bluuebunny/crossref_metadata_2025_split huggingface dataset:
Numerical simulation of the spin‐draw process of poly(ethylene terephthalate) fibers
Authors: Oh Tae Hwan 
Published: February 2007

AbstractNumerical simulation for the calculation of the profile developments of the spin‐draw process in the melt spinning of poly(ethylene terephthalate) was performed. Both spinning and drawing profiles were analyzed and included the structure development of birefringence and crystallinity in the draw line. By applying a simple model describing the continuous drawing process, we made it possible to simulate the spin‐draw process. The strain rate of the spinline had a broad distribution, and that of the draw line had a narrower peak. The calculated birefringence ranged from 0.176 to 0.192 and the crystallinity ranged from 0.37 to 0.44 with draw ratio. The birefringence profile had a similar pattern as the stress profile, and the crystallinity gently increased along the draw line more than the birefringence did. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci 104: 2522–2527, 2007
Synthesis and gas permeability of novel fluorinated poly(phenylene‐co‐naphthalimide)s
Authors: Qiu Zhiming , Zhang Suobo , Li Wenmu 
Published: February 2007

AbstractA new class of high‐performance polymers [poly(phenylene‐co‐naphthalimide)s] was prepared through the Ni(0) catalytic coupling of N‐(4‐chloro‐2‐trifluromethylphenyl)‐5‐chloro‐1,8‐naphthalimide and 2,5‐dichlorobenzophenone. The resulting copolymers exhibited high molecular weights (high inherent viscosities) and a combination of desirable properties such as good solubility in dipolar aprotic solvents, film‐forming capability, and mechanical properties. The glass‐transition temperatures of the copolymers ranged from 320 to 403°C and increased as the content of the naphthalimide moiety increased. Tough polymer films, obtained via casting from N‐methylpyrrolidone solutions, had tensile strengths of 64–107 MPa and tensile moduli of 3.4–4.7 GPa. The gas permeability coefficients of the copolymers were measured for H2, CO2, O2, CH4, and N2. They showed oxygen permeability coefficients and permeability selectivity of oxygen to nitrogen (permeability coefficient for O2/permeability coefficient for N2) in the ranges of 1.39–4.31 and 4.92–5.38 barrer, respectively. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci 104: 2395–2402, 2007
Variations of the glass‐transition temperature in the imidization of poly(styrene‐co‐maleic anhydride)
Authors: Liu He‐Yang , Cao Kun , Yao Zhen , Li Bo‐Geng , Hu Guo‐Hua 
Published: February 2007

AbstractThe imidization of poly(styrene‐co‐maleic anhydride) (SMA) was conducted, and the glass‐transition temperatures (Tg's) of the resulting products were measured with differential scanning calorimetry. The contributions from functional groups of maleic anhydride, N‐phenylmaleamic acid, and N‐phenylmaleimide to Tg were examined. Tg increased in the order of SMA < styrene–N‐phenyl maleimide copolymer < styrene–N‐phenyl maleamic acid copolymer and followed the Fox equation. Tg of the imidized products of SMA could be controlled by the conversions of both ring‐opening and ring‐closing reactions. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci 104: 2418–2422, 2007
Effects of functional groups on the thermal properties of modified polystyrene
Authors: Ahmetli Gulnare , Cerit Alaaddin 
Published: February 2007

AbstractPolystyrene is, after polyolefins, the most widespread polymer in both industry and everyday life, successfully replacing some raw natural materials. In this study, the chemical modification of polystyrenes of different molecular weights was performed with various functional group modifiers (epichlorohydrin, maleic anhydride, and acetic anhydride) in one stage and in the medium of the cationic catalyst BF3·O(C2H5)2 according to previous studies. The concentration of the functional groups bonded to the aromatic ring of the polymer as a result of the chemical modification of polystyrenes of different molecular weights depended on the molecular weight of the polymer, and more functional groups were bonded to lower molecular weight polystyrene. The effects of the functional groups bonded to the structure of the polymer on the thermal properties of modified polystyrene were investigated. The polystyrene that was modified by maleic anhydride was more stable against thermal destruction at high temperatures. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci 104: 2549–2553, 2007
Up‐regulation of metastasis‐promoting S100A4 (Mts‐1) in rheumatoid arthritis: Putative involvement in the pathogenesis of rheumatoid arthritis
Authors: Klingelhöfer Jörg , Šenolt Ladislav , Baslund Bo , Nielsen Gitte Helle , Skibshøj Inge , Pavelka Karel , Neidhart Michel , Gay Steffen , Ambartsumian Noona , Hansen Birgitte Schmidt , Petersen Jørgen , Lukanidin Eugene , Grigorian Mariam 
Published: February 2007

AbstractObjectiveTo examine the involvement of the metastasis‐inducing protein S100A4 (Mts‐1) in the pathogenesis of rheumatoid arthritis (RA).MethodsSynovial tissue, synovial fluid, and plasma were obtained from RA and osteoarthritis (OA) patients who were undergoing joint surgery. Immunohistochemical and immunofluorescence analyses and enzyme‐linked immunosorbent assays were used to determine the locations and concentrations of S100A4. The conformational structure of S100A4 in plasma and synovial fluid was determined after fractionation by size‐exclusion chromatography, protein separation by sodium dodecyl sulfate–polyacrylamide gel electrophoresis, and Western blot analysis. Expression of various S100 proteins in RA synovium was determined by immunofluorescence and double‐staining using specific anti‐S100 antibodies.ResultsWe found an up‐regulation of S100A4 in cells infiltrating RA synovial tissue. Most cell types identified by cell‐specific markers (fibroblasts, immune cells, and vascular cells) contributed to the production of S100A4 in RA synovial tissue. The pattern of S100A4 expression differed significantly from that of the proinflammatory proteins S100A9 and S100A12, which were restricted to phagocytes and granulocytes. The up‐regulation of S100A4 in RA synovial tissue was consistent with the high concentrations of the protein in RA versus OA plasma (mean 1,100 versus 211 ng/ml) and synovial fluid (mean 1,980 versus 247 ng/ml). Moreover, we found that S100A4 in RA plasma and synovial fluid was present in bioactive multimeric (M‐S100A4) conformations, whereas in OA, the majority of extracellular S100A4 was detected as the less active dimeric form. Consistent with our observations in tumor models, extracellular S100A4 stabilized the p53 tumor suppressor in RA synovial fibroblast–like cells and affected the regulation of p53 target genes, including Bcl‐2, p21WAF, and Hdm‐2, as well as matrix metalloproteinases.ConclusionOverexpression of S100A4 in RA synovial tissue and its release as M‐S100A4 can influence p53 function and modulate the expression of several genes that are potentially implicated in the disease process. Thus, S100A4 might play an important role in the pathogenesis of RA and might represent a new target for the treatment of RA.
Suppression of inflammation and structural damage in experimental arthritis through molecular targeted therapy with PPI‐2458
Authors: Hannig Gerhard , Bernier Sylvie G. , Hoyt Jennifer G. , Doyle Beth , Clark Ed , Karp Russell M. , Lorusso Jeanine , Westlin William F. 
Published: February 2007

AbstractObjectiveTo determine the disease‐modifying activity and mechanism of action of the orally available methionine aminopeptidase type 2 inhibitor, [(1R)‐1‐carbamoyl‐2‐methyl‐propyl]‐carbamic acid‐(3R,4S,5S,6R)‐5‐methoxy‐4‐[(2R,3R)‐2‐methyl‐3‐(3‐methyl‐but‐2‐enyl)‐oxiranyl]‐1‐oxa‐spiro [2.5] oct‐6‐yl ester (PPI‐2458), in a rat model of peptidoglycan–polysaccharide (PG‐PS)–induced arthritis.MethodsArthritis was induced in rats by administration of PG‐PS, causing tarsal joint swelling and histopathologic changes characteristic of rheumatoid arthritis (RA). PPI‐2458, a potent irreversible methionine aminopeptidase type 2 inhibitor, was administered orally every other day at 1, 5, or 10 mg/kg.ResultsIn an in vitro osteoclastogenesis model, PPI‐2458 potently inhibited osteoclast differentiation and bone resorption. In the rat PG‐PS arthritis model, PPI‐2458 afforded significant protection against established disease after therapeutic dosing. This in vivo activity of PPI‐2458 was linked to the inhibition of methionine aminopeptidase type 2. Histopathologic assessment of affected joints showed improvement in processes of inflammation, bone resorption, and cartilage erosion, associated with significant improvement in all clinical indices. The protective effects of PPI‐2458 against bone destruction in vivo, including the structural preservation of affected hind joints, correlated with improvements in bone histomorphometric markers, as determined by microfocal computed tomography and a significant decrease in systemic C‐telopeptide of type I collagen, suggesting decreased osteoclast activity in vivo. Moreover, PPI‐2458 prevented cartilage erosion as shown by a significant decrease in systemic cartilage oligomeric matrix protein.ConclusionThe findings of this study suggest that PPI‐2458 exerts disease‐modifying activity in experimental arthritis through its direct inhibition of several pathophysiologic processes of this disease. These results provide a rationale for assessing the potential of PPI‐2458 as a novel RA therapy.
Pharmacokinetics and pharmacodynamics of intravenous PEGylated recombinant mammalian urate oxidase in patients with refractory gout
Authors: Sundy John S. , Ganson Nancy J. , Kelly Susan J. , Scarlett Edna L. , Rehrig Claudia D. , Huang William , Hershfield Michael S. 
Published: February 2007

AbstractObjectiveTo evaluate the efficacy, immunogenicity, and tolerability of intravenous (IV) PEGylated recombinant mammalian urate oxidase (PEG‐uricase) for the treatment of severe gout.MethodsSingle infusions of PEG‐uricase (at doses ranging from 0.5 mg to 12 mg) were administered to 24 patients (6 cohorts of 4 patients each) in a phase I clinical trial. Plasma uricase activity (pUox), the plasma urate concentration (pUAc), and the uric acid–to‐creatinine ratio (UAc:Cr) in urine were monitored for 21 days after dosing. Adverse events and the IgG antibody response to PEG‐uricase were followed up for 35 days.ResultsAll patients completed the trial. Maximum pUox was linearly related to the IV dose of PEG‐uricase, the area under the curve (AUC) value increased linearly (up to a dose of 8 mg), and the pUox half‐life was 6.4–13.8 days. After doses of 4–12 mg, the pUAc fell within 24–72 hours, from a mean ± SD value of 11.1 ± 0.6 mg/dl to 1.0 ± 0.5 mg/dl; the AUC value for the pUAc was equivalent to maintaining the pUAc at 1.2–4.7 mg/dl for 21 days postinfusion. The UAc:Cr ratio in urine fell in parallel with the pUAc. IgG antibodies to PEG‐uricase, mostly IgG2 and specific for PEG, developed in 9 patients, who had more rapid enzyme clearance but no allergic reactions. All adverse events were mild to moderate, with gout flares being most common.ConclusionThe bioavailability, efficacy, and tolerability of IV PEG‐uricase were greater than the bioavailability, efficacy, and tolerability observed in a previous phase I trial of subcutaneous PEG‐uricase. Infusing 4–12 mg of PEG‐uricase every 2–4 weeks should maintain the pUAc well below the therapeutic target of 6 mg/dl and greatly reduce renal uric acid excretion. This treatment could be effective in depleting expanded tissue urate stores in patients with chronic or tophaceous gout.
Limitations of therapy and a guarded prognosis in an american cohort of takayasu arteritis patients
Authors: Maksimowicz‐McKinnon Kathleen , Clark Tiffany M. , Hoffman Gary S. 
Published: February 2007

AbstractObjectiveTo describe the clinical, laboratory, and radiographic manifestations of Takayasu arteritis (TA) in a cohort from the US, evaluate the response to interventions, remission and relapse rates, and disease progression, and compare these observations with those from other cohorts in the US, Japan, India, Italy, and Mexico.MethodsSeventy‐five patients were retrospectively studied using a uniform database that included clinical, laboratory, and imaging data. Vascular imaging studies were performed at least yearly to monitor disease progression.ResultsCommon manifestations at disease onset included loss or asymmetry of pulses (57%), limb blood pressure discrepancy (53%), and bruits (53%). Eleven percent of patients were asymptomatic prior to disease diagnosis. Initial angiographic studies showed aortic abnormalities in 79% of patients and frequent involvement of the subclavian (65%) and carotid (43%) arteries.Ninety‐three percent of longitudinally followed patients attained disease remission of any duration, but only 28% sustained remission of at least 6 months' duration after prednisone was tapered to <10 mg daily. Both angioplasty and vascular surgery were initially successful, but recurrent stenosis occurred in 78% of angioplasty and 36% of bypass/reconstruction procedures. More than two‐thirds of patients had difficulty performing routine daily activities and approximately one‐fourth of all patients were unable to work.Our cohort was similar to the National Institutes of Health, Italian, Japanese, and Mexican cohorts in terms of the predominance of female subjects and disease manifestations, but differed from the Indian cohort in that the latter group had a higher frequency of male subjects, abdominal aorta and renal artery involvement, and hypertension.ConclusionAlthough improvement of symptoms in TA usually follows glucocorticoid therapy, relapses usually occur with dosage reduction. Attempts to restore vascular patency are often initially successful, but restenosis occurs frequently. Chronic morbidity and disability occur in most patients with TA in the US.
Proinflammatory mediator–induced reversal of CD4+,CD25+ regulatory T cell–mediated suppression in rheumatoid arthritis
Authors: van Amelsfort Jocea M. R. , van Roon Joel A. G. , Noordegraaf Madelon , Jacobs Kim M. G. , Bijlsma Johannes W. J. , Lafeber Floris P. J. G. , Taams Leonie S. 
Published: February 2007

AbstractObjectiveWe previously demonstrated that CD4+,CD25+ regulatory T (Treg) cells are present in increased numbers in the synovial fluid (SF) of rheumatoid arthritis (RA) patients and display enhanced suppressive activity as compared with their peripheral blood (PB) counterparts. Despite the presence of these immunoregulatory cells in RA, chronic inflammation persists. The purpose of the present study was to investigate whether particular proinflammatory mediators that are associated with RA could abrogate CD4+,CD25+ Treg–mediated suppression.MethodsMonocyte phenotype was determined by flow cytometry and cytokine levels by enzyme‐linked immunosorbent assay. Magnetically sorted CD4+,CD25– and CD4+,CD25+ T cells derived from the PB and SF obtained from RA patients were stimulated alone or in coculture with anti‐CD3 monoclonal antibody (mAb) and autologous antigen‐presenting cells, in the absence or presence of anti‐CD28 mAb or the proinflammatory cytokines interleukin‐6 (IL‐6), tumor necrosis factor α (TNFα), or IL‐7.ResultsMonocytes from the SF of RA patients displayed increased expression of HLA class II molecules, CD80, CD86, and CD40 as compared with PB‐derived monocytes, indicating their activated status. Mimicking this increased costimulatory potential, addition of anti‐CD28 mAb to cocultures of CD4+,CD25– and CD4+,CD25+ T cells resulted in reduced CD4+,CD25+ Treg–mediated suppression in both PB and SF. Furthermore, IL‐7 and, to a limited extent, TNFα, both of which are produced by activated monocytes and were detected in SF, abrogated the CD4+,CD25+ Treg–mediated suppression. In contrast, IL‐6 did not influence Treg‐mediated suppression.ConclusionOur findings suggest that the interaction of CD4+,CD25+ Treg cells with activated monocytes in the joint might lead to diminished suppressive activity of CD4+,CD25+ Treg cells in vivo, thus contributing to the chronic inflammation in RA.
Musculoskeletal abnormalities of the tibia in juvenile rheumatoid arthritis
Authors: Felin Elena M. O. , Prahalad Sampath , Askew E. Wayne , Moyer‐Mileur Laurie J. 
Published: February 2007

AbstractObjectiveTo characterize local bone geometry, density, and strength, using peripheral quantitative computed tomography (pQCT), compared with general bone characteristics as measured using dual x‐ray absorptiometry (DXA), and to assess their relationship to disease‐related factors in children with juvenile rheumatoid arthritis (JRA).MethodsForty‐eight children ages 4–18 years with JRA (17 pauciarticular, 23 polyarticular, 8 systemic) were compared with age‐matched healthy controls (n = 266). Measurements included cortical and trabecular bone geometry, density, and strength at the distal and midshaft tibia determined by pQCT, and whole‐body, lumbar spine, and femoral neck measurements by DXA.ResultsMethotrexate (MTX) was prescribed to 23 of 48 patients (47.9%) and glucocorticoids and MTX were prescribed to 15 of 48 patients (31.3%), with the greatest use in children with systemic JRA. All JRA patients had decreased tibia trabecular bone density, cortical bone size and strength, and muscle mass. Children with systemic JRA had lower femoral neck densities. Systemic JRA was associated with a shorter, less mineralized skeleton, while a narrower, less mineralized skeleton was observed in polyarticular JRA. The tibia diaphysis was narrower with decreased muscle mass, but normal, size‐adjusted bone mineral in all subtypes indicated a localized effect of JRA on bone. Patients exposed to glucocorticoids and MTX or to glucocorticoids or MTX alone had greatly reduced trabecular density, cortical bone geometry properties, and bone mineral content, muscle mass, and bone strength.ConclusionChildren with JRA have decreased skeletal size, muscle mass, trabecular bone density, cortical bone geometry, and strength. Not surprisingly, these bone abnormalities are more pronounced in children with greater disease severity.
Tenocyte responses to mechanical loading in vivo: A role for local insulin‐like growth factor 1 signaling in early tendinosis in rats
Authors: Scott Alexander , Cook Jill L. , Hart David A. , Walker David C. , Duronio Vincent , Khan Karim M. 
Published: February 2007

AbstractObjectiveTo investigate tenocyte regulatory events during the development of overuse supraspinatus tendinosis in rats.MethodsSupraspinatus tendinosis was induced by running rats downhill at 1 km/hour for 1 hour a day. Tendons were harvested at 4, 8, 12, and 16 weeks and processed for brightfield, polarized light, or transmission electron microscopy. The development of tendinosis was assessed semiquantitatively using a modified Bonar histopathologic scale. Apoptosis and proliferation were examined using antibodies against fragmented DNA or proliferating cell nuclear antigen, respectively. Insulin‐like growth factor 1 (IGF‐1) expression was determined by computer‐assisted quantification of immunohistochemical reaction. Local IGF‐1 signaling was probed using antibodies to phosphorylated insulin receptor substrate 1 (IRS‐1) and ERK‐1/2.ResultsTendinosis was present after 12 weeks of downhill running and was characterized by tenocyte rounding and proliferation as well as by glycosaminoglycan accumulation and collagen fragmentation. The proliferation index was elevated in CD90+ tenocytes in association with tendinosis and correlated with increased local IGF‐1 expression by tenocytes and phosphorylation of IRS‐1 and ERK‐1/2. Both apoptosis and cellular inflammation were absent at all time points.ConclusionIn this animal model, early tendinosis was associated with local stimulation of tenocytes rather than with extrinsic inflammation or apoptosis. Our data suggest a role for IGF‐1 in the load‐induced tenocyte responses during the pathogenesis of overuse tendon disorders.
Primary necrotizing lymphocytic central nervous system vasculitis due to perforin deficiency in a four‐year‐old girl
Authors: Moshous Despina , Feyen Oliver , Lankisch Petra , Schwarz Klaus , Schaper Jörg , Schneider Marion , Dilloo Dagmar , Laws Hans‐Jürgen , Schwahn Bernd C. , Niehues Tim 
Published: February 2007

AbstractWe report the case of a 4‐year‐old girl who presented with headaches, ataxia, and visual disturbances. Cranial magnetic resonance imaging showed multiple supra‐ and infratentorial lesions with peripheral contrast enhancement and central necrosis. Brain biopsy revealed necrotizing lymphocytic vasculitis of undetermined etiology. Perforin expression was found to be significantly reduced in the patient's peripheral blood cells, and sequence analysis of the patient's perforin gene showed a compound heterozygous state with 1 nonsense mutation and 2 missense alterations in exon 2. Central nervous system (CNS) vasculitis was thus attributed to the perforin deficiency, and the patient was successfully treated by transplantation of stem cells from an HLA‐identical brother. The findings described herein indicate that, even in the absence of classic non‐neurologic symptoms of hemophagocytic lymphohistiocytosis, measurement of perforin expression should be one of the diagnostic tests used to identify the cause of unexplained CNS vasculitis, since this may have profound implications regarding therapy.
Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression
Authors: Brechter Anna Bernhold , Lerner Ulf H. 
Published: February 2007

AbstractObjectiveBradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin‐1 (IL‐1)–induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation‐induced bone loss. The present study was undertaken to study 1) the role of the kinin B1 and B2 receptors in the synergistic interaction with IL‐1 and tumor necrosis factor α (TNFα), 2) the molecular mechanisms involved in synergistic enhancement of PG formation, and 3) the effects of kinins on cytokine‐induced expression of RANKL, RANK, and osteoprotegerin (OPG) (the latter being crucial molecules in osteoclast differentiation).MethodsFormation of PGs, expression of enzymes involved in arachidonic acid metabolism, and expression of RANKL, RANK, and OPG were assessed in the human osteoblastic cell line MG‐63 and in mouse calvarial bones. The role of NF‐κB and MAP kinases was studied using pharmacologic inhibitors.ResultsPGE2formation and cyclooxygenase 2 (COX‐2) protein expression were induced by IL‐1β and potentiated by kinins with affinity for the B1 or B2 receptors, resulting in PGE2‐dependent enhancement of RANKL. The enhancements of PGE2formation and COX‐2 were markedly decreased by inhibition of p38 and JNK MAP kinases, whereas inhibition of NF‐κB resulted in abolishment of the PGE2response with only slight inhibition of COX‐2.ConclusionKinin B1 and B2 receptors synergistically potentiate IL‐1– and TNFα‐induced PG biosynthesis in osteoblasts by a mechanism involving increased levels of COX‐2, resulting in increased RANKL. The synergistic stimulation is dependent on NF‐κB and MAP kinases. These mechanisms might help to explain the enhanced bone resorption associated with inflammatory disorders, including that in rheumatoid arthritis.