bluuebunny/crossref_metadata_2025 huggingface dataset:
Structure control of polyphenylene sulfide membrane prepared by thermally induced phase separation
Authors: Ding Huaiyu , Zhang Qiang , Wang Fuming , Tian Ye , Wang Lihua , Shi Yanqiao , Liu Biqian
Published: May 2007

Porous membranes were prepared through thermally induced phase separation (TIPS) of polyphenylene sulfide (PPS)/diphenyl ketone mixtures. The phase diagram of PPS/diphenyl ketone system was drawn by cloud point temperature and dynamic crystallization temperature. SEM images and porosity were used to characterize PPS membrane structures. According to the analysis of phase diagram, three main effecting factors including polymer concentration, cooling rate, and nucleating agent could control the pore structure and pore size for the preparation of symmetry and asymmetry membranes. The experimental results are coincident with the theory prediction. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Fracture surface morphology in thermosets modified with hollow microspheres
Authors: Kim Ho Sung
Published: May 2007

Fracture surface morphology in relation with toughening of thermosets modified with hollow microspheres was studied. Two different toughening methods were employed—one was with (MEH) and the other without (ME) compressive residual stresses around microspheres, respectively. The compressive residual stresses were to increase effective stress intensity factor. Various conditions arising from toughening method, properties of constituent materials, bonding between matrix and microspheres, relativity between bonding and microsphere strengths, and plane stress/strain were derived for part of generalization of fracture surface morphology. Mohr circle representations were employed for relative stress components analysis. New deformation mechanisms contributing to toughening were proposed. A major difference in toughening mechanism between ME and MEH methods was found to be in the location of plastic deformation under plane strain. The plastic deformation of ME was dominantly in matrix and appeared in the form of matrix cavitation. In the case of MEH, it was dominantly in microspheres. It was suggested that compressive residual stress promotes plastic deformation of microspheres caused by “extrusion” effect. The microsphere deformation in MEH was found also under plane stress although it was not as much as under plane strain. Matrix cavitation in ME under plane stress, however, was not found. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Thermal decomposition of copolymers used in dental resins formulations photocured by ultra blue IS
Authors: Rigoli Isabel C. , Cavalheiro Carla C. S. , Neumann Miguel G. , Cavalheiro Éder T. G.
Published: May 2007

Kinetics of thermal decomposition of acrylates copolymers used in dental resins formulations were studied with dynamic thermogravimetric analysis experiments. The kinetic parameters, including activation energy, pre‐exponential factor, and 60 min half‐life temperature, which were calculated by the Flynn and Wall method, are presented. The results indicate that thermal decomposition of the material occurred in three different stages characterized by different mechanism. These three events were separated and the kinetics parameters were determined. The loss mass was observed in the onset of the thermal decomposition for the all of copolymers studied. When the copolymers were submitted to thermal treatment before of thermal analysis was not observed the loss mass in the beginning of the process. The analysis of intermediates by GC of the condensed material extracted after thermal treatment at TB copolymers showed the presence of the methacrylic acid and 2‐hydroxyethyl methacrylate, which are products of decomposition of BisGMA and triethyleneglycol dimethacrylate monomers. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Etherification of hemicelluloses from sugarcane bagasse
Authors: Ren Jui‐Li , Sun Run‐Cang , Liu Chan‐Fu
Published: May 2007

Conditions 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

Objective

Single‐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.

Methods

SNPs 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.

Results

Whereas 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.

Conclusion

Our 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

Microscopic 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

Objective

Increased 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.

Methods

A 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.

Results

FMD%, 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.

Conclusion

Small 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

Objective

To evaluate opioid receptor function as a basis for novel antinociceptive therapy in arthritis.

Methods

We 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.

Results

A 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.

Conclusion

Our 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

Objective

To 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.

Methods

TLRs 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.

Results

TLRs 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.

Conclusion

These 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

Objective

To identify pathogenic and/or disease‐specific short peptides in sera from patients with systemic sclerosis (SSc).

Methods

Serum 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.

Results

A 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.

Conclusion

This 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

Objective

In 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.

Methods

The 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.

Results

KM‐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.

Conclusion

Apoptosis‐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

Objective

To 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.

Methods

Seven 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.

Results

The 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).

Conclusion

The 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

Objective

Several 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.

Methods

Aortic 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.

Results

Mononuclear 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.

Conclusion

Among 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

Objective

Accumulating 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.

Methods

Peripheral 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.

Results

In 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.

Conclusion

These 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

Objective

The 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.

Methods

Serum 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.

Results

SAP 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.

Conclusion

We 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.
Bronchoalveolar lavage cellular profiles in patients with systemic sclerosis–associated interstitial lung disease are not predictive of disease progression
Authors: Goh Nicole S. L. , Veeraraghavan Srihari , Desai Sujal R. , Cramer Derek , Hansell David M. , Denton Christopher P. , Black Carol M. , du Bois Roland M. , Wells Athol U.
Published: May 2007

Objective

To evaluate the prognostic value of bronchoalveolar lavage (BAL) cellular profiles in patients with systemic sclerosis–associated interstitial lung disease (SSc‐ILD).

Methods

BAL cellularity was examined in relation to mortality (n = 141), serial pulmonary function findings (n = 134), and “progression‐free survival” (n = 134), by proportional hazards analysis. Baseline severity was quantified according to the extent of disease on high‐resolution computed tomography, the diffusing capacity for carbon monoxide, and the presence or absence of pulmonary hypertension. Mortality was subclassified into overall mortality (during 10 years of followup), early mortality (occurring within 2 years of presentation), and late mortality (occurring 2–10 years after presentation).

Results

Overall mortality was associated with neutrophilia on BAL (hazard ratio 2.23 [95% confidence interval 1.20–4.14], P = 0.01), but this effect was lost when disease severity was taken into account. Early mortality was associated with neutrophilia on BAL (hazard ratio 8.40 [95% confidence interval 1.91–36.95], P = 0.005), independent of disease severity. Late mortality was not associated with neutrophilia on BAL. The presence of neutrophilia on BAL was not associated with time to decline in pulmonary function or progression‐free survival. Neither eosinophilia nor lymphocytosis on BAL was associated with mortality, rapidity of functional deterioration, or progression‐free survival. These findings were unaltered when treatment status was taken into account.

Conclusion

BAL findings provide only limited prognostic information in SSc‐ILD. Neutrophilia on BAL is linked to early mortality, but BAL findings are not linked to long‐term survival or the rapidity of progression of lung disease. The usefulness of BAL to define alveolitis in SSc is questionable.
Impairment of endothelial cell differentiation from bone marrow–derived mesenchymal stem cells: New insight into the pathogenesis of systemic sclerosis
Authors: Cipriani P. , Guiducci S. , Miniati I. , Cinelli M. , Urbani S. , Marrelli A. , Dolo V. , Pavan A. , Saccardi R. , Tyndall A. , Giacomelli R. , Matucci Cerinic M.
Published: May 2007

Objective

Systemic sclerosis (SSc) is a disorder characterized by vascular damage and fibrosis of the skin and internal organs. Despite marked tissue hypoxia, there is no evidence of compensatory angiogenesis. The ability of mesenchymal stem cells (MSCs) to differentiate into endothelial cells was recently demonstrated. The aim of this study was to determine whether impaired differentiation of MSCs into endothelial cells in SSc might contribute to disease pathogenesis by decreasing endothelial repair.

Methods

MSCs obtained from 7 SSc patients and 15 healthy controls were characterized. The number of colony‐forming unit–fibroblastoid colonies was determined. After culture in endothelial‐specific medium, the endothelial‐like MSC (EL‐MSC) phenotype was assessed according to the surface expression of vascular endothelial growth factor receptors (VEGFRs). Senescence, chemoinvasion, and capillary morphogenesis studies were also performed.

Results

MSCs from SSc patients displayed the same phenotype and clonogenic activity as those from controls. In SSc MSCs, a decreased percentage of VEGFR‐2+, CXCR4+, VEGFR‐2+/CXCR4+ cells and early senescence was detected. After culturing, SSc EL‐MSCs showed increased expression of VEGFR‐1, VEGFR‐2, and CXCR4, did not express CD31 or annexin V, and showed significantly decreased migration after specific stimuli. Moreover, the addition of VEGF and stromal cell–derived factor 1 to cultured SSc EL‐MSCs increased their angiogenic potential less than that in controls.

Conclusion

Our data strongly suggest that endothelial repair may be affected in SSc. The possibility that endothelial progenitor cells could be used to increase vessel growth in chronic ischemic tissues may open up new avenues in the treatment of vascular damage caused by SSc.
Low number of regulatory T cells in skin lesions of patients with cutaneous lupus erythematosus
Authors: Franz B. , Fritzsching B. , Riehl A. , Oberle N. , Klemke C.‐D. , Sykora J. , Quick S. , Stumpf C. , Hartmann M. , Enk A. , Ruzicka T. , Krammer P. H. , Suri‐Payer E. , Kuhn A.
Published: May 2007

Objective

To define the phenotype and function of CD4+,CD25+ regulatory T cells (Treg) in patients with cutaneous lupus erythematosus (CLE), a heterogeneous autoimmune disease characterized primarily by inflammatory skin lesions.

Methods

The number of Treg in skin specimens obtained from patients with various subtypes of CLE was investigated by immunohistochemical analysis, using anti‐Foxp3 and anti‐CD4 monoclonal antibodies. Furthermore, characterization of peripheral blood CD4+,CD25+ Treg from normal healthy donors and patients with CLE was carried out by flow cytometry, analyzing the expression of Foxp3 and Treg subpopulations. We also purified CD4+,CD25high Treg obtained from patients with CLE and tested the sensitivity of these cells to CD95L‐mediated apoptosis.

Results

Quantitative analysis of CD4+ T cells in skin lesions from patients with CLE revealed that the number was similar to that in lesions from patients with other chronic inflammatory diseases, but the number of Foxp3+ Treg in CLE was significantly reduced. There was no correlation between disease subtype and the frequency of Foxp3+ Treg in the skin of patients with CLE. In peripheral blood, no significant differences were observed in the number and phenotype of CD4+,CD25+ Treg or in the sensitivity to apoptosis of CD4+,CD25high Treg derived from patients with CLE and those derived from normal healthy donors.

Conclusion

These data suggest that an organ‐specific abnormality of Treg in the skin underscores the importance of analyzing Treg in the affected tissue. Such a local process might give insight into the pathogenic mechanisms of CLE and differs from a global peripheral dysfunction as reported for patients with a systemic manifestation of the disease.
Epidemiology of juvenile idiopathic arthritis in a multiethnic cohort: Ethnicity as a risk factor
Authors: Saurenmann R. K. , Rose J. B. , Tyrrell P. , Feldman B. M. , Laxer R. M. , Schneider R. , Silverman E. D.
Published: May 2007

Objective

To study the influence of ethnicity on the risk of developing juvenile idiopathic arthritis (JIA) in a multiethnic community of patients with unrestricted access to health care.

Methods

A questionnaire on ethnicity was distributed to all patients with JIA being followed up at the Hospital for Sick Children in Toronto, Ontario, Canada. Of 1,082 patients, 859 (79.4%) responded to the questionnaire. To calculate the relative risk (RR) of developing JIA in this study cohort, the results were compared with data from the age‐matched general population of the Toronto metropolitan area (TMA) as provided in the 2001 census from Statistics Canada.

Results

European descent was reported by 69.7% of the patients with JIA compared with a frequency of 54.7% in the TMA general population, whereas a statistically significantly lower than expected percentage of the patients with JIA reported having black, Asian, or Indian subcontinent origin. Children of European origin had a higher RR for developing any of the JIA subtypes except polyarticular rheumatoid factor (RF)–positive JIA, and were particularly more likely to develop the extended oligoarticular and psoriatic subtypes. A higher frequency of enthesitis‐related JIA was observed among patients of Asian origin, while those of black origin or native North American origin were more likely to develop polyarticular RF‐positive JIA.

Conclusion

In this multiethnic cohort, European descent was associated with a significantly increased risk of developing JIA, and the distribution of JIA subtypes differed significantly across ethnic groups.
Coffee consumption and risk of incident gout in men: A prospective study
Authors: Choi Hyon K. , Willett Walter , Curhan Gary
Published: May 2007

Objective

Coffee is one of the most widely consumed beverages in the world and may affect the risk of gout via various mechanisms. We prospectively evaluated the relationship between coffee intake and the risk of incident gout in a large cohort of men.

Methods

Over a 12‐year period, we studied 45,869 men with no history of gout at baseline. Intake of coffee, decaffeinated coffee, tea, and total caffeine was assessed every 4 years through validated questionnaires. We used a supplementary questionnaire to ascertain whether participants met the American College of Rheumatology survey criteria for gout.

Results

We documented 757 confirmed incident cases of gout. Increasing coffee intake was inversely associated with the risk of gout. The multivariate relative risks (RRs) for incident gout according to coffee consumption categories (0, <1, 1–3, 4–5, and ≥6 cups per day) were 1.00, 0.97, 0.92, 0.60 (95% confidence interval [95% CI] 0.41–0.87), and 0.41 (95% CI 0.19–0.88), respectively (P for trend = 0.009). For decaffeinated coffee, the multivariate RRs according to consumption categories (0, <1, 1–3, and ≥4 cups per day) were 1.00, 0.83, 0.67 (95% CI 0.54–0.82), and 0.73 (95% CI 0.46–1.17), respectively (P for trend = 0.002). Total caffeine from all sources and tea intake were not associated with the risk of gout.

Conclusion

These prospective data suggest that long‐term coffee consumption is associated with a lower risk of incident gout.
Use of accommodations for valued life activities: Prevalence and effects on disability scores
Authors: Katz Patricia P. , Morris Anne
Published: May 2007

Objective

To describe the prevalence of using 4 specific behavioral accommodations (assistive devices, personal assistance, limits on the amount or kind of activities, and taking more time to perform activities) in the performance of valued life activities (VLAs), and to examine the impact of accounting for these accommodations on VLA disability scores.

Methods

Data were from a panel study of 467 individuals with rheumatoid arthritis (RA) interviewed annually by telephone. VLA disability was assessed using a 29‐item scale, rating difficulty performing each activity and asking whether the 4 types of accommodations were used. An unadjusted difficulty score based solely on difficulty ratings was calculated, as well as 3 adjusted scores accounting for use of assistance or devices, use of assistance, devices, or limitations in activities, and use of all 4 accommodations.

Results

Accommodations were widely used by individuals with RA to perform daily activities. Limits and more time were used for more activities than assistance and devices. Adjustment for accommodations produced substantial increases in disability scores (e.g., the mean total VLA difficulty score increased by 84% after adjustment for all 4 accommodations).

Conclusion

The accommodations included on the Health Assessment Questionnaire, the most commonly used measure of functioning for RA, include only assistive devices and personal assistance, which were not the accommodations most frequently used in our sample. If assessments are intended to estimate total disease burden, they should include use of a broader range of accommodations to develop a more complete picture of how daily function is affected.
Early aggressive care and delayed recovery from whiplash: Isolated finding or reproducible result?
Authors: Côté Pierre , Hogg‐Johnson Sheilah , Cassidy J. David , Carroll Linda , Frank John W. , Bombardier Claire
Published: May 2007

Objective

To test the reproducibility of the finding that early intensive care for whiplash injuries is associated with delayed recovery.

Methods

We analyzed data from a cohort study of 1,693 Saskatchewan adults who sustained whiplash injuries between July 1, 1994 and December 31, 1994. We investigated 8 initial patterns of care that integrated type of provider (general practitioners, chiropractors, and specialists) and number of visits (low versus high utilization). Cox models were used to estimate the association between patterns of care and time to recovery while controlling for injury severity and other confounders.

Results

Patients in the low‐utilization general practitioner group and those in the general medical group had the fastest recovery even after controlling for important prognostic factors. Compared with the low‐utilization general practitioner group, the 1‐year rate of recovery in the high‐utilization chiropractic group was 25% slower (adjusted hazard rate ratio [HRR] 0.75, 95% confidence interval [95% CI] 0.54–1.04), in the low‐utilization general practitioner plus chiropractic group the rate was 26% slower (HRR 0.74, 95% CI 0.60–0.93), and in the high‐utilization general practitioner plus chiropractic combined group the rate was 36% slower (HRR 0.64, 95% CI 0.50–0.83).

Conclusion

The observation that intensive health care utilization early after a whiplash injury is associated with slower recovery was reproduced in an independent cohort of patients. The results add to the body of evidence suggesting that early aggressive treatment of whiplash injuries does not promote faster recovery. In particular, the combination of chiropractic and general practitioner care significantly reduces the rate of recovery.
Assessment of American College of Rheumatology quality criteria for rheumatoid arthritis in a pre–quality criteria patient cohort
Authors: Kahn K. L. , MacLean C. H. , Wong A. L. , Rubenstein L. Z. , Liu H. , Fitzpatrick D. M. , Harker J. O. , Chen W. P. , Traina S. B. , Mittman B. S. , Hahn B. H. , Paulus H. E.
Published: May 2007

Objective

To evaluate the American College of Rheumatology (ACR) starter set of quality measures for rheumatoid arthritis (RA) in an actual patient cohort that preceded publication of the quality measures.

Methods

We retrospectively applied the 2006 ACR quality criteria to a prospectively studied cohort of 568 patients with RA treated by 1,932 unique physicians including 255 different rheumatologists between the years 1999 and 2003. Data on performance were obtained from self‐report surveys and medical record review within 12 months.

Results

At least 1 joint examination was performed in 98% of patients. Patient and physician global assessments were reported for 79% and 74% of patients, respectively. A total of 85% of patients received disease‐modifying antirheumatic drugs (DMARDs). DMARD adjustments were made for 50% of patients in whom increasing disease activity was noted at least once and for 64% of patients in whom increasing disease activity was noted during 2 (of 4) 3‐month periods within the year. Compared with self‐report surveys, medical records substantially underreported performance on quality measures.

Conclusion

The ACR‐endorsed quality measures for RA can be assessed using available data sources. When both self‐report and medical record data are used, adherence rates, designed to serve as minimum standards of care, were moderate or high for most measures. Prior to using indicators to compare quality across groups, specific strategies for operationalizing measures and for using accurate data sources to assess adherence to the measures should be defined.
Long‐term treatment with methotrexate or tumor necrosis factor α inhibitors does not increase epstein‐barr virus load in patients with rheumatoid arthritis
Authors: Balandraud Nathalie , Guis Sandrine , Baptiste Meynard Jean , Auger Isabelle , Roudier Jean , Roudier Chantal
Published: May 2007

Objective

We previously demonstrated that patients with rheumatoid arthritis (RA) have a 10‐fold systemic Epstein‐Barr virus (EBV) overload, very similar to that observed in healthy organ transplant recipients. Our objective was to monitor EBV load over time in patients with RA receiving methotrexate, infliximab, or etanercept to detect possible immunosuppression‐associated EBV dysregulation, as described in posttransplant lymphoproliferative disease.

Methods

The EBV load in the peripheral blood mononuclear cells (PBMCs) from 19 patients receiving methotrexate, 68 patients receiving infliximab, and 48 patients receiving etanercept was monitored for durations ranging from 6 months to 5 years using a real‐time polymerase chain reaction assay previously developed for that purpose. The effect of treatment duration on EBV load and the link between the Disease Activity Score in 28 joints and EBV load were analyzed by generalized estimating equations.

Results

Methotrexate tended to decrease EBV load over time, but this did not reach significance. Tumor necrosis factor α (TNFα) inhibitors did not significantly modify EBV load over time. Finally, high disease activity was significantly associated with high EBV load.

Conclusion

Long‐term usage of methotrexate or TNFα inhibitors in patients with RA does not significantly influence EBV load in PBMCs.
Alcohol‐Vapor Inclusion in Single‐Crystal Adsorbents [MII2(bza)4(pyz)]n (M=Rh, Cu): Structural Study and Application to Separation Membranes
Authors: Takamizawa Satoshi , Kachi‐Terajima Chihiro , Kohbara Masa‐aki , Akatsuka Takamasa , Jin Tetsuro
Published: May 2007

The vapor absorbency of the series of alcohols methanol, ethanol, 1‐propanol, 1‐butanol, and 1‐pentanol was characterized on the single‐crystal adsorbents [MII2(bza)4(pyz)]n (bza=benzoate, pyz=pyrazine, M=Rh (1), Cu (2)). The crystal structures of all the alcohol inclusions were determined by single‐crystal X‐ray crystallography at 90 K. The crystal‐phase transition induced by guest adsorption occurred in the inclusion crystals except for 1‐propanol. A hydrogen‐bonded dimer of adsorbed alcohol was found in the methanol‐ and ethanol‐inclusion crystals, which is similar to a previous observation in 2⋅2EtOH (S. Takamizawa, T. Saito, T. Akatsuka, E. Nakata, Inorg. Chem. 2005, 44, 1421–1424). In contrast, an isolated monomer was present in the channel for 1‐propanol, 1‐butanol, and 1‐pentanol inclusions. All adsorbed alcohols were stabilized by hydrophilic and/or hydrophobic interactions between host and guest. From the combined results of microscopic determination (crystal structure) and macroscopic observation (gas‐adsorption property), the observed transition induced by gas adsorption is explained by stepwise inclusion into the individual cavities, which is called the “step‐loading effect.” Alcohol/water separation was attempted by a pervaporation technique with microcrystals of 2 dispersed in a poly(dimethylsiloxane) membrane. In the alcohol/water separation, the membrane showed effective separation ability and gave separation factors (alcohol/water) of 5.6 and 4.7 for methanol and ethanol at room temperature, respectively.