bluuebunny/crossref_metadata_2025_split huggingface dataset:
The flocculation and rheological characteristics of hydrolyzed and unhydrolyzed grafted sodium alginate in aqueous solutions
Authors: Biswal D. R. , Singh R. P. 
Published: September 2004

AbstractSodium alginate is a natural anionic polysaccharide obtained from natural and microbial resources. It is also used as a flocculating agent and thickener. It is grafted with polyacrylamide, in the presence of ceric ammonium nitrate (CAN) as an initiator. The graft copolymer (SAG‐g‐PAM) is again hydrolyzed with some amount of alkali. The flocculation characteristics of hydrolyzed graft copolymer (Hyd SAG‐g‐PAM) are compared with that of the unhydrolyzed ones, in 5 wt % kaolin and 10 wt % iron ore suspensions. The flocculation characteristics of the hydrolyzed graft copolymer are also compared with those of some of the commercial flocculants. The SAG‐g‐PAM and Hyd SAG‐g‐PAM are characterized by IR and intrinsic viscosity measurements. The rheological properties of aqueous solutions of hydrolyzed and unhydrolyzed graft copolymers are measured by Advanced AR‐1000 Rheometer. There is drastic enhancement in flocculation and viscosifying characteristics on hydrolysis of the graft copolymers. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1480–1488, 2004
Mechanical properties and morphological structures relationship of blends based on sulfated EPDM ionomer and polypropylene
Authors: Su Zhanpai , Jiang Pingkai , Li Qiang , Wei Ping , Wang Genlin , Zhang Yong 
Published: September 2004

AbstractThe mechanical properties and morphological structures of blends based on Zn2+ neutralized low degree sulfated ethylene propylene diene monomer rubber (Zn–SEPDM) ionomer and polypropylene (PP) were studied. It was found that Zn2+ neutralized low degree sulfated EPDM ionomer and PP blends, which are new thermoplastic elastomeric materials, have better mechanical properties than those of PP/EPDM blend. Theoretical analysis of tensile data suggests that there is an increase of the extent of interaction between PP and EPDM in the presence of a low degree of Zn2+, which is also an indicator of better interfacial adhesion between PP and Zn–SEPDM than that between PP and EPDM. SEM results proved that the finer dispersed phase sizes and the shorter interparticle distances are the main reasons for the improved mechanical properties of the PP/EPDM blend. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1504–1510, 2004
Graft copolymerization of methacrylamide onto acrylic fibers initiated by benzoyl peroxide
Authors: Çelik Meltem 
Published: September 2004

AbstractAcrylic fibers were graft copolymerized with methacrylamide in aqueous media, using benzoyl peroxide as a free‐radical initiator. The grafting reactions were carried out within the 75–95°C temperature range, and the effect of initiator, monomer concentrations, and the amount of fiber on the graft yield were also investigated. The maximum graft yield was reached at the benzoyl peroxide concentration of 3.0 × 10−3 mol/L and the optimum temperature of 85°C. The activation energy of the reaction was found to be 33.8 kcal/mol at the temperature interval of 80–95°C. The grafted fibers were characterized with infrared spectroscopy, scanning electron microscopy, and thermogravimetry. The thermogravimetric analysis results revealed that the degradation temperature of the acrylic fibers increased with grafting. The scanning electron photographs showed that the homogeneous appearance of the fiber surface changed and a shell‐like heterogeneous structure occurred at the surface with an increasing degree of grafting. The moisture content and water absorption of grafted acrylic fibers was highly enhanced by grafting. © 2004 Wiley Periodicals, Inc. J Appl Polym Sci 94: 1519–1525, 2004
Sympathetic nervous system regulation of liver repair
Authors: Oben Jude A. , Diehl Anna Mae 
Published: September 2004

AbstractThis chapter reviews recent evidence that the sympathetic nervous system (SNS) regulates liver repair by modulating the phenotypes of hepatic stellate cells (HSCs), the liver's principal fibrogenic cells, and hepatic epithelial progenitors, i.e., oval cells. SNS nerve fibers touch HSCs and these cells express adrenoceptors, suggesting that HSCs may be targets for SNS neurotransmitters. HSCs also contain catecholamine biosynthetic enzymes, release norepinephrine (NE), and are growth‐inhibited by adrenoceptor antagonists. In addition, HSCs from mice with reduced levels of NE grow poorly in culture and exhibit inhibited activation during liver injury. Finally, growth and injury‐related fibrogenic responses are rescued by adrenoceptor agonists. Thus, certain SNS inhibitors (SNSIs) protect experimental animals from cirrhosis. Conversely, SNSIs enhance the hepatic accumulation of oval cells (OCs) in injured livers. This response is associated with improved liver injury. Because SNSIs do not affect the expression of cytokines, growth factors, or growth factor receptors that are known to regulate OCs, and OCs express adrenoceptors, it is conceivable that catecholamines influence OCs by direct interaction with OC adrenoceptors. Given evidence that the SNS regulates the viability and activation of HSCs and OCs differentially, SNSIs may be novel therapies to improve the repair of damaged livers. © 2004 Wiley‐Liss, Inc.
Hyperkeratosis in cystathionine beta synthase‐deficient mice: An animal model of hyperhomocysteinemia
Authors: Robert Karine , Maurin Nicole , Ledru Aurélie , Delabar Jean , Janel Nathalie 
Published: September 2004

AbstractCystathionine beta synthase (CBS) is a crucial regulator of plasma concentrations of homocysteine. Severe hyperhomocysteinemia due to CBS deficiency confers diverse clinical manifestations. Patients with severe hyperhomocysteinemia have fine hair and thin skin, but it is unclear whether these changes are related to CBS deficiency or are coincidental. To investigate these aspects of hyperhomocysteinemia, we characterized skin abnormalities of CBS‐deficient mice, a murine model of severe hyperhomocysteinemia. Histological and histomorphometric analyses revealed that CBS‐deficient mice have wrinkled skin with hyperkeratinosis of the epidermis and thinning of the dermis. © 2004 Wiley‐Liss, Inc.
Modeling of the D2 Dopamine Receptor Arylpiperazine Binding Site for 1‐{2‐[5‐(1H‐benzimidazole‐2‐thione)]ethyl}‐4‐arylpiperazines
Authors: Šukalović Vladimir , Zlatović Mario , Andrić Deana , Roglić Goran , Kostić‐Rajacčić Sladjana , Šoškić Vukić 
Published: September 2004

AbstractDocking of several 1‐{2‐[5‐(1H‐benzimidazole‐2‐thione)]ethyl}‐4‐ and 1‐benzyl‐arylpiperazines to the D2 dopamine receptor (DAR) was examined. The binding pocket of the D2 DAR defined according to Teeter and DuRand [1] was extended using the Insight II software. It was found that (i) the interaction of the protonated N1 of the piperazine ring with Asp86, (ii) the hydrogen bond formation between the benzimidazole part of the ligand and Ser141, as well as Ser122, and (iii) the edge‐to‐face interactions of the aromatic ring or arylpiperazine part of the ligand with Phe178, Tyr216 and Trp182 of the receptor represent the mayor stabilizing forces. Besides, the hydrogen bond acceptor group in position 2 of the phenylpiperazine aromatic ring could form one more hydrogen bond with Trp182. Bulky substituents in position 4 are not tolerated, due to the unfavorable sterical interaction with Phe178. Substituents in positions 2 and 3 are sterically well tolerated. Electron‐attractive groups (F, Cl, CF3, and NO2) decreased, while electron donors (‐OMe) and the second aromatic ring (naphthyl) increased the binding affinity, as compared to that of the parent compound 1. This can be explained by strong edge‐to‐face interactions of negative electrostatic surface potential (ESP) in the center of aromatic residues of the ligand with positive‐ESP protons in the aromatic residues of the receptor. Thus, besides the salt bridges and hydrogen bonds, edge‐to‐face interactions significantly contribute to arylpiperazine ligands forming complexes with the D2 DAR.
A genome‐wide scan for juvenile rheumatoid arthritis in affected sibpair families provides evidence of linkage
Authors: Thompson Susan D. , Moroldo Marta B. , Guyer Laura , Ryan Mary , Tombragel Esther M. , Shear Edith S. , Prahalad Sampath , Sudman Marc , Keddache Mehdi A. , Brown W. Mark , Giannini Edward H. , Langefeld Carl D. , Rich Stephen S. , Nichols William C. , Glass David N. 
Published: September 2004

AbstractObjectiveJuvenile rheumatoid arthritis (JRA) represents a heterogeneous group of disorders with a complex genetic component. A genome scan was performed to detect linkage to JRA in 121 families containing 247 affected children in North America (the JRA Affected Sibpair [ASP] Registry).MethodsGenotype data collected for HLA–DR and 386 microsatellite markers were subjected to multipoint nonparametric linkage analysis. Following analysis of the entire set of families, additional analyses were performed after a priori stratification by disease onset type, age at onset, disease course, and selected HLA–DRB1 alleles.ResultsLinkage of JRA to the HLA region was confirmed (logarithm of odds [LOD] score 2.26). Additional evidence supporting linkage of JRA was observed at 1p36 (D1S214; LOD 1.65), 19p13 (D19S216; LOD 1.72), and 20q13 (D20S100; LOD 1.75). For early‐onset polyarticular disease, evidence of linkage was found at chromosome 7q11 (D7S502; LOD 3.47). For pauciarticular disease, evidence supporting linkage was observed on chromosome 19p13 (D19S216; LOD 2.98), the same marker that supported linkage to the “JRA” phenotype. Other regions supporting linkage with JRA disease subtype included 20q13, 4q24, 12q24, and Xp11. Stratification of families based on the presence of the HLA–DR8 allele in affected siblings resulted in significant linkage observed at 2p25 (D2S162/D2S305; LOD 6.0).ConclusionThese data support the hypothesis that multiple genes, including at least 1 in the HLA region, influence susceptibility to JRA. These findings for JRA are consistent with findings for other autoimmune diseases and support the notion that common genetic regions contribute to an autoimmune phenotype.
Down‐regulation of FLIP sensitizes rheumatoid synovial fibroblasts to Fas‐mediated apoptosis
Authors: Palao Guillermo , Santiago Begoña , Galindo María , Payá Mónica , Ramirez Juan C. , Pablos José L. 
Published: September 2004

AbstractObjectiveHyperplasia of fibroblast‐like synoviocytes (FLS) contributes to chronic inflammation and joint destruction in rheumatoid arthritis (RA). FLICE‐inhibitory protein (FLIP) is an antiapoptotic protein that might prevent apoptotic elimination of FLS in response to death ligands such as tumor necrosis factor α (TNFα) or Fas ligand, which are present in RA synovium. Previous studies on FLIP expression by osteoarthritis (OA) and RA FLS have shown variable results, and the specific role of FLIP as an apoptosis inhibitor in these cells remains unclear. We undertook this study to investigate the expression and antiapoptotic function of FLIP in FLS.MethodsWe studied the expression of FLIP by immunohistochemistry and immunoblotting in synovial tissues or cultured FLS from RA and OA patients. FLS apoptosis was induced by an agonistic anti‐Fas monoclonal antibody and FLS were then quantified. We studied the effects of cycloheximide (CHX), TNFα, and FLIP antisense oligonucleotide on FLIP expression and FLS apoptotic susceptibility.ResultsFLIPL was the isoform mainly expressed in lining synoviocytes and cultured FLS. Synovial tissues and cultured FLS from OA and RA tissues displayed similar patterns and levels of expression of FLIP. Fas‐induced apoptosis was variable in different FLS lines, but differences between OA and RA groups were not detected. TNFα induced increases in FLIPL and FLIPS expression and protected RA FLS from apoptosis, while CHX induced the opposite effects. Down‐regulation of FLIP by antisense oligonucleotide strongly sensitized RA FLS to Fas‐mediated apoptosis.ConclusionApoptosis susceptibility and FLIP expression are similar in OA and RA FLS. Down‐regulation of FLIP sensitizes RA FLS to Fas‐mediated apoptosis and may be a valuable tool for targeting RA FLS hyperplasia.
Triptolide, an active component of the Chinese herbal remedy Tripterygium wilfordii Hook F, inhibits production of nitric oxide by decreasing inducible nitric oxide synthase gene transcription
Authors: Wang B. , Ma L. , Tao X. , Lipsky P. E. 
Published: September 2004

AbstractObjectiveThe ethyl acetate (EA) extract of Tripterygium wilfordii Hook F (TWHF) and its major active component, triptolide, have been reported to be effective in the treatment of rheumatoid arthritis and other autoimmune inflammatory diseases. Nitric oxide (NO) has been recognized as an important mediator of inflammation. This study was therefore undertaken to examine the effects of the EA extract and triptolide on the production of NO and inducible NO synthase (iNOS) gene expression and transcription in vivo and in vitro.MethodsPeritoneal macrophages from C57BL/6J mice treated orally with the EA extract of TWHF were assayed for NO production and iNOS messenger RNA (mRNA) expression by reverse transcriptase–polymerase chain reaction. The murine fibroblast cell line NIH3T3 was also assessed for NO production and iNOS mRNA expression, as well as for iNOS promoter activation, Oct‐1 nuclear binding capacity, and Oct‐1 protein content by transient transfection, electrophoretic mobility shift assay, and immunoblotting, respectively.ResultsNO production and iNOS mRNA expression by macrophages from C57BL/6J mice immunized with trinitrophenyl–bovine serum albumin in Freund's complete adjuvant were significantly inhibited by oral administration of the EA extract (52.3% and 59.8% of control, respectively, at one‐eighth of the dose that is lethal for 50% of the animals [LD50] and 21.0% and 38.1% of control, respectively, at one‐fourth the LD50). Moreover, the EA extract and triptolide significantly inhibited NO production in vitro in activated peritoneal macrophages, which reflected a decreased level of iNOS mRNA. Finally, triptolide inhibited promoter activity of the iNOS gene and induction of the activity of the regulator of iNOS transcription, Oct‐1.ConclusionThe EA extract of TWHF and triptolide inhibit transcription of the iNOS gene. This may contribute to the antiinflammatory effects of this traditional herbal remedy.
Polyglutamation of methotrexate with common polymorphisms in reduced folate carrier, aminoimidazole carboxamide ribonucleotide transformylase, and thymidylate synthase are associated with methotrexate effects in rheumatoid arthritis
Authors: Dervieux Thierry , Furst Daniel , Lein Diana Orentas , Capps Robert , Smith Katie , Walsh Michael , Kremer Joel 
Published: September 2004

AbstractObjectiveMethotrexate (MTX) enters cells through the reduced folate carrier (RFC‐1) and exerts part of its effects through polyglutamation to MTX polyglutamates (MTXPGs) and inhibition of 5‐aminoimidazole‐4‐carboxamide ribonucleotide transformylase (ATIC) and thymidylate synthase (TS). We investigated the contribution of common genetic polymorphisms in RFC‐1 (G80A), ATIC (C347G), and TS (28‐bp tandem repeats located in the TS enhancer region [TSER*2/*3]) and of MTXPGs to the effect of MTX in patients with rheumatoid arthritis.MethodsThe study was cross‐sectional. All patients received MTX for at least 3 months. The numbers of tender and swollen joints, the Visual Analog Scale (VAS) scores for the physician's global assessment of disease activity, and the modified Health Assessment Questionnaire scores were collected. Using the VAS score for the physician's assessment of patient's response to MTX, the population of patients was dichotomized into responders to MTX (VAS score ≤2 cm) and nonresponders to MTX (VAS score >2 cm). A pharmacogenetic index was calculated as the sum of homozygous variant genotypes (RFC‐1 AA + ATIC 347GG + TSER *2/*2) carried by the patients. MTXPG concentrations were measured in red blood cells (RBCs) by high‐performance liquid chromatography.ResultsThe dose of MTX was not associated with the effects of MTX (P > 0.05). In contrast, increased RBC long‐chain MTXPG concentrations (median 40 nmoles/liter; range <5–131 nmoles/liter) and an increased pharmacogenetic index were associated with a lower number of tender and swollen joints (P < 0.05) and a lower score for the physician's global assessment of disease activity (P ≤ 0.001). Patients with RBC MTXPG levels of >60 nmoles/liter and carriers of a homozygous variant genotype were 14.0‐fold (95% confidence interval [95% CI] 3.6–53.8) and 3.7‐fold (95% CI 1.7–9.1), respectively, more likely to have a good response to MTX (P ≤ 0.01).ConclusionThese data suggest that measuring RBC MTXPG levels and/or the common polymorphisms in the folate–purine–pyrimidine pathway may help in monitoring MTX therapy.
The influence of genetic variation in the HLA–DRB1 and LTA–TNF regions on the response to treatment of early rheumatoid arthritis with methotrexate or etanercept
Authors: Criswell Lindsey A. , Lum Raymond F. , Turner Kevin N. , Woehl Blanche , Zhu Yuanqing , Wang Jinyi , Tiwari Hemant K. , Edberg Jeffrey C. , Kimberly Robert P. , Moreland Larry W. , Seldin Michael F. , Bridges S. Louis 
Published: September 2004

AbstractObjectiveTo examine the roles of specific genetic polymorphisms as predictors of response to treatment of early rheumatoid arthritis (RA).MethodsSubjects included 457 patients with early RA (duration of ≤3 years) who participated in a randomized controlled trial comparing weekly methotrexate and 2 dosages of etanercept (10 mg twice weekly and 25 mg twice weekly). Our primary outcome measure was achievement of 50% improvement in disease activity according to the criteria of the American College of Rheumatology (ACR50 response) after 12 months of treatment. Subjects were genotyped for HLA–DRB1 alleles and polymorphisms in the following genes: TNF, LTA, TNFRSF1A, TNFRSF1B, FCGR2A, FCGR3A, and FCGR3B. Univariate and multivariate analyses were performed to define the impact of specific polymorphisms and haplotypes on response to treatment. Covariates for the multivariate analyses included sex, ethnicity, age, disease duration, and baseline values for rheumatoid factor and the tender and swollen joint counts.ResultsThe presence of 2 HLA–DRB1 alleles encoding the shared epitope (SE) (compared with 1 or 0 copies) was associated with response to treatment with standard‐dose etanercept (odds ratio [OR] 4.3, 95% confidence interval [95% CI] 1.8–10.3). Among Caucasian patients, 2 extended haplotypes that included the HLA–DRB1 alleles *0404 and *0101 (both of which encode the SE) and 6 single‐nucleotide polymorphisms in the LTA–TNF region were associated with response to treatment. In a multivariate model that included treatment received and the aforementioned covariates, the ORs for the association of these haplotypes with achievement of an ACR50 response at 12 months were 2.5 (95% CI 0.8–7.3) and 4.9 (95% CI 1.5–16.1) for the *0404‐ and *0101‐containing haplotypes, respectively.ConclusionGenetic variation in the HLA–DRB1 and the LTA–TNF regions is significantly associated with response to treatment of early RA. These findings may have clinical application through the identification of patients who are most likely to benefit from treatment with methotrexate or etanercept.
Expression of chemokine and fibrosing factor messenger RNA in the urinary sediment of patients with lupus nephritis
Authors: Chan Rebecca Wing‐Yan , Lai Fernand Mac‐Moune , Li Edmund Kwok‐Ming , Tam Lai‐Shan , Wong Teresa Yuk‐Hwa , Szeto Carol Yi‐Ki , Li Philip Kam‐Tao , Szeto Cheuk‐Chun 
Published: September 2004

AbstractObjectiveLupus nephritis is characterized by intrarenal inflammation. To assess the extent and severity of disease activity and renal involvement, this study examined the expression of transforming growth factor β (TGFβ) and monocyte chemoattractant protein 1 (MCP‐1) in the urinary sediment of patients with systemic lupus erythematosus (SLE).MethodsWe studied 106 patients with SLE who were classified according to their disease status as those with active disease, those with disease in remission, and those with nonrenal SLE. Ten healthy subjects were used as controls. Lupus activity was assessed by the SLE Disease Activity Index (SLEDAI). If renal biopsy was performed, the histologic activity index and chronicity index were determined, and a morphometry analysis of renal scarring was performed. The urinary expresssion of TGFβ and MCP‐1 messenger RNA (mRNA) was studied by real‐time quantitative polymerase chain reaction, and the corresponding protein concentrations of TGFβ and MCP‐1 in the urine were measured by enzyme‐linked immunosorbent assay (ELISA).ResultsExpression of TGFβ and MCP‐1 mRNA in the urinary sediment was significantly elevated in the active disease group (P < 0.001 for both). These expression levels of TGFβ and MCP‐1 mRNA correlated with the SLEDAI score (TGFβ r = 0.71, P < 0.001; MCP‐1 r = 0.72, P < 0.001), and also significantly correlated with the histologic activity index (TGFβ r = 0.487, P = 0.004; MCP‐1 r = 0.357, P = 0.038). The urinary protein concentration of MCP‐1, but not of TGFβ, correlated with the SLEDAI score (r = 0.66, P < 0.001). However, neither the protein concentration of TGFβ nor that of MCP‐1 as measured by ELISA in the urine correlated with the histologic activity index.ConclusionThe measurement of urinary mRNA expression may be a noninvasive method for the assessment of lupus disease activity and the severity of renal involvement in patients with lupus nephritis.
Effective treatment of a mouse model of Sjögren's syndrome with eyedrop administration of anti‐CD4 monoclonal antibody
Authors: Hayashi Yuki , Ishimaru Naozumi , Arakaki Rieko , Tsukumo Shin‐ichi , Fukui Hitomi , Kishihara Kenji , Shiota Hiroshi , Yasutomo Koji , Hayashi Yoshio 
Published: September 2004

AbstractObjectiveTo determine whether eyedrop administration of an anti‐CD4 monoclonal antibody (mAb) is effective in the treatment of Sjögren's syndrome (SS) using a mouse model of the disease.MethodsThe anti‐CD4 mAb was administered daily into the eyes of mice with SS from ages 4 to 8 weeks or ages 10 to 12 weeks. During treatment, tear volume was monitored and after final treatment, histologic features of the lacrimal and salivary glands, the phenotypes and function of T cells, and serum titers of anti–α‐fodrin antibody were examined.ResultsEyedrop administration of anti‐CD4 mAb before the onset of SS prevented the autoimmune pathology seen in the lacrimal glands but not that in the salivary glands. Furthermore, eyedrop administration of anti‐CD4 mAb after the development of SS inhibited mononuclear cell infiltration and the destruction of parenchyma only in the lacrimal glands. Eyedrop administration of anti‐CD4 mAb suppressed the local activation of CD4+ T cells rather than deleting CD4+ T cells, which reduced the expansion of pathologic CD4+ T cells against α‐fodrin.ConclusionThese results demonstrate the remarkable efficacy of anti‐CD4 mAb eyedrops in the treatment of SS eye symptoms, which illustrates a new antibody‐based therapeutic strategy for patients with eye problems caused by SS as well as other diseases.