bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nomenklatur der Lignane und Neolignane
Authors: Schomburg Dietmar 
Published: April 2005

AbstractLignane und Neolignane sind eine große Gruppe von Naturstoffen, in denen zwei C6C3‐Einheiten miteinander verknüpft vorliegen. Für Nomenklaturzwecke wird die C6C3‐Einheit als Propylbenzol behandelt, die Ringatome werden, beginnend bei der Propylgruppe, mit 1–6 nummeriert, die Atome der Propylgruppe mit 7–9, beginnend am Benzolring. Für die zweite C6C3‐Einheit werden einfach gestrichene Nummern verwendet. Wenn die beiden C6C3‐Einheiten durch eine Bindung zwischen den Positionen 8 und 8′ verbunden sind, wird die Substanz als Lignan bezeichnet. Wenn die Verknüpfung dagegen über andere Positionen erfolgt, ist die Substanz ein Neolignan; dabei kann C‐8 oder C‐8′ sehr wohl an der Verknüpfung beteiligt sein. Gibt es keine direkte C‐C‐Bindung zwischen den C6C3‐Einheiten, sondern eine O‐Brücke, wird die Substanz Oxyneolignan genannt. Das Nomenklatursystem sieht die Benennung von weiteren Ringen und von Modifizierungen gemäß Standardverfahren der organischen Nomenklatur für Naturstoffe vor. Die Benennung der höheren Homologe wird ebenfalls behandelt: Sesquineolignane bestehen aus drei, Dineolignane aus vier C6C3‐Einheiten.
Differential effects of the immunosuppressant FK‐506 on human α2(I) collagen gene expression and transforming growth factor β signaling in normal and scleroderma fibroblasts
Authors: Asano Yoshihide , Ihn Hironobu , Yamane Kenichi , Jinnin Masatoshi , Mimura Yoshihiro , Tamaki Kunihiko 
Published: April 2005

AbstractObjectiveTo investigate the effects of FK‐506 on the expression of the human α2(I) collagen gene and transforming growth factor β (TGFβ) signaling in normal and scleroderma fibroblasts.MethodsThe expression levels of type I procollagen protein and α2(I) collagen messenger RNA (mRNA) were analyzed by immunoblotting and Northern blotting, respectively. The promoter activities of α2(I) collagen gene and 3TP‐Lux were determined by transient transfection assay. Interaction between TGFβ receptor type I and FK‐506 binding protein 12 (FKBP12) was evaluated by immunoprecipitation.ResultsFK‐506 did not affect the basal expression of type I procollagen protein or α2(I) collagen mRNA, but it significantly reduced the TGFβ1‐induced expression of type I procollagen protein and α2(I) collagen mRNA in normal fibroblasts. The effect of FK‐506 was regulated posttranscriptionally, but not transcriptionally. In scleroderma fibroblasts, FK‐506 significantly reduced the expression of type I procollagen protein and α2(I) collagen mRNA through posttranscriptional regulation, but not transcriptional regulation. FK‐506 increased the basal activity of the 3TP‐Lux promoter, but it did not affect the TGFβ1‐induced promoter activity in normal fibroblasts. In contrast, FK‐506 did not affect the basal or the TGFβ1‐induced 3TP‐Lux promoter activity in scleroderma fibroblasts. Furthermore, FKBP12, which protects TGFβ receptor type I from ligand‐independent activation by TGFβ receptor type II, constitutively dissociated from TGFβ receptor type I in scleroderma fibroblasts.ConclusionFK‐506 inhibits α2(I) collagen gene expression by reducing the stability of mRNA without exhibiting its activation effect on TGFβ signaling in scleroderma fibroblasts.
Pain, stiffness, and fatigue in juvenile polyarticular arthritis: Contemporaneous stressful events and mood as predictors
Authors: Schanberg Laura E. , Gil Karen M. , Anthony Kelly K. , Yow Eric , Rochon James 
Published: April 2005

AbstractObjectiveTo analyze patterns of stress, mood, disease symptoms, and activity reduction in children with polyarticular arthritis, using a prospective daily diary method.MethodsFor a 2‐month period, 51 children with polyarticular arthritis (mean age 12.4 years, 65% female) completed daily diaries that included measures of symptoms of pain, stiffness, and fatigue, as well as stress, mood, and activity reduction. Functional status and disease activity were assessed at the initial and followup evaluations with use of the Childhood Health Assessment Questionnaire, physician global assessment, joint count, and laboratory testing.ResultsChildren reported having pain, stiffness, and fatigue on >70% of days, with significant variability in symptom levels. Results revealed significant same‐day relationships between stress, mood, and disease symptoms, after controlling for covariates. Specifically, daily fluctuations in both stress and mood were predictive of increased pain, stiffness, and fatigue. Increases in daily stress, mood, and disease symptoms were also significantly related to decreased participation in social activities on a day‐to‐day basis. Only mood and stiffness were predictors of a cutback in school attendance.ConclusionStress and mood are important predictors of daily disease symptoms in children with polyarticular arthritis. Moreover, daily fluctuations in stress, mood, and disease symptoms are predictive of aspects of daily function, including participation in school and social activities. Thus, health care providers should solicit daily symptom reports when making decisions regarding clinical management. Nonpharmacologic interventions such as cognitive‐behavioral therapy and stress management may be useful adjuvant therapy when treating the disease symptoms of children with polyarticular arthritis.
Interleukin‐1 blockade by anakinra improves clinical symptoms in patients with neonatal‐onset multisystem inflammatory disease
Authors: Lovell Daniel J. , Bowyer Suzanne L. , Solinger Alan M. 
Published: April 2005

AbstractNeonatal‐onset multisystem inflammatory disease (NOMID) is a rare, childhood‐onset disease that is characterized by chronic, systemic inflammation. The purpose of this report is to describe the effects of interleukin‐1 (IL‐1) blockade on the clinical symptoms of 2 patients with NOMID. At the time of this report, the patients had been treated with anakinra (Kineret), a recombinant human IL‐1 receptor antagonist, for 1.5 and 2 years, respectively. Both patients demonstrated rapid improvement in clinical symptoms and laboratory markers of inflammation. The use of anakinra in these patients seemed to be effective, without any safety concerns. These observations suggest that IL‐1 plays a critical role in the pathogenesis of this inflammatory disease, and that blockade with anakinra should be further studied as a treatment for patients with NOMID and related disorders.
Factors associated with hip cartilage volume measured by magnetic resonance imaging: The Tasmanian Older Adult Cohort Study
Authors: Zhai Guangju , Cicuttini Flavia , Srikanth Velandai , Cooley Helen , Ding Changhai , Jones Graeme 
Published: April 2005

AbstractObjectiveTo compare associations between anthropometric and lifestyle factors and femoral head cartilage volume/thickness and radiographic features of osteoarthritis (OA) and to provide evidence of construct validity for magnetic resonance imaging (MRI) assessment of femoral cartilage volume and thickness.MethodsWe studied a cross‐sectional sample of 151 randomly selected subjects (79 men, 72 women; mean age 63 years) from the Tasmanian Older Adult Cohort Study. A sagittal T1‐weighted fat‐suppression MRI scan of the right hip was performed to determine femoral head cartilage volume, cartilage thickness, and size. An anteroposterior radiograph of the pelvis with weight bearing was performed and scored for radiographic evidence of OA in the right hip. Other factors measured were height, weight, leg strength, serum vitamin D levels, and bone mineral density.ResultsHip cartilage volume was significantly associated with female sex, body mass index, and femoral head size, whereas hip cartilage thickness was significantly associated only with the size of the femoral head. Only female sex was significantly associated with the total radiographic OA score and the joint space narrowing (JSN) score, but not the osteophyte score. Radiographic JSN of the hip, especially axial JSN (but not osteophytes), was significantly correlated with hip cartilage volume and thickness.ConclusionFemoral head cartilage volume and thickness have modest but significant construct validity when correlated with radiographic findings. Furthermore, the generally stronger associations with volume compared with radiographic OA suggest that MRI may be superior at identifying risk factors for hip OA.
Expression of interleukin‐22 in rheumatoid arthritis: Potential role as a proinflammatory cytokine
Authors: Ikeuchi Hidekazu , Kuroiwa Takashi , Hiramatsu Noriyuki , Kaneko Yoriaki , Hiromura Keiju , Ueki Kazue , Nojima Yoshihisa 
Published: April 2005

AbstractObjectiveInterleukin‐22 (IL‐22) is a novel cytokine of the IL‐10 family. Although its pathophysiologic function is largely unknown, induction of acute‐phase responses by IL‐22 has suggested proinflammatory properties. In this study, we sought to examine whether IL‐22 plays a role in the pathogenesis of rheumatoid arthritis (RA).MethodsExpression of IL‐22 and IL‐22 receptor 1 (IL‐22R1) was examined by reverse transcription–polymerase chain reaction (RT‐PCR), Western blot, and immunohistochemical analysis. The effects of recombinant IL‐22 (rIL‐22) on cultured synovial fibroblasts derived from RA patients (RASF), with regard to the proliferation of synovial fibroblasts and production of monocyte chemoattractant protein 1 (MCP‐1), were examined by alamer blue assay and enzyme‐linked immunosorbent assay, respectively.ResultsIL‐22 messenger RNA was detected by RT‐PCR in RA synovial tissues and mononuclear cells isolated from RA synovial fluid samples. High levels of IL‐22 were expressed both in the lining and the sublining layers of RA synovial tissues. Staining for vimentin and CD68, as markers of synovial fibroblasts and macrophages, respectively, showed that the majority of IL‐22–positive cells were synovial fibroblasts and macrophages. IL‐22R1 was also expressed in both the lining and the sublining layers of RA synovial tissues. The majority of cells expressing IL‐22R1 were positive for vimentin, but not for CD68. Expression of IL‐22 and IL‐22R1 in RASF was confirmed by RT‐PCR and Western blot analysis. In vitro, rIL‐22 significantly increased proliferation of RASF and production of MCP‐1 by RASF above the value of medium controls. Moreover, MAPK activation was induced in RASF in response to IL‐22 stimulation.ConclusionThese data suggest that IL‐22, produced by synovial fibroblasts and macrophages, promotes inflammatory responses in RA synovial tissues by inducing the proliferation and chemokine production of synovial fibroblasts.
A new haplotype of PDCD1 is associated with rheumatoid arthritis in Hong Kong Chinese
Authors: Kong Eric Kai‐Pang , Prokunina‐Olsson Ludmila , Wong Wilfred Hing‐Sang , Lau Chak‐Sing , Chan Tak‐Mao , Alarcón‐Riquelme Marta , Lau Yu‐Lung 
Published: April 2005

AbstractObjectiveThe programmed death 1 (PD‐1) molecule is a negative regulator of T cells, and a genetic association between PD‐1 and systemic lupus erythematosus and rheumatoid arthritis (RA) in Caucasians has been reported. The aim of this study was to investigate the association of PDCD1 polymorphisms and haplotypes with RA in the Chinese population.MethodsThree single‐nucleotide polymorphisms (SNPs), PD‐1.1 G/A, PD‐1.3 G/A, and PD‐1.5 C/T, were genotyped in 180 patients with RA and 647 healthy controls in a case–control association study. Analyses of the association of genotypes and alleles with disease, haplotype construction, and linkage disequilibrium (LD) were performed.ResultsWe constructed haplotypes with the alleles of markers PD‐1.1 G/A and PD‐1.5 C/T and found that the GT haplotype was overrepresented in patients with RA (31%) compared with controls (23%) (P = 0.001, odds ratio [OR] 1.54, 95% confidence interval [95% CI] 1.18–1.99). Among GT double homozygotes the risk of RA was increased even further (OR 2.31, 95% CI 1.31–4.08, P = 0.006). We also observed that the AA genotype of SNP PD‐1.1 was associated with a decreased risk for developing RA (OR 0.38, 95% CI 0.15–0.99, P = 0.034). No association for SNP PD‐1.5 in RA was found, and SNP PD‐1.3 was nonpolymorphic in the Chinese population.ConclusionOur results support the involvement of PDCD1 as a susceptibility gene for RA in the Chinese population. © 2005, American College of Rheumatology
Risk factors for functional decline in older adults with arthritis
Authors: Dunlop Dorothy D. , Semanik Pamela , Song Jing , Manheim Larry M. , Shih Vivian , Chang Rowland W. 
Published: April 2005

AbstractObjectiveFunctional limitation is a major factor in medical costs. This study was undertaken to evaluate the prevalence of functional limitation among adults with arthritis and the frequency of functional decline over 2 years, and to investigate factors amenable to public health intervention that predict functional decline.MethodsLongitudinal data (1998–2000) from a cohort of 5,715 adults ages 65 years or older with arthritis from a national probability sample were analyzed. Function was defined based on ability to perform basic activities of daily living (ADL) tasks and instrumental ADL. Adjusted odds ratios (ORs) from a multiple logistic regression model were used to estimate the associations between functional decline and comorbid conditions, health behaviors, and economic factors.ResultsOverall, 19.7% of this cohort had functional limitation at baseline, including 12.9% with ADL limitations. Over the subsequent 2 years, function declined in 13.6% of those at risk. Functional decline was most frequent among women (15.0%) and minorities (18.0% Hispanics, 18.7% African Americans) with arthritis. Lack of regular vigorous physical activity, the most prevalent risk factor (64%), almost doubled the odds of functional decline (adjusted OR 1.9, 95% confidence interval 1.5–2.4) after controlling for all risk factors. It was found that if all subjects engaged in regular vigorous physical activity, the expected functional decline could be reduced as much as 32%. Other significant predictors included older age, cognitive impairment, depressive symptoms, diabetes, physical limitations, no alcohol use, stroke, and vision impairment.ConclusionLack of regular vigorous physical activity is a potentially modifiable risk factor that could substantially reduce functional decline and associated health care costs. Prevention/intervention programs should include regular vigorous physical activity, weight maintenance, and medical intervention for health needs. © 2005, American College of Rheumatology
MRL/Mp CD4+,CD25− T cells show reduced sensitivity to suppression by CD4+,CD25+ regulatory T cells in vitro: A novel defect of T cell regulation in systemic lupus erythematosus
Authors: Monk C. R. , Spachidou M. , Rovis F. , Leung E. , Botto M. , Lechler R. I. , Garden O. A. 
Published: April 2005

AbstractObjectiveTo investigate the hypothesis that loss of suppression mediated by peripheral CD4+,CD25+ regulatory T cells is a hallmark of systemic lupus erythematosus (SLE).MethodsMice of the MRL/Mp strain were studied as a polygenic model of SLE. Following immunomagnetic selection, peripheral lymphoid CD25+ and CD25− CD4+ T cells were cultured independently or together in the presence of anti‐CD3/CD28 monoclonal antibody–coated beads. Proliferation was assessed by measuring the incorporation of tritiated thymidine.ResultsWhile MRL/Mp CD4+,CD25+ regulatory T cells showed only subtle abnormalities of regulatory function in vitro, syngeneic CD4+,CD25− T cells showed significantly reduced sensitivity to suppression, as determined by crossover experiments in which MRL/Mp CD4+,CD25− T cells were cultured with H‐2–matched CBA/Ca CD4+,CD25+ regulatory T cells in the presence of a polyclonal stimulus.ConclusionOur findings highlight a novel defect of peripheral tolerance in SLE. Identification of this defect could open new opportunities for therapeutic intervention.
Relationship between anti–double‐stranded DNA antibodies and exacerbation of renal disease in patients with systemic lupus erythematosus
Authors: Linnik Matthew D. , Hu Jay Z. , Heilbrunn Kenneth R. , Strand Vibeke , Hurley Frank L. , Joh Tenshang ,   LJP 394 Investigator Consortium
Published: April 2005

AbstractObjectiveTo examine the relationship between changes in anti–double‐stranded DNA (anti‐dsDNA) antibody levels and the risk of renal flare in patients with systemic lupus erythematosus (SLE), using data from 2 randomized, controlled trials.MethodsAnalyses were based on 487 patients with SLE and a history of lupus nephritis who had an anti‐dsDNA antibody titer ≥15 IU/ml at baseline, as measured by Farr assay. Results are presented for the combined population of patients, the placebo arms, and the drug treatment arms in which a dsDNA‐based bioconjugate (abetimus sodium; LJP 394) was used.ResultsChanges in anti‐dsDNA antibody levels were inversely correlated with changes in the C3 level (P < 0.0001 in both trials). Cox proportional hazards regression models showed that changes in anti‐dsDNA antibody levels correlated with the risk of renal flare. The models predicted that a point estimate of a 50% reduction in anti‐dsDNA antibody levels is associated with a 52% reduction (95% confidence interval [95% CI] 26–68%, nominal P = 0.0007) and a 53% reduction (95% CI 33–69%, nominal P < 0.0001) in the risk of renal flare in the 2 trials, respectively. In the 2 trials, the incidence of renal flare was lower in patients with sustained reductions in anti‐dsDNA antibodies (3.0% and 4.1%, respectively) than in patients with stable or increasing antibody levels (21.3% and 20.3%, respectively).ConclusionChanges in anti‐dsDNA antibody levels were directly correlated with the risk of renal flare and inversely correlated with changes in the C3 level. Reducing anti‐dsDNA antibody levels may represent a therapeutic objective in SLE patients with lupus nephritis, because it is associated with a reduced risk of renal flare.
Pregabalin for the treatment of fibromyalgia syndrome: Results of a randomized, double‐blind, placebo‐controlled trial
Authors: Crofford Leslie J. , Rowbotham Michael C. , Mease Philip J. , Russell I. Jon , Dworkin Robert H. , Corbin Ann E. , Young James P. , LaMoreaux Linda K. , Martin Susan A. , Sharma Uma ,   Pregabalin 1008‐105 Study Group
Published: April 2005

AbstractObjectiveFibromyalgia syndrome (FMS) is characterized by widespread musculoskeletal pain and lowered pain threshold. Other prominent symptoms include disordered sleep and fatigue. FMS affects an estimated 2% of the population, predominantly women. This trial was designed to evaluate the efficacy and safety of pregabalin, a novel α2‐δ ligand, for treatment of symptoms associated with FMS.MethodsThis multicenter, double‐blind, 8‐week, randomized clinical trial compared the effects of placebo with those of 150, 300, and 450 mg/day pregabalin on pain, sleep, fatigue, and health‐related quality of life in 529 patients with FMS. The primary outcome variable was the comparison of end point mean pain scores, derived from daily diary ratings of pain intensity, between each of the pregabalin treatment groups and the placebo group.ResultsPregabalin at 450 mg/day significantly reduced the average severity of pain in the primary analysis compared with placebo (−0.93 on a 0–10 scale) (P ≤ 0.001), and significantly more patients in this group had ≥50% improvement in pain at the end point (29%, versus 13% in the placebo group; P = 0.003). Pregabalin at 300 and 450 mg/day was associated with significant improvements in sleep quality, fatigue, and global measures of change. Pregabalin at 450 mg/day improved several domains of health‐related quality of life. Dizziness and somnolence were the most frequent adverse events. Rates of discontinuation due to adverse events were similar across all 4 treatment groups.ConclusionPregabalin at 450 mg/day was efficacious for the treatment of FMS, reducing symptoms of pain, disturbed sleep, and fatigue compared with placebo. Pregabalin was well tolerated and improved global measures and health‐related quality of life.
Innate immunity and arthritis: Neutrophil Rac and toll‐like receptor 4 expression define outcomes in infection‐triggered arthritis
Authors: Zhang Xiang , Glogauer Michael , Zhu Fei , Kim Tae‐Hwan , Chiu Basil , Inman Robert D. 
Published: April 2005

AbstractObjectiveThe role of innate immunity in Chlamydia‐induced arthritis has not been defined. The purpose of this study was to examine the role of neutrophils in experimental arthritis in mice with targeted elimination of the small GTPases Rac1 and Rac2, as well as the role of Toll‐like receptors (TLRs) in this model.MethodsArthritis was induced by intraarticular inoculation of synoviocyte‐packaged Chlamydia trachomatis. The degree of arthritis was assessed according to joint swelling and pathology scores. The persistence of Chlamydia in joints was assessed by immunoassay. The expression of TLR‐2 and TLR‐4 in neutrophils was detected by semiquantitative reverse transcription–polymerase chain reaction.ResultsIn the acute phase, wild‐type mice developed more severe arthritis than did Rac‐deficient mice, with abundant infiltration of neutrophils into the joint. In the chronic phase, the Rac‐deficient mice developed more severe arthritis and demonstrated defective clearance of the pathogen from the joint. In vitro stimulation of neutrophils with Chlamydia up‐regulated the expression of TLR‐4, but not TLR‐2, in wild‐type mice. However, neutrophils from Rac‐deficient mice did not show this up‐regulation of TLR‐4. Sustained TLR‐4 expression in neutrophils was found to be dependent on the expression of Rac. Mice genetically deficient in TLR‐4 demonstrated more severe arthritis than did the controls. Thus, Rac expression plays a profound role in infection‐triggered arthritis and demonstrates a bimodal influence on the disease process, exacerbating acute joint inflammation but controlling chronic arthritis. Rac deficiency was associated with diminished TLR‐4 expression, impaired host clearance of the pathogen, and more severe chronic arthritis.ConclusionIn infection‐triggered arthritis, innate immunity plays a critical role. Effective host clearance of an arthritogenic pathogen depends on intact expression of Rac and appropriate expression of TLR‐4 by neutrophils.