bluuebunny/crossref_metadata_2025_split huggingface dataset:
Some recombinant human cytokines stimulate glycosaminoglycan synthesis in human synovial fibroblast cultures and inhibit it in human articular cartilage cultures
Authors: Yaron Ilana , Meyer Frank A. , Dayer Jean‐Michel , Bleiberg Ilan , Yaron Michael 
Published: February 2007

AbstractRecombinant human cytokines were compared for their effects on glycosaminoglycan (GAG) synthesis in human synovial fibroblast cultures and human articular cartilage explant cultures. In fibroblast cultures, recombinant human interleukin‐1α (rHuIL‐1α), rHuIL‐1β, and recombinant human tumor necrosis factor α (rHuTNFα) stimulated hyaluronic acid (HA) production and, to a lesser extent, sulfated GAG production, while recombinant human γ‐interferon did not have a significant effect. Half‐maximal stimulation of HA by rHuIL‐1β was 0.14 pM, while stimulation for rHuIL‐1α and rHuTNFα was 1.6 pM and 32 pM, respectively. Indomethacin (10 μg/ml) had no influence on HA stimulation by cytokines, while hydrocortisone (2–10 μg/ml) caused a significant reduction. In articular cartilage cultures, the cytokines inhibited production of sulfated GAGs. The activity of rHuIL‐1β was greater than that of rHuIL‐1α (half‐maximal inhibition at 0.71 pM and 4.7 pM, respectively) and both were considerably more active than rHuTNFα; γ‐interferon again had no significant effect. Neither indomethacin nor hydrocortisone influenced cytokine‐induced inhibition by either rHuIL‐1 preparation. These studies indicate that cytokines released during an inflammatory process may affect GAG synthesis in human joint tissues and may have opposite effects on GAG synthesis in different types of connective tissues.
Reversal of neutropenia with methotrexate treatment in patients with felty's syndrome. Correlation of Response with Neutrophil‐Reactive IgG
Authors: Fiechtner Justus J. , Miller Donald R. , Starkebaum Gordon 
Published: February 2007

AbstractWe evaluated the clinical and hematologic response to methotrexate (MTX) in 4 women with Felty's syndrome (FS) who had had neutropenia for 1–3 years. Since immune complexes or antineutrophil antibodies are implicated in the pathogenesis of the neutropenia of FS, we also measured both direct and indirect levels of neutrophil‐reactive IgG. All 4 patients showed a prompt and dramatic increase in neutrophil counts within 1–2 months of starting MTX therapy. In 3 patients, the symptoms of arthritis also improved; in the fourth patient, arthritis worsened. Recurring infections ceased in 3 patients. Neutrophil‐reactive IgG levels, which were elevated in all patients prior to treatment, decreased toward normal while the patients were receiving MTX therapy. We conclude that MTX is effective in treating the neutropenia of FS, in part by lowering neutrophil‐reactive IgG.
Home central venous hyperalimentation in fifteen patients with severe scleroderma bowel disease
Authors: Ng Swee Cheng , Clements Philip J. , Paulus Harold E. , Berquist William E. , Furst Daniel E. 
Published: February 2007

AbstractFifteen patients with severe scleroderma bowel disease began receiving home central venous hyperalimentation (HCVH) between 1979 and 1987. The major reasons for instituting HCVH were intestinal pseudo‐obstruction, malabsorption, and malnutrition. Eleven patients had an improved quality of life. Serious complications encountered over these 15,700 catheter‐use days were 2 episodes of septicemia and 2 episodes of superior vena cava obstruction. Seven patients died, but none directly from their gastrointestinal disease or from the HCVH.
Is it mandatory to examine synovial fluids promptly after arthrocentesis?
Authors: Kerolus Ghaly , Clayburne Gilda , Schumacher H. Ralph 
Published: February 2007

AbstractFifty synovial fluid (SF) samples from patients with various types of arthritis were examined promptly after joint aspiration and after storage at room temperature (22°C) or at refrigerator temperature (4°C) for 1 hour, 2 hours, 3 hours, 6 hours, 1 day, and 3 days, then weekly for 3 weeks and monthly for 2 months. We found that the leukocyte count (white blood cell [WBC] count) decreased within a few hours. In 4 SF samples from patients with mild inflammation (initial range 3,150–6,200 WBC/mm3), the WBC count decreased into a “noninflammatory” range (<2,000/mm3) within 5–6 hours. In 3 of 5 SF samples that on the first day were found to be laden with crystals of calcium pyrophosphate dihydrate (CPPD), the crystals were much less abundant and were difficult to recognize by the next day. CPPD crystals dissolved completely in all SF samples by 3–8 weeks of the study. Monosodium urate crystals remained detectable throughout the 8 weeks of study, but they became smaller, less birefringent, and less numerous with time. Clumps of apatite‐like crystals persisted for several months. Most SF samples initially negative for apatite‐like crystals remained negative over time. New, artifactual crystals, including alizarin red S–positive clumps or star‐shaped arrays, plate‐like structures, positively birefringent Maltese crosses, and hematoidin crystals, developed with time. Because of these observations, we urge prompt examination of SF specimens to avoid the problems of misdiagnosing borderline inflammatory fluids, missing CPPD crystals that dissolve with time, or over‐interpreting the findings because of the new, artifactual crystals.
Expression of an endogenous retroviral transcript is associated with murine lupus
Authors: Krieg Arthur M. , Khan Arifa S. , Steinberg Alfred D. 
Published: February 2007

AbstractWe have been investigating whether murine lupus is associated with endogenous type C retroviral expression. We used Northern blot analyses and oligonucleotide probes, which are able to distinguish the envelope genes of the xenotropic and mink cell focusforming (MCF) classes of type C retroviruses. Xenotropic expression in the spleen varied markedly among inbred mouse strains; although all strains expressed a 1.8‐kb transcript, only one‐half expressed one or more larger transcripts (8.4, 7.2, and/or 3.0 kb). Autoimmune disease did not correlate with expression of any of the xenotropic transcripts. Xenotropic and MCF transcripts were expressed independently among the mouse strains studied. Splenic RNA from all strains contained 7.2‐, 3.0‐, and 1.8‐kb MCF transcripts. Some strains also expressed 8.4‐kb MCF splenic RNA. There was a strong association between murine lupus and expression of 8.4‐kb MCF transcripts: 6 of 6 lupus‐prone strains, but only 2 of 11 nonautoimmune strains, had detectable 8.4‐kb MCF RNA. The xid and Yaa mutations had minimal effects on expression of 8.4‐kb MCF‐related transcripts, despite their major and opposite effects on disease. Moreover, New Zealand black mice highly expressed this RNA from day 1 of life, before disease development. The data suggest that expression of 8.4‐kb MCF endogenous retroviral transcripts is a primary feature of murine lupus and is not secondary to disease expression.
Genetic analysis of CR1 expression on erythrocytes of patients with systemic lupus erythematosus
Authors: Cohen Jacques H. M. , Caudwell Valérie , Levi‐Strauss Matthieu , Bourgeois Pierre , Kazatchkine Michel D. 
Published: February 2007

AbstractThe role of genetic factors in decreased expression of CR1 in patients with systemic lupus erythematosus (SLE) was investigated by assessing the frequency of genotypes determining the numbers of CR1 on erythrocytes obtained from 52 patients with SLE and from 84 normal individuals. The expression of CR1 was quantitated using flow cytometry. Genotypes were determined by analyzing the CR1 gene restriction fragment length polymorphism using the CR1.1 complementary DNA probe and the Hind III restriction enzyme. In normal subjects, the distribution of the HH, HL, and LL genotypes fit the Hardy‐Weinberg law. The frequency for the H allele did not differ between the 2 groups. No individual homozygous for the LL genotypes was found among the SLE patient population. Taken together, data from this and previous studies indicate an under‐representation of the LL homozygous genotype in patients with SLE. SLE patients expressed decreased numbers of CR1 per erythrocyte within each genotype compared with these numbers in normal subjects. The results suggest that defective expression of CR1 in SLE patients is acquired and that the presence of the L allele is not linked to a genetic susceptibility for SLE.
Antilymphocyte antibodies against CD4+2H4+ cell populations in patients with systemic lupus erythematosus
Authors: Tanaka Shinsuke , Matsuyama Takami , Steinberg Alfred D. , Schlossman Stuart F. , Morimoto Chikao 
Published: February 2007

AbstractIn previous studies, we demonstrated that patients with active systemic lupus erythematosus (SLE) had significantly decreased percentages of circulating CD4+2H4+ suppressor/inducer cells. The decrease in this T cell subset was most frequent and most marked in patients with active SLE and renal disease. In the present study, we attempted to determine whether SLE patients had plasma antilymphocyte antibodies preferentially reactive with the CD4+2H4+ subset. We found that many SLE patients did have these specifically reactive antibodies. Furthermore, the presence of anti‐lymphocyte antibodies reactive with CD4+2H4+ cells correlated with disease activity in these patients. Also, in vitro functional studies revealed that suppressor/inducer function was eliminated in the pokeweed mitogen–driven IgG synthesis system after the treatment of CD4 cells with patient plasma antilymphocyte antibodies and complement. These results suggest that antilymphocyte antibodies play a role in the elimination of CD4+2H4+ cells in patients with active SLE.
The expression and function of CD3 and CD5 in patients with primary sjögren's syndrome
Authors: Dauphinée Michael J. , Tovar Zair , Ballester Ana , Talal Norman 
Published: February 2007

AbstractWe studied the expression and function of 2 cell surface markers that induce T cell activation, CD3 and CD5, in 19 patients with primary Sjögren's syndrome (SS). The expression of CD3+ lymphocytes was normal, but CD3 function was moderately reduced, as measured by anti‐CD5–induced T cell proliferation. Anti‐CD3–induced stimulation of T cell help for Ig production and non–major histocompatibility complex–restricted (natural) killing were normal. In contrast, there was reduced expression and function of the CD5 molecule on peripheral blood lymphocytes of the SS patients. The ratio of CD5+ to CD3+ lymphocytes was 0.45 in SS patients compared with 0.85 in normal subjects, indicating that the CD3+ cells are relatively CD5‐deficient in SS patients. Anti‐CD5 monoclonal antibody did not augment suboptimal anti‐CD3 stimulation of whole peripheral blood lymphocytes or of purified T lymphocytes from SS patients, which indicated impaired functioning of the CD5 molecule. A significant impairment in proliferation was found in response to phorbol myristate acetate and to ionomycin in combination, suggesting defective intracellular signaling. Findings from serial studies of individual patients suggested that normal or low expression of CD5 on T cells can be stable over periods as long as 2 years. However, in 2 patients who required systemic therapy, a correction of the CD5 lymphocyte abnormality occurred in association with clinical remission, which suggests the potential reversibility of this condition. Our findings suggest a possible defect in intracellular signaling in primary SS, related in part to the CD5 molecule, which may provide a molecular explanation for the T cell hyporesponsiveness that is characteristic of this disease.
Cross‐reactive epitope with Klebsiella pneumoniae nitrogenase in articular tissue of HLA–B27+ patients with ankylosing spondylitis
Authors: Husby Gunnar , Tsuchiya Naoyuki , Schwimmbeck Peter L. , Keat Andrew , Pahle Jon A. , Oldstone Michael B. A. , Williams Ralph C. 
Published: February 2007

AbstractSynovial tissues from patients with ankylosing spondylitis or reactive arthritis were examined by an immunoperoxidase technique, using antisera to synthetic peptides representing antigens shared between HLA–B27.1 and Klebsiella pneumoniae nitrogenase. With either antiserum, all HLA–B27+ patients with synovial inflammation showed strong immunoperoxidase staining in synovial lining cells, vascular endothelium, and infiltrating inflammatory cells. These findings indicate that antigens showing cross‐reactivity between HLA–B27.1 and Klebsiella nitrogenase epitopes are strongly expressed within inflamed synovial tissues of HLA–B27+ patients.
CHANGES IN THE VISCOSITY OF HYALURONIC ACID AFTER EXPOSURE TO A MYELOPEROXIDASE‐DERIVED OXIDANT
Authors: Baker Mark S. , Green Simon P. , Lowther Denis A. 
Published: February 2007

AbstractBoth purified hyaluronic acid (HA) and bovine synovial fluid react with OCl‐, the major oxidant produced by the myeloperoxidase (MPO)/H2O2/Cl‐ system, resulting in a decrease in their specific viscosity. This reaction is inhibited in the presence of excess methionine. H2O2 alone decreases the viscosity of HA, presumably by the Fenton reaction, in the absence (but not in the presence) of the iron chelator, diethyltriaminepentacetic acid (DETAPAC). In the presence of DETAPAC, incubation of HA with the complete MPO/H2O2/Cl‐ system lowered the viscosity of HA. Analysis of 3H‐HA exposed to OCl‐ by gel filtration chromatography indicated that cleavage of HA occurred only at higher OCl‐ concentrations. We suggest that the reduction in viscosity of HA by the MPO/H2O2/Cl‐ system may be due to a combination of oxidative cleavage and changes in the conformation of the molecule. We speculate that the changes in the molecular size of rheumatoid synovial fluid HA may be due to the action of the neutrophil MPO/H2O2/Cl‐ system.
Work disability among women with rheumatoid arthritis. The relative importance of disease, social, work, and family factors
Authors: Reisine Susan T. , Grady Kathleen E. , Goodenow Carol , Fifield Judith 
Published: February 2007

AbstractYelin and others have shown social work factors to be more important than disease factors in predicting work disability among arthritis patients; however, the effects of family factors on work role functioning have not been considered in previous explanatory models. In this study, we use Yelin's model to explain work disability among 122 women with rheumatoid arthritis and to incorporate family factors into the model. Using logistic regression, we found, as with previous studies, that work autonomy, social factors, and disease factors are important predictors of work disability. In the logistic regression model, self‐assessed health status seemed to be more important than work factors in predicting work status. Further, family factors significantly contributed to the explanatory model, in that having more home responsibilities was associated with lower risk of work disability.
Synovial fluid characteristics and the lupus erythematosus cell phenomenon in drug‐induced lupus. Findings in three patients and review of pertinent literature
Authors: Vivino Frederick B. , Ralph Schumacher H. 
Published: February 2007

AbstractThe characteristics of synovial fluid obtained from 3 patients with drug‐induced lupus erythematosus are described. Two patients had “inflammatory” counts of synovial leukocytes, in the range of 2,500–39,000/mm3, with mononuclear predominance in 1 patient and neutrophil predominance in the other. The third patient had “noninflammatory” fluid, with mononuclear predominance. Lupus erythematosus cells formed in vivo were observed in the synovial fluid of 2 of the patients. Biopsy of the synovium of 1 patient showed nonspecific chronic inflammatory changes. Our findings in these patients with drug‐induced lupus are indistinguishable from those previously described in patients with idiopathic lupus erythematosus.
DNA polymorphism of immunoglobulin kappa confers risk of rheumatoid arthritis
Authors: Moxley George 
Published: February 2007

AbstractTo examine the hypothesis that a hereditary factor linked to the immunoglobulin kappa constant segment (Cκ) contributes to risk of rheumatoid arthritis (RA), white persons with RA were examined for Sac I restriction site polymorphisms. RA patients were more likely to have the 5/5‐kb Cκ genotype than white control subjects (relative risk 2.8, P < 0.02). A subgroup of RA patients who were positive for serum rheumatoid factor had a relative risk of 2.4 (P < 0.05). The subgroup without serum rheumatoid factor had an even higher relative risk of 9.7 (P < 0.05). The results suggest that immunoglobulin kappa is an important component in the genetic predisposition toward RA.
Lack of association between serum keratan sulfate concentrations and cartilage changes of osteoarthritis after transection of the anterior cruciate ligament in the dog
Authors: Brandt Kenneth D. , Thonar Eugene J‐M. A. 
Published: February 2007

AbstractTo determine whether the serum keratan sulfate (KS) concentration reflected the status of degenerating articular cartilage in a commonly used model of osteoarthritis (OA), serum KS levels were measured in 9 dogs prior to transection of the anterior cruciate ligament, 4 weeks later, and when the dogs were killed 8–14 weeks after surgery, at which time mild OA was present. In all cases, the serum KS levels were within the normal range. Values were not related to the cartilage uronic acid concentration, the rate of net 35SO4 glycosaminoglycan synthesis, or the histopathologic changes of OA. Although the serum KS concentration was not helpful as an indicator of the current status of the articular cartilage abnormality in the OA knee, serial samples from 6 dogs showed an increase of at least 10% over the baseline KS level at both timepoints following surgery (P = 0.031 and 0.027). This presumably reflects changes in proteoglycan metabolism in the unstable knee, although the possibility of a systemic change in proteoglycan metabolism following cruicate ligament transection can not be excluded.
Expression and regulation of the hla–dr antigen on circulating monocytes isolated from patients with rheumatoid arthritis
Authors: Hassan Jaythoon , Feighery Conleth , Bresnihan Barry , Whelan Alex 
Published: February 2007

AbstractUsing a modified radioimmunoassay, surface labeling of HLA–DR antigens on monocytes revealed reduced densities in patients with active rheumatoid arthritis (RA) (P < 0.001) and in gold‐treated patients (P < 0.01) versus normal controls. Significant enhancement of DR antigen expression (P = 0.01), with values similar to those of normal monocytes, occurred in patient monocytes preincubated at 37°C overnight, but not in monocytes preincubated at 4°C. This suggested that a temperature‐dependent metabolic process is required to enhance antigen expression. The addition of cycloheximide totally inhibited the enhancement of DR antigen density. Incubation of monocytes with exogenous prostaglandin E2 (10−‐5M final concentration) caused a reduction of DR densities on control and on RA monocytes, although this decrease was more marked in the controls. Addition of indomethacin did not affect DR antigen levels on control monocytes, but greatly enhanced the expression of DR antigens on RA monocytes. When HLA–DR antigen levels were estimated in detergent‐solubilized membrane preparations, monocytes from patients with active RA demonstrated normal‐to‐increased densities compared with control monocytes. Thus, although RA monocytes possess a normal ability to synthesize DR molecules, surface expression of these molecules is inhibited; this inhibition may be mediated by prostaglandin 2 acting as a negative suppressive signal.
High‐Dose, pulse intravenous methylprednisolone enhances fcγ receptor–mediated mononuclear phagocyte function in systemic lupus erythematosus
Authors: Salmon Jane E. , Kapur Sandip , Meryhew Nancy L. , Runquist Olaf A. , Kimberly Robert P. 
Published: February 2007

AbstractThe benefit of high‐dose, pulse intravenous methylprednisolone (IVMP) for some patients with active lupus nephritis would appear paradoxical, since active nephritis is associated with profound abnormalities in Fcγ receptor function, and several studies have demonstrated that glucocorticoids decrease monocyte Fcγ receptor expression and phagocytic function. To resolve this paradox, we investigated the possibility that pulse IVMP might enhance monocyte Fcγ receptor function in patients with systemic lupus erythematosus (SLE). Circulating immune complex (CIC) levels, Fcγ receptor–mediated clearance, and Fcγ receptor–dependent monocyte function were analyzed in 23 SLE patients before and after pulse IVMP (1 gm daily for 3 days). A biphasic response in CIC levels, determined by a staphylococcal protein A binding assay, was observed. Initially, CIC levels increased within 2–4 hours after the first dose of pulse IVMP and then decreased by 50% within 24–48 hours after the completion of therapy. Fcγ receptor–mediated binding and phagocytosis of IgG‐sensitized erythrocytes (EA) by monocytes in vitro were significantly enhanced 24 hours after the final dose of pulse IVMP (pre‐IVMP versus post‐IVMP 43 ± 14% versus 53 ± 12% EA rosettes, P < 0.01; 3.00 ± 1.04 versus 3.99 ± 1.30 EA ingested/monocyte, P < 0.01). In contrast, there was no change in the phagocytosis of an Fcγ receptor–independent probe, neuraminidasetreated erythrocytes. This enhancement of monocyte Fcγ receptor function may reflect a synergism between glucocorticoids and a suitably primed mononuclear phagocyte in SLE. Glucocorticoid‐induced augmentation of Fcγ receptor function in the presence of γ‐interferon, which may be elevated in SLE, has been shown. The enhancement of monocyte Fcγ receptor function that we observed may contribute to the therapeutic efficacy of pulse IVMP in lupus nephritis.
Hydroxyapatite pseudopodagra. A syndrome of young women
Authors: Fam Adel G. , Rubenstein Joel 
Published: February 2007

AbstractSix women with acute calcific periarthritis of the first metatarsophalangeal joint (hydroxyapatite pseudopodagra) are described, and 10 previously reported cases (8 female patients and 2 male patients) are reviewed. The onset was characterized by acute pain, swelling, erythema, tenderness, and limitation of movement of the first metatarsophalangeal joint, symptoms indistinguishable from those of gouty podagra, which is associated with transient amorphous calcific deposits in the vicinity of the joint. Based on these results it appears that hydroxyapatite pseudopodagra is a disorder that predominantly affects premenopausal women.
Sex‐Linked differences in susceptibility of cynomolgus monkeys to type II collagen–induced arthritis. Evidence that epitope‐specific immune suppression is involved in the regulation of type II collagen autoantibody formation
Authors: Terato Kuniaki , Arai Haruyoshi , Shimozuru Yasunori , Fukuda Taneo , Tanaka Hiroshi , Watanabe Hideto , Nagai Yutaka , Fujimoto Koji , Okubo Fumio , Cho Fumiaki , Honjo Shigeo , Cremer Michael A. 
Published: February 2007

AbstractTo determine whether sex‐linked factors are important in the susceptibility and resistance of cynomolgus monkeys to type II collagen–induced arthritis, we immunized 5 males and 10 females with chick type II collagen (CII) and studied their clinical and immune responses. All 10 females developed overt arthritis and produced antibodies to CII and cross‐reactive antibodies to monkey type II collagen (MkII). In contrast, only 1 male monkey developed arthritis, which was transient and mild in severity. Examination of antisera obtained from the male monkeys disclosed high titers of antibody to CII, but little antibody to MkII. The cyanogen bromide peptide recognition patterns varied markedly from animal to animal, implying that monkeys are capable of recognizing multiple arthritogenic determinants on CII.