bluuebunny/crossref_metadata_2025 huggingface dataset:
Abnormalities in the content of nucleic acids of peripheral blood mononuclear cells from patients with systemic lupus erythematosus. Relationship to dna antibodies
Authors: Alarcón‐Segovia Donato , Llorente Luis , Fishbein Eugenia , Díaz‐Jouanen Efraín
Published: February 2007

We have completed 59 cytofluorographic studies of DNA/RNA content in acridine orange‐stained peripheral blood mononuclear cells from 44 patients with systemic lupus erythematosus, most of whom received no medications. Most such cells were in resting phases of the cell cycle, particularly those from patients with inactive disease. Nine patients with systemic lupus erythematosus had increased percentages of these cells in the synthesis and postsynthesis phases of the cell cycle; the B lymphocytes had the greatest proportions of activated cells. In 11 patients, we found that cells, particularly T lymphocytes, had increased RNA content without a proportional increase in DNA. This DNA block occurred primarily in patients with serum antibodies to DNA and it could be reproduced in normal mitogen‐stimulated mononuclear cells incubated in heat‐inactivated sera from patients with systemic lupus erythematosus whose own cells showed abnormalities of DNA/RNA content or in purified native DNA antibody. The DNA blocking potential of the DNA antibody was dependent on its Fc portion and on the presence of Fc receptors on T cells. Thus, saturation of Fc receptors by pretreatment with aggregated IgG or incubation with the whole antibody in the cold prevented the DNA block, indicating that it was an active process.
Suppression of the normal autologous mixed leukocyte reaction by sera from patients with systemic lupus erythematosus
Authors: Hahn Bevra H. , Pletscher L. Susan , Muniain Miguel , Macdermott Richard P.
Published: February 2007

Sera from 15 patients with active systemic lupus erythematosus and 7 patients with inactive lupus were added to normal autologous mixed leukocyte reaction (MLR) cultures. Twelve of the 22 sera reduced autologous T cell proliferative responsiveness to B plus null (B+N) cells or macrophages by 50% or more. This inhibition correlated with defective autologous MLR in fresh mononuclear cells from those patients. When normal responding and stimulating cell populations were preincubated with suppressive lupus sera, then added to autologous MLR cultures that contained normal serum, proliferative responses were also reduced; inhibitors are directed against participating mononuclear cell subpopulations. The suppressive serum factors were directed variously against monocyte/macrophage (MΦ), B+N, or T cell populations; MΦ/T interactions were suppressed most frequently. The inhibitors were not removed by high‐speed centrifugation or by depletion of antibodies to DNA, and they did not correlate with the presence of lymphocytotoxic antibodies. The presence of serum inhibitors of normal MΦ/T and B+N/T autologous MLR may be an immunologic abnormality important in the initiation, perpetuation, or exacerbation of systemic lupus erythematosus.
Autologous and allogeneic mixed lymphocyte reactions in progressive systemic sclerosis
Authors: Morse Jane H. , Bodi Betsy S.
Published: February 2007

The autologous and allogeneic mixed lymphocyte reactions (MLR), observed when peripheral blood mononuclear cells from 20 patients with progressive systemic sclerosis were used, were compared with those of age‐, sex‐, and race‐matched normal controls. Such cells were separated by gradient centrifugation of sheep red blood cell (E) rosettes into stimulator (E‐ or non‐T cell) and responder (E+ or T cell) populations. The autologous MLR of both the progressive systemic sclerosis and normal peripheral blood mononuclear cells varied widely but there was no statistical difference between the means of each group. In the allogeneic MLR, proliferation between progressive systemic sclerosis non‐T cells and normal T cells was significantly less than that of normal non‐T cells and progressive systemic sclerosis T cells (P = 0.001). A decreased autologous MLR, while noted with other autoimmune diseases, was lacking in progressive systemic sclerosis. This suggests a different defect. The differences in the allogeneic MLR also suggest that either progressive systemic sclerosis non‐T cells were poor stimulators or T cells associated with this disease were better responders when compared with similarly prepared cell populations from normal individuals. The MLR differences could have also resulted from compositional subset alterations or the sharing of a common antigen. HLA—DR5 was found in 9 of the 17 white patients with progressive systemic sclerosis. Although these individuals were evenly distributed as low, medium, and high responders, this finding showed that some progressive systemic sclerosis non‐T cells shared a common antigen.
Serum interferon levels in patients with systemic lupus erythematosus
Authors: Ytterberg Steven R. , Schnitzer Thomas J.
Published: February 2007

Levels of interferon (IFN) were measured in 81 serum samples from 23 patients with systemic lupus erythematosus (SLE) by a plaque‐reduction method and correlated retrospectively with clinical records of disease activity, anti‐DNA binding, and serum complement measurements. IFN titers were found to correlate with both clinical disease activity and anti‐DNA binding, but no relation was found to serum complement. Most (76.6%, 31 of 41) serum samples obtained during periods of active disease contained measureable amounts of IFN, but only 9.1% (2 of 22) of results of tests on samples obtained during periods of disease quiescence were positive (P < 0.005). Of samples with clearly elevated anti‐DNA binding (> 40%), 69.7% (23 of 33) had positive results for IFN, but 57.1% (8 of 14) had negative results when the anti‐DNA binding was normal (< 20%) (P < 0.005). Measurement of serum IFN titers in patients with SLE, therefore, provides another serologic marker of disease activity. Contrary to the findings of previous studies, the IFN found in the present study was characterized as IFN‐α, or Type I IFN, on the basis of acid stability and neutralization by antibody to IFN‐α. Of interest are the questions raised about the origin of IFN in the sera of patients with SLE and what role IFN might have in the pathogenesis of the autoimmune disease in view of the many documented immunomodulating effects of IFN.
Immune functions of human synovial cells. phenotypic and t cell regulatory properties of macrophage‐like cells that express hla–dr
Authors: Klareskog Lars , Forsum Urban , Kabelitz Dieter , Plöen Leif , Sundström Christer , Nilsson Kenneth , Wigren Anders , Wigzell Hans
Published: February 2007

Normal and rheumatoid synovial cells have been analyzed in frozen sections and in suspension. HLA–DR‐expressing, macrophage‐like cells are demonstrated in normal synovial intima and in rheumatoid tissue. Suspended normal synoviocytes equaled peripheral blood non–T lymphocytes as stimulators of mixed lymphocyte reactions, whereas adherent rheumatoid synovial cells were extremely efficient as such stimulators and in presenting soluble antigens to autologous T lymphocytes. This HLA–DR‐dependent T lymphocyte regulation might provide a cellular basis for the HLA–D haplotype–arthritis associations.
Seronegative rheumatoid arthritis.
Authors: AlarcóN Graciela S. , Koopman William J. , Acton Ronald T. , Barger Bruce O.
Published: February 2007

Measurement of serum rheumatoid factor (RF) by conventional methods in patients with rheumatoid arthritis (RA) has repeatedly identified a subpopulation of patients without detectable RF. Previous investigators have consistently confirmed the association of HLA–DR4 with seropositive RA, but studies of seronegative RA have been limited and contradictory. We studied 140 randomly selected patients from Alabama, all of whom had either classic or definite RA, and we were able to obtain complete HLA typing for 110 of these individuals. Eighty were consistently seropositive (on at least 2 separate occasions) and 30 were consistently seronegative (on at least 3 separate determinations). There was no statistically significant difference between the seronegative RA patients and 123 control subjects in the distribution of DR antigens. In seropositive RA, there was a significant increase in DR4 (P<0.001; relative risk = 8.02; attributable risk = 49.2%) and a significant decrease in DR3 (P<0.001; relative risk = 0.14) and DR7 (0.01>P>0.001; relative risk = 0.33). The clinical data also distinguished between seropositive RA and seronegative RA; subcutaneous nodules (37.5%) and vasculitis (6.3%) were present only in seropositive RA. DR4 positivity did not correlate with any of the clinical variables measured in the seropositive RA group. In contrast, DR4 in the seronegative RA group was associated with more destructive disease. The data suggest that seronegative RA represents a disease entity clinically and immunogenetically distinct from seropositive RA. Moreover, our results indicate that DR4 may be a previously undisclosed marker for disease severity in seronegative RA.
The role of cell surface proteins in platelet stimulation by monosodium urate crystals
Authors: Jaques Bryon C. , Ginsberg Mark H.
Published: February 2007

To test whether urate crystal‐membrane protein interactions mediate platelet stimulation, platelet membrane proteins were radiolabeled by lactoperoxidase, extracted with 1% Triton X–100, and incubated with urate crystals. The crystal‐associated and supernate fractions were isolated and analyzed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS–PAGE) and by 2‐dimensional isoelectric focusing followed by SDS‐PAGE. Four of the lactoperoxidaseradiolabeled polypeptides that associated with urate crystals had reduced molecular weights and pIs of Mr = 105,000, pI 4.9; Mr = 123,000, pI = 4.9; Mr = 123,000, pI = 5.3; and Mr = 132,000, pI = 4.8–6.3, respectively. These proteins were characterized with regard to their labeling intensities, apparent isoelectric points, apparent molecular weights (reduced and nonreduced), lectin‐binding properties, carbohydrate‐ and protein‐staining characteristics, and presence or absence in Glanzmann's thrombasthenia. They have been identified as derived from glycoproteins Ib, IIb, and III (Phillips‐Agin nomenclature) and an unidentified membrane protein. To test whether removal of these proteins would result in a diminution of platelet response to urate, intact platelets were digested with chymotrypsin, resulting in cleavage of more than 80% of these proteins and a 5‐fold reduction in secretory responsiveness to urate crystals. Response to a second platelet stimulus, collagen, was unaffected, indicating an intact secretory mechanism. In addition, when platelets were preincubated with F(ab′)2 fragments of an antibody directed against these proteins, platelet secretory response to urate was inhibited by 50%, whereas the responses to collagen and thrombin were unaffected. Thus, membrane proteins appear to mediate platelet stimulation by urate crystals.
Immunosuppression by fractionated total lymphoid irradiation in collagen arthritis
Authors: McCune W. Joseph , Buckley Judith A. , Belli James A. , Trentham David E.
Published: February 2007

Treatments with fractionated total lymphoid irradiation (TLI) and cyclophosphamide were evaluated for rats injected with type II collagen. Preadministration of TLI and repeated injections of cyclophosphamide suppressed the severity of arthritis and lowered antibody titers to collagen significantly. TLI initiated at the onset of collagen arthritis decreased humoral and cellular responses to collagen but did not affect the severity of arthritis. These data demonstrate that both TLI and cyclophosphamide are immunosuppressive in an experimentally inducible autoimmune disease.
Clinical responses during gold therapy for rheumatoid arthritis. changes in synovitis, radiologically detectable erosive lesions, serum proteins, and serologic abnormalities
Authors: Sharp John T. , Lidsky Martin D. , Duffy Joseph
Published: February 2007

Gold therapy given to 73 patients with rheumatoid arthritis was associated with remission of synovitis for 3 months or longer in 27 patients and 50% or greater improvement in 20 patients. New joint deformities did not develop in patients who experienced remission, and progression of radiologically detectable erosive changes was prevented. Serum protein and serologic abnormalities were improved in all groups, but patients who had a good response experienced the greatest improvement. No single clinical or laboratory feature in the pretreatment assessment predicted response, but, as a group, the patients with the best response also ranked best for most prognostic indicators.
Estrogen and glucocorticoid receptors in adult canine articular cartilage
Authors: Young PETER C. M. , Stack Michael T.
Published: February 2007

The cytoplasmic and crude nuclear fractions of adult mongrel dog articular cartilage contained estradiol‐ and dexamethasone‐binding components which had properties of physiologic steroid receptors. The equilibrium dissociation constants averaged 0.37 nM for estradiol and 2.27 nM for dexamethasone. The concentrations of estrogen receptors ranged from below 6 to 101 fmol/mg protein in the cytosols and from below 2.8 to 17.5 fmol/μg DNA in the nuclear fractions. Glucocorticoid receptors were detected in only 4 of 13 cytosols (range: 61.2–132 fmol/mg protein), whereas 10 of 13 nuclear fractions contained 0.8 to 46.8 femtomoles of the receptors for each microgram of DNA. There appeared to be no marked difference between the contents of either steroid receptor in female or male dog cartilage. No receptors were detected for androgen and progesterone.
Prior gold therapy does not influence the adverse effects of D‐penicillamine in rheumatoid arthritis
Authors: Kean Walter F. , Lock Colin J. L. , Howard‐Lock Helen E. , Buchanan W. Watson
Published: February 2007

One hundred fourteen patients with definite or classic rheumatoid arthritis were followed prospectively between January 1976 and April 1981 to monitor their toxicity pattern to D‐penicillamine. The influence of previous sodium aurothiomalate therapy on the toxicity pattern of D‐penicillamine is described. There was no significant difference in overall outcome of the patients treated with D‐penicillamine with respect to adverse effects, whether they had previous gold toxicity, previous gold therapy but no toxicity, or no previous gold therapy. The time from gold toxicity to the start of D‐penicillamine therapy was greater in those who did not develop D‐penicillamine toxicity compared with those who did. This difference just reached statistical significance. Total gold salt received had no effect on eventual outcome of D‐penicillamine treatment, and the toxicity pattern of D‐penicillamine in those patients who had previous gold therapy was similar to those patients who had never received gold therapy.
Ultrastructure of arthritis induced by a caprine retrovirus
Authors: Brassfield Alberta L. , Adams D. Scott , Crawford Timothy B. , Mcguire Travis C.
Published: February 2007

The ultrastructure of early retrovirus‐induced arthritis was studied sequentially in 20 goat kids inoculated with caprine arthritis—encephalitis virus. Synovial lesions began as intercellular edema and collagen fragmentation and continued as progressive mononuclear cell infiltration and lining cell hyperplasia, hypertrophy, and necrosis. At 18 through 45 days after the inoculation, lining cells contained small accumulations of virus‐like particles similar to virus seen in infected tissue culture cells. No virus was seen budding from infected lining cell membranes.
Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis
Authors: Borenstein David G. , Gibbs Christina A. , Jacobs Robert P.
Published: February 2007

Nonvolatile short‐chain fatty acids from 80 synovial fluids were quantified by gas‐liquid chromatography. Succinic acid was detectable in all 23 septic synovial fluids infected with either gram‐positive or gramnegative organisms and in only 5 of 57 nonseptic synovial fluids. Lactic acid was present in all of the effusions but was correlated with septic arthritis only when present in concentrations greater than 250 mg%. Neither short‐chain fatty acid was more sensitive than high white blood cell counts (>50,000 mm3) or depressed glucose concentration (<40 mg/dl) in diagnosing septic arthritis before antibiotic therapy; however, the detection of succinic acid was helpful in identifying patients with septic arthritis who had been given antibiotic treatment before arthrocentesis. Thus, gas‐liquid chromatography, a rapid and sensitive method for the detection of short‐chain fatty acids, may complement the currently available methods used to diagnose septic arthritis.
Nailfold capillary abnormalities and clinical outcome in childhood dermatomyositis
Authors: Spencer‐Green George , Crowe William E. , Levinson Joseph E.
Published: February 2007

The nailfold capillary pattern was observed in a population of patients with childhood dermatomyositis. Distinctive nailfold capillary loop abnormalities were found in 11 of 19 childhood dermatomyositis patients and in none of 2 control populations (P < 0.001). By a retrospective analysis of the childhood dermatomyositis patients, we found that the presence of nailfold capillary abnormalities correlates with more severe forms of the disease (ulcerative and chronic types), as opposed to limited type of disease. These changes occurred independently of disease activity or of cutaneous abnormalities.
Interrelationships of HLA‐DR, MB, AND MT phenotypes, autoantibody expression, and clinical features in systemic lupus erythematosus
Authors: Ahearn Joseph M. , Provost Thomas T. , Dorsch Carole A. , Stevens Mary Betty , Bias Wilma B. , Arnett Frank C.
Published: February 2007

The interrelationships of serologic and clinical features and the HLA–DR, MB, and MT specificities were examined in 70 white patients with systemic lupus erythematosus. HLA–DR2 and MB1 were significantly increased when compared with controls from the Eighth International Histocompatibility Testing Workshop but not with local controls. DR2 and DR3 correlated with increased seroreactivity (anti‐Ro, antiDNA, rheumatoid factor, and hyperglobulinemia), and anti‐Ro with clinically overt sicca complex. Thus, DR2 and DR3 may be markers of a major histocompatibility complex–mediated immune hyperresponsiveness that affects expression of systemic lupus erythematosus.
Serum pepsinogen i in rheumatic diseases. reduced levels in sjögren's syndrome
Authors: Maury C. Peter J. , Räsänen VESA , Teppo Anna‐Maija , Helve Tapani , Wegelius Otto
Published: February 2007

Group I pepsinogens were measured by radioimmunoassay in the sera of 93 patients with rheumatic diseases and 99 controls. Patients with rheumatoid arthritis and systemic lupus erythematosus had levels of pepsinogen I similar to controls, whereas patients with Sjögren's syndrome had levels significantly lower than either controls (P<0.001) or patients with rheumatic diseases not associated with sicca syndrome (P<0.001). The concentrations of serum pepsinogen I were lower in patients with sicca syndrome alone than in those with sicca syndrome associated with some other connective tissue disease (P<0.05). In patients with Sjögren's syndrome, a negative correlation was found between serum concentrations of β2‐microglobulin and pepsinogen I (r = −0.46, P<0.05).
STRAIN and sex variation in the susceptibility to streptococcal CELL WALL–INDUCED POLYARTHRITIS IN THE RAT
Authors: Wilder Ronald L. , Calandra Gary B. , Garvin A. Julian , Wright Karen D. , Hansen Carl T.
Published: February 2007

Sixteen inbred rat strains were examined for susceptibility and resistance to group A streptococcal cell wall–induced polyarthritis. The findings indicated that 2 or more genetic loci, as well as sex‐related factors, played a major role in determining susceptibility to arthritis in this model. Breeding studies demonstrated that susceptibility was a dominant or codominant trait. A positive association between the severity of arthritis and the development of chronic inflammation in multiple tissues was also observed. In strains that were relatively resistant to arthritis, chronic inflammation was generally limited to the spleen. Since translocation of the poorly degradable and phlogogenic streptococcal cell walls to the synovium and other tissues appears to initiate inflammation, these studies suggested that susceptibility might be the result of a defect in host mechanisms limiting cell wall dissemination.
HUMAN COMPLEMENT ACTIVATION BY SELF‐ASSOCIATED IgG RHEUMATOID FACTORS
Authors: Brown Paul B. , Nardella Francis A. , Mannik Mart
Published: February 2007

IgG rheumatoid factors (IgG–RFs) undergo concentration‐dependent self‐association into dimers and higher polymers, as previously reported. The interactions of purified IgG–RF from the plasma of 3 patients with rheumatoid arthritis, with guinea pig and human complement were studied. Self‐associating IgG–RFs were isolated by affinity columns and gel filtration. These preparations contained no detectable IgM and were composed only of IgG subclasses known to fix complement. Complement utilization of IgG–RF was compared with that of monomeric IgG, heat‐aggregated IgG, and soluble rabbit IgG immune complexes. Although incubation of IgG–RF or monomeric IgG with 3 units of guinea pig or human complement resulted in decreased hemolysis of sheep erythrocytes sensitized with IgM hemolysin, these substances were less than 100 times as effective as heat‐aggregated IgG or soluble immune complexes. The ability of human or guinea pig complement that had been incubated with IgG–RF to restore hemolytic activity to C4‐deficient guinea pig serum served to distinguish Clq binding from complement cascade activation. IgG–RFs and monomeric IgG did not activate guinea pig complement cascade in contrast to aggregated IgG. IgG–RFs, however, activated human complement cascade; monomeric IgG only bound human Clq. These results indicate that self‐associated IgG–RFs can activate human complement in fluid phase, but less effectively than aggregated IgG or large‐latticed immune complexes.
Immune complexes in progressive systemic sclerosis (scleroderma)
Authors: Seibold James R. , Medsger Thomas A. , Winkelstein Alan , Kelly Robert H. , Rodnan Gerald P.
Published: February 2007

Serum immune complexes were measured in 92 patients with progressive systemic sclerosis, and elevated levels were found as follows: Raji cell assay 72% (59% after pronase treatment of Raji cells), agarose gel electrophoresis 52%, and C1q binding 24%. Fortythree (47%) had abnormal results on two or more of these tests, but only 17 (18%) had normal results by all three assays. Computer‐assisted analysis of immune complex results and extensive clinical and laboratory data compiled on these patients revealed that the patients with abnormal Raji cell assays more often had diffuse scleroderma, tendon friction rubs, and positive serum antinuclear antibody tests than did patients with negative results on Raji cell assays. Individuals with immune complexes detected by C1q binding had evidence of pulmonary involvement and positive serum rheumatoid factor more frequently than did patients whose C1q tests were negative.
Circulating immune complexes in patients with progressive systemic sclerosis
Authors: Siminovitch K. , Klein M. , Pruzanski W. , Wilkinson S. , Lee P. , Yoon Sung‐Ja , Keystone E.
Published: February 2007

Forty‐one patients with progressive systemic sclerosis were studied for the presence of immune complexes by the fluid‐ and solid‐phase C1q binding, C1 activation, and the fluid‐phase conglutinin assays. Complement activation and autoantibodies were also studied. Immune complexes were detected in only 6 patients (15%); activation of complement was found in 5 others. The clinical and serologic features of patients with complexes were compared with those in whom complexes were not identified. No significant difference was found with respect to serology. Organ involvement was generally more frequent in the group with immune complexes, but the difference was statistically significant only with respect to lung involvement. The present data suggest that, although complement‐fixing immune complexes are infrequently detected in progressive systemic sclerosis, they may play a role in the pathogenesis of lung lesions associated with the disease.
Effect of purified growth factors on rabbit articular chondrocytes in monolayer culture. II. sulfated proteoglycan synthesis
Authors: Prins A. Pieter A. , Lipman Jack M. , Mcdevitt Cahir A. , Sokoloff Leon
Published: February 2007

The effect of 3 purified peptide growth factors—platelet‐derived growth factor (PDGF), epidermal growth factor (EGF), pituitary fibroblast growth factor (FGF)—heat‐inactivated fetal bovine serum (FBS), insulin, and 0.2 mM ascorbate on synthesis of sulfated proteoglycan by rabbit articular chondrocytes was studied in monolayer culture. Growth of the cells increased linearly as the concentration of heat‐inactivated FBS rose from 0 to 30%. Glycosaminoglycan (GAG) synthesis (35SO4/μg DNA) was enhanced as the concentration of heat‐inactivated FBS went from 0 to 5%. At higher levels of serum, radiosulfate incorporation declined progressively. Two modes of study of the test factors were used: 1) the dose of the factor was increased while the serum concentration was fixed at a low basal level (1% heat‐inactivated FBS); 2) the dose of the test factor was kept constant but the level of heat‐inactivated FBS varied from 0 to 10%. There was an inverse relationship between GAG and DNA synthesis when proliferation of cells was increased by EGF and platelet lysate. PDGF (1 U/ml) stimulated radiosulfate incorporation as well as DNA formation in the serum‐free medium; the values for GAG synthesis did not increase as the serum concentration increased, but the cell mass did. The action of FGF was intermediate between that of EGF and PDGF: with 50 ng FGF/ml, increasing concentrations of serum caused a large progressive reduction of radiosulfate incorporation as growth was stimulated. In basal medium, however, FGF caused mild enhancement of GAG synthesis. Insulin increased aggregatable proteoglycan production far out of proportion to its growth‐promoting activity in the presence of 1% heat‐inactivated FBS. The response was effaced when higher concentrations of serum were employed. Ascorbate had a unique anabolic effect, increasing both cell growth and proteoglycan synthesis that is not suppressed by higher concentrations of serum. The content of serum and its several peptide and hormonal components thus have divergent effects on growth and proteoglycan synthesis in cell culture. This phenomenon must be taken into account in studying biochemical processes and pharmacologic reactions of articular chondrocytes in vitro.
Evidence for the local production and utilization of immune reactants in rheumatoid arthritis
Authors: Cecere F. , Lessard J. , Mcduffy S. , Pope R. M.
Published: February 2007

Immunoglobulins, including rheumatoid factors, are produced by the rheumatoid synovial membrane. A significant contribution of the synovial membrane to the total IgG and IgM detected in the synovial fluid has been documented. The present study was designed to examine the contribution of the synovial membrane to the rheumatoid factors detected in the synovial fluid. Analysis of the data demonstrated that the synovial membrane was the source of a significant component of the total synovial fluid IgA rheumatoid factor and IgM rheumatoid factor. While some fluids possessed extremely elevated concentrations of the IgG rheumatoid factor, the data suggested that IgG rheumatoid factor was preferentially reduced, relative to total IgG, by the rheumatoid inflammatory process. These observations suggest a potentially important role for IgG rheumatoid factor in rheumatoid synovitis.
Nonreducible rotational head tilt and lateral mass collapse. a prospective study of frequency, radiographic findings, and clinical features in patients with rheumatoid arthritis
Authors: Halla James T. , Fallahi Sohrab , Hardin Joe G.
Published: February 2007

Of 126 hospitalized, but otherwise unselected, patients with rheumatoid arthritis, 12 (10%) had a persisting nonreducible rotational head tilt deformity (NRRHT). These 12 were grouped with an additional 12 similar subjects, previously found to have the same condition, and all 24 were compared with the remaining 114 who did not have head tilt. Patients with NRRHT differed significantly from the others in that the former were more likely to have a destructive peripheral arthritis, headache, limited neck motion, and various cervical subluxations. All 24 subjects with NRRHT had predominately unilateral collapse of the lateral masses of the atlas and/or axis, compared with only 2 of the 114 with normal head position. The head always tilted to the side of the lateral mass collapse, which appeared to be the sole or major cause of the abnormal head position.
Functional aberration of t cell subsets in patients with behclet's disease
Authors: Sakane Tsuyoshi , Kotani Hiroyuki , Takada Shinsuke , Tsunematsu Tokugoro
Published: February 2007

Abnormalities of concanavalin A–induced suppressor activity and autologous mixed lymphocyte reaction (which is part of the regulatory role of T cells on lymphocyte functions) were observed in patients with preactive Behçet's disease. However, both the functions returned to normal when the patients entered an active or inactive phase of disease. Thus, a diminution of suppressor function appears to be necessary for the initiation or potentiation of autoimmune and/or inflammatory abnormalities in Behçet's disease. Results of studies of T cell subsets and their functional analysis in patients with preactive Behçet's disease provide further evidence in support of this hypothesis.
Serum eosinophilotactic activity in eosinophilic fasciitis
Authors: Wasserman Stephen I. , Seibold James R. , Medsger Thomas A. , Rodnan Gerald P.
Published: February 2007

Serum eosinophil chemotactic activity was determined by the Boyden chamber technique in 20 patients with eosinophilic fasciitis. Increased eosinophil chemotactic activity (>125% of background) was found in all 20 patients (mean 297% ± 129), whereas sera of 20 controls with systemic sclerosis and diffuse scleroderma had increased eosinophil chemotactic activity in only 6 (30%) instances (mean 96% ± 47, P<0.001). Although serum eosinophil chemotactic activity decreased over time in all 8 eosinophilic fasciitis patients studied longitudinally, this activity returned to normal in only 3, all of whom received prolonged courses of corticosteroids. Preliminary data suggest the existence of a eosinophilotactic serum factor common to patients with eosinophilic fasciitis.
Increased endothelial cell adherence, aggregation, and superoxide generation by neutrophils incubated in systemic lupus erythematosus and felty's syndrome sera
Authors: Hashimoto Yoshimi , Ziff Morris , Hurd Eric R.
Published: February 2007

The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated. PMN from normal healthy donors were incubated in sera from 19 patients with active SLE, 12 with inactive SLE, 20 with Felty's, 24 with rheumatoid arthritis, and 34 normal persons. After incubation, the degree of adherence of the PMN to human endothelial cells in culture, their aggregation, and superoxide (O2‐) generation were determined. Sera from patients with both active SLE and Felty's syndrome induced significantly increased PMN adherence to endothelial cells and PMN aggregation in vitro, compared with normal sera. This increased adherence to endothelial cells was maintained after heat treatment (56°C for 30 minutes) of the sera. In O2‐ generation experiments, sera from patients with active SLE induced significantly increased O2‐ release from normal PMN using both fresh and heat‐treated sera. Sera from Felty's patients demonstrated the same effect with heattreated sera but not with fresh sera. When sera from patients with active SLE and Felty's syndrome were used, all three parameters correlated significantly with each other in individual patients. In contrast, sera from the 12 patients with inactive SLE and 24 rheumatoid arthritis patients without Felty's failed to induce significant differences in the three parameters studied when compared with 34 normal controls. Fractionation of 3 SLE sera and 1 Felty's serum on Sephadex G‐200 demonstrated that the adherence enhancing factor was present in both IgG and IgG‐excluded fractions. The observed increased adhesiveness of PMN induced by SLE and Felty's sera may, at least in part, contribute to the neutropenia which is common in these diseases. Increased O2‐ release associated with PMN adherence may contribute to endothelial cell damage and vascular injury, which is also a common manifestation of these diseases.
Articular cartilage in the degenerative arthropathy of hemochromatosis
Authors: Schumacher H. Ralph
Published: February 2007

Iron was readily demonstrated in chondrocytes in 3 of 4 hemochromatosis articular cartilages studied. Either apatite, calcium pyrophosphate dihydrate crystals, or both were found in all cartilages including those of 3 patients who had no radiographic or light microscopic evidence of calcification. These crystals, which may be secondary to degenerative changes or may play a role in cartilage degeneration, were not seen in any consistent morphologic relationship with the iron deposits. In fact, apatite was found in one cartilage in which no iron was identified in the sections studied. If iron, as demonstrated in the chondrocytes, is contributing to the calcium crystal deposition, it would most likely do so indirectly, for example by altering chondrocyte enzymes or connective tissue components.
Anticentromere antibody
Authors: Mccarty Gale Anne , Rice John R. , Bembe Mary L. , Barada Franc A.
Published: February 2007

The presence of antibody to the chromosomal centromere appears to be associated with a subset of patients with the limited CREST form of scleroderma. To further define the prognostic value of this autoantibody, 27 patients, who were identified as having anticentromere antibody by screening antinuclear antibody tests using HEp‐2 cell substrates, were followed clinically and serologically for 2 years. The presence of anticentromere antibody is common in the limited CREST forms of systemic sclerosis, and it is often the only autoantibody specificity present in the sera of patients with the CREST variant. When compared with other patients who exhibit speckled or nucleolar antinuclear antibody patterns, those with anticentromere antibody had significantly less major organ system involvement.
Rheumatoid synovial cell morphologic changes induced by a mononuclear cell factor in culture
Authors: Baker Daniel G. , Dayer Jean‐Michel , Roelke Merrilee , Schumacher H. Ralph , Krane Stephen M.
Published: February 2007

Adherent rheumatoid synovial cells in culture produce large amounts of prostaglandin E2 (PGE2) and collagenase. When exposed to a monocyte‐derived factor, such cells exhibit marked increases in PGE2 and collagenase production. In addition, cellular morphology becomes more stellate. In the presence of this factor, indomethacin inhibits both PGE2 production and the stellate changes, whereas collagenase production usually continues at a high rate. Addition of PGE2 to cultures reproduces the stellate change as does the cyclic adenosine monophosphate (cAMP) analog 8‐bromo‐cAMP. Colchicine inhibits morphologic transformation induced by the monocyte‐derived factor, whereas cytochalasin B has no effect. It appears that the stellate morphology is dependent upon PGE2‐induced cAMP stimulation and is not related to collagenase production per se.
Differential release of plasminogen activator and latent collagenase from mononuclear cell‐stimulated synovial cells
Authors: Golds Elaine E. , Ciosek Carl P. , Hamilton John A.
Published: February 2007

Independent studies have previously shown that mononuclear cell supernatants stimulate the release of plasminogen activator and latent collagenase from synovial cell monolayer cultures. Simultaneous secretion of these enzymes could be an important pathway for tissue destruction under inflammatory conditions, since plasminogen activator can cause activation of latent collagenase in the presence of plasminogen. We investigated the kinetics of release of the two enzymes from synovial cells in response to the addition of mononuclear cell supernatants and retinoic acid. Synovial cells derived from osteoarthritic and rheumatoid arthritic patients responded similarly. Plasminogen activator is released within a few hours of stimulation, and secretion usually stops when the stimulus is removed. In contrast, significant amounts of collagenase are secreted only after an initial lag period of 1–2 days, and secretion is sustained long after removal of mononuclear cell supernatant. Another difference in regulation of the secretion of these two neutral proteinases is that the addition of all‐trans retinoic acid to the same synovial cell culture elevates plasminogen activator secretion while suppressing that of latent collagenase. Differential regulation of these enzymes under conditions of chronic inflammation may allow for continual accumulation of latent enzyme(s) which are activated during short periods of plasminogen activator release.
Anemia associated with rheumatoid disease
Authors: Harvey Andrew R. , Clarke Bryan J. , Chui David H. K. , Kean Walter F. , Watson Buchanan W.
Published: February 2007

Cell culture techniques were used to evaluate the number of erythroid colonies formed by circulating progenitor cells from 24 patients with rheumatoid disease and controls. A highly significant inverse correlation was demonstrated between erythroid colony counts and serum IgM and rheumatoid factor concentrations in the rheumatoid patients. The potential role of these factors in the pathogenesis of the anemia of rheumatoid disease is discussed.
HLA antigens in juvenile arthritis
Authors: Førre Øystein , Dobloug Jan H. , Høyeraal HANS M. , Thorsby Erik
Published: February 2007

Serologic HLA typing was performed in 77 patients with juvenile arthritis (JA). The frequency of the DR4 antigen was significantly increased in the seropositive but decreased in the seronegative patients—53% and 17%, respectively (P < 0.025)—compared with 27% in healthy Norwegians. An increased frequency of the HLA‐DR4 antigens was also found in polyarticular onset JA (50% compared with 27%, P < 0.05). The frequency of both the HLA‐B27 (21%) and the DR5 antigen (21%) was increased in the whole patient group compared with controls (10% and 9%, respectively, P < 0.01). The DR5 antigen was also increased in the systemic onset patients (40%, P < 0.05). Both the DR5 and the DR8 antigens were increased in the pauciarticular onset group (P < 0.05 and P < 0.01, respectively). The results support the view that seropositive and seronegative JA are different disease entities and also that seropositive JA may be an early form of seropositive rheumatoid arthritis. The association between the DR4 antigen and IgM rheumatoid factor suggests that the HLA‐DR4 gene or a closely linked gene may regulate autoimmune responses to self IgG.
Familial systemic lupus erythematosus in males
Authors: Lahita Robert G. , Chiorazzi Nicholas , Gibofsky Allan , Winchester Robert J. , Kunkel Henry G.
Published: February 2007

Several families in which systemic lupus erythematosus predominates in males are presented. The disease primarily manifested itself in the sons and in the male parents. Females in some of the families had other autoimmune diseases such as idiopathic thrombocy‐topenic purpura or symptoms suggestive of a lupus diathesis. It is suggested that the sons inherited the disease from their fathers in these families. The disease in the patients had some similarity to the disease in BXSB mice.
Collagenase and collagenolytic activity in human osteoarthritic cartilage
Authors: Pelletier Jean‐Pierre , Martel‐Pelletier Johanne , Howell David S. , Ghandur‐Mnaymneh Latifa , Enis Jerry E. , Frederick Woessner J.
Published: February 2007

Forty‐nine specimens of human cartilage were taken from 3 sites on the tibial plateau (center of osteoarthritic lesion, edge of lesion, and remote site) and graded histologically by the scale of Mankin. The tissue was homogenized and centrifuged to obtain an insoluble pellet. This was resuspended in buffer and incubated at 37°C, pH 7.5. Collagen digestion was quantitated by the release of hydroxyproline‐containing peptides. The highest collagenolytic activity (4.6%) was found in the center of lesions, declining in remote sites to 2.4% and in controls to 1.1%. Moderately severe disease of grade 6–9 had the highest collagenolytic activity. Approximately 55% of the metal‐dependent collagenolytic activity was in a latent form, activatable by amino‐phenylmercuric acetate; the remainder was self‐active. A method was developed for the extraction of collagenase from cartilage; the extracted enzyme produced the typical 75:25 cleavage products of type I collagen.
Tuberculosis of the greater trochanteric bursa
Authors: Rehm‐Graves Susan , Weinstein Allan J. , Calabrese Leonard H. , Cook Sebastian A. , Boumphrey Francis R. S.
Published: February 2007

A patient with tuberculosis of the greater trochanteric bursa is described, and the clinical and radiographic characteristics of the infection are reviewed. Despite the infrequency of skeletal tuberculosis, this infection should be considered in the differential diagnosis of chronic hip pain.
Effects of dietary enrichment with eicosapentaenoic acid upon autoimmune nephritis in female NZBXNZW/F1 MICE
Authors: Prickett James D. , Robinson Dwight R. , Steinberg Alfred D.
Published: February 2007

A menhaden oil diet, rich in eicosapentaenoic acid, protected female NZBxNZW/F1 mice from autoimmune nephritis. Only 15% of mice treated with the diet from weaning had died with severe renal disease at 19 months, versus 98% of controls on a beef tallow diet. The menhaden oil also protected these mice from renal disease when instituted at 4 and 5 months of age and, under these conditions, levels of anti‐native DNA antibodies were similar in both dietary groups. Our data suggest that the menhaden oil diet may act primarily to reduce inflammation via the ability of eicosapentaenoic acid to alter the production of prostaglandins and leukotrienes.
Capacity to solubilize immune complexes in sera and synovial fluids from patients with rheumatoid arthritis
Authors: Dayer E. , Gerster J. C. , Aguado M. T. , Lambert P. H.
Published: February 2007

Fifty‐six sera and 33 synovial fluids from rheumatoid arthritis patients were studied to evaluate their capacity to solubilize immune complexes. A decreased function was found in 65% of rheumatoid synovial fluids when compared with 13 osteoarthritis synovial fluids. The decrease of immune complex solubilization capacity correlated with the decrease of hemolytic activity of the alternative complement pathway (P < 0.001) and inversely with the level of immune complexes (P < 0.05). Synovial fluids with low and normal immune complex solubilization capacity were compared; the results confirmed a possible role of the synovial complement system in modulating the size and thus the diffusion and clearance of locally generated immune complexes.
Elevation of creatine kinase in amyotrophic lateral sclerosis
Authors: Harrington Thomas M. , Cohen Marc D. , Bartleson John D. , Ginsburg William W.
Published: February 2007

Serum creatine kinase (CK) levels were recorded in 100 patients with amyotrophic lateral sclerosis (ALS). CK concentrations were elevated in 43% of the patients, with a mean level of 240 U/liter and a range of 59–1,327 U/liter (male normal <95 U/liter, female normal <59 U/liter). All patients with elevated CK had muscle weakness. Seven patients were initially misdiagnosed as having polymyositis and given high dose corticosteroids without clinical benefit, prior to the diagnosis of ALS. Such diagnostic confusion can be avoided by an awareness that CK levels cannot be used to reliably differentiate between ALS and primary muscle disease such as polymyositis.
Morphologic observations in the early phase of the cartilage‐pannus junction
Authors: Shiozawa Shunichi , Shiozawa Kazuko , Fujita Takuo
Published: February 2007

The 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

IgG 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

The 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.