bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cigarette smoking and the risk of systemic lupus erythematosus: A meta‐analysis
Authors: Costenbader Karen H. , Kim Daniel J. , Peerzada Jehanna , Lockman Shahin , Nobles‐Knight Dolores , Petri Michelle , Karlson Elizabeth W. 
Published: March 2004

AbstractObjectiveExisting studies present conflicting evidence for the role of cigarette smoking as a risk factor in the development of systemic lupus erythematosus (SLE). We performed an extensive search of the medical literature for all studies examining this relationship, and performed a meta‐analysis to arrive at a more precise estimate of effect.MethodsWe performed a computerized literature search for all studies (in all languages), using Medline and EMBASE (1966 to present) and the Cochrane Collaboration database, and completed hand searches of relevant bibliographies and abstracts of conference proceedings. Several investigators systematically extracted data from the relevant studies. Unpublished data were obtained from the author of one abstract. Studies were examined in aggregate for heterogeneity and publication bias. The relationships of current smoking and past smoking (prior to the onset of SLE) to development of SLE were analyzed separately.ResultsFifty‐two studies were identified and chosen for detailed review. Of these, 9 (7 case–control and 2 cohort studies) were appropriate for inclusion in our meta‐analyses. For current smokers compared with nonsmokers, the odds ratio (OR) for development of SLE was significantly elevated (OR 1.50, 95% confidence interval [95% CI] 1.09–2.08). Former smokers, compared with nonsmokers, did not demonstrate an increased risk of SLE (OR 0.98, 95% CI 0.75–1.27). Several subgroups were also analyzed.ConclusionOur meta‐analysis of the 7 existing case–control and 2 cohort studies revealed a small but statistically significant association between current smoking and development of SLE. However, no association between past smoking and development of SLE was observed.
Sjögren's syndrome associated with systemic lupus erythematosus: Clinical and laboratory profiles and comparison with primary Sjögren's syndrome
Authors: Manoussakis Menelaos N. , Georgopoulou Chryssoula , Zintzaras Elias , Spyropoulou Marilyn , Stavropoulou Aikaterini , Skopouli Fotini N. , Moutsopoulos Haralampos M. 
Published: March 2004

AbstractObjective.To address the clinical, serologic, pathologic, and immunogenetic features of sicca syndrome that occurs in systemic lupus erythematosus (SLE), as well as its similarities to, and differences from, sicca syndrome that occurs in primary Sjögren's syndrome (SS).Methods.A cohort of 283 consecutive unselected SLE patients was evaluated for the presence of associated SS using the American–European classification criteria. Clinical and laboratory parameters in SLE patients with SS (SLE–SS) were compared with those in SLE patients without SS (SLE–no SS) and with a group of 86 unselected patients with primary SS.Results.SS was identified in 26 SLE patients (9.2%); the SS preceded the development of lupus in 18 of them (69.2%). Compared with the SLE–no SS group, patients with SLE–SS were significantly older, had a higher frequency of Raynaud's phenomenon, anti‐Ro/SSA, anti‐La/SSB, and rheumatoid factor, but had a significantly lower frequency of renal involvement, lymphadenopathy, and thrombocytopenia. Compared with the primary SS group, SLE–SS patients displayed a clinically similar sicca syndrome, but were significantly younger and had an increased frequency of perivascular infiltrates in the salivary glands associated with anticardiolipin antibodies in the serum. SLE–SS patients had a high frequency of the DRB1*0301 allele. This HLA profile distinguished the SLE–SS group from the SLE–no SS group, who had an increased frequency of DRB1*1501 and DQB1*0602 alleles, but was similar to the HLA profile of the primary SS group, who had an increased frequency of DRB1*0301.Conclusion.SLE–SS appears to constitute a subgroup of patients with distinct clinical, serologic, pathologic, and immunogenetic features, in whom SS is expressed as an overlapping entity and is largely similar to primary SS.
Is α‐actinin a target for pathogenic anti‐DNA antibodies in lupus nephritis?
Authors: Mason Lesley J. , Ravirajan Chelliah T. , Rahman Anisur , Putterman Chaim , Isenberg David A. 
Published: March 2004

AbstractObjectiveFollowing recent reports that pathogenic murine anti‐DNA antibodies bind to α‐actinin, it was obviously of interest to assess the ability of human pathogenic anti–double‐stranded DNA (anti‐dsDNA) antibodies to bind this antigen. Both human monoclonal anti‐DNA antibodies and antibodies affinity purified from the sera of patients with systemic lupus erythematosus (SLE) were investigated.MethodsAn enzyme‐linked immunosorbent assay was established to measure immunoglobulin binding to α‐actinin. Antibodies binding dsDNA were purified from the sera of SLE patients who either had active renal disease or had never had renal disease. Serum samples were selected at times when the patients' sera exhibited high IgG binding to dsDNA. The binding of supernatants from 3 high‐affinity human anti‐dsDNA IgG hybridomas (RH14, B3, and DIL‐6) and 7 human IgM anti‐DNA hybridomas was also investigated.ResultsA greater proportion of anti‐dsDNA IgG–binding antibodies purified from patients with renal disease bound to α‐actinin than did those purified from the sera of patients without renal disease. The specificity of binding to the 100‐kd α‐actinin molecule was confirmed by Western blotting. The pathogenic human antibodies RH14 and B3 bound strongly to α‐actinin, while nonpathogenic DIL‐6 bound very weakly. RT84, the IgM antibody that binds dsDNA with the highest affinity, exhibited the greatest binding to α‐actinin.ConclusionThe results of our study support the findings of previous studies using murine anti‐DNA monoclonal antibodies, which suggest that pathogenic anti‐dsDNA antibodies cross‐react with α‐actinin.
In vivo imaging of experimental arthritis with near‐infrared fluorescence
Authors: Hansch Andreas , Frey Oliver , Sauner Dieter , Hilger Ingrid , Haas Michael , Malich Ansgar , Bräuer Rolf , Kaiser Werner A. 
Published: March 2004

AbstractObjectiveTo visualize early experimental arthritis with near‐infrared fluorescence (NIRF) imaging in a murine model of antigen‐induced arthritis (AIA).MethodsThe target of NIRF was the F4/80 antigen present on the surface of macrophages infiltrating the inflamed synovial membrane. Imaging was performed using anti‐F4/80 monoclonal antibodies (mAb) labeled with Cy5.5 fluorochrome. On day 7 of AIA, 6 mice received an intravenous (IV) injection of labeled mAb; control AIA mice (n = 6) received an IV injection of Cy5.5‐labeled isotype control antibody. NIRF imaging was performed before injection (baseline) and until 72 hours thereafter. Histologic evaluation of arthritis severity and immunohistochemical assessment of F4/80 antigen density were also performed on day 7.ResultsNIRF imaging showed an accumulation of fluorochrome probes in the inflamed knee joints and, to a lesser extent, in the contralateral (nonarthritic) knee joints. The signal induced by mAb F4/80 was clearly higher than that generated by the isotype control. Accumulation of fluorochrome probes in the joints was confirmed histologically by confocal laser scanning microscopy.ConclusionThe use of fluorochromes allows imaging of arthritis in the near‐infrared range. Accumulation in the contralateral, nonarthritic knee joints can be explained by the presence of sentinel macrophages in normal synovium or by a mild contralateral response due to systemic activation or neurogenic mechanisms.
Lack of response to anakinra in rheumatoid arthritis following failure of tumor necrosis factor α blockade
Authors: Buch Maya H. , Bingham Sarah J. , Seto Yohei , McGonagle Dennis , Bejarano Victoria , White Jo , Emery Paul 
Published: March 2004

AbstractObjective.In patients with rheumatoid arthritis (RA) treated with tumor necrosis factor α (TNFα)– blocking therapy, there is heterogeneity of response. This raises the possibility that in certain circumstances, cytokines such as interleukin‐1 (IL‐1) may dominate the drive toward joint inflammation. This study was undertaken to investigate whether blocking the action of IL‐1 with an IL‐1 receptor antagonist (IL‐1Ra) is efficacious in patients with disease that did not respond to TNFα blockade.Methods.We identified 26 RA patients whose disease had failed to respond to TNFα‐blocking therapy, defined as failure to achieve or sustain a 20% improvement in disease activity according to the criteria of the American College of Rheumatology (ACR20 response). These patients were then treated with anakinra (100 mg/day subcutaneously) for 12 weeks, and their levels of response were assessed.Results.After 3 months of anakinra therapy, only 2 of 26 patients (8%) achieved an ACR20 response; none achieved an ACR50 or ACR70 response. A rise in the mean C‐reactive protein level and an increase in the mean swollen joint count were noted during the study period.Conclusion.This study demonstrates that patients with disease that fails to respond to TNFα blockade also do not respond to IL‐1Ra. These data do not provide evidence of a dominant role for IL‐1 in patients who do not respond to TNFα blockade, but they do not exclude a role for other proinflammatory mediators.
Haplotype analysis in simplex families and novel analytic approaches in a case–control cohort reveal no evidence of association of the CTLA‐4 gene with rheumatoid arthritis
Authors: Barton Anne , Jury Francine , Eyre Stephen , Bowes John , Hinks Anne , Ward Daniel , Worthington Jane 
Published: March 2004

AbstractObjectiveCytotoxic T lymphocyte–associated antigen 4 (CTLA‐4) is a negative regulator of T cells and is, therefore, a strong candidate susceptibility gene for T cell–mediated autoimmune diseases. The association of CTLA‐4 single‐nucleotide polymorphisms (SNPs) with rheumatoid arthritis (RA) has been investigated previously, with inconsistent results. Recently, SNPs mapping to the gene (and not previously investigated in RA) have been associated with both type 1 diabetes mellitus and Graves' disease. The aim of this study was to investigate the association of the CTLA‐4 polymorphism with RA.MethodsPrimer extension methods were used to genotype 5 haplotype‐tagging SNPs (htSNPs) (−1722 T/C, −1661 A/G, −658 C/T, −319 C/T, and +49 A/G), and the TaqMan 5′ allelic discrimination assay was used to genotype an additional 2 SNPs (CT60 and rs1863800) mapping to the CTLA‐4 gene. Association to the 5 htSNPs was investigated using the transmission disequilibrium test in RA simplex families (n = 122). Allele frequencies for the htSNPs were also investigated in affected sibling pairs (n = 96) and unrelated controls (n = 173). For the SNPs CT60 and rs1863800, unrelated patients with RA (n = 759) were compared with controls (n = 755).ResultsNo evidence for association to single markers or haplotypes of the 5 htSNPs was detected in either RA simplex families or the affected sibling–control cohort. Neither of the 2 SNPs recently associated with Graves' disease showed evidence for association in the unrelated patient–control cohort.ConclusionNo evidence for association of CTLA‐4 with RA was detected using family or case–control methods.
Endothelial and platelet microparticles in vasculitis of the young
Authors: Brogan P. A. , Shah V. , Brachet C. , Harnden A. , Mant D. , Klein N. , Dillon M. J. 
Published: March 2004

AbstractObjectiveMicroparticles are released from endothelial cells in response to a variety of injurious stimuli and recently have been shown to be increased in a number of diseases associated with endothelial dysfunction. This study examined endothelial microparticle (EMP) and platelet microparticle (PMP) profiles in children with systemic vasculitis to test the hypothesis that EMPs may provide a noninvasive means of examining endothelial activation or injury.MethodsThe study cohort comprised 39 children with systemic vasculitis at various stages of disease activity, 24 control children with febrile disease, and a control group of 43 healthy subjects. Plasma was ultracentrifuged at 17,000g for 60 minutes, and the microparticle pellets were examined using flow cytometry.ResultsPlasma from patients with active systemic vasculitis contained significantly higher numbers of E‐selectin–positive EMPs compared with that from patients in remission, healthy controls, or febrile disease controls (P = 0.000 for each). A similar result was obtained for the numbers of EMPs expressing the marker CD105. There was also a significant increase in PMPs expressing CD42a in the active vasculitis group as compared with the other groups, but this difference was not significant for PMPs expressing P‐selectin. The EMP counts correlated with the Birmingham Vasculitis Activity Score and the acute‐phase reactant levels in the patients with systemic vasculitis, but there was a poor correlation overall between EMP counts and the acute‐phase reactant levels in the febrile disease controls.ConclusionEMPs may provide a window to the activated endothelium and could provide important pathophysiologic insights into the vascular injury associated with vasculitis of the young.
Enumeration and phenotypic characterization of synovial fluid multipotential mesenchymal progenitor cells in inflammatory and degenerative arthritis
Authors: Jones Elena A. , English Anne , Henshaw Karen , Kinsey Sally E. , Markham Alex F. , Emery Paul , McGonagle Dennis 
Published: March 2004

AbstractObjectiveTo evaluate synovial fluid (SF) for the presence of mesenchymal progenitor cells (MPCs), to compare SF MPCs with bone marrow (BM) MPCs, and to enumerate these cells in both inflammatory arthritis and osteoarthritis (OA).MethodsSF from 100 patients with arthritis (53 rheumatoid arthritis [RA], 20 OA, and 27 other arthropathies) was evaluated. To establish multipotentiality, polyclonal and single cell–derived cultures of SF fibroblasts were examined by standard and quantitative differentiation assays. Their phenotype before and after expansion was determined by multiparameter flow cytometry. A colony‐forming unit–fibroblast assay was used for SF MPC enumeration.ResultsRegardless of the nature of the arthritis, both polyclonal and single cell–derived cultures of SF fibroblasts possessed trilineage mesenchymal differentiation potentials. The number of MPCs in a milliliter of SF was higher in OA (median 37) than in RA (median 2) (P < 0.00001). No significant differences in MPC numbers were found between early and established RA (median 3 and 2 cells/ml, respectively). Culture‐expanded SF and BM MPCs had the same phenotype (negative for CD45 and positive for D7‐FIB, CD13, CD105, CD55, and CD10). Rare, uncultured SF fibroblasts were CD45low and expressed low‐affinity nerve growth factor receptor, similar to in vivo BM MPCs.ConclusionOur findings prove the presence of rare tripotential MPCs, at the single‐cell level, in the SF of patients with arthritis. SF MPCs are clonogenic and multipotential fibroblasts that, despite the pathologic environment within a diseased joint, have a phenotype similar to that of uncultured BM MPCs. The higher prevalence of MPCs in OA SF suggests their likely origin from disrupted joint structures. These findings could determine the role of MPCs in the pathogenesis of inflammatory arthritis, together with their role in attempted joint regeneration in degenerative arthritis, which has yet to be established.
Signal transduction via the NF‐κB pathway: a targeted treatment modality for infection, inflammation and repair
Authors: Ali Shakir , Mann Derek A. 
Published: March 2004

AbstractActivation of transcription factors plays a pivotal role in many signal transduction pathways. Of particular interest is NF‐κB, which is present in the cytoplasm in an inactive form, where it can be activated in response to many different stress conditions such as infection, inflammation, heat shock etc. It has also been associated with apoptosis and tissue repair. Modulation of signal transduction events that mediate activation of NF‐κB seems to have a great potential in not only treating many disease conditions, but also in tissue repair. The present review article is an attempt to put together many different conditions where the NF‐κB activation pathway appears to be crucial in transducing signals under stress conditions, and to explore the possibility of its modulation as a targeted treatment modality. Copyright © 2004 John Wiley & Sons, Ltd.
About the CRAZED sequence
Authors: Branca Rosa T. , Capuani Silvia , Maraviglia Bruno 
Published: March 2004

AbstractIn this article we report a detailed and understandable analysis of the evolution of various coherence orders in a Correlated 2D spectroscopy Revamped by Asymmetric Z‐gradient Echo Detection (CRAZED) like pulse sequence, used to select a signal from intermolecular Multi Quantum Coherences (iMQCs). Because the signal to‐noise‐ratio of iMQC is much lower than the signal from conventional single quantum coherence (SQC), an optimization of experimental parameters is a necessity when measurements are made with iMQC. For this purpose a phase cycle is shown that not only allows a simpler selection of a particular quantum coherence order, but also removes receiver artifacts. © 2004 Wiley Periodicals, Inc. Concepts Magn Reson Part A 21A: 22–36, 2004
A microscopic view of chemical exchange: Monte Carlo simulation of molecular association
Authors: Lippens G. , Caron L. , Smet C. 
Published: March 2004

AbstractThe well‐known phenomenon of exchange broadening, described in macroscopic terms by the modified Bloch equations, is re‐examined from the point of view of the individual molecules. Defining two possible states, we use a simple Monte Carlo algorithm to calculate the time trajectory of all molecules. After assigning distinct frequencies to the two states, the spectrum of an individual molecule can be calculated. The ensemble average describes well the broadening that is experimentally observed. © 2004 Wiley Periodicals, Inc. Concepts Magn Reson Part A 21A: 1–9, 2004
Residual dipolar coupling constants: An elementary derivation of key equations
Authors: Kramer F. , Deshmukh M.V. , Kessler H. , Glaser S.J. 
Published: March 2004

AbstractResidual dipolar couplings have recently found a wide range of applications in high‐resolution NMR of biomolecules in the liquid state. A nonisotropic orientational distribution of a molecule of interest results in nonzero average dipolar coupling constants. Here, we present an intuitive introduction to the alignment tensor and an elementary derivation of key equations. © 2004 Wiley Periodicals, Inc. Concepts Magn Reson Part A 21A: 10–21, 2004
Pulsed saturation of the standard two‐pool model for magnetization transfer. Part I: The steady state
Authors: Helms Gunther , Hagberg Gisela E. 
Published: March 2004

AbstractA general framework for magnetization transfer (MT) of a two‐pool system with linear exchange for arbitrary saturation by periodic radio‐frequency pulses was derived. It is based on a novel parameterization adapted to the time evolution of saturation recovery. The conditions in tissue permit a description in analogy to partial saturation of a homogeneous liquid. In this approximation, the direct saturation of bulk water is amplified by MT. Rapid transfer equilibrates the saturation of the pools in the early phase of free evolution. This kinetic “pre‐equilibrium” relaxes slowly with a common relaxation rate. © 2004 Wiley Periodicals, Inc. Concepts Magn Reson Part A 21A: 37–49, 2004
Pulsed saturation of the standard two‐pool model for magnetization transfer. Part II: The transition to steady state
Authors: Helms Gunther , Dathe Henning , Hagberg Gisela E. 
Published: March 2004

AbstractThe transition of the tissue signal to steady state under periodic selective saturation of macromolecular magnetization can be observed by single‐shot echo‐planar imaging. The general solution for a two‐pool system with linear exchange kinetics contains two transient components. The rapid minor transient causes an initial delay of the transition for fast pulse repetition (PR) and weak saturation. The slow major transient combines progressive direct saturation and transferred saturation. Its PR‐dependence provides similar information as the steady state, but is less sensitive to direct saturation and fitting errors. Sampling at different PR allows to quantify all system parameters. © 2004 Wiley Periodicals, Inc. Concepts Magn Reson Part A 21A: 50–62, 2004
Human cardiovascular and gustatory brainstem sites observed by functional magnetic resonance imaging
Authors: Topolovec Jane C. , Gati Joseph S. , Menon Ravi S. , Shoemaker J. Kevin , Cechetto David F. 
Published: March 2004

AbstractThe reflex control and relay to higher brain sites of visceral sensory information within the central nervous system is mediated via discrete sites in the brainstem. Anatomical characterization of these sites in humans has been limited due to the invasive nature of such research. The present study employed 4 Tesla functional magnetic resonance imaging (fMRI) to characterize brainstem sites involved in autonomic control in the human. Eight subjects performed tasks that activate the general visceral (the isometric hand‐grip, maximal inspiration, Valsalva maneuver) or special visceral sensory systems (sucrose administration to the tongue). Activation of the nucleus of the solitary tract and parabrachial nucleus was consistently observed with all general visceral tasks. Periaqueductal gray area activation was observed during the maximal inspiration and Valsalva maneuver conditions and raphe activation was present in response to isometric hand‐grip and maximal inspiration tasks. The activation in the nucleus of the solitary tract was consistently more rostral in the medulla during sucrose administration than during performance of the other experimental tasks. This finding is consistent with what has been previously demonstrated in animals. This is the first study to image the human brainstem with respect to visceral control and demonstrates the feasibility of using high‐resolution fMRI to study the functional organization of the human brainstem. J. Comp. Neurol. 471:446–461, 2004. © 2004 Wiley‐Liss, Inc.