bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determination of swelling behavior and morphological properties of poly(acrylamide‐co‐itaconic acid) and poly(acrylic acid‐co‐itaconic acid) copolymeric hydrogels
Authors: Pulat Mehlika , Eksi Haslet 
Published: September 2006

AbstractPoly(acrylamide‐co‐itaconic acid) (PAAmIA) and poly(acrylic acid‐co‐itaconic acid) (PAAIA) copolymeric hydrogels were prepared with different compositions via free‐radical polymerization. Ethylene glycol dimethacrylate (EGDMA) was used as an original crosslinker for these monomers. Gelation percentages of the monomers were studied in detail and it was found that addition of IA into the monomer mixture decreased the gelation percentage. The variation in swelling values (%) with time, temperature, and pH was determined for all hydrogels. PAA, which is the most swollen hydrogel, has the swelling percentage value of 2000% at pH = 7.4, 37°C. Swelling behaviors were explained with detailed SEM micrographs, which show the morphologic differences between dry and swollen hydrogels. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 102: 5994–5999, 2006
Fabrication of discontinuous fibers of poly (N‐vinylpyrrolidone) containing metalloporphyrin molecules
Authors: Jin Yuwei , Lu Xiaofeng , Wang Ce 
Published: September 2006

AbstractThis study described the preparation of discontinuous fibers of poly (N‐vinylpyrrolidone) (PVP) containing metalloporphyrin (Manganese (III) tetrakis (1‐methyl‐4‐pyridyl) porphyrin pentachloride) molecules using electrospinning method. SEM images showed that before adding the metalloporphyrin molecules, the electrospun nanofibers are straight and smooth, while after adding metalloporphyrin molecules into the PVP solutions, the SEM images clearly showed that there were two different types of fibers: the thinner fibrous phase and the thicker discontinuous fibers. The chemical composition of the resulting PVP/metalloporphyrin composite fibers was characterized by Fourier‐transform infrared (FTIR) and energy dispersive X‐ray (EDX) analysis. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 102: 6017–6022, 2006
Stabilization of epidermal growth factor on thermal and proteolytic degradation by conjugating with low molecular weight chitosan
Authors: Chung Kyu Hwan , Park Se Hoon , Kim Mi Kyung , Park Hyung Dal , Son Tae Il 
Published: September 2006

AbstractEpidermal growth factor (EGF, 5900 Da) has been reported to have the high efficiency of wound repair. However, the half‐life of EGF in the body is too short to exert the biological activity effectively when applied in free forms. Conjugation of the low molecular weight chitosan (LMC) to EGF was carried out to enhance its stability. EGF was conjugated with LMC activated by water‐soluble carbodiimide. The formation of EGF–LMC was quantitatively measured by indirect enzyme‐linked immunosorbent assay (ELISA). In a study of the thermal and the proteolytic stability of free EGF and EGF–LMC, EGF covalently attached to LMC was found to be more stable than free EGF in thermal and proteolytic stabilities. In animal experiments of which free EGF (control), EGF–LMC (test) and LMC (carrier) diluted in viscous carboxymethyl cellulose (CMC) solution (vesicle) were applied to the incisional wounds in rats, the EGF–LMC conjugates are considered to be potent wound healing agent with mitogenicity and wound‐healing property. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 102: 5072–5082, 2006
Discovery of Novel Aldose Reductase Inhibitors Characterized by an Alkoxy‐Substituted Phenylacetic Acid Core
Authors: Rakowitz Dietmar , Gmeiner Andreas , Matuszczak Barbara 
Published: September 2006

AbstractIn continuation of our effort aimed towards the development of novel aldose reductase inhibitors, several phenylacetic acids bearing an alkoxy substituent in position 3 or 4, respectively, were prepared and screened. The latter represent formal ring opening products of the cyclohexylmethyloxyphenylacetic acids IIa and IIb, recently elaborated in our group. Out of these series, compounds 4aa and 4ba characterized by an n‐heptyloxy subunit turned out to be the most potent inhibitors. Based on these unexpected results, we suggest that such an alkyl side chain acts as a useful surrogate for the 4‐bromo‐2‐fluorobenzyl residue often found in potent aldose reductase inhibitors.
Oral salmon calcitonin reduces Lequesne's algofunctional index scores and decreases urinary and serum levels of biomarkers of joint metabolism in knee osteoarthritis
Authors: Manicourt Daniel‐Henri , Azria Moïse , Mindeholm Linda , Thonar Eugene J.‐M. , Devogelaer Jean‐Pierre 
Published: September 2006

AbstractObjectiveTo evaluate the effects of oral salmon calcitonin (sCT) on Lequesne's algofunctional index scores and on biomarkers of joint metabolism in knee osteoarthritis.MethodsIn this randomized, double‐blind trial, patients received either placebo (n = 18), 0.5 mg of sCT (n = 17), or 1 mg of sCT (n = 18) daily for 84 days. Biomarkers included C‐telopeptide of type II collagen (CTX‐II), type II collagen neoepitope C2C, collagenases (matrix metalloproteinase 1 [MMP‐1], MMP‐8, and MMP‐13), stromelysin (MMP‐3), tissue inhibitors of metalloproteinases 1 and 2, and hyaluronan. Statistical analysis included nonparametric tests.ResultsA total of 41 patients completed the study (13 in the group receiving 0.5 mg of sCT and 14 in each of the other 2 other groups). Although, on day 84, patients in both the placebo group and the group receiving 1 mg of sCT exhibited a similar significant decrease in pain scores, a significant reduction in the function score was observed only in the 2 sCT groups. On day 84, there was no significant decrease in biomarker levels in the placebo group, whereas significant reductions in the levels of both MMP‐3 and hyaluronan were observed in the 2 sCT groups. The group of patients receiving 1 mg of sCT exhibited significant decreases in the levels of CTX‐II, C2C, and MMP‐13.ConclusionBy improving functional disability and by reducing levels of biomarkers that are thought to be predictive of joint space narrowing (and thus cartilage loss), oral sCT at a dose of 1 mg might be a useful pharmacologic agent in human knee OA.
In vitro and in vivo efficacy of a recombinant immunotoxin against folate receptor β on the activation and proliferation of rheumatoid arthritis synovial cells
Authors: Nagai Taku , Tanaka Masashi , Tsuneyoshi Yasuhiro , Matsushita Kakushi , Sunahara Nobuhiko , Matsuda Takemasa , Yoshida Hiroki , Komiya Setsuro , Onda Masanori , Matsuyama Takami 
Published: September 2006

AbstractObjectiveTo investigate the effects of the recombinant immunotoxin dsFv anti‐FRβ‐PE38, which consists of the disulfide‐stabilized Fv fragment (dsFv) of the anti–folate receptor β (anti‐FRβ) antibody and the 38‐kd portion of Pseudomonas exotoxin A (PE38), on the activation and proliferation of cells that function in inflammatory and degradative processes in rheumatoid arthritis (RA) synovial tissue.MethodsThe Ig VH‐PE38 fusion protein and the Ig VL protein were produced in Escherichia coli, and then joined with a disulfide bond by engineering cysteine residues in the framework regions of these proteins. The effects of dsFv anti‐FRβ‐PE38 on the activation and proliferation of cells in RA synovial tissue were investigated by immunohistochemistry; the numbers of cells expressing CD68, vascular cell adhesion molecule 1, angiopoietin 1, CD34, proliferating cell nuclear antigen, and interleukin‐6 and the numbers of apoptotic cells were counted in RA synovial tissue engrafted into SCID mice treated or not treated with dsFv anti‐FRβ‐PE38. The effects of dsFv anti‐FRβ‐PE38 on the generation of osteoclasts from RA adherent synovial mononuclear cells in vitro was investigated by counting the number of resorption pits on dentin slices treated or not treated with dsFv anti‐FRβ‐PE38.ResultsAdministration of dsFv anti‐FRβ‐PE38 reduced the numbers of macrophages, activated fibroblast‐like cells, endothelial cells, and proliferating cells and increased the numbers of apoptotic cells in RA synovial tissue engrafted into SCID mice. In vitro, the generation of osteoclasts from RA adherent synovial mononuclear cells was largely suppressed by treatment with dsFv anti‐FRβ‐PE38.ConclusionOur findings show that dsFv anti‐FRβ‐PE38 immunotoxin would be a promising tool for the treatment of RA synovitis, especially when administered intraarticularly.
Influence of male sex on disease phenotype in familial rheumatoid arthritis
Authors: Jawaheer Damini , Lum Raymond F. , Gregersen Peter K. , Criswell Lindsey A. 
Published: September 2006

AbstractObjectiveTo examine sex differences in clinical, demographic, and genetic characteristics among a large cohort of patients with familial rheumatoid arthritis (RA).MethodsWe studied 1,004 affected members of 467 Caucasian multicase RA families recruited from the North American Rheumatoid Arthritis Consortium. Standardized information about demographic and clinical characteristics was collected from all patients. Affected individuals also underwent radiography of the hands and were genotyped for markers in the HLA region. Sex differences were assessed using contingency table analysis (for categorical variables) and Student's t‐tests for (continuous variables), and by multivariate logistic and linear regression analysis.ResultsMale patients had a significantly later onset of RA, were more likely to be seropositive for RF, and had significantly higher titers of anti–cyclic citrullinated peptide (anti‐CCP) antibodies compared with female patients, even after adjustment for covariates in multivariate analyses. Male patients were also significantly more likely to have a history of smoking and to be HLA–DRB1 shared epitope (SE) positive. Interestingly, female patients with an affected male sibling had significantly higher titers of anti‐CCP antibodies and were more likely to be SE positive compared with female patients without affected male siblings. Multivariate analyses indicated that the presence of the SE did not fully explain the increased anti‐CCP antibody titers observed in these families.ConclusionSex has an important influence on the disease phenotype in RA, including the age at disease onset and autoantibody production. Furthermore, families with affected male members are characterized by higher titers of autoantibodies, particularly anti‐CCP antibodies. Our results indicate that these findings are not fully explained by differences in exposure to tobacco smoke, presence of the HLA–DRB1 SE, or other HLA region genetic variation. Thus, other genetic or nongenetic factors also contribute to sex differences in the RA phenotype.
Changes in Health Assessment Questionnaire disability scores over five years in patients with rheumatoid arthritis compared with the general population
Authors: Sokka Tuulikki , Kautiainen Hannu , Hannonen Pekka , Pincus Theodore 
Published: September 2006

AbstractObjectiveTo analyze longitudinal data over 5 years for changes in Health Assessment Questionnaire (HAQ) scores in patients with rheumatoid arthritis (RA) and age‐ and sex‐matched controls from the general population.MethodsIn 2000 and 2005, identical self‐report questionnaires were mailed to a cohort of patients with RA and control cohort from the community. The questionnaire included the HAQ, which was used to assess functional status. Changes in HAQ scores over 5 years were analyzed.ResultsIn 2000, 73% of 1,495 patients with RA and 77% of 2,000 general population controls responded to the questionnaire. In 2005, 84% of 2,022 patients with RA and 77% of 1,817 controls responded. A total of 863 patients with RA and 1,176 community controls responded in both 2000 and 2005 and were included in the analyses. Mean baseline HAQ scores were significantly higher in patients with RA than in controls (0.71 versus 0.17; P < 0.001). Over 5 years, the HAQ scores increased by 0.01 units per year in both the RA cohort and the community population; in both cohorts, the net change was primarily attributable to individuals over age 70 years. Changes in HAQ scores were similar in patients and controls who had low HAQ scores at baseline. Female patients with baseline HAQ scores of ≥0.5 had less potential for improvement than did controls. Among subjects in both groups who had HAQ scores >2, death was a common outcome over the next 5 years.ConclusionCurrently, progression of functional disability among patients with RA and among persons in the general population is largely explained by the aging process. Our results showing stable function scores over 5 years in most patients with RA who are younger than age 70 years provide further evidence of improved status of RA patients today compared with the major declines observed in previous decades.
Regulation of Mcl‐1 expression in rheumatoid arthritis synovial macrophages
Authors: Liu Hongtao , Huang QiQuan , Shi Bo , Eksarko Polikseni , Temkin Vladislav , Pope Richard M. 
Published: September 2006

AbstractObjectiveResistance to apoptosis may be an important mechanism contributing to the persistence of rheumatoid arthritis (RA). This study was undertaken to characterize the expression, regulation, and function of the antiapoptotic Bcl‐2 family member Mcl‐1 in macrophages isolated from the joints of patients with RA.MethodsMononuclear cells were isolated from the synovial fluid (SF) of patients with RA. Mcl‐1 expression was documented by intracellular staining of CD14+ cells using flow cytometry, and by real‐time polymerase chain reaction or immunoblot analysis of isolated macrophages. The expression of Mcl‐1 was suppressed with small interfering RNA (siRNA) or chemical inhibitors of the phosphatidylinositol 3‐kinase (PI 3‐kinase)/Akt‐1 and signal transducer and activator of transcription 3 (STAT‐3) pathways. Apoptosis was defined by the loss of mitochondrial transmembrane potential and by DNA fragmentation.ResultsThe expression of Mcl‐1 was increased in CD14+ macrophages from the SF of patients with RA compared with normal in vitro–differentiated macrophages. Inhibition of the PI 3‐kinase/Akt‐1 or STAT‐3 pathways significantly reduced the percentage of CD14+ cells within the SF and resulted in the reduction of Mcl‐1 and the induction of apoptosis of synovial macrophages. Transfection of RA synovial macrophages with Mcl‐1 siRNA resulted in apoptotic cell death.ConclusionMcl‐1 is critical for the survival of macrophages in the joints of patients with RA, and is therefore a potential therapeutic target in this disease.
Bim deficiency leads to exacerbation and prolongation of joint inflammation in experimental arthritis
Authors: Scatizzi John C. , Bickel Emily , Hutcheson Jack , Haines G. Kenneth , Perlman Harris 
Published: September 2006

AbstractObjective:Rheumatoid arthritis (RA) is characterized by hyperplasia of the synovial lining, inflammation, and destruction of cartilage and bone. Since there are only a few detectable cells undergoing apoptosis in the joint, it is possible that a defect in apoptosis may contribute to synovial hyperplasia. This study sought to identify and characterize the direct role of apoptotic regulators in a mouse model of inflammatory arthritis.MethodsUsing a serum transfer model, experimental arthritis was induced in mice lacking the proapoptotic Bcl‐2 family genes Bak (Bak−/−), Bax (Bax−/−), or Bim (Bim−/−), as compared with wild‐type (WT) control mice. Physical examination for edema of the ankles and histopathologic analysis of ankle sections were used to determine the severity of arthritis. The serum and ankles were examined for production of chemokines and cytokines using enzyme‐linked immunosorbent or Luminex‐based assays.ResultsBim−/− mice displayed increased severity and prolongation of arthritis. In contrast, Bak−/− and Bax−/− mice showed no difference in the severity of arthritis as compared with WT mice. In addition, Bim−/− mice had elevated levels of proinflammatory chemokines and cytokines, decreased joint and serum production of antiinflammatory cytokines, fewer TUNEL‐positive cells, and reduced levels of active caspase 3 as compared with WT mice.ConclusionThese studies are the first to demonstrate a role for the proapoptotic Bcl‐2 protein Bim in the effector phase of RA. The findings indicate that Bim potentially functions to repress the effector phase of arthritis by regulating the milieu of the joint and serum, and by inducing apoptosis.
Fluctuation in self‐perceived stress and increased risk of flare in patients with lupus nephritis carrying the serotonin receptor 1A –1019 G allele
Authors: Birmingham Daniel J. , Nagaraja H. N. , Rovin Brad H. , Spetie Lacramioara , Zhao Yanxing , Li Xiaobai , Hackshaw Kevin V. , Yu C. Yung , Malarkey William B. , Hebert Lee A. 
Published: September 2006

AbstractObjectiveStress is believed to be a risk factor for systemic lupus erythematosus (SLE) flare. Two serotonin‐related gene polymorphisms, the serotonin receptor 1A (5‐HT1A) polymorphism at –1019C>G and the serotonin transporter LS polymorphism, have been reported to affect stress‐related behaviors. The purpose of this study was to assess the relationship between self‐perceived stress (SPS), variability in SPS, and the 2 serotonin‐related gene polymorphisms as risk factors for SLE flare.MethodsSeventy‐seven SLE patients (50 with lupus nephritis) were evaluated every 2 months (mean ± SD total followup 18.5 ± 8.5 months), and patients recorded their daily SPS levels (0–10 scale). Values for mean SPS and coefficient of variation (CV) for SPS were calculated from the 60‐day block of daily measurements between study visits. Serotonin‐related gene polymorphism genotypes were determined by polymerase chain reaction–based methods.ResultsOf the 77 patients, 53 experienced 80 flares of SLE (32 renal flares) based on prespecified criteria. Multivariate analysis revealed that whereas neither the serotonin‐related gene polymorphisms nor the mean SPS was predictive of an SLE flare, an increased CV for SPS was predictive (P = 0.0031). Interaction between the CV for SPS and the 5‐HT1A –1019C>G polymorphism was also found to be a predictor of SLE flare (P = 0.0039). Subset analysis revealed that only in lupus nephritis patients were increasing CVs for SPS (P = 0.0002) and the interaction between CVs for SPS and 5‐HT1A (P < 0.0001) predictive of a flare. Odds ratio curves demonstrated that the predictive effect of increasing CVs for SPS required the presence of the 5‐HT1A –1019 G allele, but appeared to be independent of the G allele number.ConclusionFluctuation in the level of SPS is a risk factor for the onset of flare in SLE patients with major renal manifestations when it occurs on the background of a stress‐related susceptibility gene (the 5‐HT1A –1019 G allele).
Effect of hormone therapy on risk of hip and knee joint replacement in the women's health initiative
Authors: Cirillo Dominic J. , Wallace Robert B. , Wu LieLing , Yood Robert A. 
Published: September 2006

AbstractObjectiveTo determine the effect of hormone therapy on arthroplasty rates.MethodsWe examined data from the Women's Health Initiative placebo‐controlled, double‐blind, randomized trials. Community‐dwelling women ages 50–79 years were enrolled at 40 US clinics. Women with prior arthroplasty were excluded, yielding a sample size of 26,321 subjects. Women who had had hysterectomies (n = 10,272) were randomly assigned to receive 0.625 mg/day conjugated equine estrogens (n = 5,076), or placebo (n = 5,196), with a mean followup of 7.1 years. Those who had not had hysterectomies (n = 16,049) were randomly assigned to receive estrogen plus progestin (n = 8,240), given as 0.625 mg/day conjugated equine estrogens plus 2.5 mg/day medroxyprogesterone acetate, or placebo (n = 7,809), with a mean followup of 5.6 years. Participants reported hospitalizations, and arthroplasties were identified by procedure codes. Arthroplasties due to hip fracture were censored. Cox proportional hazards regression was used to assess hazard ratios (HRs) and 95% confidence intervals (95% CIs) using intent‐to‐treat methods and outcome of time to first procedure.ResultsIn the estrogen‐alone trial, women receiving hormone therapy had significantly lower rates of any arthroplasty (HR 0.84 [95% CI 0.70–1.00], P = 0.05). However, this effect was borderline statistically significant for hip arthroplasty (HR 0.73 [95% CI 0.52–1.03], P = 0.07), and not significant for knee arthroplasty (HR 0.87 [95% CI 0.71–1.07], P = 0.19). In the estrogen‐plus‐progestin trial, there was no association for total arthroplasty (HR 0.99 [95% CI 0.82–1.20], P = 0.92) or for individual hip (HR 1.14 [95% CI 0.83–1.57], P = 0.41) or knee (HR 0.91 [95% CI 0.72–1.15], P = 0.41) arthroplasties.ConclusionThese data suggest that hormone therapy may influence joint health, but this observed decrease in risk may be limited to unopposed estrogen and may possibly be more important in hip than in knee osteoarthritis.
CTLA‐4IG suppresses reactive oxygen species by preventing synovial adherent cell–induced inactivation of rap1, a ras family GTPASE mediator of oxidative stress in rheumatoid arthritis T cells
Authors: Remans P. H. J. , Wijbrandts C. A. , Sanders M. E. , Toes R. E. , Breedveld F. C. , Tak P. P. , van Laar J. M. , Reedquist K. A. 
Published: September 2006

AbstractObjectiveOxidative stress contributes to the inflammatory properties of rheumatoid arthritis (RA) synovial T lymphocytes. This study was undertaken to investigate the mechanisms leading to production of reactive oxygen species (ROS) and oxidative stress in RA synovial T lymphocytes.MethodsROS production in T lymphocytes from the peripheral blood (PB) of healthy donors and from the PB and synovial fluid (SF) of RA patients was measured by ROS‐dependent fluorescence of 6‐carboxy‐2′,7′‐dichlorofluorescein. Rap1 GTPase activation was assessed by activation‐specific probe precipitation. Proliferation of RA PB and SF T lymphocytes was assayed by 3H‐thymidine incorporation. In some experiments, RA PB T cells were preincubated with autologous SF or with PB or SF adherent cells. Experiments were performed in the absence or presence of transwell membranes or CTLA‐4Ig fusion proteins. Short‐ and long‐term stimulations of healthy donor PB T lymphocytes were performed with inflammatory cytokines, in the absence or presence of activating anti‐CD28 antibodies.ResultsT lymphocyte ROS production and Rap1 inactivation were mediated by cell–cell contact with RA synovial adherent cells, and this correlated with T cell mitogenic hyporesponsiveness. CTLA4‐Ig blockade of synovial adherent cell signaling to CD28 T cells reversed the inhibition of Rap1 activity and prevented induction of ROS. Introduction of active RapV12 into T cells also prevented induction of ROS production. Coincubation of T cells with stimulating anti‐CD28 antibodies and inflammatory cytokines synergistically increased T cell ROS production.ConclusionCell–cell contact between T cells and RA synovial adherent cells mediates Rap1 inactivation and subsequent ROS production in T lymphocytes following exposure to inflammatory cytokines. This process can be blocked by CTLA4‐Ig fusion protein.