bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐distance running causes site‐dependent decrease of cartilage glycosaminoglycan content in the knee joints of beagle dogs
Authors: Arokoski Jari , Kiviranta Ilkka , Jurvelin Jukka , Tammi Markku , Helminen Heikki J. 
Published: February 2007

AbstractObjective. To study the effects of a long‐term (1‐year) program of running exercise (up to 40 km/day) on the thickness and glycosaminoglycan (GAG) content of articular cartilage in the knee and humeral head cartilage of young dogs.Methods. Samples for histologic analysis were obtained from 12 different locations of the joints. We conducted a detailed, area‐specific analysis, measuring the thickness of articular cartilage and analyzing the distribution of Safranin O stain that binds stoichiometrically to GAG as determined by quantitative microspectrophotometry.Results. Running exercise decreased the GAG content of the uncalcified articular cartilage in the weight‐bearing summits of the femoral condyles by 5–13% (P < 0.05), while at margins of these areas the GAG content was equivalent to control levels. In the lateral condyle of the femur, the reduction was most prominent in the superficial zone (up to 28% decrease; P < 0.05), and extended into the intermediate zone (11% decrease; P < 0.05). GAG content was also significantly reduced in the superficial zone at the lateral condyle of the tibia and the head of the humerus, by 35% (P < 0.01) and 15% (P < 0.05), respectively. Running did not alter GAG concentration in the patellofemoral region.Conclusion. The GAG depletion caused by 40‐km/day running exercise is restricted to prominent weight‐bearing areas of the joint and begins from the superficial cartilage without signs of degeneration. The different degree and type of joint loading can explain the site‐dependent cartilage response to long‐distance running. The loss of GAGs was possibly due to breakdown of proteoglycans, which could not be compensated for by neosynthesis of molecules. With time, this may affect the condition of articular cartilage, especially if the joint is exposed to loading for lengthy periods.
Myopathy with mitochondrial alterations in patients with primary biliary cirrhosis and antimitochondrial antibodies
Authors: Varga John , Heiman‐Patterson Terry , Muñoz Santiago , Love Lori A. 
Published: February 2007

AbstractObjective. To describe a syndrome of severe progressive myopathy, cardiomyopathy, and gastrointestinal dysmotility in 2 patients with asymptomatic primary biliary cirrhosis (PBC) and circulating anti‐mitochondrial autoantibodies, and to review pertinent literature concerning this syndrome.Methods. Clinical, electrophysiologic, serologic, and pathologic studies of the 2 affected patients were conducted.Results. Skeletal muscle involvement was manifested by progressive weakness of the proximal muscles, marked diaphragmatic dysfunction with consequent hypoventilation and respiratory failure, and moderately elevated levels of muscle‐associated enzymes. Serum from both patients contained antimitochondrial antibodies that reacted with components of the mitochondrial keto acid dehydrogenase enzyme complex. Results of electromyography were consistent with a myopathic process. The microscopic and ultrastructural changes in the skeletal muscles were distinct from those of typical myositis, and were notable for striking subsarcolemmal aggregation of abnormal mitochondria in the absence of significant inflammation.Conclusion. Severe skeletal muscle, cardiac, and gastrointestinal pathology with abnormalities of the muscle mitochondria develops in a subset of patients with mild PBC and antimitochondrial antibodies. The pathogenesis of this syndrome is unclear, but may be related to the presence of the antimitochondrial autoantibodies.
Regulation of human normal and osteoarthritic chondrocyte interleukin‐1 receptor by antirheumatic drugs
Authors: Pelletier Jean‐Pierre , Mccollum Robert , Dibattista John , Loose Leland D. , Cloutier Jean‐Marie , Martel‐Pelletier Johanne 
Published: February 2007

AbstractObjective. To determine the effect of antirheumatic drugs and corticosteroids on interleukin‐1 receptor (IL‐1R) levels in, and IL‐1–stimulated metalloprotease synthesis and expression by, normal and osteoarthritic (OA) human articular chondrocytes.Methods. IL‐1R affinity and density of human chondrocytes were determined using radioligand binding experiments. Collagenase and stromelysin synthesis activities were analyzed by 14C‐labeled type I collagen and Azocoll assays, respectively. Their messenger RNA (mRNA) levels were determined by Northern blot analysis. IL‐1α, IL‐1β, IL‐1 receptor antagonist, and β2‐microglobulin were measured using enzyme‐linked immunosorbent assays. Protein synthesis was determined by 3H‐leucine incorporation.Results. Antirheumatic drugs reduced the IL‐1R level in normal and OA chondrocytes in a dose‐dependent manner. In normal chondrocytes, tenidap reduced the IL‐1R level by 44% at 5 μg/ml to 88% at 100 μg/ml (50% inhibition constant [IC50] 10.1 μg/ml), indomethacin reduced IL‐1R by 6% at 1.5 μg/ml to 43% at 60 μg/ml, and naproxen reduced IL‐1R by 10% at 10 μg/ml to 41% at 300 μg/ml; the effects observed with indomethacin and naproxen occurred only when the drugs were used at levels above their therapeutic concentrations. In OA chondrocytes, the effect of indomethacin and naproxen on the IL‐1R level was greatly reduced, whereas tenidap still had a marked effect (IC50 22.5 μg/ml). Dexamethasone and hydrocortisone had no consistent effect on the IL‐1R level. At a therapeutic concentration (20 μg/ml), tenidap was found to reduce the IL‐1R level in a time‐dependent manner, with maximum inhibition (98%) by 48 hours. Tenidap was also found to markedly reduce collagenase and stromelysin synthesis and mRNA levels in IL‐1–stimulated chondrocytes.Conclusion. The suppressive effects of tenidap on IL‐1–stimulated metalloprotease synthesis and expression in OA and normal chondrocytes are likely related to a decrease in IL‐1R levels. At therapeutic concentrations, tenidap has a greater effect on the IL‐1R level than is seen with indomethacin or naproxen, and glucocorticoids have no effect on IL‐1R.
A canadian study of the total medical costs for patients with systemic lupus erythematosus and the predictors of costs
Authors: Clarke Ann E. , Esdaile John M. , Bloch Daniel A. , Lacaille Diane , Danoff Deborah S. , Fries James F. 
Published: February 2007

AbstractObjective. We conducted a cost identification analysis on 164 consecutive patients with systemic lupus erythematosus (SLE) who entered the Montreal General Hospital Lupus Registry between January 1977 and January 1990, compared their costs to the population of Quebec, and determined the predictors of cost.Methods. In January 1990 and 1991, participants completed questionnaires on health services utilization and on employment history over the preceding 6 months, as well as on functional, psychological, and social well‐being. The societal burden of SLE was determined in terms of direct costs (all resources consumed in patient care) and indirect costs (wages lost due to lack of work force participation because of morbidity).Results. The mean total annual cost for 1989, as assessed in January 1990 and expressed in 1990 Canadian dollars, was $13,094. Although only 44% of the patients were fully employed, indirect costs were responsible for 54% of this total ($7,071). Ambulatory costs, primarily diagnostic procedures, medications, and visits to health care professionals, comprised 55% of direct costs ($3,331). The results of the 1990 cost determination were similar. On average, hospitalizations among SLE patients were 4 times more frequent than among the general population of Quebec (matched for age and sex), and the number of ambulatory visits to physicians was double that for the average resident of Quebec. Higher 1989 values of creatinine and a poorer level of physical functioning were the best predictors of higher 1990 direct costs (R2 = 0.29). A poorer SLE well‐being score, a combination of education and employment status, and a weaker level of social support were the best predictors of higher indirect costs (R2 = 0.29).Conclusion. The direct and indirect costs for patients with SLE are substantial, and their respective predictors are distinct. Direct costs arise from organic complications which induce functional disability. Predictors of indirect costs are potentially amenable to psychological or social interventions and may be more easily modified than the determinants of direct costs, thereby improving patient outcome while simultaneously reducing disease costs.
Isolated congenital heart block. long‐term outcome of mothers and characterization of the immune response to ss‐a/ro and to ss‐b/la
Authors: Julkunen Heikki , Kurki Pekka , Kaaja Risto , Heikkilä Ritva , Immonen Ilkka , K. L. Chan Edward , Wallgren Eric , Friman Claes 
Published: February 2007

AbstractObjective. To study the long‐term outcome of mothers of children with isolated congenital heart block (CHB) and to characterize the maternal autoantibody response to SS‐A/Ro and SS‐B/La.Methods. A retrospective clinical study of 33 mothers a mean of 11.2 years (SD 9.2 years, range 0–32 years) after the delivery of their first child with CHB. A clinical and immunologic study of 31 of these mothers, compared with 89 healthy mothers, 45 mothers with systemic lupus erythematosus (SLE), and 19 mothers with primary Sjögren's syndrome (SS), all of whom had healthy children. The specificity of the autoantibody responses to SS‐A/Ro and SS‐B/La was studied by enzyme‐linked immunosorbent assays using purified human recombinant antigens and affinity‐purified antigens.Results. By the time of the analysis, 2 (6%) of the 33 mothers of CHB children had died and 6 (18%) had met the criteria for SLE. As a group, mothers of CHB children had clinical and immunologic characteristics more closely related to primary SS than to SLE or any other connective tissue disease. The predominant autoantibody response was to the SS‐A/Ro antigens, notably to the 52‐kd SS‐A/Ro protein (prevalence 97%). Compared with controls with SLE, mothers of CHB children had higher titers of antibodies to recombinant 52‐kd and 60‐kd SS‐A/Ro proteins and to the affinity‐purified SS‐A/Ro antigen (P < 0.05, P < 0.01, and P < 0.001, respectively). Compared with controls with primary SS, the autoantibody responses were similar.Conclusion. The predominant autoimmune disorder in mothers of children with CHB is subclinical primary SS. Antibodies to SS‐A/Ro appear to be a prerequisite for the development of CHB.
U1—70‐kd autoantibody–positive mixed connective tissue disease in children. A longitudinal clinical and serologic analysis
Authors: Hoffman Robert W. , Cassidy James T. , Takeda Yoshihiko , Smith‐Jones Elaine I. , Wang Grace S. , Sharp Gordon C. 
Published: February 2007

AbstractObjective. To obtain longitudinal data on the clinical, serologic, and immunogenetic features of children with mixed connective tissue disease (MCTD).Methods. Eleven children with MCTD were followed up for a mean of 9.8 years. Enzyme‐linked immunosorbent assay and immunoblotting were used to analyze sera for autoantibodies to small nuclear ribonucleoprotein polypeptides. HLA types were determined in 9 patients, by microcytotoxicity and DNA typing.Results. All 11 children had anti–U1–70‐kd autoantibodies. Six of 9 were positive for HLA–DR2, 4 of 9 for HLA–DR4, and 9 of 9 for either HLA–DR2 or DR4. Outcomes were favorable with no functional impairment in 8 of the 11 children and were poor in 3.Conclusion. The frequency of HLA–DR2/DR4 is increased among children with anti–U1–70‐kd autoantibody positive MCTD.
Inflammatory polyarthritis in mice transgenic for human t cell leukemia virus type i
Authors: Yamamoto Hiroaki , Sekiguchi Toyozo , Itagaki Keiko , Saijo Shinobu , Iwakura Yoichiro 
Published: February 2007

AbstractObjective. We have recently reported that arthropathy develops in high incidence among transgenic mice carrying the pX region of human T cell leukemia virus type I (HTLV‐I). In the present study, the histopathologic features of the joints in these mice were examined in order to compare the animal disease with rheumatoid arthritis (RA) in humans.Methods. Paraffin sections of limbs (right and left fingers, wrists, elbows, shoulders, toes, knees, and ankles) were stained with hematoxylin and eosin, periodic acid–Schiff, azan‐Mallory, or phosphotungstic acid hematoxylin, and examined by light microscopy.Results. Abnormalities of the limbs began to occur as early as 3 weeks of age, and the incidence gradually increased until the mice were 12 months old. The incidence of arthropathy was 22% (48 of 217) at 3 months of age and 28% (18 of 64) at 6 months. The severity of the histopathologic changes in the joints of the transgenic mice ranged from grade I to grade IV.Conclusion. The major histopathologic features in the joints of HTLV‐I transgenic mice are similar to those in humans with RA. Thus, these mice may represent a useful model for the study of the disease in humans.
Management of work disability. resources for vocational rehabilitation
Authors: Allaire Saralynn H. , Partridge Alison J. , Andrews Howard F. , Liang Matthew H. 
Published: February 2007

AbstractObjective. To review the state–federal vocational rehabilitation (SF‐VR) system and its utilization by persons with rheumatic conditions.Methods. SF‐VR system instruction manuals, and literature on rheumatology rehabilitation, work disability, and rehabilitation counseling were reviewed. National and Massachusetts state SF‐VR system data on persons with “arthritis and rheumatism” were analyzed.Results. The SF‐VR system is used by a small proportion of persons with rheumatic diseases. Fifty‐two percent of clients with arthritis are employed after receiving services.Conclusion. Although evidence indicates that VR services for persons with rheumatic conditions improves their chances for reemployment, the SF‐VR system is underutilized.
Incidence of rheumatoid arthritis in central massachusetts
Authors: Chan Kin‐Wei A. , Felson David T. , Yood Robert A. , Walker Alexander M. 
Published: February 2007

AbstractObjective. To determine whether there is a secular decline in the incidence of rheumatoid arthritis (RA), as has been suggested by previous studies.Methods. In the absence of comprehensive data in the United States population, we estimated RA incidence in a health maintenance organization population from 1987 through 1990 and compared the rates with those in an earlier, similarly performed study from Rochester, Minnesota, which covered the years 1950 through 1974. RA estimates were based on our review of medical records of patients who had been diagnosed as having RA or related diseases during the period of January 1, 1987 through December 31, 1990.Results. Annual age‐standardized incidence of classic or definite RA (according to the American College of Rheumatology [formerly, the American Rheumatism Association] 1958 criteria) in patients aged 18 or older was 22 per 100,000 in men and 60 per 100,000 in women. The incidence of RA increased with age, with a marked increase in women older than 50.Conclusion. We found no secular change in RA incidence compared with the similarly ascertained historical data.
Generalized osteoarthritis associated with increased insulin‐like growth factor types i and ii and transforming growth factor β in cortical bone from the iliac crest. possible mechanism of increased bone density and protection against osteoporosis
Authors: Dequeker J. , Mohan S. , Finkelman R. D. , Aerssens J. , Baylink D. J. 
Published: February 2007

AbstractObjective. To investigate whether growth factors stored in bone might explain the increased bone density and resistance to osteoporosis in generalized osteoarthritis.Methods. Levels of insulin‐like growth factor (IGF) types I and II and transforming growth factor β (TGFβ) were measured in extracts of cortical bone from the iliac crest obtained at necropsy from subjects with or without osteoarthritis of the hands.Results. Concentrations of IGF‐I, IGF‐II, and TGFβ were significantly higher in extracts of bone powder from subjects in the osteoarthritis group than in extracts from subjects in the control group.Conclusion. The results suggest that the increased bone density and resistance to osteoporosis in patients with osteoarthritis may be associated with increased skeletal concentrations of IGF‐I, IGF‐II, and TGFβ and may reflect a generally increased biosynthetic activity of osteoblasts in these patients.
Physician Variation in Diagnostic Testing for Low Back Pain. Who You See Is What You Get
Authors: Cherkin Daniel C. , Deyo Richard A. , Wheeler Kimberly , Ciol Marcia A. 
Published: February 2007

AbstractObjective. This study examined patterns of diagnostic test use for patients with low back pain. Three specific questions were addressed: 1) What tests do physicians recommend for patients with 3 common types of low back pain? 2) Do physicians in various specialties differ in the tests they would order? and 3) How appropriate are physicians' choices of tests, based on current medical knowledge and expert recommendations?Methods. A stratified national random sample of 2,604 physicians in 8 specialties was mailed questionnaires asking about the tests they would order for hypothetical patients with acute back pain, sciatica, or chronic low back pain. Physicians were also asked which procedures they generally used to evaluate suspected lumbar nerve root compression. These responses were compared with guidelines that have been suggested by the Quebec Task Force on Spinal Disorders, based on comprehensive evaluation of the scientific literature.Results. Approximately 1,100 physicians responded to the survey (43% response rate). Magnetic resonance imaging was the most frequently used procedure for evaluating suspected lumbar nerve root compression, although a majority of neurosurgeons would still use myelography. Neurosurgeons and neurologists were twice as likely as other specialists to order an imaging study for patients with acute nonradiating pain or chronic back pain. Physiatrists and neurologists were more than 3 times as likely as other specialists to order electromyograms for acute back pain with sciatica or chronic back pain. Rheumatologists were almost twice as likely as other specialists to order laboratory tests for both acute and chronic back pain. The reported use of imaging and electrodiagnostic tests was generally premature and more extensive than that recommended by the Quebec Task Force.Conclusion. There is little consensus, either within or among specialties, on the use of diagnostic tests for patients with back pain. Thus, the diagnostic evaluation depends heavily on the individual physician and his or her specialty, and not just the patient's symptoms and findings. Furthermore, many physicians may be ordering imaging studies too early and for patients who do not have the appropriate clinical indications. These results suggest a need for additional clinical guidelines as well as better adherence to existing guidelines.
Enhanced Synthesis of Cysteinyl Leukotrienes in Juvenile Rheumatoid Arthritis
Authors: Fauler J. , Thon A. , Tsikas D. , Hardt H. Von Der , Frölich J. C. 
Published: February 2007

AbstractObjective. Endogenous synthesis of cysteinyl leukotrienes in juvenile rheumatoid arthritis (JRA) was investigated.Methods. Cysteinyl leukotriene synthesis was assessed by measuring the excretion of leukotriene E4 (LTE4) in urine by radioimmunoassay. The identity of urinary LTE4 was investigated by gas chromatography—mass spectrometry (GC‐MS), and 2,3‐dinor‐thromboxane B2 was measured with GC‐MS.Results. Excretion of LTE4 into urine was significantly (P < 0.05) enhanced in children with JRA compared with that in healthy children (n = 10). Aspirin, in a dosage of 2.5 gm/day, had no effect on urinary LTE4 levels, but it reduced urinary 2,3‐dinorthromboxane B2 levels by more than 85% in healthy adults. There was a positive correlation between LTE4 excretion and the number of affected joints.Conclusion. This study demonstrates a markedly enhanced cysteinyl leukotriene synthesis and a positive correlation between LTE4 excretion and the number of affected joints in children with JRA.
Human Osteoarthritic Chondrocytes Possess an Increased Number of Insulin‐Like Growth Factor 1 Binding Sites but are Unresponsive to its Stimulation
Authors: Doré Sylvain , Pelletier Jean‐Pierre , Dibattista John A. , Tardif Ginette , Brazeau Paul , Martel‐Pelletier Johanne 
Published: February 2007

AbstractObjective. To characterize the insulin‐like growth factor 1 (IGF‐1) receptor in human osteoarthritic (OA) and normal adult chondrocytes. The biologic response of chondrocytes to IGF‐1 stimulation was examined, as was the presence and synthesis of IGF binding proteins (IGFBP) in these cells.Methods. Binding studies, Northern blot, immunohistochemical analysis, and affinity cross‐linking experiments were performed for characterization of the IGF receptor, and the latter method was also used for IGFBP determination. The biologic response was estimated via the incorporation of radiolabeled proline into a newly synthesized protein.Results. Binding experiments revealed a single class of binding sites. The mean ± SEM affinity (Kd) of normal chondrocytes was 1.4 ± 0.4 nM, with 26.8 ± 5.5 x 103 binding sites/cell. OA chondrocytes had a lower affinity (Kd 15.4 ± 4.7 nM) and a higher density (1,178.3 ± 299.5 x 103 binding sites/cell) compared with normal cells (P < 0.004 and P < 0.001, respectively). Immunohistochemical studies with a monoclonal antibody (MAb) against the type 1 IGF receptor (αIR3) showed increased staining in OA cartilage compared with normal tissue. Biologic responses of chondrocytes after IGF‐1 stimulation revealed that OA chondrocytes were unresponsive, whereas a 2.5‐fold increase in new protein synthesis was observed in normal cells. Competition studies in normal chondrocytes revealed that both IGF‐1 and IGF‐2 displaced radiolabeled IGF‐1 in a comparable manner; however, insulin at high concentration weakly competes. Moreover, MAb αIR3 effectively blocked specific binding in normal chondrocytes (77%), but not in OA chondrocytes (26%). Northern blot and covalent cross‐linking analyses revealed the specific band characteristic of type 1 receptor. With the latter technique, other bands corresponding to the IGFBPs were also detected. Comparison between normal and OA chondrocytes showed increased intensity of the IGFBP bands, particularly those corresponding to the IGFBP‐3 doublet.Conclusion. It is shown that type 1 IGF receptor is expressed in human articular cartilage and that the level of binding sites is significantly increased in OA chondrocytes. Interestingly, despite the higher level of binding sites in OA cells, no response to IGF‐1 stimulation was found in these cells. Our data suggest that this increase in specific binding may involve not only the type 1 IGF receptor but also IGFBP on the cell surface. The latter, by binding the IGF‐1, will diminish the bioavailability of IGF‐1 and thus prevent its anabolic action.