bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphologic observations in the early phase of the cartilage‐pannus junction
Authors: Shiozawa Shunichi , Shiozawa Kazuko , Fujita Takuo 
Published: February 2007

AbstractThe early phase of cartilage destruction by active cellular pannus in rheumatoid joints was observed under light and electron microscopy. In the early phase of pannus formation, cartilage was covered by several layers of fibroblast‐like cells. This was also the case at the advancing edge of the pannus. Invasion of the cartilage by macrophage‐like cells has been observed to start beneath this layer. Observations under electron microscope demonstrated that the main cells participating in the cartilage destruction at the cartilage‐pannus junction were either fibroblast‐like or macrophage‐like cells, and suggested the possibility that these two types of cells were derived from synovial type A and type B cells. Morphologic observations also suggested a possibility of transformation of the fibroblast‐like cell into the macrophage‐like cell at the cartilage‐pannus junction.
Clinical characteristics of patients with rheumatic disorders who possess antibodies against ribonucleoprotein particles
Authors: Williamson Gerald G. , Pennebaker James , Boyle John A. 
Published: February 2007

AbstractIgG was purified from 91 serum samples obtained from patients with systemic rheumatic diseases and examined for the presence of antinuclear antibodies reactive with small ribonucleoprotein (RNP) complexes. Antibody specificity was determined by autoradiographic detection of 32P labeled RNA which had been separated by polyacrylamide gel electrophoresis. This RNA was extracted from immune complexes formed by adding purified IgG to a homogenate of 32P labeled HeLa cells. Anti‐RNP antibodies were detected in 70% of these samples. Specific antibodies detected were anti‐(U1)‐RNP (35%), anti‐Sm (30%), anti‐Ro (24%), and anti‐La (10%). Other antibodies (9%) were reactive with structures containing 5S and 5.8S RNA or 4S RNA. There was a significant relationship between the presence of anti‐RNP antibodies in patients with systemic lupus erythematosus (SLE) (78%) as opposed to their presence in patients with non‐SLE rheumatic disorders (45%). However, taken individually, anti‐Ro was the only antibody whose presence in SLE patients (30%) was significantly greater than its presence in non‐SLE patients (5%). Vasculitis was the only clinical manifestation found to correlate with the presence of a particular antibody, anti‐(U1)RNP. There is some suggestion of a racial distribution of antibody types.
Granulopoiesis in systemic lupus erythematosus
Authors: Yamasaki Kazuo , Niho Yoshiyuki , Yanase Toshiyuki 
Published: February 2007

AbstractThe pathogenesis of granulopoietic failure in systemic lupus erythematosus (SLE) was studied. In 16 Japanese women with SLE, a decreased number of granulocyte/monocyte progenitor cells (CFU‐C) in the bone marrow was demonstrated, and the number of CFU‐C correlated significantly with the peripheral blood granulocyte/monocyte count. The peripheral and bone marrow T lymphocytes suppressed the colony formation of autologous or allogeneic bone marrow CFU‐C. These findings suggest that the decreased marrow CFU‐C may be due to suppression by T lymphocytes, an event that may play an important role in the pathogenesis of granulopoietic failure in SLE.
Relationship between matrix proteoglycan content and the effects of salicylate and indomethacin on articular cartilage
Authors: Palmoski Marshall J. , Brandt Kenneth D. 
Published: February 2007

AbstractWhen 160 γg/ml sodium salicylate was added to the culture medium, glycosaminoglycan synthesis in slices of normal articular cartilage from habitually loaded areas of canine femoral condyles was diminished by 24% (P ≤ 0.01). Although glycosaminoglycan synthesis in cartilage from habitually unloaded regions of the same joints was similar to that in cartilage from loaded sites, the mean uronic acid content of the former was about 25% less, and salicylate suppressed glycosaminoglycan synthesis in unloaded cartilage to a much greater extent (42% of control) than it did in loaded cartilage (P ≤ 0.01). Furthermore, 1.5 γg/ml indomethacin, which had no effect on cartilage from loaded regions, suppressed glycosaminoglycan synthesis in cartilage from unloaded regions by 31%. However, if cartilage from loaded regions was treated with testicular hyaluronidase, indomethacin inhibited glycosaminoglycan synthesis, and inhibition of glycosaminoglycan metabolism by salicylate in hyaluronidase‐treated cartilage was greater than in untreated cartilage. The data suggest that the effects of nonsteroidal antiinflammatory drugs on glycosaminoglycan metabolism in articular cartilage are dependent on proteoglycan content of the extracellular matrix.
Neutrophil Aggregation Induced by Sera from Patients with Active Systemic Lupus Erythematosus
Authors: Abramson Steven B. , Given William P. , Edelson Henry S. , Weissmann Gerald 
Published: February 2007

AbstractActivated complement components and immune complexes cause neutrophil (PMN) aggregation in vitro and in vivo, as in dialysis‐induced neutropenia and adult respiratory distress syndrome. To investigate the possible role of PMN aggregation in systemic lupus erythematosus (SLE), we studied the capacity of 59 sera from 53 patients to induce aggregation of normal PMN in vitro. Neutrophil aggregating activity (NAA) was present in the sera of 26 of 28 patients with active SLE. The mean NAA in this group was significantly greater than that found in 13 patients with inactive SLE, 20 patients with rheumatoid arthritis, and 17 normal controls. In patients with SLE there was a positive correlation between disease severity and the quantitative measure of NAA. NAA did not correlate with serum C3 or C4 nor with the presence or absence of circulating immune complexes. High levels of NAA were particularly characteristic of central nervous system lupus. These data suggest that the formation of intravascular leukoaggregates may contribute to morbidity in SLE.
Arthropathy of Lowe's (Oculocerebrorenal) Syndrome
Authors: Athreya Balu H. , Schumacher H. Ralph , Getz Harry D. , Norman Michael E. , Iv Spencer Borden, , Witzleben Camillus L. 
Published: February 2007

AbstractWe describe 3 children with Lowe's syndrome who developed joint manifestations—‐a previously rarely recognized feature. Two children had swelling and contractures of large and small joints; the third child had a small joint effusion and hypermobile joints. None of them had antinuclear antibody or rheumatoid factor; synovial effusions and biopsies showed no evidence of inflammatory cell infiltration. By light microscopy, profuse fibrous tissue and sparse synovial lining cells were found. Electron microscopy of the synovium of 2 patients showed large amounts of normal appearing collagen, unidentified thin fibrils, and focal profuse granular and fibrillar basement membrane‐like material around small vessels, similar to findings described in other tissues in this syndrome. Whether these clinical and pathologic findings are results of the still incompletely understood basic metabolic defect or not, they should be recognized as features that may be seen in patients with Lowe's syndrome.
T Lymphocyte Subsets in Systemic Lupus Erythematosus
Authors: Bakke Antony C. , Kirkland Purnell A. , Kitridou Rodanthi C. , Quismorio Francisco P. , Rea Thomas , Ehresmann Glenn R. , Horwitz David A. 
Published: February 2007

AbstractThe contribution of immune regulation to the etiology of systemic lupus erythematosus (SLE) is poorly understood. Using the monoclonal antibodies OKT4 and OKT8, we quantitated, by flow cytometry, T inducer/helper and T cytotoxic/suppressor cells in patients with SLE. Serologically active patients, who had clinical manifestations such as arthritis or rash and were not receiving prednisone, were characteristically lymphopenic due to a marked reduction in OKT4+ cells. Prednisone therapy produced the same phenomenon. Untreated patients, who were serologically inactive, demonstrated no abnormalities. These studies have thus revealed two presumably independent factors that can produce similar immunoregulatory aberrations.
Spinal Fractures Complicating Ankylosing Spondylitis
Authors: Hunter Thomas , Dubo Hyman I. C. 
Published: February 2007

AbstractTwenty‐two spinal fractures in 20 patients with chronic ankylosing spondylitis are reported. Nineteen fractures occurred in the cervical region. Fourteen of the fractures were caused by minor falls, 3 by falls down steps, 4 by motor vehicle accidents, and 1 by cardiopulmonary resuscitation. Long‐term followup (mean 3.2 years) of 9 fractures diagnosed early and managed conservatively showed bony union of all fractures. No patient deteriorated neurologically and 3 patients made major recovery. Long‐term followup is also reported on 6 patients in whom the diagnosis was delayed. The difficulties in diagnosis and management are discussed.
The Radiographic Diagnosis of Sacroiliitis
Authors: Ryan Lawrence M. , Carrera Guillermo F. , Lightfoot Robert W. , Hoffman Raymond G. , Kozin Franklin 
Published: February 2007

AbstractConventional radiography is the standard method of objectively identifying sacroiliitis. Single views of the sacroiliac joints can be unequivocally interpreted in 70‐80% of patients with low back pain. A series of views usually correctly resolves the ambiguity in the remaining 20—30% of patients (67% correct). Computed tomography will be helpful in the few patients in whom a series of views produces equivocal interpretation.
Hyaluronate Synthesis by Synovial Villi in Organ Culture
Authors: Myers Stephen L. , Christine Theresa A. 
Published: February 2007

AbstractIndividual canine synovial villi were used to establish short‐term synovial organ cultures. These villi incorporated 3H‐glucosamine into highly‐polymerized 3H‐hyaluronic acid (3H‐HA), which was the only 3H‐glycosaminoglycan identified in the culture medium. Some 3H‐HA, and larger amounts of other 3H‐glycosaminoglycans, were recovered from cultured tissues. Culture medium 3H‐HA content was proportional to the surface area of cultured villi. Organ cultures of nonvillous synovium were compared with villi; nonvillous cultures synthesized less 3H‐HA per mm2 of their synovial intimal surface than villi. These cultures complement cell culture techniques for in vitro studies of synovial lining cell function.
Benoxaprofen stimulates proteoglycan synthesis in normal canine knee cartilage in vitro
Authors: Palmoski Marshall J. , Brandt Kenneth D. 
Published: February 2007

AbstractSeveral nonsteroidal antiinflammatory drugs which are cyclooxygenase inhibitors (e.g., salicylates, fenoprofen, ibuprofen) have been shown to suppress proteoglycan synthesis by normal joint cartilage in vitro. We examined the effect of benoxaprofen, a long‐acting proprionic acid derivative which inhibits lipoxygenase in addition to causing moderate cyclooxygenase inhibition. When added to the culture medium in concentrations comparable with those obtainable in serum of patients treated with the drug (e.g., 10 and 50 μg/ml), benoxaprofen increased proteoglycan synthesis in slices of normal canine knee cartilage to 126% and 135%, respectively, of control levels. These concentrations of the drug augmented net protein synthesis to 154% and 123%, respectively, of control levels. Incorporation of 3H glucosamine into 9‐aminoacridine precipitable material was increased by benoxaprofen, showing that it stimulates net proteoglycan synthesis, and not merely sulfation. At concentrations of either 10 or 50 μg/ml, the drug had no effect on proteoglycan catabolism or on the ability of proteoglycans to interact with cartilage hyaluronic acid to form macromolecular aggregates. Nordi‐hydroguaiaretic acid, a free radical scavenger which, like benoxaprofen, inhibits the lipoxygenase as well as cyclooxygenase pathways of arachidonic acid metabolism, also increased 35S glycosaminoglycan synthesis in cartilage slices. The stimulation of glycosaminoglycan and protein synthesis by benoxaprofen suggests that its action on the chondrocyte may be different from that of most other nonsteroidal antiinflammatory drugs.
Clinical characteristics of fibrositis
Authors: Campbell Stephen M. , Clark Sharon , Tindall Elizabeth A. , Forehand Mary E. , Bennett Robert M. 
Published: February 2007

AbstractTwenty‐two patients with fibrositis, selected from a general medical outpatient population by a screening questionnaire and subsequent evaluation, were compared with age‐, sex‐, and clinic‐matched patients without fibrositis. Although there was a high prevalence of musculoskeletal complaints in both groups, the fibrositis patients had a uniform constellation of symptoms, including axial pain, severe aching and stiffness, morning fatigue, and modulation by specific factors. They also had a higher incidence of tension headache and irritable bowel syndrome. The use of a dolorimeter demonstrated that fibrositis patients had many more areas of localized tenderness than control patients, but also that fibrositis patients did not have diffusely diminished pain threshold and tolerance. Using the criteria of this study, fibrositis appears to be a common and readily definable syndrome within the spectrum of soft tissue rheumatism.
Biochemical and morphologic studies of cartilage from the adult human sacroiliac joint
Authors: Paquin Julie D. , Rest Michel Van Der , Marie Pierre J. , Mort John S. , Pidoux Isabelle , Robin Poole A. , Roughley Peter J. 
Published: February 2007

AbstractThe cartilage of the adult sacroiliac joint contains type II collagen and a high concentration of glycosaminoglycan. Furthermore, large aggregating proteoglycans and link proteins were extracted from the sacral cartilage. In these respects the sacroiliac cartilage is similar to that in the peripheral joints. However, while the organization of the collagen in the sacral cartilage is typical of an articular cartilage, the organization of the ilial cartilage is very different, and throughout its depth it possesses narrow collagen fibrils arranged parallel to the articular surface.
The pathology of the involved tendons in patients with familial arthropathy and congenital camptodactyly
Authors: Ochi Takahiro , Iwase Rokuro , Okabe Norikazu , Fink Chester W. , Ono Keiro 
Published: February 2007

AbstractIn 2 sisters with congenital camptodactyly and joint effusions, abnormalities in tendons were restricted to the portion within synovia sheaths. This implied a disease of the tenosynovium, rather than one of the tendon itself. In areas of chronic involvement, some tendons were replaced by fibrous tissue. Significant portions of the tendons in fingers with camptodactyly were replaced by hard scars. Congenital camptodactyly is probably the result of an intrauterine tenosynovitis, rather than an isolated congenital anomaly.
Natural killing activity in sjögren's syndrome
Authors: Miyasaka N. , Seaman W. , Bakshi A. , Sauvezie B. , Strand V. , Pope R. , Talal N. 
Published: February 2007

AbstractNatural killing (NK) by peripheral blood mono‐nuclear cells (PBMC) against K562 cells was examined in 27 patients with Sjögren's syndrome and 17 normal controls. NK activity in the patients was significantly reduced compared with normal controls (34.6 ± 3.4% versus 52.2 ± 3.4%, P < 0.001). Patients with secondary Sjögren's had lower cytotoxicity compared with those who had primary Sjögren's (28.5 ± 5.5% versus 37.3 ± 4.2%, P < 0.01). The proportion of PBMC with characteristics of NK cells was not decreased in the patients. NK by normal PBMC was diminished both in the presence of sera from patients with reduced NK and when the effector cells were pretreated with the sera. Pretreatment of target K562 cells did not alter NK activity. Suppression of NK by sera from patients did not correlate with levels of immune complexes or with antilymphocyte antibodies. Some patients had adherent cells which inhibited NK function. Addition of either indomethacin or catalase partially restored NK activity in such patients, indicating that both prostaglandins and hydrogen peroxide play a role in suppression. These data suggest that multiple mechanisms are involved in the defective NK activity seen in patients with Sjögren's syndrome. The reduction of NK activity in Sjögren's syndrome may contribute to the increased incidence of lymphoid malignancy.
Esophageal abnormalities and dysphagia in polymyositis and dermatomyositis
Authors: Merieux Paula De , Anthony Verity M. , Clements P. J. , Paulus Harold E. 
Published: February 2007

AbstractStructural or functional abnormalities of the distal esophagus were demonstrated by cineradiography in 14 of 16 patients with polymyositis or dermatomyositis who had been incompletely responsive to high dose corticosteroids and, in some cases, immunosuppressive therapy, or who had adverse effects associated with these therapies. These distal abnormalities occurred in the absence of proximal esophageal skeletal muscle dysfunction in 70% of patients, usually were more frequent with increasing disease duration, and were functionally similar to abnormalities reported in scieroderma. Symptomatic improvement occurred in some patients with administration of antacids and measures designed to decrease esophageal reflux, but improved esophageal symptoms did not correlate with improvement in the myositis. In 18 autopsy subjects with similar histories, distal esophageal smooth muscle atrophy and fibrosis occurred in only 1 and 2 cases, respectively. Of 5 in whom distal esophageal dysmotility had been documented ante‐mortem, only 1 had fibrosis and none had smooth muscle atrophy. These findings suggest that factors other than fibrosis and muscle atrophy may contribute to distal esophageal dysmotility in polymyositis and dermatomyositis.
Isolation of an interleukin‐1‐like factor from human joint effusions
Authors: Wood D. D. , Ihrie E. J. , Dinarello C. A. , Cohen P. L. 
Published: February 2007

AbstractInterleukin‐1 (IL‐1) is a macrophage derived mediator whose properties suggest that it could play a role in the pathology of arthritis. To test this hypothesis, joint fluids from patients with several different arthritides were tested. Small amounts of IL‐1‐like activity were recovered from many of these joint fluids after affinity chromatography over a column of rabbit anti‐human IL‐1. Positive fluids were obtained from patients with rheumatoid arthritis, psoriatic arthritis, Reiter's syndrome, osteoarthritis, gout, and traumatic arthritis. Upon gel filtration, the joint derived factor displayed a molecular weight distribution similar to that of IL‐1 derived from human monocytes stimulated in vitro. These results suggest that IL‐1 is present in joint effusions and, therefore, might contribute to joint destruction.
Pain in the rheumatic diseases
Authors: Kazis Lewis E. , Meenan Robert F. , Anderson Jennifer J. 
Published: February 2007

AbstractThe importance of pain in the health status and health behavior of patients with chronic rheumatic disease was evaluated. The Arthritis Impact Measurement Scales were used to estimate physical disability, psychological status, and pain in a large set of rheumatic disease patients. Explanatory regression models were built to explore the contribution of pain in physician and patient assessments of overall health, medication usage, and changes in health status over time. Results confirm that pain makes a highly significant contribution to explaining both physician and patient overall health assessments (P < 0.001). Pain is also the most important of the 3 health status components in explaining medication usage (P < 0.001). Finally, using prospective data, it is shown that current pain, rather than current physical or psychological disability, is the best predictor of subsequent pain (P < 0.001). Current pain also is most associated with subsequent physical disability (P < 0.05). These findings confirm the importance of pain in determining the health status and health behavior of individuals with chronic rheumatic disease, and suggest that doctors and other health professionals should continue to solicit and address the patient's complaints of pain.
The significance of thrombocytopenia in systemic lupus erythematosus
Authors: Miller Marian H. , Urowitz Murray B. , Gladman Dafna D. 
Published: February 2007

AbstractThe significance of thrombocytopenia in systemic lupus erythematosus (SLE) is unclear. Some researchers have found it associated with severe disease, others with mild disease. Thrombocytopenia (platelets < 100,000) occurred in 21 patients seen at an SLE clinic over 18 months. Prospective assessment of 19 (non‐SLE causes excluded) revealed 2 distinct subgroups. Seven were thrombocytopenic only during severe multisystem flares. Twelve had chronic thrombocytopenia with intermittent mild flares in other systems. Serious bleeding was rare in both subgroups. It was concluded that thrombocytopenia clearly is not a prognostic indicator.
Impaired natural killer cell function in systemic lupus erythematosus
Authors: Sibbitt Wilmer L. , Likar Laura , Spellman Craig W. , Bankhurst Arthur D. 
Published: February 2007

AbstractImmune regulation requires clonal expansion of regulatory T cells which is dependent on the presence of interleukin‐2 (IL‐2). Previously, both natural killer (NK) cell function and IL‐2 production were found to be depressed in systemic lupus erythematosus (SLE). This study was designed to determine the relationship between IL‐2 production and NK cell activity in SLE. NK activity as determined by a standard 4‐hour51Cr‐release assay was impaired in SLE (11.0 ± 5.1 lytic units/107cells) compared with controls (25.1 ± 7.1 lytic units/107cells) (P< 0.05). IL‐2 production was induced with concanavalin A and phorbol ester and quantitated using the IL‐2 dependent cell line HT‐2. IL‐2 production was impaired in only 1 SLE patient, despite concomitant abnormalities in NK function in the SLE group as a whole. Moreover, in patients with impaired NK activity, incubation of lymphocytes with exogenous IL‐2 did not restore NK activity to normal levels. These findings demonstrate that impaired NK activity in SLE is independent of IL‐2 production and that defects in IL‐2 production in SLE may not be as common as previously reported.
Connective tissue activation
Authors: Cabral A. , Castor C. W. 
Published: February 2007

AbstractFour normal (NF) and 4 scleroderma skin fibro‐blast (SF) strains were compared with respect to 1) basal 14C‐glucosamine and 35SO4‐labeled glycosaminoglycan (GAG) synthesis, 2) responsiveness to autacoid mediators, and 3) performance following maximal stimulation. Under basal conditions, SF synthesized and secreted 2–3 times more radioactive hyaluronic acid than the NF (P < 0.001); molecular volume by gel chromatography was similar and suggested a high molecular weight product. SF were essentially as responsive to normal lymphoid and platelet factors as were NF. No consistent qualitative or quantitative differences in sulfated GAG synthesis were noted between the 2 groups of cells. Incubation of NF and SF with a false “core protein” such as p‐nitrophenyl‐β‐D‐xyloside suggested that synthesis of the core protein was rate limiting; SF and NF were equally facile in SO4‐GAG chain synthesis in the presence of a β‐xyloside. SF appear to retain in vitro a partially activated state for many generations, at least with respect to hyaluronic acid synthesis.