bluuebunny/crossref_metadata_2025_split huggingface dataset:
Study of polyethylene solution fractionation and resulting fractional crystallization behavior
Authors: Kong Jie , Fan Xiaodong , Jia Mei 
Published: July 2004

AbstractSolution fractionation for four different polyethylenes including high‐density polyethylene (HDPE), low‐density polyethylene (LDPE), linear low‐density polyethylene (LLDPE), and very low‐density polyethylene (VLDPE) are conducted by stepwise controlling both the temperature and the amount of precipitant. The size exclusion chromatograph (SEC) measurements indicate that solution fractionation technique can successfully separate all the polyethylene samples in accordance with their molecular weight and molecular‐weight distributions. In addition, infrared spectroscopy analysis shows that the degree of short‐chain branching for each fraction of each polyethylene varies with the fraction's molecular weight. The effect of the molecular weight with different short‐chain branching on each fraction's crystallinity represents the characteristics of chain components for different polyethylenes. The crystallinities of HDPE, LLDPE, and LDPE decrease with the increase in their molecular weights; however, for VLDPE, its crystallinity increases with the increase in the molecular weight. The research revealed that the degree of short‐chain branching, together with the molecular weight, can greatly affect the crystallinity of polyethylene. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 93: 2542–2549, 2004
Cementum‐like tissue deposition on the resorbed enamel surface of human deciduous teeth prior to shedding
Authors: Sahara Noriyuki , Ozawa Hidehiro 
Published: July 2004

AbstractPrior to the shedding of human deciduous teeth, odontoclastic resorption takes place at the pulpal surface of the coronal dentin, and this resorption occasionally extends coronally from the dentinoenamel junction into the enamel. After the end of resorption, however, the resorbed enamel surface is repaired by the deposition of a cementum‐like tissue. Using this phenomenon as an observation model, in this study we examined the sequence of cellular and extracellular/matrix events involved in the enamel resorption repair by light and electron microscopy. As the odontoclast terminated its resorption activity, it detached from the resorbed enamel surface; thereafter, numerous mononuclear cells were observed along the resorbed enamel surface. Most of these mononuclear cells made close contact with the resorbed enamel surface, and coated pits or patches were observed on their plasma membrane facing this surface. Furthermore, they frequently contained thin needle‐ or plate‐like enamel crystals in their cytoplasmic vacuoles as well as secondary lysozomes. Following the disappearance of these monononuclear cells, the resorbed enamel surface now displayed a thin coat of organic matrix. Ultrastructurally, this organic layer was composed of a reticular and/or granular organic matrix, but contained no collagen fibrils. Energy‐dispersive X‐ray microanalysis of this thin organic layer in undecalcified sections revealed small spectral peaks of Ca and P. Cementum‐like tissue initially formed along this thin organic layer, increased in width, and appeared to undergo mineralization as time progressed. The results of our observations demonstrate that regardless of type of matrix of dental hard tissues, tooth repair may be coupled to tooth resorption, and suggest that mononuclear cells and an organic thin layer found on the previously resorbed enamel surface may play an important role in the repair process initiated after resorption of the enamel. © 2004 Wiley‐Liss, Inc.
Etanercept in Sjögren's syndrome: A twelve‐week randomized, double‐blind, placebo‐controlled pilot clinical trial
Authors: Sankar Vidya , Brennan Michael T. , Kok Marc R. , Leakan Rose Anne , Smith Janine A. , Manny Joan , Baum Bruce J. , Pillemer Stanley R. 
Published: July 2004

AbstractObjectiveTo assess the safety and potential efficacy of etanercept in the treatment of Sjögren's syndrome (SS).MethodsThis pilot study was a 12‐week randomized, double‐blind, placebo‐controlled trial of etanercept, with 14 subjects in each group. Patients received 25 mg of etanercept or placebo (vehicle) by twice‐weekly subcutaneous injection. Patients met the American‐European Consensus Group criteria for SS. The primary outcome required at least 20% improvement from baseline values for at least 2 of the following 3 domains: subjective or objective measures of dry mouth, subjective or objective measures of dry eyes, and IgG level or erythrocyte sedimentation rate (ESR).ResultsOf the 14 patients taking etanercept, 11 had primary SS and 3 had SS secondary to rheumatoid arthritis. Baseline measures did not differ between the 2 groups. Three etanercept‐treated patients and 1 placebo‐treated patient did not complete the trial. Five etanercept‐treated patients and 3 placebo‐treated patients showed improvement from baseline in the primary outcome variable at 12 weeks, but the difference was not statistically significant. There were no significant differences between the groups for changes in subjective measures of oral or ocular symptoms (by visual analog scale), the IgG level, Schirmer I test result, van Bijsterveld score, or salivary flow. At 12 weeks, the ESR had decreased in the etanercept group compared with baseline (P = 0.004); however, the mean reduction was only 18.6%.ConclusionWe found no evidence to suggest that treatment with etanercept at a dosage of 25 mg twice weekly for 12 weeks was clinically efficacious in SS. A larger trial will be necessary to definitively address the efficacy of etanercept in the treatment of SS.
Genetic studies in familial ankylosing spondylitis susceptibility
Authors: Zhang Ge , Luo Jingchun , Bruckel Jane , Weisman Michael A. , Schumacher H. Ralph , Khan Muhammad A. , Inman Robert D. , Mahowald Maren , Maksymowych Walter P. , Martin Tammy M. , Yu David T. Y. , Stone Millicent , Rosenbaum James T. , Newman Patricia , Lee Juwon , McClain Jo A. , West O. Clark , Jin Li , Reveille John D. 
Published: July 2004

AbstractObjectiveTo define the genetic basis of susceptibility to ankylosing spondylitis (AS), especially non–major histocompatibility complex (MHC) genes.MethodsThe study group comprised 244 affected sibling pairs from 180 pedigrees of primarily European ancestry. Sibling pairs were concordant for AS by the modified New York criteria and had available sacroiliac radiographs. The subjects were genotyped for 400 markers in ABI PRISM linkage map MD‐10 and for 17 additional markers on chromosomes 6p, 6q, and 11q (including HLA–B, DRB1, DQA1, DQB1, and DPB1 alleles). Two‐point and multipoint nonparametric linkage (NPL) analyses were conducted using the NPL statistic and 1‐parameter allele‐sharing model logarithm of odds (LOD) scores, calculated using the Allele‐Sharing Model (ASM) computer program.ResultsLinkage of the MHC region was supported by both 2‐point and multipoint analyses, with the strongest peak (45.90 cM) in the MHC at the HLA–DRB1 locus (NPL score 8.720, ASM LOD score 20.49; P = 6.8 × 10−20 for 2‐point analysis). A second region was found to have positive linkage at the q arm of chromosome 6 (D6S441) in 2‐point analysis; this was supported by a 39.13‐cM region (135.58–174.71 cM) in multipoint analysis, with the smallest P value (4.2 × 10−3) at 166.39 cM. A third region was found on chromosome 11q, with the strongest evidence for linkage for D11S4094 at 123 cM (NPL score 2.235, ASM LOD score 1.939) and, on transmission disequilibrium test analysis, D11S4090 at 105.74 cM (P = 6.2 × 10−5). Linkage in this area was supported by multipoint analysis, spanning 22.19 cM continuously from 101.68 cM to 123.87 cM, with the strongest peak at 112.33 cM (P = 0.014); this was confirmed by subsequent fine mapping studies.ConclusionThus, this genome‐wide scan implicates, in addition to the MHC, regions outside the MHC in AS susceptibility, especially on chromosomes 6q and 11q.
Diagnostic value of magnetic resonance imaging of the forefeet in early rheumatoid arthritis when findings on imaging of the metacarpophalangeal joints of the hands remain normal
Authors: Ostendorf Benedikt , Scherer Axel , Mödder Ulrich , Schneider Matthias 
Published: July 2004

AbstractObjectiveTo investigate the diagnostic role of magnetic resonance imaging (MRI) of the forefeet in patients with early rheumatoid arthritis (RA) in whom findings on MR images of the hands are normal and conventional radiographs of the hands and feet do not show erosions.MethodsThe study group comprised 25 patients with early RA (disease duration of <12 months) in whom erosions were not demonstrated on conventional radiographs of the hands and feet. These patients underwent MRI of the clinically dominant hand to detect signs of arthritis. If results of MRI of the hand were normal according to the Outcome Measures in Rheumatology Clinical Trials (OMERACT) RA‐MRI scoring system (RAMRIS), MRI of the dominant forefoot was performed. The MRI protocol comprised coronal and sagittal T1‐weighted spin‐echo (before and after administration of contrast medium), coronal fat‐suppressed short tau inversion recovery sequences, coronal and sagittal T2‐weighted turbo spin‐echo sequences, and axial fat‐suppressed T1‐weighted spin‐echo sequences after administration of contrast medium. MRI of the forefeet was analyzed on the basis of a modified RAMRIS.ResultsMRI revealed pathologic findings in the hands of 15 of 25 patients (edema in 9 patients, synovitis in 12, erosions in 6, defects in 3). In 10 patients with a mean disease duration of 9.4 weeks, hand MRI scans were normal according to RAMRIS. Four of these 10 patients had tenosynovitis of the finger flexor tendons (there was no OMERACT criterion for tenosynovitis). RAMRIS analysis of the corresponding MRI scans of the forefeet of these patients revealed signs of edema in 7 patients, synovitis in all 10 patients (at the third metatarsophalangeal [MTP] joint in 7, at the fourth MTP joint in 6, at the first MTP joint in 4, and at the fifth MTP joint in 2 patients), tenosynovitis of the foot flexor tendons in 2 patients, erosions at the second and third MTP joints in 1 patient, and a single defect at the first MTP joint in 1 patient.ConclusionRAMRIS analysis of MRI scans of the forefeet detected synovitis and bone edema in patients with early RA in whom MRI of the finger joints was normal. MRI of the forefeet contributes an additional tool aimed at earlier and more accurate diagnosis and thus might allow an earlier decision to start appropriate medication in patients with early RA.
Association between HLA class II genes and autoantibodies to cyclic citrullinated peptides (CCPs) influences the severity of rheumatoid arthritis
Authors: Van Gaalen Floris A. , Van Aken Jill , Huizinga Tom W. J. , Schreuder Geziena M. Th. , Breedveld Ferdinand C. , Zanelli Eric , Van Venrooij Walther J. , Verweij Cornelis L. , Toes René E. M. , De Vries René R. P. 
Published: July 2004

AbstractObjectiveThe functional role of HLA class II molecules in the pathogenesis of rheumatoid arthritis (RA) is unclear. HLA class II molecules are involved in the interaction between T and B lymphocytes required for long‐lived B cell responses and generation of high‐affinity IgG antibodies. We undertook this study to investigate the relationship between HLA class II gene polymorphisms and RA‐specific IgG antibodies against cyclic citrullinated peptides (anti‐CCP antibodies).MethodsHigh‐resolution HLA–DR and DQ typing and anti–CCP‐2 antibody testing were performed on 268 RA patients from the Early Arthritis Clinic cohort at the Department of Rheumatology of the Leiden University Medical Center. The presence of anti‐CCP antibodies was analyzed in carriers of the different DR and DQ alleles. Disease progression was measured over a period of 4 years by scoring radiographs of the hands and feet using the Sharp/van der Heijde method.ResultsCarriership of the individual alleles HLA–DRB1*0401, DRB1*1001, DQB1*0302, and DQB1*0501 was associated with the presence of anti‐CCP antibodies. Carriers of DQ–DR genotypes containing proposed RA susceptibility alleles were significantly more often anti‐CCP antibody positive. Carriership of one or two HLA–DRB1 shared epitope (SE) alleles was significantly associated with production of anti‐CCP antibodies (odds ratio [OR] 3.3, 95% confidence interval [95% CI] 1.8–6.0 and OR 13.3, 95% CI 4.6–40.4, respectively). An increased rate of joint destruction was observed in SE+, anti‐CCP+ patients (mean Sharp score 7.6 points per year) compared with that in SE−, anti‐CCP+ patients (2.4 points per year) (P = 0.04), SE+, anti‐CCP− patients (1.6 points per year) (P < 0.001), and SE−, anti‐CCP− patients (1.6 points per year) (P < 0.001).ConclusionHLA class II RA susceptibility alleles are associated with production of anti‐CCP antibodies. Moreover, more severe disease progression is found in RA patients with both anti‐CCP antibodies and SE alleles.
Ultrasonography of the metatarsophalangeal joints in rheumatoid arthritis: Comparison with magnetic resonance imaging, conventional radiography, and clinical examination
Authors: Szkudlarek Marcin , Narvestad Eva , Klarlund Mette , Court‐Payen Michel , Thomsen Henrik S. , Østergaard Mikkel 
Published: July 2004

AbstractObjectiveTo compare ultrasonography (US) with magnetic resonance imaging (MRI), conventional radiography, and clinical examination in the evaluation of bone destruction and signs of inflammation in the metatarsophalangeal (MTP) joints of patients with rheumatoid arthritis (RA).MethodsTwo hundred MTP joints of 40 patients with RA and 100 MTP joints of 20 healthy control subjects were assessed with B‐mode US, contrast‐enhanced MRI, conventional radiography, and clinical examination for signs of bone destruction and joint inflammation.ResultsWith MRI considered the reference method, the sensitivity, specificity, and accuracy of US for the detection of bone erosions were 0.79, 0.97, and 0.96, respectively, while the corresponding values for radiography were 0.32, 0.98, and 0.93. The sensitivity, specificity, and accuracy of US for the detection of synovitis were 0.87, 0.74, and 0.79, while for clinical examination, the corresponding values were 0.43, 0.89, and 0.71. Erosive disease was identified in 26 patients by US, compared with 20 patients by MRI and 11 patients by radiography. Evaluation by US indicated signs of inflammation in 36 patients, while MRI and clinical examination revealed signs of inflammation in 31 patients and 20 patients, respectively. US and MRI volume‐based gradings of synovitis showed intraclass correlation coefficients of 0.56–0.72 (P < 0.0001). The MRI and radiographic visualizations of US‐detected bone changes were closely related to their size‐based gradings on US.ConclusionUS enables detection and grading of destructive and inflammatory changes in the MTP joints of patients with RA. By comparison with MRI, US was found to be markedly more sensitive and accurate than clinical examination and conventional radiography. Considering the early and frequent involvement of the MTP joints, evaluation of these joints by US may be of major clinical importance in RA.
Involvement of chemokines and Th1 cytokines in the pathogenesis of mucocutaneous lesions of Behçet's disease
Authors: Ben Ahmed M. , Houman H. , Miled M. , Dellagi K. , Louzir H. 
Published: July 2004

AbstractObjectiveTo investigate a possible pathogenic role of cytokines in Behçet's disease (BD) by focusing on the analysis of cytokine gene expression within mucocutaneous BD lesions.MethodsThe study group comprised 20 patients with active BD. In this group, a set of chemokines as well as Th1 and Th2 cytokines in biopsy specimens obtained from oral and genital ulcers, pseudofolliculitis lesions, and lesions at the site of pathergy testing were studied using real‐time quantitative reverse transcriptase–polymerase chain reaction.ResultsWe observed important increases in the expression of interleukin‐8 (IL‐8) (∼700‐fold), monocyte chemoattractant protein 1 (∼65‐fold), interferon‐γ (∼71‐fold), and IL‐12 (∼69‐fold) messenger RNA in BD lesions compared with normal skin. Except for IL‐10 (∼75‐fold increase), Th2 cytokines (i.e., IL‐4 and IL‐13) were absent.ConclusionOur data suggest a direct role of Th1 lymphocytes in the pathogenesis of mucocutaneous BD lesions.
Etanercept treatment of psoriatic arthritis: Safety, efficacy, and effect on disease progression
Authors: Mease Philip J. , Kivitz Alan J. , Burch Francis X. , Siegel Evan L. , Cohen Stanley B. , Ory Peter , Salonen David , Rubenstein Joel , Sharp John T. , Tsuji Wayne 
Published: July 2004

AbstractObjectiveEtanercept has been shown to improve the articular and cutaneous manifestations of psoriatic arthritis (PsA). In this study, we further evaluated the safety, efficacy, and effect on radiographic progression of etanercept in patients with PsA.MethodsPatients with PsA (n = 205) were randomized to receive placebo or 25 mg etanercept subcutaneously twice weekly for 24 weeks. Patients continued to receive blind‐labeled therapy in a maintenance phase until all had completed the 24‐week phase, then could receive open‐label etanercept in a 48‐week extension. Efficacy and safety were evaluated at 4, 12, and 24 weeks and at 12‐week intervals thereafter. Radiographs of the hands and wrists were assessed at baseline and 24 weeks, at entry to the open‐label phase, and after 48 weeks in the study.ResultsEtanercept significantly reduced the signs and symptoms of PsA and psoriasis. At 12 weeks, 59% of etanercept patients met the American College of Rheumatology 20% improvement criteria for joint response, compared with 15% of placebo patients (P < 0.0001), and results were sustained at 24 and 48 weeks. At 24 weeks, 23% of etanercept patients eligible for psoriasis evaluation achieved at least 75% improvement in the Psoriasis Area and Severity Index, compared with 3% of placebo patients (P = 0.001). Radiographic disease progression was inhibited in the etanercept group at 12 months; the mean annualized rate of change in the modified total Sharp score was −0.03 unit, compared with +1.00 unit in the placebo group (P = 0.0001). Etanercept was well tolerated.ConclusionEtanercept reduced joint symptoms, improved psoriatic lesions, inhibited radiographic progression, and was well tolerated in patients with PsA.
Outer surface lipoproteins ofBorrelia burgdorferivary in their ability to induce experimental joint injury
Authors: Batsford Stephen , Dunn John , Mihatsch Michael 
Published: July 2004

AbstractObjectiveTo examine the ability of bacterial lipoproteins from the spirocheteBorrelia burgdorferito cause in vivo tissue injury (arthritis).MethodsOuter surface proteins (OSPs) fromB burgdorferiwere used in a rat model of antigen‐induced allergic arthritis. Intraarticular challenge with recombinant OspA, OspB, and OspC in nonlipidated (peptide) and lipidated forms was performed in the left knee joint; the contralateral joint received buffer as control. Inflammation was monitored by technetium scintigraphy and histology.ResultsNonlipidated (peptide) OspA, OspB, and OspC did not induce arthritis; the only exception was polymerized OspA, which was tested in preimmunized rats. Lipidated OspA from 2 different strains and lipidated OspC induced severe arthritis, whereas lipidated OspB failed to induce injury. A synthetic analog of the OSP lipid modification, lipopeptide Pam3Cys‐Ser‐Lys4‐OH, either alone or coupled to bovine serum albumin, also failed to induce injury. Injury did not develop in control groups that were given the appropriate buffers or lipopolysaccharide. This showed that lipidated borrelial OSPs can be potent arthritogens but vary greatly with respect to their injury‐inducing potential. The possession of a lipid modification is essential but is not sufficient to render an OSP arthritogenic.ConclusionThis is the first study to demonstrate that individual lipoproteins fromB burgdorferican induce experimental joint injury in vivo. These results may help elucidate the pathogenesis of Lyme arthritis and, above all, underline the importance of bacterial lipoproteins as major virulence factors.
Amplification of the synovial inflammatory response through activation of mitogen‐activated protein kinases and nuclear factor κB using ligation of CD40 on CD14+ synovial cells from patients with rheumatoid arthritis
Authors: Harigai Masayoshi , Hara Masako , Kawamoto Manabu , Kawaguchi Yasushi , Sugiura Tomoko , Tanaka Michi , Nakagawa Miki , Ichida Hisae , Takagi Kae , Higami‐Ohsako Satomi , Shimada Katsuhiko , Kamatani Naoyuki 
Published: July 2004

AbstractObjectiveTo determine the signal transduction pathways in CD14+ synovial cells from patients with rheumatoid arthritis (RA) after CD40 ligation, and to examine their role in amplifying synovial inflammation in affected joints.MethodsExpression of messenger RNA was analyzed using quantitative reverse transcription–polymerase chain reaction. Cytokines and chemokines were measured using enzyme‐linked immunosorbent assay. Activation of kinases was detected using Western blotting. Nuclear translocation of NF‐κB was examined using immunohistochemistry. CD14+ synovial cells were enriched using magnetic cell sorting. Fibroblast‐like synoviocytes (FLS) were obtained by passaging primary synovial cell culture.ResultsStimulation of CD14+ synovial cells from RA patients by recombinant soluble CD154 (rsCD154) significantly induced expression of tumor necrosis factor α (TNFα), interleukin‐1α (IL‐1α), and IL‐1β. CD14+ RA synovial cells stimulated with rsCD154 plus interferon‐γ (IFNγ) induced significantly higher production of IL‐6, IL‐8, and monocyte chemoattractant protein 1 by FLS compared with unstimulated CD14+ synovial cells, through TNFα‐, IL‐1α−, and IL‐1β–mediated pathways. Stimulation with rsCD154 plus IFNγ induced the activation of ERK‐1/2, p38 MAPK, and NF‐κB. Specific inhibitors of MAPK/ERK‐1/2 kinases and p38 MAPK significantly reduced the production of TNFα and IL‐1β by rsCD154 plus IFNγ–stimulated CD14+ synovial cells, and also inhibited production of these cytokines by freshly isolated synovial cells from RA patients.ConclusionThese data indicate that the CD40–CD154 interaction activates the ERK, p38, and NF‐κB pathways in CD14+ synovial cells from RA patients to produce TNFα, IL‐1α, and IL‐1β, which in turn amplifies inflammatory responses by stimulating FLS. Inhibition of the CD40–CD154 interaction or its signal transduction pathways would be a strong and efficient strategy for the management of synovial inflammation in RA.