bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preparation and electroluminescence of CaS: (Ce, Eu and Cu) phosphors
Authors: Arterton B. W. , Viney I. V. F. , Ray B. , Brightwell J. W. 
Published: May 2005

AbstractDoped CaS powder samples were prepared using two methods: (i) a metathesis reaction of carbonate with H2S at 1200°C; (ii) reaction with Na2Co3/S flux at 1000°C in nitrogen, followed by washing in an alkaline solution, drying and sieving to give 20–30 μm particles.Powders produced from both reactions were strongly photoluminescent and singificant AC electroluminescence (ACEL) was observed when samples produced by the metathesis reactions were copper coated. Samples prepared using the flux technique on pre‐copperdoped carbonate also showed ACEL.The EL excitation process in the flux grown material differs from that in samples prepared using H2S; this stems from Cu2S microdeposits on the particle surfaces of the former. The formation of the needle‐like deposit results from precipitation of copper from solid solution with decreasing temperature. The EL emission arises from observable point sources rather than the more uniform emission from copper‐coated samples.
ZnCdS films for solar cell and photodetector applications deposited by In Situ chemical doping of CdS with Zn
Authors: Sebastian P. J. 
Published: May 2005

AbstractZnCdS films were formed by in situ chemical doping of CdS with Zn in a chemical bath. The X‐ray diffraction (XRD) patterns of CdS films after Zn doping showed a more disordered nature, consisting of reflections from Zn0.049Cd0.951S (JCPDS 40‐834) as well as CdS greenockite (hexagonal, JCPDS 41‐1049) and hawleyite (cubic, JCPDS 10‐0454) phases. A comparison of the optical transmittance spectra for undoped and Zn‐doped films showed that the cut‐off wavelength was modified after Zn doping, indicating the presence of impurity states in the band gap. Zn‐doped films showed an increase in dark conductivity after annealing at about 200°C. These films exhibit promising characteristics for application in solar cell and photodetector structures.
Electrical, optical and photoelectrochemical properties of natural enargite, Cu3AsS4
Authors: Pauporté Th. , Lincot D. 
Published: May 2005

AbstractThe semiconducting properties of natural samples of enargite, a copper and arsenic suphide (Cu3AsS4), have been studied. They have been found to be p‐type semiconductors with a resistivity of about 7 Ω cm, a doping level of about 1017 cm−3 and a mobility of 9 cm2V−1 s−1. The variation of the resistivity as a function of temperature allows to determine an activation energy of 0.11 eV. Two optical transitions have been determined, an indirect one at 1.19 eV and a direct one at 1.44 eV. The samples, mounted as working electrodes in a photoelectrochemical set‐up, are photosensitive and behave as p‐type photocathodes. The two transitions are found again from the analysis of photocurrent spectra. The direct band gap value is close to the ideal value required for photovoltaic applications. However the quantum efficiencies obtained here are still low.
Clinical relevance of the expression of P‐glycoprotein on peripheral blood lymphocytes to steroid resistance in patients with systemic lupus erythematosus
Authors: Tsujimura Shizuyo , Saito Kazuyoshi , Nakayamada Shingo , Nakano Kazuhisa , Tanaka Yoshiya 
Published: June 2005

AbstractObjectiveP‐glycoprotein (P‐gp) of membrane transporters leads to drug resistance by the exclusion of intracellular drugs, including corticosteroids. Some patients with highly active systemic lupus erythematosus (SLE) show poor response to corticosteroids; however, the mechanisms of steroid resistance remain unclear. The aim of this study was to elucidate the clinical relevance of P‐gp expression on lymphocytes to steroid resistance in patients with active SLE.MethodsFlow cytometric analyses of the expression of P‐gp on peripheral blood lymphocytes from 20 normal volunteers and 80 SLE patients were performed. Steroid‐exclusion analysis of peripheral blood mononuclear cells (PBMCs) was conducted by using radioisotope‐labeled dexamethasone.ResultsP‐gp was expressed at significantly high levels on most of the peripheral blood lymphocytes from SLE patients, whereas normal lymphocytes had only marginal expression. The quantity of P‐gp on SLE lymphocytes correlated with the disease activity in each patient, as estimated by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Furthermore, in SLE patients whose SLEDAI scores were >12 despite taking >0.5 mg/kg/day of prednisolone, P‐gp expression on lymphocytes was markedly increased, and intracellular dexamethasone in their PBMCs was significantly decreased. However, intensive immunosuppressive treatment in these SLE patients resulted in successful control of disease activity, which occurred in parallel with a marked reduction of P‐gp on lymphocytes.ConclusionThe overexpression of P‐gp on lymphocytes might lead to exclusion of corticosteroids from lymphocytes, resulting in steroid resistance in patients with highly active SLE. Reduction of P‐gp expression achieved by intensive immunosuppressive treatment overcame the steroid resistance. We therefore propose that measurement of P‐gp expression on lymphocytes is useful in the assessment of steroid resistance and is a good marker for indicating the need for intensive immunosuppressive treatment in patients with highly active SLE.
Amelioration of rat adjuvant‐induced arthritis by Met‐RANTES
Authors: Shahrara Shiva , Proudfoot Amanda E. I. , Woods James M. , Ruth Jeffrey H. , Amin M. Asif , Park Christy C. , Haas Christian S. , Pope Richard M. , Haines G. Kenneth , Zha Yuan Yuan , Koch Alisa E. 
Published: June 2005

AbstractObjectiveCC chemokines and their receptors play a fundamental role in trafficking and activation of leukocytes at sites of inflammation, contributing to joint damage in rheumatoid arthritis. Met‐RANTES, an amino‐terminal–modified methionylated form of RANTES (CCL5), antagonizes the binding of the chemokines RANTES and macrophage inflammatory protein 1α (MIP‐1α; CCL3) to their receptors CCR1 and CCR5, respectively. The aim of this study was to investigate whether Met‐RANTES could ameliorate adjuvant‐induced arthritis (AIA) in the rat.MethodsUsing immunohistochemistry, enzyme‐linked immunosorbent assay, real‐time reverse transcription–polymerase chain reaction, Western blot analysis, adoptive transfer, and chemotaxis, we defined joint inflammation, bony destruction, neutrophil and macrophage migration, Met‐RANTES binding affinity to rat receptors, proinflammatory cytokine and bone marker levels, CCR1 and CCR5 expression and activation, and macrophage homing into joints with AIA.ResultsAdministration of Met‐RANTES as a preventative reduced the severity of joint inflammation. Administration of Met‐RANTES to ankles with AIA showed decreases in inflammation, radiographic soft tissue swelling, and bone erosion. Met‐RANTES significantly reduced the number of neutrophils and macrophages at the peak of arthritis compared with saline‐injected controls. Competitive chemotaxis in peripheral blood mononuclear cells demonstrated that Met‐RANTES inhibited MIP‐1α and MIP‐1β at 50% inhibition concentrations of 5 nM and 2 nM, respectively. Furthermore, levels of tumor necrosis factor α, interleukin‐1β, macrophage colony‐stimulating factor, and RANKL were decreased in joints with AIA in the Met‐RANTES group compared with the control group. Interestingly, the expression and activation of CCR1 and CCR5 in the joint were down‐regulated in the Met‐RANTES group compared with the control group. Functionally, Met‐RANTES administration decreased adoptively transferred peritoneal macrophage homing into the joint.ConclusionThe data suggest that the targeting of Th1‐associated chemokine receptors reduce joint inflammation, bone destruction, and cell recruitment into joints with AIA.
Effects of combination M40403 and dexamethasone therapy on joint disease in a rat model of collagen‐induced arthritis
Authors: Cuzzocrea Salvatore , Mazzon Emanuela , Paola Rosanna Di , Genovese Tiziana , Muià Carmelo , Caputi Achille P. , Salvemini Daniela 
Published: June 2005

AbstractObjectiveTo investigate the effects of combination therapy with M40403, a superoxide dismutase mimetic (SODm), and dexamethasone (DEX) on collagen‐induced arthritis (CIA) in rats.MethodsCIA was elicited in Lewis rats by an intradermal injection of 100 μl of an emulsion of bovine type II collagen (CII) in Freund's incomplete adjuvant (IFA) at the base of the tail. On day 21, a second injection of CII in IFA was administered at the base of the tail.ResultsLewis rats developed erosive arthritis of the hind paw when immunized with an emulsion of CII in IFA. The histopathology of CIA included erosion of the articular cartilage at the joint margins and subchondral bone resorption. Immunohistochemical analysis for nitrotyrosine, poly(ADP‐ribose) polymerase (PARP), inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX‐2) revealed positive staining in inflamed joints of collagen‐treated rats. The combination therapy with M40403 2 mg/kg and DEX 0.01 mg/kg significantly reduced the development of the inflammatory process and reduced the degree of staining for iNOS, COX‐2, nitrotyrosine, and PARP. No significant difference in the degree of staining between the combination therapy and the higher dose of DEX (0.1 mg/kg) was found. Furthermore, radiographic evidence of protection from bone resorption was apparent in the tibiotarsal joints of rats that received the combination therapy.ConclusionThis study shows that combination therapy with M40403 and DEX reduced the degree of chronic inflammation and tissue and bone damage associated with CIA in the rat. It supports the possible use of SODm in combination with steroids to reduce the dose necessary and the side effects related to the use of steroids in the management of chronic diseases such as rheumatoid arthritis.
Interaction of pyrin with 14.3.3 in an Isoform‐specific and phosphorylation‐dependent manner regulates its translocation to the nucleus
Authors: Jéru Isabelle , Papin Stéphanie , L'Hoste Sébastien , Duquesnoy Philippe , Cazeneuve Cécile , Camonis Jacques , Amselem Serge 
Published: June 2005

AbstractObjectivePyrin, the familial Mediterranean fever gene product, exists in several isoforms of unknown functions. The recombinant full‐length isoform (pyrin.fl) is cytoplasmic, whereas an alternatively spliced isoform lacking exon 2 (pyrin.ΔEx2) concentrates in the nucleus. Native pyrin, mainly consisting of pyrin.fl, is also cytoplasmic in monocytes but is predominantly nuclear in other cell types. To understand pyrin‐dependent biologic pathways and to decipher the mechanisms accounting for such different patterns of subcellular compartmentalization, binding partners and posttranslational modifications of pyrin were assessed.MethodsA yeast 2‐hybrid screen was performed with pyrin.fl as the bait. The interaction identified between pyrin.fl and 14.3.3 proteins was confirmed by immunoprecipitation of 35S‐radiolabeled protein complexes; similar experiments were performed with pyrin.ΔEx2, pyrin.fl after alkaline phosphatase treatment, and pyrin.fl mutants in which several exon 2–encoded serine residues were replaced by nonphosphorylatable alanines. The subcellular localization of the different wild‐type and mutated pyrin proteins was assessed by immunofluorescence.ResultsTwo members of the 14.3.3 protein family were identified as pyrin partners. Whereas pyrin.fl interacted with 14.3.3τ and 14.3.3ϵ, these interactions did not occur with pyrin.ΔEx2. Pyrin.fl was phosphorylated, and this modification mediated 14.3.3 binding. Serines 208, 209, and 242, within exon 2, acted as critical residues in the interaction between pyrin.fl and 14.3.3. When an S208–S209–S242A pyrin.fl triple mutant or wild‐type pyrin.fl in the presence of an inhibitor of 14.3.3–ligand interactions was used, promotion of nuclear translocation of pyrin was observed.ConclusionThese results disclose the role played by 14.3.3 in the regulation of the subcellular compartmentalization of pyrin in a phosphorylation‐ and isoform‐dependent manner. They also reconcile the observations made in vitro with those made in vivo, while providing a direct link between 14.3.3‐dependent pathways and pyrin.
Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis: A randomized clinical trial
Authors: Wanders Astrid , Heijde Désirée van der , Landewé Robert , Béhier Jéhan‐Michel , Calin Andrei , Olivieri Ignazio , Zeidler Henning , Dougados Maxime 
Published: June 2005

AbstractObjectiveA 2‐year randomized controlled trial was performed to test the hypothesis that long‐term, continuous treatment with nonsteroidal antiinflammatory drugs (NSAIDs), in comparison with NSAID treatment on demand only, influences radiographic progression in patients with ankylosing spondylitis (AS).MethodsPatients with AS (n = 215), who had previously participated in a 6‐week, randomized, double‐blind clinical trial that compared celecoxib, ketoprofen, and placebo, were randomly allocated to receive either continuous treatment with NSAIDs or on‐demand treatment with NSAIDs for a period of 2 years. All patients began treatment with celecoxib, at a starting dosage of 100 mg twice daily; patients could increase this dosage to 200 mg twice daily or could switch to another NSAID while maintaining the same treatment strategy. Structural changes were assessed by radiographs of the lumbar and cervical spine and scored according to the modified Stoke Ankylosing Spondylitis Spine Score by one observer who was blinded to the treatment strategy and temporal order of the radiographs. Statistical analyses included a between‐group comparison of 1) radiographic progression scores (by Mann‐Whitney U test), 2) time‐averaged values of variables reflecting signs and symptoms of AS (by linear regression analysis), and 3) the frequency of reported site‐specific adverse events (by chi‐square test or Fisher's exact test, as appropriate).ResultsComplete sets of radiographs were available for 76 of the 111 patients in the continuous‐treatment group and for 74 of the 104 patients in the on‐demand group. The mean ± SD scores for radiographic progression were 0.4 ± 1.7 in the continuous‐treatment group and 1.5 ± 2.5 in the on‐demand treatment group (P = 0.002). Parameters reflecting signs and symptoms were not statistically significantly different between groups. The between‐group difference in radiographic progression did not disappear after adjusting for baseline values of radiographic damage or disease activity variables and for time‐averaged values of disease activity variables, nor after imputation of missing data. Relevant adverse events tended to occur more frequently in the continuous‐treatment group than in the on‐demand group (for hypertension, 9% versus 3%; for abdominal pain, 11% versus 6%; for dyspepsia, 41% versus 38%), but the differences were not statistically significant.ConclusionA strategy of continuous use of NSAIDs reduces radiographic progression in symptomatic patients with AS, without increasing toxicity substantially.
The involvement of Vα14 natural killer T cells in the pathogenesis of arthritis in murine models
Authors: Chiba Asako , Kaieda Shinjiro , Oki Shinji , Yamamura Takashi , Miyake Sachiko 
Published: June 2005

AbstractObjectiveTo examine the physiologic role of natural killer T (NKT) cells bearing Vα14 T cell receptor (TCR) in the pathogenesis of collagen‐induced arthritis (CIA) and antibody‐induced arthritis in mice.MethodsNKT cells were stained with α‐galactosylceramide–loaded CD1 dimer, and then assessed using flow cytometry. CIA was induced in mice by immunization on days 0 and 21 with type II collagen (CII) emulsified with an equal volume of Freund's complete adjuvant. Anti‐CII antibodies were measured by enzyme‐linked immunosorbent assay. For antibody‐induced arthritis, mice were injected with anti‐CII monoclonal antibodies (mAb) followed by lipopolysaccharide, or with serum from KRN TCR–transgenic mice crossed with nonobese diabetic mice (K/BxN). The severity of arthritis was monitored with a macroscopic scoring system.ResultsThe number of NKT cells increased in the liver at the peak of the clinical course of CIA. Administration of anti‐CD1 mAb inhibited development of CIA. The severity of CIA in NKT cell–deficient mice was reduced compared with that in wild‐type mice. The IgG1:IgG2a ratio of anti‐CII was elevated and production of interleukin‐10 from draining lymph node cells was increased in NKT cell–deficient mice. NKT cell–deficient mice were significantly less susceptible to antibody‐induced arthritis.ConclusionNKT cells contribute to the pathogenesis of arthritis by enhancing autoantibody‐mediated inflammation. NKT cells also contribute to the disease process in a deleterious way, due, at least in part, to the alteration of the Th1/Th2 balance in T cell response to CII.
Whole‐genome screening for susceptibility genes in multicase families with Behçet's disease
Authors: Karasneh Jumana , Gül Ahmet , Ollier William E. , Silman Alan J. , Worthington Jane 
Published: June 2005

AbstractObjectiveBehçet's disease is generally considered to be a multifactorial disease with important genetic and environmental components. A strong association between an HLA class I antigen, HLA–B51, and Behçet's disease has long been known. However, analysis of multicase families has suggested a substantial contribution of non‐HLA loci. The aim of this study was to perform a whole‐genome linkage analysis for identification of other susceptibility loci for Behçet's disease in multicase families.MethodsThe study group comprised a total of 193 individuals (90 male, 103 female) from 28 multicase families of Turkish origin; 83 of the subjects (50 males, 33 females) fulfilled the International Study Group criteria for Behçet's disease. Three hundred ninety‐five highly informative microsatellite markers spanning the genome were genotyped using fluorescent polymerase chain reaction primers and a fully automated electrophoresis platform. After the first analysis, 33 additional markers that were located close to the peak linkage areas were genotyped in all individuals. Nonparametric multipoint linkage analysis was carried out using GeneHunter version 2.1 software.ResultsEvidence for linkage (P ≤ 0.05) was obtained in 16 chromosome regions: 1p36, 4p15, 5q12, 5q23, 6p22–24, 6q16, 6q25–26, 7p21, 10q24, 12p12–13, 12q13, 16q12, 16q21–23, 17p13, 20q12–13, and Xq26–28. After the addition of further markers, the maximum nonparametric linkage score increased from 3.5 to 3.94 at 12p12–13 (D12S77; P = 0.0002) and from 3.07 to 3.70 at 6p22–24 (D6S285; P = 0.0005).ConclusionThis study is the first systematic genome screen in Behçet's disease and provides evidence of linkage to several non‐HLA susceptibility loci in a cohort of Turkish multicase families. This represents the first step toward the identification of novel Behçet's disease susceptibility genes.
Rapid responses to anakinra in patients with refractory adult‐onset Still's disease
Authors: Fitzgerald Avril A. , LeClercq Sharon A. , Yan Alexander , Homik Joanne E. , Dinarello Charles A. 
Published: June 2005

AbstractObjectiveTo assess the efficacy of anakinra treatment in patients with adult‐onset Still's disease (AOSD) that is refractory to corticosteroids, methotrexate (MTX), and etanercept.MethodsFour patients with AOSD were treated with prednisone and MTX and 2 patients were also treated with etanercept for worsening symptoms and indicators of systemic inflammation. White blood cells (WBCs), C‐reactive protein (CRP) levels and/or erythrocyte sedimentation rate, and ferritin levels were measured and, in 1 patient, serum creatinine levels were determined. Treatment with anakinra at 100 mg/day was initiated.ResultsThe index patient's disease was refractory to treatment with prednisone (30 mg/day) and MTX, with spiking fevers, rash, synovitis, a serum ferritin level of 8,400 ng/ml (normal ≤200), and a CRP level of 86 mg/liter (normal <8). Levels of interleukin‐1β (IL‐1β), IL‐1α, IL‐6, IL‐1 receptor antagonist, and IL‐18 were elevated. Just prior to anakinra treatment, the WBC count was 14,600/mm3, the CRP level was 86 mg/liter, and the ferritin level was 573 ng/ml, with daily spiking fevers to 104°F, rash, and swollen joints. Within hours of the first injection, the patient was afebrile and asymptomatic; within days, the WBC count, ferritin level, and CRP level decreased into the normal range. On 2 occasions, anakinra was withheld. Within a few days, the WBC count rose to >20,000/mm3with prominent neutrophilia, the CRP level rose to >200 mg/liter, and the ferritin level rose to >3,000 ng/ml. Upon restarting anakinra, the patient became afebrile, the WBC count fell to 8,000/mm3, the CRP level fell to <3 mg/liter, and the ferritin level fell to <300 ng/ml. Three additional patients with refractory AOSD who experienced rapid reductions in fever, symptoms, and markers of inflammation when treated with anakinra are reported.ConclusionRefractory AOSD appears to be IL‐1–mediated since anakinra decreases hematologic, biochemical, and cytokine markers and also produces rapid reductions in systemic and local inflammation. Reported efficacy of tumor necrosis factor–blocking therapies in AOSD may be due to a reduction in IL‐1.
Human β‐defensin 3 mediates tissue remodeling processes in articular cartilage by increasing levels of metalloproteinases and reducing levels of their endogenous inhibitors
Authors: Varoga Deike , Pufe Thomas , Harder Jürgen , Schröder Jens‐Michael , Mentlein Rolf , Meyer‐Hoffert Ulf , Goldring Mary B. , Tillmann Bernhard , Hassenpflug Joachim , Paulsen Friedrich 
Published: June 2005

AbstractObjectiveBeta‐defensins are broad‐spectrum antimicrobial peptides (APs) that are components of innate immunity. Recent investigations showed the induction of β‐defensins in synovial membranes of osteoarthritic (OA) joints and suggested that they have functions other than the ability to kill microbes. As a result of these findings, we undertook this study to investigate the production of human β‐defensin 3 (HBD‐3) in OA cartilage and to determine its influence on chondrocyte function.MethodsHealthy and OA cartilage were assessed for HBD‐3 expression by reverse transcriptase–polymerase chain reaction (RT‐PCR) and immunohistochemistry. HBD‐3 expression in C28/I2 chondrocytes after administration of tumor necrosis factor α (TNFα) and interleukin‐1 (IL‐1) was determined by real‐time RT‐PCR and immunodot blot. Enzyme‐linked immunosorbent assay experiments were used to study the effects of HBD‐3 in cultured articular chondrocytes and in healthy and OA cartilage discs. Immunohistochemical analyses were performed to study the expression of mouse β‐defensins (MBDs) in OA cartilage of STR/Ort mice.ResultsHBD‐3 was induced in OA cartilage without bacterial challenge. Cytokines involved in the pathogenesis of OA, namely, TNFα and IL‐1, were strong inducers of HBD‐3 in cultured chondrocytes. Application of the recombinant HBD‐3 protein to cultured chondrocytes and cartilage discs resulted in increased production of cartilage‐degrading matrix metalloproteinases and in down‐regulation of their endogenous regulators, tissue inhibitors of metalloproteinases 1 and 2. Furthermore, STR/Ort mice, which are genetically predisposed to develop OA‐like lesions in the knee joint, demonstrated an increased expression of MBDs 3 and 4 in cartilage compared with that in healthy animals.ConclusionThese findings widen our knowledge of the functional spectrum of APs and demonstrate that HBD‐3 is a multifunctional AP with the ability to link host defense mechanisms and inflammation with tissue‐remodeling processes in articular cartilage. Moreover, our data suggest that HBD‐3 is an additional factor in the pathogenesis of OA.