bluuebunny/crossref_metadata_2025_split huggingface dataset:
The production of collagenase by adherent mononuclear cells cultured from human peripheral blood
Authors: Louie James S. , Weiss Judy , Ryhänen Lasse , Nies Kenneth M. , Rantala‐Ryhänen Sirpa , Uitto Jouni 
Published: February 2007

AbstractMononuclear cells were isolated from human peripheral blood by Ficoll‐Hypaque centrifugation, and the cells adherent to plastic substrata were cultured in serum‐free media supplemented with lactalbumin hydrolysate. These cell cultures, which consisted predominantly of monocyte‐macrophages as judged by nonspecific esterase staining, accumulated collagenase in the medium. This collagenase resembled other vertebrate collagenases in that it cleaved native triple‐helical type I collagen at a locus 3/4‐length away from the amino‐terminal end of the molecule. The collagenase activity was inhibited by Na2EDTA, dithiothreitol, and fetal calf serum, while the addition of Ca++ or N‐ethylmaleimide enhanced the enzyme activity. The accumulation of collagenase in the culture media was markedly enhanced by the incubation of cells with concanavalin A or phorbol myristic acetate. In the presence of cycloheximide, the levels of collagenase activity were markedly reduced, suggesting that active protein synthesis was required to express the enzyme activity. In additional experiments, monocytes were further purified by counterflow centrifugation‐elutriation. The collagenase production was markedly increased in cultures enriched in monocyte‐macrophages and devoid of polymorphonuclear leukocytes. The accumulation of collagenase in monocyte cultures incubated for 48 hours in the presence of concanavalin A or phorbol myristic acetate was of the same order of magnitude as in parallel cultures containing the same number of polymorphonuclear leukocytes purified by Ficoll‐Hypaque centrifugation and Plasmagel sedimentation. The demonstration of collagenase activity in the monocyte cultures appears to reflect the increased diversity of monocyte functions which may play an important role in the tissue damage in chronic inflammatory diseases such as rheumatoid arthritis.
The lupus anticoagulant. A disease marker in antinuclear antibody negative lupus that is cross‐reactive with autoantibodies to double‐stranded DNA
Authors: Colaco C. Bernard , Elkon Keith B. 
Published: February 2007

AbstractThe lupus anticoagulant (LA) was demonstrated in 37% of 52 consecutive systemic lupus erythematosus (SLE) patients and patients with lupus‐like syndromes, who were referred to our unit. The LA was found to be associated with a biologic false‐positive VDRL (P < 0.005), and the apparently paradoxical association of LA with vascular thromboses was confirmed (P < 0.05). The presence of LA and a biologic false‐positive VDRL defined a group of 7 antinuclear antibody negative patients with characteristic features of recurrent thromboses, spontaneous abortions, neurologic involvement, and renal disease. Further studies on 6 selected sera demonstrated LA in all 6 IgM fractions and in 3 of 6 IgG fractions. Inhibition of LA was shown in 6 of 9 Ig fractions after absorption with double‐stranded DNA (dsDNA). Anticardiolipin antibody was shown by immunodiffusion in 3 LA positive IgG fractions from VDRL negative sera. Cardiolipin micelles partially inhibited anti‐dsDNA binding of 4 IgG fractions, 3 of which were LA negative. In this report we discuss the overlapping specificities due to cross‐reactivity between LA, anticardiolipin, and anti‐dsDNA antibodies in human SLE, and we suggest that LA be considered equivalent to the biologic false‐positive VDRL as a criterion for the diagnosis of SLE.
Cartilage nucleoside triphosphate pyrophosphohydrolase. II. role in extracellular pyrophosphate generation and nucleotide metabolism
Authors: Ryan Lawrence M. , Wortmann Robert L. , Karas Barbara , McCarty Daniel J. 
Published: February 2007

AbstractExtracellular generation of inorganic pyrophosphate (PPi) in cartilage organ culture is markedly augmented by ATP. ATP, not an ATP metabolite (ADP, AMP, adenosine), is necessary for this augmentation. Excess PPi production is effectively blocked by known inhibitors of nucleoside triphosphate (NTP) pyrophosphohydrolase (EDTA, EGTA, dithiothreitol). Excess 32P‐PPi is generated directly from γ32P‐ATP by cartilage, as substrate and product have similar specific activities. These findings strongly favor ecto‐NTP pyrophosphohydrolase as the source of extracellular PPi generation in the presence of NTP. Additionally, active nucleotide and nucleoside catabolism is demonstrated in these cartilage organ cultures.
Blastomycosis presenting as monarticular arthritis. The role of synovial fluid cytology
Authors: George Jr. Alfred L. , Hays J. Taylor , Graham Barney S. 
Published: February 2007

AbstractJoint complaints are common among patients with blastomycosis; however, true arthritis is infrequently documented by synovial fluid analysis. Of 72 individuals with blastomycosis who were patients at the Vanderbilt School of Medicine affiliated hospitals during the period 1957–1983, 6 (8%) had arthritis at presentation. In 5 patients (7%), monarticular arthritis was the chief complaint leading to hospitalization. Cytologic examination of synovial fluid was performed in 4 patients and demonstrated characteristic organisms each time. Three patients had negative 10% potassium hydroxide smears, and 2 had negative synovial fluid cultures. Blastomycosis should be considered in the differential diagnosis of acute arthritis. In patients with blastomycotic arthritis, cytologic examination of synovial fluid can add to the diagnostic yield of synovial fluid fungal cultures and potassium hydroxide preparations.
Etiopathogenesis of the rheumatoid arthritis–like disease in MRL/1 mice. I. The histomorphologic basis of joint destruction
Authors: O'sullivan Frank X. , Fassbender Hans‐Georg , Gay Steffen , Koopman William J. 
Published: February 2007

AbstractMRL/1 mice spontaneously develop a hindlimb arthropathy, as well as a number of immunologic abnormalities, including circulating rheumatoid factors. Although previous studies have suggested that this arthropathy is primarily an inflammatory process, we performed a comprehensive histomorphologic study which indicated that inflammation is a late manifestation of MRL/1 arthritis. The pathologic changes that occur in the joints of these mice can be divided into 3 stages. The first stage develops between the ages of 7 and 13 weeks and consists of synovial cell proliferation in the joint recesses. The second stage is characterized by continued proliferation of synovial cells which take on an appearance similar to that of transformed mesenchymal cells. The earliest destructive changes occur in the second stage and include marginal erosions, followed soon after by progressive destruction of articular and meniscal cartilage. The final stage is characterized by a diminution of synovial cell proliferation, extensive cartilage destruction, formation of scar tissue and fibrocartilage, and a very moderate infiltration of the synovial stroma by mononuclear and polymorphonuclear inflammatory cells. Throughout the disease progression there is a striking dissociation between inflammatory cell infiltration or exudation and tissue destruction. The histomorphologic similarities between human rheumatoid synovitis and the arthritis of MRL/1 mice, as well as the presence of rheumatoid factors, make this mouse strain an excellent model for studying human rheumatoid arthritis.
The autologous mixed lymphocyte reaction is decreased in Freund's adjuvant–injected rats of arthritis‐susceptible and ‐insusceptible strains
Authors: Crowe William E. , Crowe William E. , Battisto Jack R. , Smith R. N. 
Published: February 2007

AbstractWe examined the T–non‐T cell autologous mixed lymphocyte reaction (AMLR) of spleen cells from rats with arthritis induced by Freund's complete adjuvant in an effort to establish an animal model for the study of the relationship between the AMLR and autoimmune disease. We found that the splenic T–non‐T AMLR was markedly decreased in rats with adjuvant‐induced arthritis and that this decrease was mediated by suppressor cells within the nylon‐wool–adherent stimulator cell population. However, we also found a similar decrease in the AMLR of arthritis‐resistant Fisher 344 rats that received Freund's complete adjuvant but did not develop arthritis. Control animals with local inflammation induced by turpentine, a nonarthritogenic inflammatory substance, had normal AMLR, whereas other controls given Freund's incomplete adjuvant, also a nonarthritogenic substance, had a modest responder cell–mediated decrease in AMLR. These studies help to clarify the relationship between the decreased AMLR and the pathogenesis of adjuvant‐induced arthritis by demonstrating that: 1 the acute‐phase inflammatory response does not reduce the AMLR; and 2 the decreased AMLR can occur in the absence of overt autoimmune disease. This latter observation calls into question the proposed pathogenetic relationship between the AMLR and autoimmune disease states.
Proteoglycan depletion, rather than fibrillation, determines the effects of salicylate and indomethacin on osteoarthritic cartilage
Authors: Palmoski Marshall J. , Brandt Kenneth D. 
Published: February 2007

AbstractThe effects of salicylate and indomethacin on glycosaminoglycan (GAG) synthesis by atrophic and osteoarthritic (OA) canine cartilage were examined in vitro by transecting distal femora at the metaphysis and incubating the knuckle, with its overlying cap of articular cartilage, in medium containing sodium salicylate or indomethacin, and 35SO4. Atrophic cartilage had an intact articular surface, but its uronic acid content averaged 65% of the control level, and GAG synthesis was decreased to 50% of control values. Both salicylate and indomethacin decreased net GAG synthesis in the atrophic cartilage by an additional 10%. OA cartilage showed surface disruption, a uronic acid content 49% of the control value, and a 49% increase in net GAG synthesis. Salicylate and indomethacin profoundly decreased GAG synthesis in the OA cartilage. However, GAG synthesis and uronic acid content of cartilage which had been lacerated in vitro immediately prior to culture (to stimulate fibrillation) were normal and not affected by either drug. The data emphasize the importance of matrix proteoglycan content in protecting the chondrocyte from the suppressive effects of salicylate and indomethacin on GAG metabolism, and suggest that the lower proteoglycan content of OA cartilage may be more important than fibrillation in rendering it vulnerable to the metabolic effects of these drugs.
The specificity of antibodies to the F(ab′)2 fragment of human IgG
Authors: Heimer Ralph , Wolfe Lawrence D. , Abruzzo John L. 
Published: February 2007

AbstractThe specificity of IgG anti‐F(ab′)2 antibodies was examined in unfractionated sera of patients with rheumatoid arthritis and also with affinity‐purified antibody preparations. Examination of the sera by an enzyme‐linked immunosorbent assay, using pooled human F(ab′)2 fragments absorbed to microtiter plates, revealed that IgG anti‐F(ab′)2 antibodies cross‐react with human and rabbit IgG and rabbit F(ab′)2. IgG anti‐F(ab′)2 antibodies were purified by affinity chromatography and, when tested by a fluid‐phase inhibition enzyme‐linked immunosorbent assay, were found to be of 2 types. One fraction, similar to pepsin agglutinator, reacted with human F(ab′)2 fragment alone. The other fraction was cross‐reactive with human IgG and yet failed to react with idiotopes on Fab or epitopes on Fc fragments. The IgG anti‐F(ab′)2 antibodies we purified had no reactivity toward a human immune complex prepared from tetanus toxoid and antitoxoid.
Collagen synthesis regulation by the aminopropeptide of procollagen i in normal and scleroderma fibroblasts
Authors: Perlish Jerome S. , Timpl Rupert , Fleischmajer Raul 
Published: February 2007

AbstractThe effect of the aminopropeptide of type I procollagen, Col 1(1), on collagen synthesis by normal and scleroderma fibroblasts was investigated. Collagen synthesis was inhibited by about 42% when normal fibroblasts were labeled with 3H‐proline in the presence of 4 μM Col 1(I). In contrast, collagen synthesis by scleroderma fibroblasts was inhibited to a lesser degree, about 19%. Furthermore, scleroderma fibroblasts with elevated rates of collagen synthesis (2.5–5 times normal) were inhibited by only about 10%. The data suggest that the increased accumulation of collagen in the skin of scleroderma patients may be related to a defect in the regulation of collagen synthesis by the aminopropeptide.
The effect of D‐penicillamine on pulmonary findings in systemic sclerosis
Authors: Steen Virginia D. , Owens Gregory R. , Redmond Carol , Medsger Thomas A. 
Published: February 2007

AbstractD‐penicillamine has been used for the treatment of systemic sclerosis for 2 decades. Forty‐four systemic sclerosis patients who received a mean dose of 636 mg of D‐penicillamine for 2.3 years and 48 untreated patients, who had repeat pulmonary function tests performed after a mean of 3.5 and 4.8 years, respectively, were evaluated. There were no significant changes in the vital capacity or the forced expiratory volumes during this time in either group. However, the diffusing capacity for carbon monoxide improved from 76% of predicted to 87% of predicted in D‐penicillamine‐treated patients. Untreated patients changed slightly, from 73% of predicted to 76% of predicted. When multiple logistic regression analysis was used to account for factors which could have biased treatment comparisons, the improvement related to use of the D‐penicillamine was significant (P < 0.05). This improvement in the D‐penicillamine‐treated patients was associated with no further progression of dyspnea or fibrosis on chest radiograph, as well as reduced skin thickening. These data suggest that D‐penicillamine may be useful in the treatment of systemic sclerosis that involves the lung; however, further studies are needed.
Computed tomography in the diagnosis of early ankylosing spondylitis
Authors: Fam Adel G. , Rubenstein Joel D. , Chin‐Sang Hyacinth , Leung Frances Y. K. 
Published: February 2007

AbstractComputed tomography (CT) was compared with plain radiography and quantitative sacroiliac (SI) scintigraphy in 28 patients with early ankylosing spondylitis (AS) of ⩽10 years duration. Compared with conventional radiography, CT improved delineation of the SI joints and revealed more abnormalities and higher grades of sacroiliitis; this was significant in patients with early AS of ⩽3 years duration. Quantitative sacroiliac scintigraphy showed higher SI joint:sacrum ratios of radioisotope uptake in patients with AS compared with controls. However, its diagnostic usefulness was limited by the frequency of inconsistent results and the lack of specificity. CT examination of the SI joints may be a useful adjunct in the diagnosis of early AS.
Different defects of T cell regulation of epstein‐barr virus‐induced B cell activation in rheumatoid arthritis
Authors: Kahan Alice , Kahan André , Amor Bernard , Menkes Charles J. 
Published: February 2007

AbstractSeveral reports have shown a defective Epstein‐Barr virus (EBV)‐specific suppressor T cell function in rheumatoid arthritis (RA), suggesting that EBV may have a role in the pathogenesis of RA. EBV‐specific T cell regulation was studied in 47 EBV‐immune RA patients and in 14 EBV‐immune control subjects by comparing the secretion of IgM into supernatants of 28‐day cultures of B cells alone and cocultures of B and autologous T cells. In control subjects, autologous T cells mediated a significant decrease in the secretion of IgM by B cells at 12 and 16 days of culture. Analysis of individual responses demonstrated the existence of 3 subgroups of RA patients: group I (18 patients) had a suppressor T cell function similar to that of controls; group II (21 patients) had a defective T cell function; group III (8 patients) was characterized by a “late help phenomenon.” Moreover, in RA group III, IgM secretion in cultures of B cells alone was lower than that seen in controls, RA group I, or RA group II. Differences in the duration or severity of the disease, or in the use of slow‐acting therapeutic agents, corticosteroids, and nonsteroidal antiinflammatory drugs could not account for these subdivisions. Thus, our study demonstrates that several immunoregulatory defects exist in subgroups of RA patients.
The clinical features of elderly‐onset rheumatoid arthritis. A comparison with younger‐onset disease of similar duration
Authors: Deal Chad L. , Meenan Robert F. , Goldenberg Don L. , Anderson Jennifer J. , Sack Burton , Pastan Robert S. , Cohen Alan S. 
Published: February 2007

AbstractPatients with elderly‐onset rheumatoid arthritis (EORA) may represent a clinical subset of individuals who differ prognostically and therapeutically from patients with younger‐onset disease (YORA). In order to test this hypothesis, we reviewed the records of 212 patients with rheumatoid arthritis and grouped them according to age at onset above or below 60 years old. Seventy‐eight EORA patients and 134 YORA patients with disease duration of ⩽10 years were used for a comparison of presenting features and disease outcome. Abrupt onset occurred somewhat more frequently in EORA, but was not associated with a significantly different clinical course than was an insidious presentation in this older group. There were no differences between the EORA and YORA groups in terms of mean initial joint score, although the scores for the YORA group had wider variation. An initial clinical presentation resembling polymyalgia rheumatica (PMR) was 4 times as frequent in EORA. Elderly patients were less likely to have subcutaneous nodules or rheumatoid factor at disease onset. At the final examination, the EORA patients had lower joint scores and higher health assessments despite similar courses of treatment. These outcome differences persisted when patients with PMR‐like presentations were excluded. Multivariate analyses indicated that joint scores and disease duration made important contributions to a better outcome of EORA, whereas PMR presentation and abrupt onset did not. After an adjustment was made for these 4 features, age at onset was an important contribution to joint score outcome. These results confirm the existence of important differences in onset, clinical features, and prognosis between patients with EORA and those with YORA.
Crystal‐induced endogenous pyrogen production. A further look at gouty inflammation
Authors: Malawista Stephen E. , Duff Gordon W. , Atkins Elisha , Cheung Herman S. , McCarty Daniel J. 
Published: February 2007

AbstractWe found previously that crystals of sodium urate and silicon dioxide (silica) can stimulate the production of endogenous pyrogen (EP), now called interleukin‐1 (IL‐1), the polypeptide mediator of fever and other aspects of inflammation. We have confirmed and extended the work with urate crystals and have examined 2 other crystals associated with joint problems, hydroxyapatite (HA) and calcium pyrophosphate dihydrate (CPPD). The crystals were added to suspensions of human blood leukocytes (2.5 × 106 monocytes/dose, with 10% fresh autologous plasma); after 18 hours of incubation, the EP content of the supernatants was assayed in the rabbit pyrogen test. HA and CPPD crystals neither induced EP production nor reduced the amount of staphylococci‐induced EP. Presized (10‐40 μm) urate crystals were pyrogenic, but less so than the unsized and aggregated urate crystals investigated previously and reexamined here. On ultrasonication, the aggregated urate crystals became first more pyrogenic and then less so as the crystals were dispersed and broken down. Ultrasound did not impart pyrogenicity to HA or CPPD crystals: their failure to stimulate EP/IL‐1 production from leukocytes in vitro indicates a difference in their phlogistic properties, compared with crystals of urate or silica. The results with urate crystals have pathogenetic implications in a number of areas of gouty inflammation: initiation of the acute attack, other aspects of the acute‐phase response, polyarticular involvement, and the inflammatory consequences of chronic stimulation by tophaceous material.
How many joints in the hands and wrists should be included in a score of radiologic abnormalities used to assess rheumatoid arthritis?
Authors: Sharp John T. , Young Donald Y. , Bluhm Gilbert B. , Brook Andrew , Brower Anne C. , Corbett Mary , Decker John L. , Genant Harry K. , Gofton J. Philip , Goodman Neal , Larsen Arvi , Lidsky Martin D. , Pussila Pekka , Weinstein Aaron S. , Weissman Barbara N. , Sharp John T. , Young Donald Y. , Bluhm Gilbert B. , Brook Andrew , Brower Anne C. , Corbett Mary , Decker John L. , Genant Harry K. , Gofton J. Philip , Goodman Neal , Larsen Arvi , Lidsky Martin D. , Pussila Pekka , Weinstein Aaron S. , Weissman Barbara N. 
Published: February 2007

AbstractNumerous methods for reading abnormalities of rheumatoid arthritis in hand and wrist radiographs have been proposed over the past several decades. There are many differences among these methods, one of the more striking of which is the variation in the number of joints that are scored. In this study, we tested the number of joints that need to be read in order to represent abnormalities accurately and reproducibly, using the scores of multiple observers. Thirteen rheumatologists and radiologists each read a set of 41 hand and wrist films from patients with rheumatoid arthritis. Ten of 13 readers scored 27 joints in each hand and wrist; the other 3 readers scored fewer areas. Fourteen combinations of joints were selected based on the frequency of involvement and the technical adequacy of routine films in assessing a given area. After testing these 14 different combinations, 1 scheme, which included 17 areas read for erosions and 18 areas read for joint space narrowing, was tested further. The correlation coefficients for 10 intraobserver scores derived from this modified scheme compared with the original scores were between 0.981 and 0.997. Seventy‐one of 78 interobserver comparisons were better using the new scheme than using the original scheme. These data indicate that the simplified scheme, using a combination of 17 joints to score erosions and 18 to score joint space narrowing, more accurately reflects the extent of abnormalities perceived by a panel of experts than does the original scheme. This abbreviated number of joints shortens the amount of time required to read a set of films and simplifies the scoring of films, since a number of areas that are difficult to read are eliminated from radiographic assessment.
Cancer and systemic sclerosis. An epidemiologic study
Authors: Roumm Alan D. , Medsger Thomas A. 
Published: February 2007

AbstractThe association between systemic sclerosis and malignancy was evaluated in the Pittsburgh standard metropolitan statistical area during 1971–1982 and compared with data for this geographic area from the Third National Cancer Survey of 1969‐1971. Fourteen malignancies were detected in 262 systemic sclerosis patients (5%) during a followup period that included 1, 335 patient‐years. After adjustment for age and sex, the expected number of malignancies was 7.72 (relative difference = 1.81; P = 0.05). This increased relative difference was predominantly due to an increase in observed lung cancer (relative difference = 4.4; P < 0.05), which occurred in the setting of long‐standing pulmonary fibrosis but was not associated with cigarette smoking. Although breast cancer was no more frequent than expected, it tended to occur in close temporal relationship with the onset of systemic sclerosis. These findings suggest a biologic relationship between systemic sclerosis and certain malignant neoplasms.