bluuebunny/crossref_metadata_2025_split huggingface dataset:
Eosinophilia‐myalgia syndrome due to l‐tryptophan ingestion: report of four cases and review of the Maryland experience
Authors: Roubenoff Ronenn , Coté Timothy , Watson Rosemarie , Levin Michael L. , Hochberg Marc C. 
Published: February 2007

AbstractEosinophilia‐myalgia syndrome (EMS) is a recently described clinical entity that has been ascribed to taking over‐the‐counter preparations of the amino acid L‐tryptophan. We describe 4 patients with EMS, 3 of whom presented with eosinophilic fasciitis, and we review the epidemiology of EMS reported in Maryland and discuss the possible pathophysiology of the disease. EMS should be considered in the differential diagnosis of severe myalgia, eosinophilia, and eosinophilic fasciitis.
The effect of ethnicity on major histocompatibility complex complement allotypes and extended haplotypes in patients with systemic lupus erythematosus
Authors: Schur P. H. , Marcus‐Bagley D. , Awdeh Z. , Yunis E. J. , Alper C. A. 
Published: February 2007

AbstractPrevious studies of patients with systemic lupus erythematosus (SLE) have shown an increased frequency of certain major histocompatibility complex (MHC) markers, including HLA–DR2, DR3, and C4AQO (C4A‐null), in Caucasian patients. However, most of these studies were of randomly selected, unrelated patients; families were not included, and haplotypes were not determined. In order to define more accurately the possible role of MHC genes in lupus susceptibility, HLA–A, B, C, and DR, as well as BF, C2, C4A, C4B, and GLO, markers were determined in 62 Caucasian patients of known ethnic background, and in the members of their families. The distributions of extended haplotypes (fixed combinations of HLA–B, DR, and complotype alleles), fragments thereof, and individual alleles were determined in SLE patients and controls. The MHC distributions in all patients were compared with haplotypes in a normal Caucasian population. There were no statistically significant differences between the frequencies of any MHC marker, fragment, or extended haplotype in the patients compared with the controls. The patients were categorized into 2 groups of European ancestry (English/Irish; other Europeans), and each group was compared with a group of ethnically matched controls. There was a statistically significantly increased frequency of the alleles C4AQO and DR3 and the complotype SC01 in SLE patients of English/Irish descent as compared with ethnically matched controls. The increase in C4AQ0 and DR3 could be accounted for by the fact that they were part of the extended haplotype [HLA–B8;SC01;DR3] and/or its fragment (SC01;DR3). No increase in any MHC marker was observed in the other patients. Thus, our results suggest that SLE in patients of English/Irish ancestry is associated with an MHC extended haplotype and/or its DR‐containing fragment.
Human lupus‐type inclusions in umbilical cord blood mononuclear cells
Authors: Rich Steven A. , Gibbons William E. 
Published: February 2007

AbstractMononuclear cells purified from umbilical cord blood activated oligoadenylate synthetase and formed human lupus‐type inclusions (LI) when cultured with the purified recombinant human leukocyte interferon, IFLrA. LI frequencies increased from 0% to a low of 0.75% and a high of 6.25% in 4‐day cultures with IFLrA (100 units/ml). These interferon‐induced responses in the mononuclear cells of neonates indicate that LI are solely an intrinsic product of normal cells, and not an exogenous virus or some other environmental agent.
Pseudotumor of the craniocervical junction during long‐term hemodialysis
Authors: Rousselin BenoǐT , Helenon Olivier , Zingraff Johanna , Delons Simone , Drueke Tilman , Bardin Thomas , Moreau Jean‐FrançOis 
Published: February 2007

AbstractA systematic study of the upper cervical spine was performed using magnetic resonance imaging in 25 patients (15 men and 10 women) who had been undergoing hemodialysis for more than 10 years. Seven pseudotumors of the periodontoid soft tissue were disclosed, which were similar to the pannus recently described in rheumatoid arthritis. Bone cystic radiolucencies were observed in association with these pseudotumors in 5 patients. The radiolucencies were located in the atlas (1 in the lateral mass and 1 in the anterior branch) and in the axis (3 in the odontoid process and 1 in the vertebral body). No horizontal or vertical atlantoaxial subluxation was demonstrated. These features were observed only in patients who had amyloid arthropathy. They could be a frequent, yet thus far little‐recognized, feature of β2‐microglobulin amyloidosis.
The post‐occlusive hyperemic response in patients with systemic sclerosis
Authors: Wigley F. M. , Wise R. A. , Mikdashi J. , Schaefer S. , Spence R. J. 
Published: February 2007

AbstractWe investigated post‐ischemic hyperreactive cutaneous blood flow in patients with primary Raynaud's phenomenon and Raynaud's phenomenon secondary to systemic sclerosis (SSc). Reactive hyperemia was measured over a locally warmed area of skin, using a laser Doppler flowmeter, following 5 minutes of suprasystolic occlusion of blood flow. We found that patients with primary Raynaud's phenomenon had normal post‐ischemic blood flow compared with normal controls. In contrast, patients with SSc had reduced levels of baseline and peak blood flow compared with either the primary Raynaud's phenomenon patients or the normal subjects. Infusion of carbaprostacyclin, a potent prostacyclin analog vasodilator, did not increase blood flow in the SSc patients, nor did it restore the reactive hyperemic response. These findings are consistent with the hypothesis that patients with the nonvasoconstricted condition of SSc have fixed structural defects that limit cutaneous microvascular blood flow.
Type XI collagen‐degrading activity in human osteoarthritic cartilage
Authors: Yu Lucino P. , Smith Gerald N. , Brandt Kenneth D. , Capello William 
Published: February 2007

AbstractHomogenates of 6 samples of human osteoarthritic cartilage were shown to degrade exogenous type XI collagen. On sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, the cleavage products generated by each homogenate were similar, and they were identical to those obtained by cleavage of the substrate with purified gelatinase. Enzyme activity, which was inhibited by EDTA, was greater in extracts of fibrillated osteoarthritic cartilage than in extracts of grossly normal cartilage from the same joint or in extracts of cartilage from joints with osteonecrosis. Activation with APMA enhanced digestion, but breakdown was apparent in extracts of fibrillated osteoarthritic cartilage even without APMA. Enzymatic degradation of type XI collagen could play a significant role in the turnover of articular cartilage in health and disease states.
A subluxing arthropathy associated with the anti‐jo‐1 antibody in polymyositis/dermatomyositis
Authors: Oddis Chester V. , Medsger Thomas A. , Cooperstein Lawrence A. 
Published: February 2007

AbstractOf 180 patients with polymyositis/dermatomyositis (PM/DM) seen at the University of Pittsburgh and affiliated hospitals since 1975, 21 of 100 tested positive for the anti‐Jo‐1 antibody. Sixteen of the 21 patients were women and 18 were white. Fifteen had adult PM, 4 had myositis in overlap with scleroderma, and 2 had adult DM. Evidence of interstitial lung disease was found in 12 of 18 anti‐Jo‐1 positive patients (67%), but in only 15 of 79 anti‐Jo‐1 negative patients (19%) (P > 0.0002). The 21 anti‐Jo‐1 positive patients were divided into 3 separate groups based on the observed articular findings. Four patients had a deforming, predominantly nonerosive arthropathy with subluxations of the distal interphalangeal joints, especially the thumbs. Eight patients had a nondeforming arthropathy primarily affecting the small joints of the hands, wrists, shoulders, and knees. Those with deformities had a longer duration of arthritis compared with those with nondeforming arthropathy (mean 14.5 years versus 3.3 years). Nine anti‐Jo‐1 positive patients had no joint arthropathy. Three of 4 patients with deformities have required articular reconstructive surgery for subluxation, with 2 having associated subcutaneous calcinosis.
Human rheumatoid factor cross‐idiotypes
Authors: Barnes Joye Lynn , Goni Fernando , Heyermann Hubert , Frangione Blas , Agnello Vincent 
Published: February 2007

AbstractThe BLA cross‐idiotype (XId) is present on a unique subset of rheumatoid factors (RF) that cross‐react with DNA‐histone. In this study, prototype Bla monoclonal RF was shown from serologic investigations and N‐terminal amino acid sequence analysis to have distinct k chains related to the Vk III subgroup and VH4 heavy chains. The amino terminus of the heavy chain was cyclized, rendering the protein resistant to Edman degradation and providing a possible investigator bias to the published Ig sequence data to date. This appears to be the first definitive report of a serum IgM that expresses the VH4 gene. RF with DNA cross‐reactivity have been reported to be produced by human and mouse cloned cells that have the VH4 or homologous mouse Vh36–60 gene.
Rescue of interleukin‐1 activity by leucovorin following inhibition by methotrexate in a murine in vitro system
Authors: Segal Rafael , Yaron Michael , Tartakovsky Boris 
Published: February 2007

AbstractWe have recently shown that methotrexate (MTX) inhibits interleukin‐1 (IL‐1) activity in vitro. This effect may play an important role in the rapid antiinflammatory action of MTX in rheumatoid arthritis. In the present study, we showed that the inhibition of IL‐1 activity in vitro by MTX is dependent on folate pathways since, after the addition of leucovorin, the inhibitory effect of MTX was abolished. These findings may shed more light on the mechanism of action of MTX in rheumatoid arthritis. They also point to the fact that some IL‐1 activities may be dependent on intracellular folate pathways.
Suppression of type II collagen–induced arthritis by monoclonal antibodies
Authors: Kobayashi Seiichi , Terato Kuniaki , Harada Yoshitada , Moriya Hideshige , Taniguchi Masaru 
Published: February 2007

AbstractSome mouse monoclonal antibodies raised against chicken type II collagen suppressed or delayed the onset of chicken type II collagen–induced arthritis in DBA/1 mice. This was correlated with the suppression of anti–mouse type II collagen antibody responses following immunization with chicken type II collagen. The epitopes recognized by the suppressive antibodies were found to be present on cyanogen bromide (CB)—digested collagen peptides CB‐11 and CB‐12. This was also confirmed by the finding that administration of the CB‐11 or CB‐12 peptide suppressed the induction of arthritis.
Biologic effects of an interleukin‐1 receptor antagonist protein on interleukin‐1–stimulated cartilage erosion and chondrocyte responsiveness
Authors: Smith Robert J. , Chin Jia En , Sam Laurel M. , Justen James M. 
Published: February 2007

AbstractRecombinant human interleukin‐1α (IL‐1α) and recombinant human IL‐1β stimulate matrix proteoglycan degradation and inhibit glycosaminoglycan synthesis in bovine nasal cartilage explants. A 17‐kd human recombinant IL‐1 receptor antagonist protein (IRAP) caused a concentration‐dependent (0.2–200 ng/ml) suppression of the effects of IL‐1α and IL‐1β in cartilage organ cultures. IRAP inhibited the binding of radiolabeled IL‐1α to rabbit articular chondrocytes. Matrix metalloproteinase (collagenase, gelatinase, and stromelysin) and prostanoid production by IL‐1–activated rabbit articular chondrocytes was also suppressed by IRAP. These results could have potential significance in the development of a new antiarthritis therapy based on an IRAP.
Down‐regulation of adoptive adjuvant‐induced arthritis by suppressor factor(s)
Authors: Nanishi Fumio , Battisto Jack R. , Nanishi Fumio , Battisto Jack R. 
Published: February 2007

AbstractWe recently described a method for inducing immunologic tolerance to trinitrochlorobenzene (TNCB), a hapten that generates suppressor cells capable of down‐regulating the efferent phase of TNP‐specific contact hypersensitivity in rats. Peritoneal exudate cells (PEC) of such tolerized rats, upon being triggered by specific hapten, suppressed contact hypersensitivity to another hapten elicited at the same time. This implied that cells that mediate delayed‐type hypersensitivity of any specificity might be down‐regulated, provided that the suppressor cells are activated with specific antigen and that the unrelated delayed‐type hypersensitivity is elicited in parallel. To rigorously test this possibility, we examined the ability of TNP‐specific suppressor lymphoid cell factors to affect cells that mediate adoptively transferable adjuvant‐induced arthritis (AIA) in rats. To induce arthritis, spleen cells from Freund's complete adjuvant‐injected rats were stimulated with concanavalin A and administered to naive recipients. Prior to adoptive transfer, the cells were exposed for brief intervals to supernatants of lymphoid cells from control and hapten‐tolerized rats. Supernatants of PEC and lymph node cells from hapten‐tolerized rats were found to markedly reduce the effectiveness of cells that mediate AIA. The hapten‐tolerized cells required reexposure to hapten prior to preparation of the supernatants. Supernatants of spleen cells from hapten‐tolerized rats that had been hapten‐painted as well as hapten‐triggered and supernatants of lymph node cells and of PEC from only hapten‐painted or hapten‐triggered rats were ineffective in altering the AIA. Thus, factors from suppressor cells induced toward hapten‐coupled self‐antigens have been found to adversely affect the function of lymphoid cells that mediate a totally unrelated inflammatory response, namely, AIA. The clinical implications of these findings are discussed.
The effect of nifedipine on myocardial perfusion and metabolism in systemic sclerosis. A positron emission tomographic study
Authors: Duboc Denis , Kahan André , Maziere Bernard , Loc'H Christian , Crouzel Christian , Menkès Charles J. , Amor Bernard , Strauch Georges , Guérin François , Syrota André 
Published: February 2007

AbstractWe assessed the effect of nifedipine on myocardial perfusion and metabolism in 9 patients with systemic sclerosis, using positron emission tomography with a perfusion tracer (potassium‐38) and a metabolic tracer (18F‐fluorodeoxyglucose [18FDG]). Nifedipine, 20 mg 3 times daily for 1 week, induced a significant increase in 38K myocardial uptake, a significant decrease in 18FDG myocardial uptake, and a significant increase in the myocardial 38K:18FDG ratio. These results indicate that the increase in myocardial perfusion is associated with modifications in myocardial energy metabolism, which probably result from a beneficial anti‐ischemic effect of nifedipine in patients with systemic sclerosis.
Activation of CD16+ effector cells by rheumatoid factor complex. Role of natural killer cells in rheumatoid arthritis
Authors: Hendrich Christian , Kuipers Jens G. , Kolanus Waldemar , Schmidt Reinhold E. , Hammer Michael 
Published: February 2007

AbstractThe role of natural killer (NK) cells in rheumatoid arthritis (RA) remains unclear. A pathogenetic function of rheumatoid factors (RF) also has not been defined. In the present studies, natural killer (NK) cells were examined as a model for Feγ receptor type III‐positive (Feγ RIII+) cells, with regard to their interaction with RF. NK cell antigen CD16 (FcγRIII) and CD56 expression and functional NK and antibody‐dependent cell‐mediated cytotoxicity (ADCC) activity were compared in peripheral blood lymphocytes and autologous synovial fluid lymphocytes (SFL) of RA patients. Peripheral blood lymphocytes and SFL showed normal CD56 expression. In contrast, both the frequency and the density of CD16 antigen were decreased in SFL. Furthermore, diminished NK cytotoxicity and a significant decrease in ADCC were observed in SF NK cells. In subsequent in vitro studies with normal fresh NK cells, it was demonstrated that IgG‐containing RF complexes from RA patients induced a modulation of FCγRIII structure from the NK cell surface, a decrease in NK activity, and a complete loss of ADCC. When purified RF was incubated with NK‐enriched cell lines from RA patients, increased transcription and subsequent production of interferon‐γ and tumor necrosis factor α were observed. These data suggest a direct involvement of RF complexes in the pathogenetic process of chronic inflammation in RA.
Diversity of rheumatoid synovial tissue T cells by T cell receptor analysis. Oligoclonal expansion in interleukin‐2–responsive cells
Authors: Cooper Sheldon M. , Dier Douglas L. , Roessner Karen D. , Budd Ralph C. , Nicklas Janice A. 
Published: February 2007

AbstractThe synovitis of rheumatoid arthritis (RA) is characterized by infiltrates of CD4+ T lymphocytes. To determine the clonal diversity of these cells, we cloned T cells with interleukin‐2 (IL‐2), alone or with phytohemagglutinin (PHA), directly from actively inflamed synovial tissue obtained at synovectomy. A total of 205 clones from 4 specimens was analyzed for T cell receptor (TCR) gene rearrangements using Hind III and Eco RI digests with β chain and γ chain complementary DNA probes. A comparison of the TCR rearrangements enabled us to determine if the T cell clones arose from the same or different precursor cells. Most of the T cell clones (92%) had distinct TCR gene rearrangement patterns, indicating a unique clonal origin. However, a few clones (1 quadruplicate and 6 pairs) with identical TCR rearrangements were identified, and these clonal multiples were most commonly found in clones selected with IL‐2 alone. Mass cultures were propagated with IL‐2, alone or with PHA, and at each passage, cells were removed for TCR analysis. The later passages of the lines selected with IL‐2 had oligoclonal TCR rearrangements, whereas no oligoclonal rearrangements were found in the PHA + IL‐2‐selected cell lines. The TCR rearrangements in the later passages of the IL‐2 mass cultures were often identical to the TCR rearrangements that were found in the IL‐2‐derived clonal multiples. These findings indicate that while the majority of CD4+ T cells within the actively inflamed rheumatoid joint have diverse clonal origins, small numbers of clonal multiples and oligoclonal populations are present, and these cells may be enriched in an IL‐2‐responsive T cell subset.
Systemic sclerosis associated with cutaneous exposure to solvent: Case report and review of the literature
Authors: Brasington Richard D. , Thorpe‐Swenson Amy Jo 
Published: February 2007

AbstractSclerodermatous skin changes and systemic sclerosis have been reported to occur as a result of contact with several different organic solvents. We describe a 41‐year‐old man who developed systemic sclerosis after working for 15 years in a foundry, where he had extensive cutaneous contact with multiple organic solvents (trichloroethane, xylene, trimethylbenzene, and naphthalene). Cutaneous exposure to organic solvents may be a factor in the etiology of some cases of systemic sclerosis.
Platelet‐derived growth factor potentiates cellular responses of articular chondrocytes to interleukin‐1
Authors: Smith Robert J. , Justen James M. , Sam Laurel M. , Rohloff Norman A. , Ruppel Patricia L. , Brunden Marshall N. , Chin Jia En 
Published: February 2007

AbstractRecombinant human interleukin‐1α (IL‐1α) induced a time‐dependent (0–72 hours) and concentration‐dependent (0.01–10 ng/ml) production of metalloproteinases (collagenase, gelatinase, stromelysin) and prostaglandin E2 (PGE2) in rabbit articular chondrocytes (RAC). Exposure of RAC to recombinant human platelet‐derived growth factor homodimer BB (PDGF‐BB; 2–200 ng/ml) in the presence of stimulatory and substimulatory concentrations of IL‐1α resulted in a marked augmentation of metalloproteinase and PGE2 production. PDGF‐BB exerted no agonist effects on RAC responsiveness. PDGF‐BB up‐regulated the number of IL‐1 receptors per chondrocyte but had no effect on receptor affinity. Cycloheximide and actinomycin D caused a concentration‐dependent suppression of the PDGF‐BB–mediated potentiation of radiolabeled IL‐1α binding to RAC and cell responsiveness to IL‐1α. Similarly, IL‐1 increased the number of PDGF receptors on RAC without changing receptor affinity. These data are discussed within the context of cytokine–growth factor interactions as components of the pathogenesis of arthritic diseases.
PBC 95K, a 95‐kilodalton nuclear autoantigen in primary biliary cirrhosis
Authors: Evans Janine , Reuben Adrian , Craft Joe 
Published: February 2007

AbstractWe have identified a novel antinuclear antibody (ANA) in the sera of patients with primary biliary cirrhosis (PBC). Sera from 22 of 50 PBC patients stained the nuclei of HEp‐2 cells in a pattern of 5–20 discrete dots, on indirect immunofluorescence. Typically, the titers were higher than 1:1,280. This staining pattern was seen in only 4 of 1,240 ANA‐positive samples from patients with other connective tissue diseases, and in none of the ANA‐positive sera from 49 patients with other liver diseases. Sera which stained the nuclear dots bound a 95‐kd polypeptide in immunoblots of HeLa nuclei and in immunoprecipitates of 35S‐methionine–labeled HeLa extracts. Affinity‐purified antibodies from the 95‐kd protein reproduced the nuclear dot immunofluorescence staining pattern, demonstrating that this polypeptide is located in the nuclear dots. ANA of this type, therefore, occur in 44% of patients with PBC, and they appear to be specific for PBC. These antibodies bind a 95‐kd protein that is discrete and is scattered throughout the nucleus.
The pharmacokinetics of total and unbound concentrations of tenoxicam in synovial fluid and plasma
Authors: Day R. O. , Williams K. M. , Graham S. , Handel M. 
Published: February 2007

AbstractTenoxicam is a nonsteroidal antiinflammatory drug with an elimination half‐life of 60–80 hours; it is administered once daily. Tenoxicam concentrations were measured in plasma (10 samples) and synovial fluid (6 samples) over a 24‐hour dosage interval at steady state in 10 subjects with arthritis who had been taking the drug at a dosage of 20 mg/day for at least 2 weeks. Total tenoxicam concentrations in synovial fluid were always less than those in plasma, and there was little fluctuation in plasma or synovial concentrations over the dosage interval, although there was substantial inter‐subject variation in both concentrations. There was a significant relationship between the tenoxicam dosage when expressed as mg/kg of body weight and the average steady‐state total concentration of tenoxicam in plasma (r = 0.80, P = 0.006); this accounted for a substantial proportion of the intersubject variation. The mean ± SD steady‐state concentrations in synovial fluid and plasma were 3.9 ± 1.8 μg/ml and 9.2 ± 3.7 μg/ml, respectively, yielding a mean ± SD synovial fluid: plasma ratio of 0.43 ± 0.12. Synovial fluid:plasma ratios of total tenoxicam correlated with synovial fluid:plasma ratios of albumin (r = 0.71, P = 0.02). The synovial fluid:plasma ratio of unbound tenoxicam was 0.90 ± 0.3 (95% confidence interval 0.68–1.11), which was not significantly different from a value of 1 (t = −1.09, P = 0.31).