bluuebunny/crossref_metadata_2025_split huggingface dataset:
An experimental model for hydrogen peroxide–induced tissue damage. Effects of a single inflammatory mediator on (peri)articular tissues
Authors: Schalkwijk Joost , van den Berg Wim B. , van de Putte Levinus B. A. , Joosten Leo A. B. 
Published: February 2007

AbstractHydrogen peroxide is receiving increasing attention as a mediator of tissue damage during inflammation. To evaluate its destructive potential in vivo, we devised a model in which hydrogen peroxide is, initially, the sole mediator of tissue damage. Glucose oxidase, which was made cationic to obtain good retention in tissue, was injected intraarticularly in mouse knee joints. This enzyme produces hydrogen peroxide, using endogenous glucose as a substrate. The local production of hydrogen peroxide induced drastic vascular damage, as measured by 99mTc uptake and leakage of 125I‐albumin. The chondrocyte proteoglycan synthesis was severely inhibited, as measured by 35SO4 incorporation. Histologic examination showed impressive inflammatory and degenerative changes, including periarticular infiltration, chondrocyte death, subchondral erosions, and muscle necrosis. Intraarticular administration of catalase could inhibit these vascular effects and cartilage damage. Systemic administration of ebselen, a synthetic glutathione peroxidase‐like compound, provided partial protection. Indomethacin and piroxicam were not effective in the acute phase. We think this model is useful both for testing drugs that are purported to act as scavengers of hydrogen peroxide and for studying chronic destructive processes.
Evaluation of amitriptyline in primary fibrositis. A double‐blind, placebo‐controlled study
Authors: Carette Simon , McCain Glenn A. , Bell David A. , Fam Adel G. 
Published: February 2007

AbstractSeventy patients with primary fibrositis satisfying Smythe's criteria were studied in a 9‐week double‐blind trial comparing 50 mg amitriptyline with placebo. Fifty‐nine patients completed the trial: 27 were treated with amitriptyline, and 32 took a placebo. The patients who received amitriptyline improved significantly in their morning stiffness and pain analog scores at 5 and 9 weeks, compared with baseline scores, whereas no changes were noted in these parameters in the placebo group. Fibrositic point tenderness did not improve significantly in either of the treatment groups. When compared with the placebo group, the amitriptyline group improved significantly with respect to sleep pattern and patient and physician global assessments. Our data indicate that amitriptyline has some therapeutic benefit in patients with primary fibrositis.
The effect of sodium selenite on chondrocytes in monolayer culture
Authors: Wei Xiqin , Wright George C. , Sokoloff Leon 
Published: February 2007

AbstractThe effect of sodium selenite on DNA and sulfated proteoglycan synthesis by cultured rabbit articular and growth plate chondrocytes was studied as an in vitro model for Kashin‐Beck disease. The selenium content of a defined medium (DMEM, fibroblast growth factor, insulin, and dexamethasone) was below the limit of detection by isotope dilution mass spectrometry. The chondrocytes were viable in the Se‐free basal medium. Selenite over a range of 5 × 10−9M to 5 × 10−7M had no stimulatory effect on DNA or sulfated proteoglycan synthesis by either type of chondrocyte or skin fibro‐blasts. Proliferation of bovine endothelial cells was enhanced by 5 × 10−7M Se. At Se concentrations of ≧ 10−6M, there was progressive inhibition of cell growth and radiosulfate incorporation of the connective tissue cells; bovine endothelial cells were more resistant. Twice equimolar concentrations of vitamins C and E exerted no protective effect against the cytotoxicity of higher concentrations of Se. Se supplementation also failed to stimulate growth of human infant chondrocytes. The model enabled simulation of conditions of hyposelenosis below those encountered in nature. The data provide no evidence that chondrocytes have idiosyncratic requirements for Se, and do not support the hypothesis that Se deficiency is a major etiologic factor in Kashin‐Beck disease.
Complement‐activating abilities of defined antinuclear antibodies
Authors: Kanayama Yoshiharu , Peebles Carol , Tan Eng M. , Curd John G. 
Published: February 2007

AbstractA complement‐fixing immunofluorescence assay on HEp‐2 cells was used to assess the ability of various antinuclear antibodies (ANA) to activate complement. Sera which contained only specific antibodies to nuclear RNP, SS‐B/La, centromere, Sm antigen, double‐stranded DNA, and/or nuclear histone were selected. Relative abilities of various ANA to activate complement were determined from the ratio of titers of C3, C4, or properdin‐fixing ANA to the IgG ANA titers. Nuclear RNP‐anti‐RNP complexes activated and deposited significantly more complement C3 than other ANA (P < 0.02). Antibodies to SS‐B/La, centromere, and Sm activated more complement than anti‐DNA or antihistone (P < 0.02). Antihistone antibodies activated the least complement. These studies demonstrate that different ANA have significantly different orders of complement‐activating capabilities when bound to their respective nuclear antigens.
Increased proto‐oncogene expression in peripheral blood lymphocytes from patients with systemic lupus erythematosus and other autoimmune diseases
Authors: Boumpas D. T. , Tsokos G. C. , Mann D. L. , Eleftheriades E. G. , Harris C. C. , Mark G. E. 
Published: February 2007

AbstractUsing RNA hybridization techniques, we examined the expression of proto‐oncogenes associated with lymphocyte activation in vitro in patients with systemic lupus erythematosus and other autoimmune diseases. T and B lymphocytes from these patients were found to have significantly increased expression of c‐myc, c‐myb, and c‐raf RNA when compared with those of normal individuals. Among the mononuclear cell subpopulations, B lymphocytes expressed higher levels of RNA for these proto‐oncogenes compared with the T lymphocytes. Since prompt expression of these and other proto‐oncogenes occurs in fibroblasts and lymphocytes following mitogenic stimulation, we propose that the present findings reflect the pathologically activated state of various lymphocytic subpopulations which is observed in systemic lupus erythematosus and in other autoimmune diseases. Endogenous and exogenous factors which lead to the expression of autoimmunity might share the induction of proto‐oncogene expression as a common pathogenetic step.
Reproducibility of synovial fluid analyses. A study among four laboratories
Authors: Schumacher H. Ralph , Sieck Marie S. , Rothfuss Susan , Clayburne Gilda M. , Baumgarten Dorothy F. , Mochan Bonnie S. , Kant Jeffrey A. 
Published: February 2007

AbstractAliquots from 30 synovial fluids were submitted to 4 laboratories for comparison of leukocyte counts and differential cell counts, and to 3 laboratories for a search for and identification of crystals. Leukocyte counts showed only fair correlation (coefficients of 0.76–0.80) with the reference laboratory. In synovial fluid from 4 patients, there was sufficient difference in leukocyte counts to cause the fluids to be erroneously classified as either “inflammatory” or “noninflammatory.” In 12 of 24 fluid specimens examined, percentages of neutrophils fell outside the 95% confidence limits of the value determined by the reference laboratory. In 7 of the 11 patients with crystals reported, discrepancies were found between the reports from 1 or more laboratories. More attention to quality control of synovial fluid analyses is important.
Comparison of pain properties in fibromyalgia patients and rheumatoid arthritis patients
Authors: Leavitt Frank , Katz Robert S. , Golden Harvey E. , Glickman Paul B. , Layfer Lawrence F. 
Published: February 2007

AbstractPain properties of 50 fibromyalgia patients were examined and compared with pain properties of 50 rheumatoid arthritis patients. In both fibromyalgia and rheumatoid arthritis, pain was bilateral, involved multiple sites, and was of equal intensity (60.8 versus 58.7, respectively, on a scale of 100). Fibromyalgia pain, however, was less localized to the joints and suggested greater spatial diffusion. It involved more kinds of pain experiences (radiating, steady, spreading, spasms, gnawing, unlocalized, pricking, crushing, shooting, pressing, splitting, cramping, nagging, and pins and needles), and was dispersed over larger areas of the body. The anatomic sites best for discrimination between patients with fibromyalgia and patients with rheumatoid arthritis were the lower back, thigh, abdomen, head, and hips for fibromyalgia, and wrist, foot, and fingers for rheumatoid arthritis. The traditional clinical description of aching and stiffness does not appear to accurately describe the complexity of the fibromyalgia pain syndrome.
Arthropathy associated with factor XIII deficiency
Authors: Thakker Suman , McGehee William , Quismorio Francisco P. 
Published: February 2007

AbstractA 47‐year‐old man with congenital factor XIII deficiency developed recurrent hemarthrosis of the right ankle. He had radiologic evidence of permanent joint damage. A review of the literature revealed that hemarthrosis is not a rare manifestation of factor XIII deficiency; however, destructive changes in the joints are relatively uncommon in this disorder, in contrast with those changes seen in patients with classic hemophilia and arthropathy. The bleeding manifestations of factor XIII deficiency are readily correctable by plasma or cryoprecipitate infusions; this may account for the preservation of joint function and structure.
The safety and efficacy of the use of methotrexate in long‐term therapy for rheumatoid arthritis
Authors: Kremer Joel M. , Lee Joong Kil 
Published: February 2007

AbstractTwenty‐nine patients participated in a prospective study of the safety and efficacy of oral methotrexate in the treatment of refractory rheumatoid arthritis. Patients received a mean dosage of 12.4 mg weekly over a mean duration of 29.1 months. All patients had liver biopsies at baseline, 2 years, and annually thereafter. Patients improved significantly by all clinical measures of efficacy after 1 month; maximum improvement tended to occur after approximately 6 months of therapy. Radiographs showed improvement of erosive disease in 7 of 11 patients measured. There was a significant reduction in mean prednisone dosage. Four patients required an increase in the dosage of methotrexate after prolonged therapy, because of declining clinical response. Toxicity was noted at some time in 26 of 29 patients (90%), but reactions universally became mild and tolerable after adjustment of the dosage. No significant hepatotoxicity was found in 60 sequential liver biopsies, although elevated transaminase levels were noted at some time in 20 of 29 patients (70%).
Methotrexate metabolism analysis in blood and liver of rheumatoid arthritis patients: Association with hepatic folate deficiency and formation of polyglutamates
Authors: Kremer Joel M. , Galivan John , Streckfuss Anita , Kamen Barton 
Published: February 2007

AbstractSerum and red blood cell methotrexate (MTX) levels, as well as hepatic levels of MTX and folate, were analyzed in 24 patients who had received long‐term oral MTX weekly for the treatment of rheumatoid arthritis. The serum MTX level peaked rapidly and was insignificant after 24 hours. The red blood cell MTX level was not related to the interval from the last MTX dose. In hepatic tissue obtained by liver biopsy, MTX was found in a predominantly polyglutamated form with depleted hepatic folate stores when compared with baseline specimens. A brief period of therapy with oral folinic acid repleted hepatic folate. It is possible that MTX hepatotoxicity is related to reduced hepatic folate levels and formation of MTX polyglutamates.
Altered distribution of debrisoquine oxidation phenotypes in patients with systemic lupus erythematosus
Authors: Baer Alan N. , McAllister C. B. , Wilkinson Grant R. , Woosley Raymond L. , Pincus Theodore 
Published: February 2007

AbstractOxidative metabolism in patients with systemic lupus erythematosus (SLE) was studied using the antihypertensive drug, debrisoquine. The metabolism of this drug to its principal metabolite, 4‐hydroxy‐debrisoquine, is catalyzed by a discrete isozyme of cytochrome P‐450. The extent of this reaction exhibits genetic polymorphism, with 2 phenotypes, “poor metabolizers” and “extensive metabolizers,” discernible in the normal population. We observed the poor metabolizer debrisoquine phenotype in 9 of 42 patients with idiopathic SLE (21%), in contrast with 12 of 147 healthy volunteers (8%), which is a significant difference in frequency (P < 0.04). These data provide further evidence for altered oxidative metabolism in SLE and support the concept that genetic differences in oxidative metabolism of endogenous compounds, such as sex steroid hormones, or of xenobiotics might influence susceptibility to SLE.
The impact of childhood rheumatic diseases on the family
Authors: McCormick Marie C. , Stemmler Margaret M. , Athreya Balu H. 
Published: February 2007

AbstractMuch of the burden of providing health care and other services for children with rheumatic diseases falls on the parents, but little is known about the impact of these conditions on the family. A survey of the parents of 138 children revealed that the most important predictors of high family impact were the number of the child's activities of daily living that were limited by illness, the educational attainment of the mother, the child's sex, the mother's perception of the child's health, and the volume of medical care use. Our results provide guidelines for identifying families who are most vulnerable to the stress of having a child with a rheumatic disease.
The face scale: A brief, nonverbal method for assessing patient mood
Authors: Lorish Christopher D. , Maisiak Richard 
Published: February 2007

AbstractValidity and reliability studies were conducted on the Face Scale, a very brief, pictorial scale of mood which uses a sequence of 20 faces and does not require reading literacy. Correlational and experimental evidence of the Face Scale's construct validity is presented, as well as its test‐retest reliability. Recommendations are made for its use as a screening tool and for additional validity studies.
Aseptic arthritis in a man with toxic shock syndrome
Authors: Gertner Elie , Inman Robert D. 
Published: February 2007

AbstractSynovitis in toxic shock syndrome (TSS) is an unusual finding. A 31‐year‐old man presented with pain and swelling in both knees and was found to have TSS, secondary to a septic bursitis caused by Staphylococcus aureus. Immune complexes were not detected in serum or synovial fluid, and the S aureus was not recovered from the inflamed joints. Antibodies against the TSS toxin‐1 were detected in serum and synovial fluid, but in lower levels than would be seen in a normal control serum. Complement studies implicated alternative pathway activation by a marked diminution in C3 levels compared with C4 levels, and by lower levels of factor B than would be found in other inflammatory joint diseases. The diagnostic dilemma posed by TSS in a man is discussed.
Clinical and serologic associations of the antiribosomal P protein antibody
Authors: Bonfa Eloisa , Elkon Keith B. 
Published: February 2007

AbstractAntibodies to the ribosomal P proteins (anti‐P) were detected, by Western blot analysis, in the sera of 20 of 114 patients with various autoimmune disorders. Eighty‐five percent of the patients with anti‐P had systemic lupus erythematosus (SLE). Of 93 randomly selected patients, the frequency of anti‐P was 7 of 59 SLE patients (12%) and 0 of 34 non‐SLE patients. Approximately one‐third of the patients with anti‐P antibodies were male; approximately half were black. In contrast to the findings of some previous studies which used isolated ribosomes as antigen, an increased frequency of renal disease was not observed. Although the overall frequency of central nervous system lupus was similar in SLE patients with and those without anti‐P, 6 of 6 patients with psychosis had anti‐P antibodies. Western blotting was the most sensitive and specific method for the detection of anti‐P antibodies; counter‐immunoelectrophoresis and cytoplasmic indirect immu‐nofluorescence were positive in only 47% and 65% of the anti‐P‐positive patients, respectively. Although 53% of the SLE patients with anti‐P had concomitant anti‐Ro antibodies, none had anti‐La (as detected by counterim‐munoelectrophoresis). Anti‐P antibodies, therefore, appear to be relatively specific serologic markers for SLE and may be detected in the serum even when antibodies to double‐stranded DNA are not found.
The use of immunoblotting and immunoprecipitation of (U) small nuclear ribonucleoproteins in the analysis of sera of patients with mixed connective tissue disease and systemic lupus erythematosus: A cross‐sectional, longitudinal study
Authors: Pettersson Ingvar , Wang Grace , Smith Elaine I. , Wigzell Hans , Hedfors Eva , Horn John , Sharp Gordon C. 
Published: February 2007

AbstractAntibodies to ribonucleoproteins (RNP) and to the Sm antigen in sera from patients with mixed connective tissue disease (MCTD) and systemic lupus erythematosus were studied using the techniques of immunoblotting and immunoprecipitation of U small nuclear RNPs. A cross‐sectional study indicated that antibodies reacting with a 68K protein were associated with anti‐RNP specificity in MCTD, but rarely occurred in systemic lupus erythematosus patients' sera. A longitudinal study demonstrated the persistence of MCTD blotting patterns over many years, and the subsequent disappearance of those specificities in sera from patients who were in prolonged remission.
Intraarticular triamcinolone hexacetonide in the management of chronic arthritis in children
Authors: Allen R. C. , Gross K. R. , Laxer R. M. , Malleson P. N. , Beauchamp R. D. , Petty R. E. 
Published: February 2007

AbstractThe use of intraarticular triamcinolone hexacetonide in the management of persistent arthritis of the knee joint that is unresponsive to nonsteroidal anti‐inflammatory drugs was prospectively evaluated in 40 children with chronic arthritis. Of 49 knees that were injected, 63.3% maintained complete resolution of effusion and other signs of inflammation at the 6‐month followup. This favorable outcome correlated with a young age, a short disease duration, and a higher dose of triamcinolone hexacetonide. At the 12‐month followup, 45% of the injected knees remained in remission.
Increased calcification of growth plate cartilage as a result of compressive force in vitro
Authors: Klein‐Nulend J. , Veldhuijzen J. P. , Burger E. H. 
Published: February 2007

AbstractThe influence of intermittent compressive force (ICF) and of continuous compressive force (CCF) on calcification of growth plate cartilage was investigated, using organ cultures of fetal mouse cartilaginous long bone rudiments. Sixteen‐day‐old metatarsal rudiments, still consisting of uncalcified cartilage, were isolated and cultured for 5 days. Initial calcification of hypertrophic cartilage occurred under control conditions (atmospheric pressure), and under the influence of ICF or CCF by intermittently or continuously compressing the gas phase above the culture medium. Calcification was monitored by means of 45Ca and 32P incorporation into calcium‐phosphate mineral and by morphometric methods. Both ICF and CCF increased cartilage calcification, but ICF was about twice as effective as CCF. Killed rudiments did not calcify during the culture period, nor did ICF or CCF increase the incorporation of label. The effects of ICF and CCF on calcification could not be mimicked by increasing the Po2 and Pco2 levels in the gas phase. The length of the central zone of calcified cartilage was significantly increased by ICF and CCF. We conclude that hypertrophic chondrocytes respond directly to ICF and CCF by an increased deposition of calcium‐phosphate mineral in the matrix. Discontinuous mechanical stimulation evokes a higher cellular response than does continuous stimulation.
In vitro cell proliferation and proteoglycan synthesis of rabbit meniscal fibrochondrocytes as a function of age and sex
Authors: Webber Richard J. , Zitaglio Teresa , Hough Aubrey J. 
Published: February 2007

AbstractMeniscal fibrochondrocytes from male and female New Zealand white rabbits, ages 6, 12, and 24 months, were grown in primary and secondary monolayer cell culture. Neither age nor sex affected the majority of their cell culture characteristics. Cells from young males (6 months old) synthesized greater amounts of sulfated proteoglycans than did those from young females, but by 2 years of age, this result was reversed. All age groups synthesized 2 classes of proteoglycans, based on hydrodynamic size, but the ratio of the 2 classes changed as a function of age. Overall, the meniscal fibrochondrocytes from both skeletally immature and skeletally mature rabbits of both sexes were capable of proliferation and matrix synthesis in vitro.
Systemic lupus erythematosus is not genetically linked to the beta chain of the T cell receptor
Authors: Fronek Zdenka , Lentz Daniel , Berliner Nancy , Duby Allan D. , Klein Karen A. , Seidman J. G. , Schur Peter H. 
Published: February 2007

AbstractThe genomic DNA polymorphism of the beta chain of the T cell receptor was examined. The restriction fragment length polymorphism distribution was similar in systemic lupus erythematosus patients, their relatives, and normal controls. Our observations suggest that these genes are not coinherited with genes responsible for systemic lupus erythematosus.
Cryoglobulinemia and hepatitis B markers in north African Jews with Raynaud's disease
Authors: Horowitz Jacob , Klein Mordechai , Sukenik Shaul 
Published: February 2007

AbstractMixed cryoglobulinemia was discovered in 11 of 20 patients with Raynaud's disease. Hepatitis B surface markers were found in 10 of these patients with cryoglobulinemia. All patients with cryoglobulinemia were female, and 10 were of northern African origin. This study indicates that, in a population with a high prevalence of hepatitis B infection, mixed cryoglobulinemia is an important etiologic factor in Raynaud's disease.
Complement activation during systemic lupus erythematosus: C3A and C5a anaphylatoxins circulate during exacerbations of disease
Authors: Belmont H. Michael , Hopkins Patricia , Edelson Henry S. , Kaplan Howard B. , Ludewig Rocio , Weissmann Gerald , Abramson Steven 
Published: February 2007

AbstractTo determine whether activated complement components appear in the circulation of patients with systemic lupus erythematosus (SLE), we measured C5a and C3a by radioimmunoassay. Mean C5a concentration in the plasma of acutely ill SLE patients was 46.0 ng/ml, compared with 17.1 ng/ml in normal controls (P < 0.01). Mean C3a concentration in patients with severe disease was 526 ng/ml, compared with 134 ng/ml in controls (P < 0.01). In patients with moderately active SLE, the mean C3a concentration, but not the mean C5a concentration, was also elevated. In addition, C3a was elevated in 15 of 21 patients with active SLE, whereas low levels of C3 or C4 were noted in only 7 of these 21 patients. We conclude that the measurement of complement‐derived anaphylatoxins may be useful in the management of patients with SLE. In addition, we suggest that these circulating mediators may contribute to the pathogenesis of vascular injury in patients with the disease.