bluuebunny/crossref_metadata_2025_split huggingface dataset:
Graft copolymerization of methacrylic acid onto xanthan gum by Fe2+/H2O2 redox initiator
Authors: Kumar Rajesh , Srivastava Arti , Behari Kunj 
Published: April 2007

AbstractThe graft copolymer of xanthan gum with methacrylic acid was synthesized in inert atmosphere by using Fentos reagent as a redox initiator. The effect of reaction conditions on grafting parameters [G(%), E(%), C(%), A(%), H(%), and Rg] was investigated. Similar trend was observed on increasing the concentration of ferrous ion and hydrogen peroxide from 4.0 to 20.0 × 10−3 mol dm−3 and 2.5 to 10 × 10−3 mol dm−3 respectively, i.e., initially grafting parameters increased and after a certain range of concentration grafting parameters showed decreasing trend. Hydrogen ion shows influenced result i.e., small increment of concentration in hydrogen ion presents much increment in percent of grafting. It was observed that the [G(%), E(%), C(%), A(%), and Rg] increased upto 6.67 × 10−2 mol dm−3 concentration of methacylic acid after that it decreased. Maximum G(%) was obtained at minimum concentration of xanthan gum i.e., at 40 × 10−2 g dm−3. The optimum temperature and time duration of reaction for maximum percentage of grafting were found to be 45°C and 150 min respectively. Thermogravimetric analysis showed that the xanthan gum‐g‐methacrylic acid is thermally more stable than pure gum. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Involvement of renal tubular toll‐like receptor 9 in the development of tubulointerstitial injury in systemic lupus
Authors: Benigni Ariela , Caroli Cristina , Longaretti Lorena , Gagliardini Elena , Zoja Carla , Galbusera Miriam , Moioli Daniela , Romagnani Paola , Tincani Angela , Andreoli Laura , Remuzzi Giuseppe 
Published: April 2007

AbstractObjectiveToll‐like receptor 9 (TLR‐9), a receptor for CpG DNA, has been implicated in the activation of immune cells in lupus. We undertook this study to determine whether the expression of TLR‐9 in resident renal cells in lupus nephritis is related to the development of tubulointerstitial injury.MethodsTLR‐9 was analyzed in selectively retrieved renal tissue from (NZB × NZW)F1 mice at different stages of disease by laser capture microdissection combined with real‐time quantitative reverse transcriptase–polymerase chain reaction, and in renal biopsy specimens from lupus nephritis patients by immunohistochemistry. We investigated for the molecular component responsible for TLR‐9 activation by cultured proximal tubular cells in serum from patients with lupus.ResultsRenal tissue from NZB × NZW mice displayed robust TLR‐9 expression localized to proximal tubular cells. TLR‐9 levels correlated with proteinuria and tubulointerstitial injury to the extent that a cyclin‐dependent kinase inhibitor, while reducing proteinuria and renal structural damage, prevented tubular TLR‐9 generation in lupus mice. Consistently, exaggerated TLR‐9 staining was found in proximal tubular cells of lupus patients, which correlated with tubulointerstitial damage. DNA‐containing immune complexes purified from sera of patients with lupus induced TLR‐9 in cultured proximal tubular cells. This was prevented by CCGG‐rich short oligonucleotides, specific antagonists of CpG DNA, indicating that the DNA component of immune complexes was required for TLR‐9 stimulation.ConclusionThese findings suggest that tubular TLR‐9 activation has a pathogenetic role in tubulointerstitial inflammation and damage in experimental and human lupus nephritis, and they indicate a novel target for future therapies.
Association of DRB1 shared epitope genotypes with early mortality in rheumatoid arthritis: Results of eighteen years of followup from the early rheumatoid arthritis study
Authors: Mattey D. L. , Thomson W. , Ollier W. E. R. , Batley M. , Davies P. G. , Gough A. K. , Devlin J. , Prouse P. , James D. W. , Williams P. L. , Dixey J. , Winfield J. , Cox N. L. , Koduri G. , Young A. 
Published: April 2007

AbstractObjectiveTo determine whether the HLA–DRB1 shared epitope (SE) is associated with early mortality and specific causes of death in rheumatoid arthritis (RA).MethodsHLA–DRB1 genotyping was carried out on blood samples from 767 patients recruited for the Early RA Study (ERAS), a multicenter, inception cohort study with followup over 18 years. Dates and causes of death (n = 186) were obtained from the Office of National Statistics. The association of HLA–DRB1 alleles with risk of mortality was assessed using Cox proportional hazards regression analyses. Multivariate stepwise models were used to assess the predictive value of HLA–DRB1 genotypes compared with other potential baseline risk factors.ResultsThe SE was not significantly associated with overall mortality. However, the presence of 2 SE alleles was associated with risk of mortality from ischemic heart disease (hazard ratio [HR] 2.02 [95% confidence interval 1.04–3.94], P = 0.04), and malignancy (HR 2.18 [95% confidence interval 1.17–4.08], P = 0.01). Analysis of specific SE genotypes (corrected for age and sex) revealed that the HLA–DRB1*0101/*0401 and 0404/*0404 genotypes were the strongest predictors of mortality from ischemic heart disease (HR 5.11 and HR 7.55, respectively), and DRB1*0101/*0401 showed a possible interaction with smoking. Male sex, erythrocyte sedimentation rate, and Carstairs Deprivation Index were also predictive, but the Health Assessment Questionnaire score, rheumatoid factor, nodules, and swollen joint counts were not. Mortality due to malignancy was particularly associated with DRB1*0101 genotypes.ConclusionThe risk of mortality due to ischemic heart disease or cancer in RA is increased in patients carrying HLA–DRB1 genotypes with particular homozygous and compound heterozygous SE combinations.
CCL18 as an indicator of pulmonary fibrotic activity in idiopathic interstitial pneumonias and systemic sclerosis
Authors: Prasse Antje , Pechkovsky Dmitri V. , Toews Galen B. , Schäfer Markus , Eggeling Stephan , Ludwig Corinna , Germann Martin , Kollert Florian , Zissel Gernot , Müller‐Quernheim Joachim 
Published: April 2007

AbstractObjectiveIn diffuse parenchymal lung diseases, the evolution of pulmonary fibrosis is often devastating and may result in death. In this study the role of CCL18 as a biomarker of disease activity in idiopathic interstitial pneumonias (IIPs) and systemic sclerosis (SSc) with lung involvement was evaluated.MethodsCCL18 was assessed in supernatants of cultured bronchoalveolar lavage (BAL) cells as well as BAL fluid and serum samples from 43 patients with IIPs, 12 patients with SSc, and 23 healthy control subjects. Concentrations of CCL18 were measured by enzyme‐linked immunosorbent assay, and expression of CCL18 was assessed by flow cytometry.ResultsCCL18 concentrations were statistically significantly increased in all patients with fibrotic lung diseases. Spontaneous CCL18 production by BAL cells was negatively correlated with total lung capacity and the diffusion capacity for carbon monoxide, whereas there was a positive correlation of CCL18 concentrations with BAL neutrophil and eosinophil cell counts. Flow cytometry revealed an increase in the percentage of CCL18‐positive alveolar macrophages and an increase in the CCL18 fluorescence intensity per cell in patients with fibrotic lung diseases. In a cohort of patients who were followed up for at least 6 months (n = 40), a close negative correlation was observed between changes in the predicted total lung capacity and changes in CCL18 serum concentrations.ConclusionThese findings suggest that CCL18 production by BAL cells and serum CCL18 concentrations reflect pulmonary fibrotic activity in patients with IIPs and those with SSc. Monitoring changes in CCL18 production might be an extraordinarily useful tool in clinical practice and in studies aimed at evaluating new approaches for treatment of fibrotic lung diseases.
Mycobacterial Hsp65‐IgG–expressing tolerogenic B cells confer protection against adjuvant‐induced arthritis in Lewis rats
Authors: Satpute Shailesh R. , Soukhareva Nadejda , Scott David W. , Moudgil Kamal D. 
Published: April 2007

AbstractObjectiveTolerization of T cells directed against a target autoantigen is a desired goal of experimental approaches for the treatment of autoimmune diseases, and novel and improved methods of tolerance induction are continuously being sought. Because most traditional methods of tolerance induction using soluble antigen are effective in the prevention of autoimmunity but fail to control established disease, this study was carried out to explore an innovative tolerogenic approach for the treatment of ongoing disease, using the rat adjuvant‐induced arthritis (AIA) model of human rheumatoid arthritis.MethodsLewis (RT.1l) rats were injected subcutaneously with heat‐killed Mycobacterium tuberculosis H37Ra to induce AIA. Before or after AIA induction, Lewis rats were treated intraperitoneally (IP) with tolerogenic B cells expressing a fusion construct of mycobacterial 65‐kd heat‐shock protein (Hsp65) and IgG heavy‐chain. For comparison, control rats were treated IP with ovalbumin (OVA)–IgG–expressing B cells or soluble mycobacterial Hsp65, and the effects on AIA were observed. We also tested the immune response to mycobacterial Hsp65 in B cell–tolerized rats.ResultsAdministration of tolerogenic mycobacterial Hsp65–expressing B cells as well as soluble mycobacterial Hsp65, but not OVA‐expressing B cells, resulted in a significant decrease in the severity of subsequent AIA. However, in rats with established disease, only the B cell regimen of mycobacterial Hsp65, but not the soluble antigen, suppressed ongoing AIA.ConclusionMycobacterial Hsp65‐IgG–expressing B cells can successfully attenuate the progression of AIA. This study introduces a promising approach for the treatment of arthritis that should be further explored.
Association of Anti–Cyclic citrullinated peptide antibody levels with PADI4 haplotypes in early rheumatoid arthritis and with shared epitope alleles in very late rheumatoid arthritis
Authors: Cha Seongwon , Choi Chan‐Bum , Han Tae‐Un , Kang Changsoo Paul , Kang Changwon , Bae Sang‐Cheol 
Published: April 2007

AbstractObjectiveAnti–cyclic citrullinated peptide (anti‐CCP) antibodies are rheumatoid arthritis (RA)–specific serologic markers. RA susceptibility has been associated with HLA–DRB1 shared epitope (SE) alleles and single‐nucleotide polymorphism (SNP) haplotypes in the peptidyl arginine deiminase 4 gene (PADI4). This study was undertaken to determine whether anti‐CCP levels are associated with PADI4 haplotypes and/or SE alleles in Korean patients with RA.MethodsThree nonsynonymous SNPs in PADI4 (padi4_89, padi4_90, and padi4_92) and SE alleles were genotyped, and serum anti‐CCP levels were measured, in 311 patients with nonerosive or erosive RA. The relationships between anti‐CCP levels and PADI4 haplotypes and/or SE alleles were analyzed statistically.ResultsAnti‐CCP levels were significantly higher in patients carrying the PADI4 RA risk haplotype than in patients who did not have the risk haplotype, among anti‐CCP–positive patients with RA with a disease duration of ≤34 months (P = 0.041), but not among patients with a longer disease duration or among those who had erosive RA versus nonerosive RA. In contrast, the levels were significantly higher in SE carriers than in noncarriers among patients with RA with a disease duration of ≥141 months (P = 0.0037) and among those who had erosive RA (P = 0.000098), but not among patients who had a shorter disease duration or those who had nonerosive RA.ConclusionThe PADI4 RA risk haplotype is associated with increased anti‐CCP levels in RA patients with disease of short duration, and PADI4 may play a role in early RA. In contrast, SE alleles are associated with increased anti‐CCP levels in RA patients with very longstanding disease and in patients with erosive RA, suggesting that SE alleles play a role in very late RA.
Protection against autoimmune nephritis in MyD88‐deficient MRL/lpr mice
Authors: Sadanaga Atsushi , Nakashima Hitoshi , Akahoshi Mitsuteru , Masutani Kohsuke , Miyake Katsuhisa , Igawa Takashi , Sugiyama Naonobu , Niiro Hiroaki , Harada Mine 
Published: April 2007

AbstractObjectiveTo determine whether innate receptor signals play an important role in the development of autoimmune nephritis in MRL/lpr mice, an experimental model of lupus nephritis.MethodsMyD88 is a critical adaptor that is involved in signaling pathways through all of the Toll‐like receptors (TLRs) except TLR‐3. We therefore generated MyD88‐knockout (MyD88‐KO) MRL/lpr mice and examined them for histopathologic changes in the kidneys, cumulative survival rates, extent of lymphadenopathy and splenomegaly, serum chemistry, and immunologic parameters. In addition, to define the role of the MyD88‐independent pathway in autoimmune nephritis, we injected MyD88‐KO MRL/lpr mice intraperitoneally with either poly(I‐C) (50 or 100 μg per mouse) or phosphate buffered saline and examined them for survival as well as for histopathologic, serologic, and immunologic parameters.ResultsIn comparison with wild‐type mice, MyD88‐KO MRL/lpr mice exhibited a prolonged lifespan, with no apparent development of autoimmune nephritis. Their kidneys showed no glomerular cell proliferation or crescent formation, along with a drastic decrease in the mesangial matrix. Lymphadenopathy and splenomegaly were less pronounced. Serum titers of anti–double‐stranded DNA (anti‐dsDNA) and production of cytokines, including interferon‐α (IFNα), interleukin‐12 (IL‐12), IL‐6, and IFNγ, in splenocytes were significantly reduced in MyD88‐KO MRL/lpr mice. Interestingly, MyD88‐KO MRL/lpr mice that had been treated with the MyD88‐independent TLR‐3 ligand poly(I‐C) showed an almost complete reversion to the features of wild‐type mice, demonstrating crescentic glomerulonephritis, with significant elevation of serum anti‐dsDNA titers and increased cytokine production in splenocytes.ConclusionThe findings indicate that both MyD88‐dependent and MyD88‐independent innate signals play a crucial role in the development of autoimmune nephritis in MRL/lpr mice.
The effects of glucosamine hydrochloride on subchondral bone changes in an animal model of osteoarthritis
Authors: Wang Susanne X. , Laverty Sheila , Dumitriu Mircea , Plaas Anna , Grynpas Marc D. 
Published: April 2007

AbstractObjectiveTo quantify periarticular subchondral bone changes in a rabbit model of experimental osteoarthritis (OA), and to determine the effects of continuous administration of a clinically relevant dose of glucosamine HCl on subchondral bone changes in this model.MethodsAnterior cruciate ligament transection (ACLT) was performed on the left femorotibial joints of 16 rabbits to induce OA. Ten rabbits that did not undergo ACLT served as unoperated controls. Eight rabbits that underwent ACLT and 6 control rabbits were treated with 100 mg of glucosamine daily, and the others were given a placebo. The articular cartilage was evaluated macroscopically and graded at the time of necropsy, 8 weeks after ACLT. Bone mineral density (BMD) was measured using dual‐energy x‐ray absorptiometry on the dissected distal femur and proximal tibia. Subchondral trabecular bone turnover, architecture, and connectivity, as well as subchondral plate thickness and mineralization were studied on the undecalcified tibia sections from each animal.ResultsEight weeks after ACLT, most of the operated joints had various degrees of cartilage damage and fibrillation. Compared with the control group, the ACLT group had significantly increased subchondral bone turnover and lower BMD, bone volume, connectivity, and bone mineralization. The high bone turnover was significantly reduced in glucosamine‐treated animals that underwent ACLT. In fact, there were no significant differences between the ACLT/glucosamine group and the control/glucosamine group in most of the bone parameters studied.ConclusionThis study shows that subchondral bone turnover, structure, and mineralization are significantly altered in the early stages of experimental OA, and that these changes are attenuated by glucosamine treatment.
The effect of methotrexate and anti–tumor necrosis factor therapy on the risk of lymphoma in rheumatoid arthritis in 19,562 patients during 89,710 PERSON‐YEARS of observation
Authors: Wolfe Frederick , Michaud Kaleb 
Published: April 2007

AbstractObjectiveTo ascertain the relationship between anti–tumor necrosis factor (anti‐TNF) therapy, methotrexate (MTX), and the risk of lymphoma in patients with rheumatoid arthritis (RA). This report updates our previous report during 29,314 person‐years of followup.MethodsParticipants in the National Data Bank for Rheumatic Diseases (NDB) longitudinal study of long‐term outcomes of RA completed semiannual questionnaires from 1998 through 2005, during 89,710 person‐years of followup. Lymphoma reports were validated by medical records. The association between lymphoma and treatment was investigated using conditional logistic regression, adjusted for severity and demographic covariates.ResultsOf the 19,591 participants, 55.3% received biologic agents and 68.0% received MTX while enrolled in the NDB. The lymphoma incidence rate was 105.9 (95% confidence interval [95% CI] 86.6–129.5) per 100,000 person‐years of exposure. Compared with the SEER (Surveillance, Epidemiology, and End‐Results) lymphoma database, the standardized incidence ratio was 1.8 (95% CI 1.5–2.2). The odds ratio (OR) for lymphoma in patients who received anti‐TNF therapy compared with patients who did not receive anti‐TNF therapy was 1.0 (95% CI 0.6–1.8 [P = 0.875]). The OR for lymphoma in patients who received anti‐TNF plus MTX therapy compared with patients who received MTX treatment alone was 1.1 (95% CI 0.6–2.0 [P = 0.710]). Infliximab and etanercept considered individually also were not associated with a risk of lymphoma.ConclusionIn a study of lymphoma in 19,591 RA patients over 89,710 person‐years of followup, which included exposure to anti‐TNF therapy in 10,815 patients, we did not observe evidence for an increase in the incidence of lymphoma among patients who received anti‐TNF therapy.
Are common symptoms in childhood associated with chronic widespread body pain in adulthood?: Results from the 1958 british birth cohort study
Authors: Jones Gareth T. , Silman Alan J. , Power Chris , Macfarlane Gary J. 
Published: April 2007

AbstractObjectiveStudies have shown that common symptoms in childhood predict the onset of chronic widespread pain in the short term. However, it is unknown whether this association persists into adulthood. The aim of the current study was to examine, prospectively, whether children with common symptoms experience an increased risk of chronic widespread pain as adults.MethodsInformation on vomiting/bilious attacks, abdominal pain, and headaches/migraine was collected on 10,453 7‐year‐old children, by maternal report. Similar data were gathered when the children were ages 11 years and 16 years. Body pain at age 45 years was assessed by postal questionnaire. Poisson regression was used to examine chronic widespread pain in relation to childhood symptom reporting.ResultsOf the 10,453 subjects on whom data were obtained when they were children, 7,470 participated at age 45 years (71.5%). Children with multiple symptoms at age 7 years experienced a 50% increased risk of chronic widespread pain (relative risk 1.5 [95% confidence interval 1.03, 2.3]). This relationship persisted after adjustment for sex, recent psychological distress, and childhood and current socioeconomic status, and after excluding children with major illnesses that might have explained early symptom reporting. A similar relationship with symptoms at ages 11 and 16 years was observed, although this was not associated with additional risk compared with that found with the presence of symptoms at age 7 years. However, despite a modest increase in risk, the presence of multiple symptoms at early ages was uncommon (<1.5%), and therefore, the associated population attributable risk was low (<1%).ConclusionMultiple common symptoms in childhood are associated with an increased risk of chronic widespread pain in adulthood. However, the magnitude of this increased risk is modest, and reports of multiple symptoms in childhood are uncommon. Thus the “early pain pathway” phenomenon is applicable only to a small proportion of individuals with chronic widespread pain.
Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development
Authors: Ding Changhai , Cicuttini Flavia , Blizzard Leigh , Jones Graeme 
Published: April 2007

AbstractObjectiveTo describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoking and family history of osteoarthritis (OA).MethodsSubjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0–4 scale) were determined using T1‐weighted fat‐saturated magnetic resonance imaging. Smoking status and duration and number of cigarettes were recorded by questionnaire.ResultsIn offspring, smoking was associated with annual change in medial and lateral tibial cartilage volume (β = −2.20% and β = −1.45%, respectively, for current smokers versus former smokers and those who had never smoked; β = −0.07%/pack‐year at both tibial sites, for smoking severity) in multivariate analysis. Smoking was also associated with increases (change ≥1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoking [total of >20 pack‐years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoking and offspring–control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects.ConclusionSmoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene–environment interaction in the etiology of knee OA.