA, combination therapy with adalimumab plus MTX was significantly superior to either MTX alone or adalimumab alone in improving signs and symptoms of disease, inhibiting radiographic progression, and effecting clinical remission.
Activation of receptor for advanced glycation end products in osteoarthritis leads to increased stimulation of chondrocytes and synoviocytes
Authors: Steenvoorden Marjan M. C. , Huizinga Tom W. J. , Verzijl Nicole , Bank Ruud A. , Ronday H. Karel , Luning Hilco A. F. , Lafeber Floris P. J. G. , Toes René E. M. , DeGroot Jeroen 
Published: December 2005

AbstractObjectiveThe major risk factor for osteoarthritis (OA) is aging, but the mechanisms underlying this risk are only partly understood. Age‐related accumulation of advanced glycation end products (AGEs) could be one of these mechanisms. We undertook this study to investigate the role of the receptor for AGEs (RAGE) in mediating the cellular effects of AGEs on chondrocytes and fibroblast‐like synoviocytes (FLS).MethodsAGE levels in human cartilage were determined by fluorescence, browning, and pentosidine levels. Chondrocyte activation by AGEs was assessed as the release of proteoglycans and the synthesis of matrix metalloproteinase 1 (MMP‐1) and type II collagen messenger RNA (mRNA). The activation of FLS by AGEs was measured by MMP‐1 production and invasion through matrix proteins.ResultsPatients with focal degeneration of cartilage showed increased AGE levels in their healthy cartilage compared with the levels in healthy cartilage from donors without cartilage degeneration (P < 0.01 for both fluorescence and browning; P not significant for pentosidine content). Stimulation of bovine chondrocytes with glycated albumin increased the release of proteoglycans by 110% (P < 0.001) and the production of MMP‐1 mRNA by 200% (P = 0.028). In addition, OA FLS produced 240% more MMP‐1 when stimulated with glycated albumin (P < 0.001). Glycated matrix or albumin increased the catabolic activity of OA FLS, which was assessed as invasive behavior, by 150% and 140% (P = 0.001 and P = 0.010), respectively. Effects of stimulation with AGEs were blocked by a neutralizing antibody against RAGE, but not by an isotype control.ConclusionThis study shows that AGEs trigger RAGE on chondrocytes and FLS, leading to increased catabolic activity and therefore to cartilage degradation. AGEs, via RAGE, could therefore contribute to the development and/or progression of OA.
Increased expression of receptor for advanced glycation end products by synovial tissue macrophages in rheumatoid arthritis
Authors: Sunahori Katsue , Yamamura Masahiro , Yamana Jiro , Takasugi Koji , Kawashima Masanori , Makino Hirofumi 
Published: December 2005

AbstractObjectiveThe accumulation of advanced glycation end products (AGEs), S100A12, and high mobility group box chromosomal protein 1 has been associated with joint inflammation in rheumatoid arthritis (RA). This study was undertaken to determine the induction of the receptor for these proteins, termed receptor for AGEs (RAGE), in synovial tissue (ST) macrophages from RA patients.MethodsRAGE and CD68 expression in ST were determined by 2‐color immunofluorescence labeling. Cell surface and messenger RNA (mRNA) expression of RAGE were examined by flow cytometry and reverse transcriptase–polymerase chain reaction (PCR) or real‐time PCR, respectively.ResultsCD68+ lining macrophages, like the vasculature, expressed high levels of RAGE in inflamed ST from RA patients. RAGE mRNA expression was significantly higher in RA ST than in ST from patients with osteoarthritis. RAGE mRNA levels were significantly higher in ST macrophages and normal endothelial cells than in ST CD4+ T cells and synovial fibroblasts stimulated with tumor necrosis factor α and interleukin‐1β (IL‐1β). Cell surface RAGE was highly induced on normal monocytes after a 24‐hour incubation with a 20% concentration of RA ST cell culture supernatants. RAGE mRNA expression in adherent monocytes was augmented by various cytokines, most potently by IL‐1β.ConclusionThese results indicate that RAGE overexpression in lining macrophages may be induced, at least in part, by cytokines such as IL‐1, leading to the amplification of inflammatory responses mediated by RAGE ligands that are abundant in RA joints.
Association of higher levels of serum cartilage oligomeric matrix protein and N‐telopeptide crosslinks with the development of radiographic hip osteoarthritis in elderly women
Authors: Kelman A. , Lui L. , Yao W. , Krumme A. , Nevitt M. , Lane N. E. 
Published: December 2005

AbstractObjectiveTo examine the association of baseline concentrations of serum cartilage oligomeric matrix protein (COMP) and serum N‐telopeptide crosslinks (NTX) with the development and progression of radiographic hip osteoarthritis (RHOA) in elderly women.MethodsPelvic radiographs were obtained a mean of 8.3 years apart from white women ≥65 years of age enrolled in the Study of Osteoporotic Fractures. Random sampling from a cohort of 5,928 subjects was performed, with subjects (∼200 per group) assigned to nested case–control studies, one focusing on RHOA incidence and the other on RHOA progression. Baseline serum levels of COMP and NTX were measured by enzyme‐linked immunosorbent assay in duplicate. Odds ratios (ORs) and 95% confidence intervals (95% CIs), indicating the likelihood of baseline serum COMP and NTX levels to be predictive of the development or progression of RHOA, were calculated using logistic regression analysis, with adjustment for potential covariates.ResultsAt baseline, incident cases of RHOA were associated with higher serum levels of COMP and NTX (P < 0.05 for each) compared with the no RHOA control group. Higher baseline serum COMP and NTX levels were associated with an increased risk of incident RHOA compared with the no RHOA group, with an adjusted OR of 1.31 per SD increase in COMP (95% CI 1.02–1.68) and adjusted OR of 1.38 per SD increase in NTX (95% CI 1.07–1.79). In this community‐based cohort, progression of RHOA was modest. However, there was a trend toward increased risk of RHOA progression with higher baseline COMP and NTX levels.ConclusionThese data suggest that serum levels of COMP and NTX are modest risk markers for the development of RHOA in a community‐based cohort of elderly white women.
Fibromyalgia diagnosis: A comparison of clinical, survey, and American College of Rheumatology criteria
Authors: Katz Robert S. , Wolfe Frederick , Michaud Kaleb 
Published: December 2005

AbstractObjectiveThe American College of Rheumatology (ACR) criteria for fibromyalgia are the de facto criteria used for research. However, ACR criteria are not generally utilized by nonrheumatologists, and rheumatologists may diagnose fibromyalgia in patients who do not satisfy the ACR criteria. We undertook this study to determine concordance between ACR criteria and clinician diagnosis and between proposed survey criteria and clinician diagnosis.MethodsConsecutive patients in a clinical practice setting were evaluated by tender point examination, survey criteria for fibromyalgia (Regional Pain Scale score ≥8 and fatigue score ≥6), and clinical diagnosis.ResultsAmong the 206 patients, the clinician diagnosed fibromyalgia in 49.0%, while 29.1% satisfied ACR criteria and 40.3% satisfied survey criteria. Clinical and survey criteria were concordant in 74.8% of cases (κ = 0.49 [95% confidence interval 0.36, 0.60]). Clinical criteria and ACR criteria were concordant in 75.2% of cases (κ = 0.50 [95% confidence interval 0.35, 0.59]), and survey criteria and ACR criteria were concordant in 72.3% (κ = 0.40 [95% confidence interval 0.25, 0.51]). The ACR tender point criterion (≥11) was not a factor in clinical and survey criteria. However, the tender point count was useful in clinical diagnosis.ConclusionClinical diagnosis and ACR and survey criteria are moderately concordant (72–75%) and address a common pool of symptoms and physical findings. Because there is no gold standard for fibromyalgia diagnosis and because fibromyalgia is often viewed as a trait diagnosis, all methods of diagnosis have utility. The survey method has the advantage that it does not require physical examination.