bluuebunny/crossref_metadata_2025_split huggingface dataset:
Etherification of hemicelluloses from sugarcane bagasse
Authors: Ren Jui‐Li , Sun Run‐Cang , Liu Chan‐Fu 
Published: May 2007

AbstractConditions for the preparation of etherified hemicelluloses from sugarcane bagasse with 2, 3‐epoxypropyltrimethylammonium chloride (ETA) using sodium hydroxide as a catalyst in aqueous solution were studied comparatively. The extent of the etherification was measured by yield percentage and degree of substitution. The effects of reaction time of 3–7 h, reaction temperature of 50–80°C, temperature of alkaline activation of 30–60°C, and time of alkaline activation of 0–60 min on the reaction yield and degree of substitution were investigated in detail. The overall yield and degree of substitution were varied from 35.2 to 41.9% and from 0.14 to 0.33, respectively, by changing the reaction temperature and duration as well as time and temperature of alkaline activation. The new materials were characterized by FT‐IR and 13C NMR spectroscopy, thermal analysis as well as GPC. It was found that the thermal stability of the hemicellulosic ethers decreased after chemical modification, and the molecular weights of the etherified hemicelluloses were lower than those of the native hemicelluloses. 13C NMR spectra gave the evidence for etherification reaction and the quaternization of hemicelluloses occurred mainly at C‐3 position. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
TNF polymorphisms in psoriasis: Association of psoriatic arthritis with the promoter polymorphism TNF*‐857 independent of the PSORS1 risk allele
Authors: Reich Kristian , Hüffmeier Ulrike , König Inke R. , Lascorz Jesús , Lohmann Jörg , Wendler Jörg , Traupe Heiko , Mössner Rotraut , Reis André , Burkhardt Harald 
Published: May 2007

AbstractObjectiveSingle‐nucleotide polymorphisms (SNPs) of the tumor necrosis factor gene TNF at positions −238 and −308 have been associated with psoriasis vulgaris and psoriatic arthritis (PsA). The strong linkage disequilibrium (LD) at chromosome region 6p21, a region known to harbor risk factors for psoriasis susceptibility (PSORS1) other than just SNPs of the TNF gene, renders the interpretation of these findings difficult. The aim of this study was to analyze several SNPs of the TNF gene and its neighboring LTA gene for independent and dependent carriage of the PSORS1 risk allele.MethodsSNPs in the promoter of the TNF (−238G/A, −308G/A, −857C/T, and −1031T/C), LTA (+252A/G), TNLFRSF1A (+36A/G), and TNLFRSF1B (+676T/G) genes were genotyped in 375 psoriasis patients, 375 PsA patients, and 376 controls. The Trp‐ Trp‐Cys‐Cys haplotype of the CCHCR1 gene (CCHCR1*WWCC) was used as an estimate of the risk allele PSORS1.ResultsWhereas we were able to confirm the previously described strong association of allele TNF*‐238A with psoriasis, our study revealed that this association was completely dependent on carriage of the PSORS1 risk allele. For PsA, but not psoriasis vulgaris without joint involvement, a strong association with the allele TNF*‐857T (odds ratio 1.956 [95% confidence interval 1.334–2.881]; corrected P = 0.0025) was also detected in patients negative for the PSORS1 risk allele.ConclusionOur results indicate that there are genetic differences between psoriasis vulgaris patients with and without joint manifestations. While the previously reported association between TNF*‐238A and psoriasis seems to primarily reflect LD with PSORS1, TNF*‐857T may represent a risk factor for PsA that is independent of the PSORS1 allele.
Microscopic polyangiitis presenting as a “pulmonary‐muscle” syndrome: Is subclinical alveolar hemorrhage the mechanism of pulmonary fibrosis?
Authors: Birnbaum Julius , Danoff Sonye , Askin Frederic B. , Stone John H. 
Published: May 2007

AbstractMicroscopic polyangiitis (MPA) may present with a syndrome that resembles idiopathic pulmonary fibrosis (IPF). We describe an MPA patient with the clinical presentation of a “pulmonary‐muscle” syndrome in which interstitial lung disease antedated the onset of myopathy. Identification of vasculitis on muscle biopsy was instrumental in recognizing clinical, radiographic, and histopathologic features that were more characteristic of MPA than of IPF. Institution of glucocorticoid and cyclophosphamide therapy led to the induction of a complete remission. The histologic findings in this case implicate subclinical episodes of alveolar hemorrhage as the mechanism of interstitial lung disease in MPA.
Improvement of vascular endothelial function using the oral endothelin receptor antagonist bosentan in patients with systemic sclerosis
Authors: Sfikakis P. P. , Papamichael C. , Stamatelopoulos K. S. , Tousoulis D. , Fragiadaki K. G. , Katsichti P. , Stefanadis C. , Mavrikakis M. 
Published: May 2007

AbstractObjectiveIncreased endothelin activity may play a role in the pathogenesis of vascular injury, a primary feature of systemic sclerosis (SSc; scleroderma). Our goal was to test the hypothesis that treatment with the oral endothelin receptor antagonist bosentan might improve vascular endothelial function in SSc patients.MethodsA 4‐week, prospective, parallel‐group study compared 12 SSc patients who did not receive bosentan treatment with 12 patients who did receive treatment (125 mg/day) for pulmonary hypertension and/or digital ulcers. There were no differences in demographic and clinical characteristics or medications between the 2 groups. Baseline endothelial dysfunction was documented by decreased brachial artery ultrasound‐derived flow‐mediated dilation (FMD%; <5.5). Pulse wave analysis, venous occlusion plethysmography, and measurement of serum vascular markers were performed in parallel.ResultsFMD%, the main end point, increased significantly from a mean ± SD of 3.1 ± 1.3% to 8.4 ± 2.6% after 4 weeks of bosentan treatment (P < 0.001, compared with a change from 2.4 ± 1.6% to 2.4 ± 2.2% in control patients). Arterial blood pressure, endothelium‐independent vascular function, augmentation index, peripheral flow reserve, as well as circulating intercellular adhesion molecule 1, E‐selectin, vascular endothelial growth factor, and endothelin 1 were not significantly affected by bosentan treatment. In patients continuously treated for 4 months, during which the dosage of bosentan remained at 125 mg/day (n = 5) or increased to 250 mg/day (n = 5), the 4‐week results remained unchanged.ConclusionSmall doses of bosentan improve endothelial function without affecting hemodynamic parameters or endothelial activation–related processes, thus supporting a direct, reversible effect of endothelin in SSc‐associated vascular injury. A long‐term, controlled trial to examine the potentially global clinical benefit of endothelin receptor blockade in patients with early SSc may be warranted.
Amelioration of pain and histopathologic joint abnormalities in the Col1‐IL‐1βXATmouse model of arthritis by intraarticular induction of μ‐opioid receptor into the temporomandibular joint
Authors: Kyrkanides Stephanos , Fiorentino Paolo M. , Miller Jen‐Nie H. , Gan Yanjun , Lai Yu‐Ching , Shaftel Solomon S. , Puzas J. Edward , Piancino Maria G. , O'Banion M. Kerry , Tallents Ross H. 
Published: May 2007

AbstractObjectiveTo evaluate opioid receptor function as a basis for novel antinociceptive therapy in arthritis.MethodsWe induced human μ‐opioid receptor (HuMOR) expression in arthritic joints of mice, using the feline immunodeficiency virus (FIV) vector, which is capable of stably transducing dividing, growth‐arrested, and terminally differentiated cells. Male and female Col1‐IL‐1βXAT–transgenic mice developed on a C57BL/6J background and wild‐type littermates were studied.ResultsA single injection of FIV(HuMOR) into the temporomandibular joints of Col1‐IL‐1βXAT–transgenic mice 1 week prior to induction of arthritis prevented the development of orofacial pain and joint dysfunction, and reduced the degree of histopathologic abnormality in the joint. In addition, FIV(HuMOR) prevented the attendant sensitization of trigeminal sensory neurons and activation of astroglia in brainstem trigeminal sensory nuclei. These effects were mediated by the transduction of primary sensory neurons via transport of FIV vectors from peripheral nerve endings to sensory ganglia, as evidenced by HuMOR expression in neuronal cell bodies located in the trigeminal ganglia, as well as in their proximal and distal nerve branches located in the main sensory and subnucleus caudalis of the brainstem and joints, respectively. The presence of MOR ligands predominantly in the descending trigeminal nucleus suggested that the observed antinociception occurred at the subnucleus caudalis. Articular chondrocytes and meniscal tissue were also infected by FIV(HuMOR), which presumably exerted an antiinflammatory effect on cartilage.ConclusionOur results indicate that prophylactic therapy with MOR overexpression in joints can successfully prevent the development of pain, dysfunction, and histopathologic abnormalities in the joints in arthritis. These findings may provide a basis for the future development of spatiotemporally controlled antinociceptive and antiinflammatory therapy for arthritis.
Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7
Authors: Bobacz K. , Sunk I. G. , Hofstaetter J. G. , Amoyo L. , Toma C. D. , Akira S. , Weichhart T. , Saemann M. , Smolen J. S. 
Published: May 2007

AbstractObjectiveTo assess the presence of Toll‐like receptors (TLRs) 1–9 in human articular cartilage, and to investigate the effects of lipopolysaccharide (LPS)–induced activation of TLR‐4 on biosynthetic activity and matrix production by human articular chondrocytes.MethodsTLRs 1–9 were assessed in human articular cartilage by reverse transcription–polymerase chain reaction (RT‐PCR); TLR‐4 was also analyzed by Western blotting and immunohistochemistry. Articular chondrocytes were isolated from human donors and from wild‐type or TLR‐4−/− mice. Chondrocyte monolayer cultures were incubated with interleukin‐1β (IL‐1β) and LPS in the absence or presence of bone morphogenetic protein 7 (BMP‐7) and IL‐1 receptor antagonist (IL‐1Ra). Neosynthesis of sulfated glycosaminoglycans (sGAG) was measured by 35S‐sulfate incorporation. Endogenous gene expression of cartilage markers as well as IL‐1β was examined using RT‐PCR. The involvement of p38 kinase or p44/42 kinase (ERK‐1/2) in LPS‐mediated TLR‐4 signaling was investigated by immunoblotting, RT‐PCR, and sGAG synthesis.ResultsTLRs 1–9 were found on the messenger RNA (mRNA) level in human articular chondrocytes. The presence of TLR‐4 was also observed on the protein level. In murine and human articular chondrocytes, but not in chondrocytes derived from TLR‐4−/− mice, stimulation with LPS resulted in a decrease in total proteoglycan synthesis. IL‐1β mRNA expression was increased by TLR‐4 activation, whereas expression of aggrecan and type II collagen was significantly decreased. The presence of BMP‐7 and IL‐1Ra antagonized the anti‐anabolic effects of LPS. Blocking of p38, but not ERK‐1/2, resulted in inhibition of both LPS‐mediated IL‐1β gene expression and the negative effects of LPS on matrix biosynthesis.ConclusionThese data demonstrate the presence of TLRs in human articular cartilage. The suppressive effects of LPS on cartilage biosynthetic activity are dependent on the presence of TLR‐4, are governed, at least in part, by an up‐regulation of IL‐1β, and are mediated by p38 kinase. These in vitro data indicate an anti‐anabolic effect of TLR‐4 in articular chondrocytes that may hamper cartilage repair in various joint diseases.
Comprehensive investigation of disease‐specific short peptides in sera from patients with systemic sclerosis: Complement C3f‐des‐arginine, detected predominantly in systemic sclerosis sera, enhances proliferation of vascular endothelial cells
Authors: Xiang Yang , Matsui Toshihiro , Matsuo Kosuke , Shimada Kota , Tohma Shigeto , Nakamura Hiroshi , Masuko Kayo , Yudoh Kazuo , Nishioka Kusuki , Kato Tomohiro 
Published: May 2007

AbstractObjectiveTo identify pathogenic and/or disease‐specific short peptides in sera from patients with systemic sclerosis (SSc).MethodsSerum samples from 40 patients with SSc, 30 patients with systemic lupus erythematosus, 21 patients with rheumatoid arthritis, 30 patients with osteoarthritis, and 26 healthy donors were tested. Short peptides with molecular weights of smaller than ∼3 kd, purified from the sera by magnetic bead–based hydrophobic interaction chromatography 18, were detected and their amino acid sequences determined using matrix‐assisted laser desorption ionization–time‐of‐flight mass spectrometry. Effects of the identified peptides on fibroblasts and microvascular endothelial cells were tested using synthesized peptides and sera containing the peptides.ResultsA group of peptides with mass/charge (m/z) values of 1,865, 1,778, 1,691, 1,563, and 1,450 were detected predominantly in the SSc sera. These peptides were identified as family members of complement C3f‐des‐arginine (DRC3f) derived from C3b. The level of DRC3f (m/z 1,865) was related to vascular involvement in SSc and to SSc disease activity. The synthesized peptides of DRC3f and C3f, as well as the filtrated sera containing DRC3f, enhanced proliferation of microvascular endothelial cells, but not fibroblasts. Both DRC3f and C3f increased production of transforming growth factor β1 by dermal microvascular endothelial cells.ConclusionThis comprehensive peptidomics analysis revealed the predominance of DRC3f in the sera of patients with SSc. Investigation of DRC3f may be a useful tool for the diagnosis and evaluation of disease activity in SSc. Moreover, its demonstrated effects on endothelial cells suggest a potential role for DRC3f in the pathophysiologic mechanisms of SSc.
Apoptosis‐induced acetylation of histones is pathogenic in systemic lupus erythematosus
Authors: Dieker Jürgen W. , Fransen Justin H. , van Bavel Casandra C. , Briand Jean‐Paul , Jacobs Cor W. , Muller Sylviane , Berden Jo H. , van der Vlag Johan 
Published: May 2007

AbstractObjectiveIn systemic lupus erythematosus (SLE), inadequate removal of apoptotic cells may lead to challenge of the immune system with immunogenic self antigens that have been modified during apoptosis. We undertook this study to evaluate whether apoptosis‐induced histone modifications are targets for the immune system in SLE.MethodsThe epitope of KM‐2, a monoclonal antihistone autoantibody derived from a lupus mouse, was mapped by random peptide phage display. The reactivity of KM‐2 and plasma with (acetylated) histone H4 (H4) peptides and with nonapoptotic, apoptotic, and hyperacetylated histones was determined by immunofluorescence staining, enzyme‐linked immunosorbent assay, and Western blotting.ResultsKM‐2 recognized apoptosis‐induced acetylation of H4 at lysines 8, 12, and 16. The majority of plasma samples from SLE patients and lupus mice showed higher reactivity with triacetylated H4 peptide (residues 1–22) and with hyperacetylated and apoptotic histones than with nonacetylated H4 peptide and normal histones. Importantly, administration of triacetylated H4 peptide to lupus‐prone mice before disease onset accelerated the disease by enhancing mortality and aggravating proteinuria, skin lesions, and glomerular IgG deposition, while the nonacetylated H4 peptide had no pathogenic effect. The delayed‐type hypersensitivity response in lupus mice against the triacetylated H4 peptide was higher than that against the nonacetylated H4 peptide. Bone marrow–derived dendritic cells (DCs) cultured in the presence of hyperacetylated nucleosomes showed increased expression/production of CD40, CD86, interleukin‐6 (IL‐6), and tumor necrosis factor α compared with DCs cultured in the presence of normal nucleosomes. Finally, DCs cultured in the presence of hyperacetylated nucleosomes were able to activate syngeneic T cells, because IL‐2 production increased.ConclusionApoptosis‐induced acetylation of nucleosomes may represent an important driving force in the development of lupus.
Clinical, immunologic, and genetic features of familial systemic sclerosis
Authors: Assassi Shervin , Arnett Frank C. , Reveille John D. , Gourh Pravitt , Mayes Maureen D. 
Published: May 2007

AbstractObjectiveTo examine whether the affected first‐degree relatives within multicase systemic sclerosis (SSc; scleroderma) families are concordant for autoantibody profile, disease type, and HLA class II haplotypes and whether clinical expression and serologic characteristics of familial SSc differ from those of sporadic SSc.MethodsSeven hundred ten SSc families from the Scleroderma Family Registry and DNA Repository (Scleroderma Registry) were examined, and 18 multicase families were identified. SSc cases and their first‐degree family members underwent serologic testing for different autoantibodies. The disease type and various disease features were abstracted from the available medical records. Additionally, HLA class II typing was performed on the multicase SSc sibpairs.ResultsThe observed SSc‐specific antibody concordance within each multicase SSc family was statistically more common than expected by chance alone (P = 0.007). The autoantibody profile and disease features of familial and sporadic SSc cases did not differ significantly. The frequency of autoantibody positivity was not different between unaffected first‐degree family members of patients from multicase versus singleton SSc families. HLA haplotype sharing between SSc sibpairs was significantly more common than expected (P = 0.011).ConclusionThe affected members within multicase SSc families tend to be concordant for SSc‐specific autoantibodies and HLA haplotypes; familial SSc does not appear to be a unique disease subset.
Inflammatory rheumatic disease and smoking are predictors of aortic inflammation: A controlled study of biopsy specimens obtained at coronary artery surgery
Authors: Hollan Ivana , Scott Helge , Saatvedt Kjell , Prayson Richard , Mikkelsen Knut , Nossent Hans C. , Kvelstad Ingjerd Lien , Liang Matthew H. , Førre ØYstein T. 
Published: May 2007

AbstractObjectiveSeveral inflammatory rheumatic diseases are associated with accelerated atherosclerosis. Atherosclerosis may result from systemic and/or local vascular inflammation. The aim of this study was to evaluate the occurrence of chronic inflammatory infiltrates in the aortas of patients with and those without inflammatory rheumatic disease who had undergone coronary artery bypass graft (CABG) surgery, and to assess the relationship between the infiltrates and other factors thought to play a role in atherosclerosis, such as smoking.MethodsAortic specimens routinely removed during CABG surgery in 66 consecutive patients with inflammatory rheumatic disease and 51 control patients without inflammatory rheumatic disease were examined by light microscopy for the occurrence, location, and severity of chronic inflammatory infiltrates and atherosclerotic lesions.ResultsMononuclear cell infiltrates in the inner adventitia (apart from those localized along the epicardium) were more frequent in the group of patients with inflammatory rheumatic disease (47% versus 20%; P = 0.002, odds ratio [OR] OR 3.6, 95% confidence interval [95% CI] 1.6–8.5), and the extent of these infiltrates was greater. Multivariate analyses revealed that the occurrence of mononuclear cell infiltrates was associated with inflammatory rheumatic disease (OR 2.99, P = 0.020) and current smoking (OR 3.93, P = 0.012), and they were observed in 6 of 7 patients with a history of aortic aneurysm. Inflammatory infiltrates in the media were seen only in patients with inflammatory rheumatic disease. The frequency of atherosclerotic lesions, inflammation within the plaques, and epicardial inflammatory infiltrates in the 2 groups was equal.ConclusionAmong aortic samples collected during CABG surgery, those obtained from patients with inflammatory rheumatic disease had more pronounced chronic inflammatory infiltration in the media and inner adventitia than those obtained from control patients. Current smoking was an independent predictor of chronic inner adventitial infiltrates. The infiltrates may represent an inflammatory process that promotes atherosclerosis and formation of aneurysms.
Functional defect of circulating regulatory CD4+ T cells in patients with Wegener's granulomatosis in remission
Authors: Abdulahad Wayel H. , Stegeman Coen A. , van der Geld Ymke M. , Doornbos‐van der Meer Berber , Limburg Pieter C. , Kallenberg Cees G. M. 
Published: May 2007

AbstractObjectiveAccumulating data support the role of regulatory T cells, a subset of CD4+ T cells that expresses CD25high and the transcription factor forkhead box P3 (FoxP3), in controlling and preventing autoimmunity. In Wegener's granulomatosis (WG), an autoimmune vasculitis, up‐regulation of CD25 on circulating CD4+ T cells has been observed, even in patients in remission. The objective of this study was to test whether the frequency and/or function of Treg cells from WG patients in remission are disturbed.MethodsPeripheral blood mononuclear cells were freshly isolated from 52 WG patients in remission and from 27 age‐ and sex‐matched healthy control subjects. The proportion of circulating Treg cells was assessed by flow cytometry using CD4, CD25, FoxP3, and CD45RO markers. Anergy and suppressive function of CD25high,CD4+ T cells were determined using polyclonal stimulants and coculture assay in 10 WG patients in remission and in 10 age‐ and sex‐matched healthy controls.ResultsIn WG patients, a significant increase was observed in the percentage of circulating CD25high,CD4+ and CD25low,CD4+ T cells, whereas CD25–,CD4+ T cells were decreased, as compared with healthy controls. Among circulating CD4+ T cells, an expanded percentage of Treg cells (CD25high,FoxP3+) with memory phenotype was present in WG patients. However, when the suppressive function of CD25high,CD4+ T cells was tested, CD25high,CD4+ T cells from WG patients showed diminished or absent suppression of responder T cell proliferation. The impaired suppression was not due to responder cell resistance (as shown by crisscross experiments with T cells from healthy controls) or altered survival of Treg cells.ConclusionThese data indicate that WG patients in remission have an expanded proportion of Treg cells that are functionally defective. This observation may be relevant to the development and relapsing course of this autoimmune vasculitis.
Normal circulating serum amyloid P component concentration in systemic sclerosis
Authors: Tennent Glenys A. , Dziadzio Magdalena , Triantafillidou Eva , Davies Phillip , Gallimore J. Ruth , Denton Christopher P. , Pepys Mark B. 
Published: May 2007

AbstractObjectiveThe observation of reduced circulating concentrations of the constitutive plasma pentraxin protein, serum amyloid P component (SAP), in serum samples obtained from a small number of patients with systemic sclerosis (SSc) has been reported as confirmation of an antifibrotic role of this protein. Because neither sustained SAP depletion in humans nor SAP deficiency in mice is associated with fibrosis, we sought to establish rigorously the serum SAP concentration in well‐characterized patients with SSc.MethodsSerum concentrations of SAP were measured by electroimmunoassay in a cross‐sectional cohort of 20 patients with diffuse cutaneous SSc and 12 patients with limited cutaneous SSc, and in a separate 12‐month longitudinal cohort of 13 patients with diffuse disease and 37 patients with limited disease. The extent and severity of disease were characterized in detail at the time of serum sampling. Serum concentrations of the classic acute‐phase reactants, C‐reactive protein and serum amyloid A protein, were measured by immunonephelometric assays.ResultsSAP values were entirely within the normal range, regardless of the extent and severity of disease, apart from a very few isolated raised values associated with acute intercurrent complications causing major acute‐phase responses.ConclusionWe observed no reduced circulating concentrations of SAP in patients with SSc, nor any evidence of an association between SAP levels and the extent or severity of fibrosis.