bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synthesis and polymerization of the acrylamide derivatives of fatty compounds
Authors: Eren Tarik , Kusefoglu Selim H. 
Published: June 2005

AbstractThe Ritter reaction of plant oil triglycerides (such as soybean and sunflower oil) with acrylonitrile was used to introduce acrylamide functionality on the triglyceride. Acrylonitrile and triglycerides were reacted in the presence of H2SO4, and acrylamide derivatives were obtained in yields of 45 and 50% for sunflower oil and soybean oil, respectively. Radical initiated copolymerization of the acrylamide derivatives of the triglycerides with styrene produced semirigid polymers. Characterization of new monomers and polymers was done by 1H‐NMR, 13C‐NMR, IR, and MS. The swelling behavior of the crosslinked network polymers was determined in different solvents. Glass transiton temperature (Tg) of the cured resin was also determined by differential scanning calorimeter to be 40°C for soybean based polymer and 30°C for sunflower‐based polymer. Homo‐ and copolymerization behavior of acrylamide derivatives of methyl oleate (MOA) and methyl 10‐undecenoate (MUA) were also investigated. The reactivity ratios of these monomers with respect to styrene were determined by the Fineman–Ross method using 1H‐NMR spectroscopic data. The reactivity ratios were rsty = 1.776; rmoa = 0512 for MOA, and rsty = 1.142; rmua = 0.507 for MUA, respectively. Photopolymerization behaviors of MOA and MUA were also investigated using the photoDSC technique and the rate of polymerization of MUA is higher than that of MOA under the same conditions. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci 97: 2264–2272, 2005
Synthesis and characterization of chitosan derivatives carrying galactose residues
Authors: Zhang Can , Ping Qineng , Ding Ya 
Published: June 2005

AbstractA series of water‐soluble chitosan derivatives, carrying galactose residues, were synthesized by using an alternative method in which the galactose groups were introduced into amino groups of the derivatives. First, hydroxyethyl chitosan (HECS) and hydroxypropyl chitosan (HPCS) were synthesized under alkaline conditions by using chitosan and propylene or chitosan and ClCH2CH2OH as the starting materials, respectively. Then lactobionic acid was added into the systems so as to form galactosylated HECS (Gal‐HECS) and galactosylated HPCS (Gal‐HPCS) with substitution degrees of 53 and 47%, respectively. Lactosaminated HPCS (Lac‐HPCS) and Lactosaminated HECS (Lac‐HECS) were obtained with substitution degrees of 42 and 38%, respectively, by the reductive amination of the mixtures of lactose and HECS or lactose and HPCS with potassium borohydride present in the reaction. The chemical structures of new chitosan derivatives were characterized by FTIR, 1H NMR, 13C NMR, and elemental analysis. Some physical properties were also analyzed by wide angle X‐ray diffraction (WAXD) and differential scanning calorimetry (DSC). The novel chitosan derivatives carrying galactose residues may be used as additives for hepatic targeting delivery. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci 97: 2161–2167, 2005
Responses of the silkworm tyramine receptor to 2‐phenylethylamines and 5‐phenyloxazoles
Authors: Ohta Hiroto , Khan Md. Anwar Arfien , Nagai Idumi , Umemoto Natsuko , Hamasaki Tomohiro , Ozoe Yoshihisa 
Published: June 2005

AbstractTyramine (TA), a biogenic amine, attenuates intracellular cAMP production by acting on its receptor in insects. Several non‐biogenic amines were examined for their actions on native and heterologously expressed silkworm TA receptors. 5‐(4‐Hydroxyphenyl)oxazole, which showed an attenuating effect on cAMP production in silkworm‐head membranes, did not attenuate forskolin‐stimulated cAMP production in HEK‐293 cells expressing the silkworm TA receptor, although the compound bound to the cloned receptor. 2‐Phenylethylamines (2‐PEAs), which showed positive and negative effects on cAMP production in silkworm‐head membranes, inhibited [3H]TA binding to the cloned TA receptor. 2‐Chloro‐2‐(4‐chlorophenyl)ethylamine was the most potent inhibitor of [3H]TA binding among the 2‐PEAs tested, with an IC50 of 30.4 nM. This compound acted as an antagonist and abolished TA‐attenuation of forskolin‐stimulated cAMP production in the cloned TA receptor. The discrepancy in the effects of the non‐biogenic amines on the native and cloned TA receptors remains to be further examined. A newly synthesized 2‐PEA, 2‐chloro‐2‐(4‐hydroxyphenyl)ethylamine, attenuated forskolin‐stimulated cAMP production in the cloned TA receptor, indicating that the para‐hydroxy group is important for the agonist action. Arch. Insect Biochem. Physiol. 59:150–160, 2005. © 2005 Wiley‐Liss, Inc.
Soluble interleukin‐1 receptor accessory protein ameliorates collagen‐induced arthritis by a different mode of action from that of interleukin‐1 receptor antagonist
Authors: Smeets R. L. , Joosten L. A. B. , Arntz O. J. , Bennink M. B. , Takahashi N. , Carlsen H. , Martin M. U. , van den Berg W. B. , van de Loo F. A. J. 
Published: June 2005

AbstractObjectiveTo discern the mode of interleukin‐1 (IL‐1) inhibition of soluble IL‐1 receptor accessory protein (sIL‐1RAcP) by comparison with IL‐1 receptor antagonist (IL‐1Ra) in arthritis.MethodsAdenoviral vectors encoding either sIL‐1RAcP or IL‐1Ra were administered systemically before onset of collagen‐induced arthritis in DBA/1 mice. Anti–bovine type II collagen IgG and IL‐6 were quantified in serum. Proliferative response of splenic T cells was determined in the presence of sIL‐1RAcP or IL‐1Ra. The effect on IL‐1 inhibition of recombinant sIL‐1RAcP and IL‐1Ra was further examined in vitro, using NF‐κB luciferase reporter cell lines. Quantitative polymerase chain reaction was used to determine the relative messenger RNA expression of the IL‐1 receptors.ResultsAdenoviral overexpression of both sIL‐1RAcP and IL‐1Ra resulted in amelioration of the collagen‐induced arthritis. Both IL‐1 antagonists reduced the circulating levels of antigen‐specific IgG2a antibodies, but only IL‐1Ra was able to inhibit lymphocyte proliferation. By using purified lymphocyte populations derived from NF‐κB reporter mice, we showed that sIL‐1RAcP inhibits IL‐1–induced NF‐κB activity in B cells but not T cells, whereas IL‐1Ra inhibited IL‐1 on both cell types. A study in a panel of NF‐κB luciferase reporter cells showed that the sIL‐1RAcP inhibits IL‐1 signaling on cells expressing either low levels of membrane IL‐1RAcP or high levels of IL‐1RII.ConclusionWe show that the sIL‐1RAcP ameliorated experimental arthritis without affecting T cell immunity, in contrast to IL‐1Ra. Our results provide data in support of receptor competition by sIL‐1RAcP as an explanation for the different mode of IL‐1 antagonism in comparison with IL‐1Ra.
Intracellular free radical production in synovial T lymphocytes from patients with rheumatoid arthritis
Authors: Remans P. H. J. , van Oosterhout M. , Smeets T. J. M. , Sanders M. , Frederiks W. M. , Reedquist K. A. , Tak P. P. , Breedveld F. C. , van Laar J. M. 
Published: June 2005

AbstractObjectiveTo investigate the cellular and molecular sources of oxidative stress in patients with rheumatoid arthritis (RA) through analysis of the production of reactive oxygen species (ROS) in synovium.MethodsCytochemical procedures based on the 3,3′‐diaminobenzidine (DAB)–Mn2+ deposition technique were used on unfixed cryostat sections of synovium from RA patients and rheumatic disease controls. For immunophenotyping, sections were incubated, fixed, and stained with fluorescein isothiocyanate–labeled antibodies. Fluorescence‐activated cell sorter analysis of the ROS‐reactive dye 6‐carboxy‐2′,7′‐dichlorodihydrofluorescein diacetate‐di(acetoxymethyl ester) was used to measure intracellular ROS in T lymphocytes from peripheral blood and synovial fluid. To determine which enzymes produced ROS, different inhibitors were tested.ResultsLarge quantities of DAB precipitated in the majority of RA synovial T lymphocytes, indicative of intracellular ROS production. These ROS‐producing T lymphocytes were observed throughout the synovium. Polymerization of DAB was observed to a lesser extent in other forms of chronic arthritis, but was absent in osteoarthritis. DAB staining of cytospin preparations of purified RA synovial fluid T cells confirmed the presence of ROS‐producing cells. One of the ROS involved appeared to be H2O2, since catalase suppressed intracellular ROS production. Superoxide dismutase, which uses superoxide as a substrate to form H2O2, diphenyleneiodonium (an inhibitor of NADPH oxidase), NG‐monomethyl‐L‐arginine (an inhibitor of nitric oxide synthesis), nordihydroguaiaretic acid (an inhibitor of lipoxygenase), and rotenone (an inhibitor of mitochondrial ROS production) failed to suppress ROS production.ConclusionOur findings show that chronic oxidative stress observed in synovial T lymphocytes is not secondary to exposure to environmental free radicals, but originates from intracellularly produced ROS. Additionally, our data suggest that one of the intracellularly generated ROS is H2O2, although the oxidase(s) involved in its generation remains to be determined.
Invasiveness of fibroblast‐like synoviocytes is an individual patient characteristic associated with the rate of joint destruction in patients with rheumatoid arthritis
Authors: Tolboom Tanja C. A. , van der Helm‐Van Mil Annette H. M. , Nelissen Rob G. H. H. , Breedveld Ferdinand C. , Toes René E. M. , Huizinga Tom W. J. 
Published: June 2005

AbstractObjectiveRheumatoid arthritis (RA) is characterized by inflammation and destruction of synovial joints. Fibroblast‐like synoviocytes (FLS) harvested from synovial tissue of patients with RA can invade normal human cartilage in severe combined immunodeficient (SCID) mice and Matrigel basement membrane matrix in vitro. This study was undertaken to investigate the association of these in vitro characteristics with disease characteristics in patients with RA.MethodsSynovial tissue samples from 72 RA and 49 osteoarthritis (OA) patients were obtained. Samples of different joints were collected from 7 patients with RA. The FLS invasiveness in Matrigel was studied, and the intraindividual and interindividual differences were compared. From the patients with FLS who exhibited the most extreme differences in in vitro ingrowth (most and least invasive FLS), radiographs of the hands and feet were collected and scored according to the Sharp/van der Heijde method to determine the relationship between in vitro invasion data and estimated yearly joint damage progression.ResultsFLS from patients with RA were more invasive than FLS from patients with OA (P < 0.001). The mean intraindividual variation in FLS invasion was much less than the mean interindividual variation (mean ± SD 1,067 ± 926 and 3,845 ± 2,367 for intraindividual and interindividual variation, respectively; P = 0.035), which shows that the level of FLS invasion is a patient characteristic. The mean ± SEM Sharp score on radiographs of the hands or feet divided by the disease duration was 4.4 ± 1.1 units per year of disease duration in patients with the least invasive FLS (n = 9), which was much lower compared with the 21.8 ± 3.1 units per year of disease duration in patients with the most invasive FLS (n = 9) (P < 0.001).ConclusionThe ex vivo invasive behavior of FLS from RA patients is associated with the rate of joint destruction and is a patient characteristic, given the much smaller intraindividual than interindividual FLS variation.
The prevalence of undiagnosed pulmonary arterial hypertension in subjects with connective tissue disease at the secondary health care level of community‐based rheumatologists (the UNCOVER study)
Authors: Wigley Fredrick M. , Lima Joao A. C. , Mayes Maureen , McLain David , Chapin J. Lincoln , Ward‐Able Clive 
Published: June 2005

AbstractObjectiveMost of the data about the prevalence of pulmonary arterial hypertension (PAH) are from tertiary centers that are biased toward seeing more severe cases; therefore, the true prevalence of PAH among patients with connective tissue disease is unknown. We sought to determine the point prevalence of undiagnosed PAH in community‐based rheumatology practices.MethodsThe study design was a multicenter, prospective and retrospective survey and analysis of clinical cases in 50 community rheumatology practices. We evaluated a total of 909 patients with either scleroderma (systemic sclerosis [SSc]) or mixed connective tissue disease (MCTD). If a subject had not been diagnosed as having PAH, then a new Doppler echocardiogram was obtained to measure cardiac parameters, including estimated right ventricular systolic pressure (ERVSP), and a full review of medical records was done.ResultsOf 909 screened patients, 791 were evaluable and completed the study; 669 had not previously been studied for PAH. Of these 669 patients, 89 (13.3%) were found by Doppler echocardiography to have an ERVSP of ≥40 mm Hg. Of these 89 patients, 82 (92.1%) had SSc and 7 (7.9%) had MCTD. The total prevalence of PAH in the survey was 26.7% (211 of 791 patients, including 122 with known PAH and 89 newly diagnosed as having PAH). Doppler echocardiographic data showed 20 of 89 patients (22.5%) with ERVSP of ≥50 mm Hg, 20 of 89 patients (22.5%) with increased RV dimension, and 25 of 89 patients (28.1%) with right atrial enlargement. Patients with ERVSP ≥40 mm Hg had decreased exercise tolerance compared with those with ERVSP <40 mm Hg (27% compared with 9.5%, respectively, were severely symptomatic).ConclusionA significant number of patients with SSc or MCTD (13.3%) followed up in a community rheumatology practice setting have undiagnosed elevated ERVSP consistent with PAH.
Risk and case characteristics of tuberculosis in rheumatoid arthritis associated with tumor necrosis factor antagonists in Sweden
Authors: Askling Johan , Fored C. Michael , Brandt Lena , Baecklund Eva , Bertilsson Lennart , Cöster Lars , Geborek Pierre , Jacobsson Lennart T. , Lindblad Staffan , Lysholm Jörgen , Rantapää‐Dahlqvist Solbritt , Saxne Tore , Romanus Victoria , Klareskog Lars , Feltelius Nils 
Published: June 2005

AbstractObjectiveBecause treatment with tumor necrosis factor (TNF) antagonists may increase the risk of tuberculosis (TB), and because knowledge of the risk of TB in rheumatoid arthritis (RA) not treated with biologics is scarce and of uncertain generalizability to low‐risk populations, this study sought to determine the risk of TB among Swedish patients with RA.MethodsUsing data from Swedish nationwide and population‐based registers and data from an ongoing monitoring program of TNF antagonists, the relative risks of TB in patients with RA (versus the general population) and of TB associated with TNF antagonists (versus RA patients not treated with biologics) were determined by comparing the incidence of hospitalization for TB in 3 RA cohorts and 2 general population cohorts from 1999 to 2001. We also reviewed the characteristics of all reported cases of TB in RA patients treated with TNF antagonists in Sweden and calculated the incidence of TB per type of TNF antagonist between 1999 and 2004.ResultsDuring 1999–2001, RA patients who were not treated with TNF antagonists were at increased risk of TB versus the general population (relative risk 2.0, 95% confidence interval [95% CI] 1.2–3.4). RA patients treated with TNF antagonists had a 4‐fold increased risk of TB (relative risk 4.0, 95% CI 1.3–12) versus RA patients not treated with TNF antagonists. The reported TB cases during 1999–2004 in RA patients exposed to TNF antagonists (9 infliximab, 4 etanercept, 2 both) were predominantly pulmonary. TB occurred up to 3 years following the start of treatment.ConclusionIrrespective of whether TNF antagonists are administered, Swedish patients with RA are at increased risk of TB. During 1999–2001, TNF antagonists were associated with an increased risk of TB, up to 4‐fold in magnitude. This increased risk may persist over time during treatment and is related to both infliximab and etanercept.
Association of cartilage defects with loss of knee cartilage in healthy, middle‐age adults: A prospective study
Authors: Cicuttini Flavia , Ding Changhai , Wluka Anita , Davis Susan , Ebeling Peter R. , Jones Graeme 
Published: June 2005

AbstractObjectiveThe significance of asymptomatic knee cartilage defects in healthy individuals is not known. The aim of this study was to examine the association between cartilage defects in the knee and cartilage volume both cross‐sectionally and longitudinally in healthy, middle‐age adults.MethodsEighty‐six healthy men and women (mean ± SD age 53.8 ± 8.8 years) underwent T1‐weighted fat‐suppressed magnetic resonance imaging of their dominant knees at baseline and at the 2‐year followup visit. Knee cartilage volume was measured. Cartilage defects were scored according to a grading system (0–4) and as present (a defect score of ≥2) or absent in the medial and lateral tibiofemoral compartments.ResultsCartilage defects in the medial and lateral tibiofemoral compartments were very common (in 61% and 43% of subjects, respectively). Those with cartilage defects had a 25% reduction in medial tibial cartilage volume, a 15% reduction in lateral tibial cartilage volume, and a 19% reduction in total femoral cartilage volume relative to those with no cartilage defects in cross‐sectional analyses (all P < 0.05). In the medial tibiofemoral compartment, the annual loss of tibial cartilage in those with cartilage defects was 2.5% (95% confidence interval [95% CI] 2.2%, 3.1%) compared with an annual loss of tibial cartilage of 1.3% (95% CI 0.5%, 2.0%) in those with no defects (P = 0.028), independent of other known risk factors for osteoarthritis (OA).ConclusionThese data suggest that the presence of asymptomatic, non–full‐thickness medial tibiofemoral cartilage defects identifies healthy individuals most likely to lose knee cartilage in the absence of radiographic knee OA. Thus, interventions aimed at reducing or reversing cartilage defects may reduce the risk of subsequent knee OA.
Retroviral gene transfer of an antisense construct against membrane type 1 matrix metalloproteinase reduces the invasiveness of rheumatoid arthritis synovial fibroblasts
Authors: Rutkauskaite Edita , Volkmer Dagmar , Shigeyama Yukio , Schedel Jörg , Pap Geza , Müller‐Ladner Ulf , Meinecke Ingmar , Alexander Dorothea , Gay Renate E. , Drynda Susanne , Neumann Wolfram , Michel Beat A. , Aicher Wilhelm K. , Gay Steffen , Pap Thomas 
Published: June 2005

AbstractObjectiveMembrane type 1 matrix metalloproteinase (MT1‐MMP) is expressed prominently in rheumatoid arthritis synovial fibroblasts (RASFs), but the specific contribution of MT1‐MMP to fibroblast‐mediated destruction of articular cartilage is incompletely understood. This study used gene transfer of an antisense expression construct to assess the effects of MT1‐MMP inhibition on the invasiveness of RASFs.MethodsRetroviral gene transfer of a pLXIN vector–based antisense RNA expression construct (MT1‐MMPαS) to MT1‐MMP was used to stably transduce RASFs. Levels of MT1‐MMP RNA and protein were determined by quantitative polymerase chain reaction, Western blotting, and immunocytochemistry in MT1‐MMPαS–transduced RASFs as well as in control cells, with monitoring for 60 days. The effects of MT1‐MMPαS on the invasiveness of RASFs were analyzed in the SCID mouse coimplantation model of RA.ResultsMT1‐MMPαS–transduced RASFs produced high levels of antisense RNA that exceeded endogenous levels of MT1‐MMP messenger RNA by 15‐fold and resulted in a down‐regulation of MT1‐MMP at the protein level. Inhibition of MT1‐MMP production was maintained for 60 days and significantly reduced the invasiveness of RASFs in the SCID mouse model. Whereas prominent invasion into cartilage by nontransduced and mock‐transduced RASFs was observed (mean invasion scores 3.0 and 3.1, respectively), MT1‐MMPαS–transduced cells showed only moderate invasiveness (mean invasion score 1.8; P < 0.05).ConclusionThe data demonstrate that an antisense RNA expression construct against MT1‐MMP can be generated and expressed in RASFs for at least 60 days. Inhibition of MT1‐MMP significantly reduces the cartilage degradation by RASFs.
Infliximab, but not etanercept, induces IgM anti–double‐stranded DNA autoantibodies as main antinuclear reactivity: Biologic and clinical implications in autoimmune arthritis
Authors: de Rycke Leen , Baeten Dominique , Kruithof Elli , Van den Bosch Filip , Veys Eric M. , de Keyser Filip 
Published: June 2005

AbstractObjectiveTo analyze the clinical and biologic correlates of autoantibody induction during longer‐term tumor necrosis factor α (TNFα) blockade with either the monoclonal antibody infliximab or the soluble receptor etanercept.MethodsThirty‐four patients with spondylarthropathy (SpA) and 59 patients with rheumatoid arthritis (RA) were treated with infliximab for 2 years. Additionally, 20 patients with SpA were treated with etanercept for 1 year. Sera were blindly analyzed for antinuclear antibodies (ANAs), anti–double‐stranded DNA (anti‐dsDNA) antibodies, anti–extractable nuclear antigen (anti‐ENA) antibodies, and antihistone, antinucleosome, and anticardiolipin antibodies (aCL). The anti‐dsDNA antibodies were isotyped.ResultsHigh numbers of infliximab‐treated patients with SpA or RA had newly induced ANAs (61.8% and 40.7%, respectively) and anti‐dsDNA antibodies (70.6% and 49.2%, respectively) after 1 year, but no further increase between year 1 and year 2 was observed. In contrast, induction of ANAs and anti‐dsDNA antibodies was observed only occasionally in the etanercept‐treated patients with SpA (10% of patients each). Isotyping revealed almost exclusively IgM or IgM/IgA anti‐dsDNA antibodies, which disappeared upon interruption of treatment. Neither infliximab nor etanercept induced other lupus‐related reactivities such as anti‐ENA antibodies, antihistone antibodies, or antinucleosome antibodies, and no clinically relevant lupus‐like symptoms were observed. Similarly, infliximab but not etanercept selectively increased IgM but not IgG aCL titers.ConclusionThe prominent ANA and anti‐dsDNA autoantibody response is not a pure class effect of TNFα blockers, is largely restricted to short‐term IgM responses, and is not associated with other serologic or clinical signs of lupus. Similar findings with aCL suggest that modulation of humoral immunity may be a more general feature of infliximab treatment.
Distribution of synaptic zinc in the macaque monkey amygdala
Authors: Ichinohe Noritaka , Rockland Kathleen S. 
Published: June 2005

AbstractWe have mapped the macaque amygdala for the distribution of synaptic zinc (Zn), a co‐factor of glutamate implicated in plasticity, as well as in several excitotoxic and other pathophysiological conditions. In brief, we found that the amygdala is Zn enriched in all nuclear groups (i.e., basolateral and cortical groups, as well as central and medial nuclei) but with marked differences in density. By comparing parallel tissue series histologically reacted for Zn and parvalbumin (PV), we further found that regions high in Zn are typically low in PV neuropil. In the basolateral group, there is a particularly distinct dorsoventral gradation such that Zn levels are most dense ventrally, i.e., in the paralaminar nucleus, the ventral division of the lateral nucleus, and the parvicellular divisions of both the basal nucleus and the accessory basal nucleus. PV levels are least dense in these same regions. For the central and medial nuclei, there is a slight mediolateral gradient, with Zn levels being higher medially. PV is low overall in these nuclei. Electron microscopic results confirmed that Zn is contained in synaptic boutons. These form asymmetrical, presumably excitatory, synapses, and the postsynaptic targets are mainly spines of projection neurons. The inhomogeneous distribution of Zn in the monkey amygdala may be related to different types or degrees of plasticity among the amygdaloid subnuclei. The complementary distribution with PV parallels that of several other substances and is interesting in the context of subnuclear vulnerability for human neuronal disease, such as seizure and Alzheimer's disease. J. Comp. Neurol. 489:135–147, 2005. © 2005 Wiley‐Liss, Inc.