bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association of cerebrospinal fluid IgM index with central nervous system involvement in Behçet's disease
Authors: Hirohata Shunsei , Takeuchi Akiteru , Miyamoto Terumasa 
Published: February 2007

AbstractImmunoglobulin (IgM, IgA, and IgG) and albumin values were determined in 12 patients who had signs and symptoms of central nervous system involvement attributable to Behçet's disease. Only the cerebrospinal fluid IgM index, which was significantly elevated in patients with active neuro‐Behçet's syndrome, was found to decrease when the neurologic manifestations of the disease had disappeared. This indicates that determination of this index may be of help in the evaluation of central nervous system disease activity in neuro‐Behçet's syndrome.
Phosphoribosylpyrophosphate synthetase superactivity: A study of five patients with catalytic defects in the enzyme
Authors: Becker Michael A. , Losman Michele J. , Rosenberg Alan L. , Mehlman Ira , Levinson Dennis J. , Holmes Edward W. 
Published: February 2007

AbstractSuperactive phosphoribosylpyrophosphate (PRPP) synthetases were characterized in fibroblasts and erythrocytes from 5 unrelated men with gout and/or hyperuricemia and uric acid overproduction. The kinetic basis of enzyme superactivity in all patients was increased maximal reaction velocity. Affinities of the enzymes for substrates and activators and responsiveness to inhibitors were normal, and levels of immunoreactive enzyme in patient and control fibroblast and erythrocyte extracts were comparable. Enzymes purified to homogeneity from 2 patients confirmed the presence of isolated catalytic defects. Altered physical properties of certain of the superactive enzymes suggested the presence of several distinctive structural defects among the aberrant forms. Fibroblasts from each affected patient showed increased PRPP concentration and generation, as well as accelerated rates of all PRPP‐requiring purine nucleotide synthetic pathways. These findings support the concept that enzyme superactivity results in uric acid overproduction as a consequence of increased rates of PRPP and purine nucleotide synthesis. Cultured cells from female relatives of 2 patients showed evidence for the heterozygous carrier state, as measured both by enzyme activities and by rates of PRPP and purine synthesis. The clinical phenotype in 4 patients was limited to early adult‐onset gout and its consequences, whereas the fifth patient expressed a familial constellation of hyperuricemia, sensorineural deafness, ataxia, and renal insufficiency. The severity of the derangements in PRPP synthetase and in PRPP and purine synthesis in cells from the 5 patients, however, was comparable. The neurologic accompaniments of enzyme superactivity found in 1 family described here, and in 2 others described previously, thus may not necessarily be consequences of primary defects in PRPP synthetase.
The neurotoxic effect of gold sodium thiomalate on the peripheral nerves of the rat: Insights into the antiinflammatory actions of gold therapy
Authors: Levine Jon D. , Goldstine Joshua , Mayes Margaret , Moskowitz Michael A. , Basbaum Allan I. 
Published: February 2007

AbstractAlthough gold is one of the few therapeutic agents that has been proven effective in producing remission in patients with rheumatoid arthritis, its mechanism of action is unknown. Since nociceptive afferent and sympathetic efferent fibers of the peripheral nervous system contribute to the pathophysiology of inflammation, and since a known side effect of gold therapy is a polyneuropathy, we tested the hypothesis that gold is toxic to small‐diameter peripheral nerve fibers in the rat. We found that prolonged treatment with gold, at the same dosage reported to be effective against adjuvant‐induced arthritis in the rat, produced a significant decrease in the numbers of unmyelinated, but not of myelinated, axons. Gold treatment also elevated nociceptive thresholds in both articular and nonarticular structures. These results suggest that gold produces an antiinflammatory effect on arthritis by a neurotoxic effect on the peripheral nerves involved in neurogenic inflammation.
Urinary neopterin reflects clinical activity in patients with rheumatoid arthritis
Authors: Reibnegger Gilbert , Egg Dietmar , Fuchs Dietmar , Günther Robert , Hausen Arno , Werner Ernst R. , Wachter Helmut 
Published: February 2007

AbstractNeopterin is a marker for activation of cellular immunity. Urinary neopterin levels were measured in 106 patients with rheumatoid arthritis (RA) and in 45 patients with osteoarthritis. Levels were significantly higher in RA patients than in osteoarthritis patients and were strongly dependent on stage and activity of RA. Correlations with other laboratory parameters were weak. Multivariate analysis demonstrated that urinary neopterin levels reflected clinical activity better than did other laboratory findings. Thus, urinary neopterin determination might be useful in monitoring RA patients.
Production of a glycosaminoglycan stimulatory factor by cloned human t lymphocytes activated in vitro
Authors: Tsao Min , Zeevi Adriana , Whiteside Theresa L. 
Published: February 2007

AbstractSupernatants of mitogen‐activated mononuclear cells contain a factor which stimulates, up to fifteenfold, the synthesis of glycosaminoglycan (GAG) by cultured normal dermal fibroblasts. To demonstrate that the GAG stimulatory factor is a product of T lymphocytes, we cloned normal peripheral blood T lymphocytes that were activated in mixed lymphocyte culture. Selected alloreactive T cell clones were expanded in the presence of original stimulator cells and T cell growth factor. Only supernatants of the clones that were reactivated with irradiated stimulators (allogeneic peripheral blood lymphocytes of B cell lines) were capable of increasing, 3–7‐fold, the GAG synthesis by dermal fibroblasts. The production of GAG stimulatory activity by alloreactive T cells was restricted by HLA‐DR allorecognition. Alloactivated T cell clones produced more GAG stimulatory activity on a per cell basis than did concanavalin A‐activated mononuclear cells. These results show that cloned, activated T lymphocytes are capable of releasing soluble factors that modulate GAG synthesis by normal dermal fibroblasts.
Murine type II collagen arthritis: Association of an acute‐phase response with clinical course
Authors: Bliven Marcia L. , Wooley Paul H. , Pepys Mark B. , Otterness Ivan G. 
Published: February 2007

AbstractThe acute‐phase reactant, C‐reactive protein, is a good index of disease activity in patients with rheumatoid arthritis. We examined the murine acute‐phase reactant, serum amyloid P, as an index of disease in type II collagen‐induced arthritis in 3 mouse strains. The onset of type II collagen‐induced arthritis, which is characterized by paw swelling, is associated with a significant, but transient, elevation of serum amyloid P. Anticollagen antibody titers are not temporally associated with the onset of disease. Although murine type II collagen arthritis fails to show the chronic acute‐phase reactant elevation that is characteristic of arthritis in humans, the transient elevation of the acute‐phase reactant is a reliable indicator of the onset of disease.
Heterogeneity of proteoglycans extracted before and after collagenase treatment of human articular cartilage: II. Variations in composition with age and tissue source
Authors: Kuijer Roel , Van De Stadt Rob J. , Van Kampen G. P. Jos , De Koning Margret H. M. T. , Van De Voorde‐Vissers Els , Van Der Korst Jan K. 
Published: February 2007

AbstractProteoglycans (A1 fractions) were extracted with 4M guanidine hydrochloride (GuHCl) from human articular cartilage samples of a wide age range. Distinctions were made between hip and knee, and upper and lower layers. The residues of these extractions were digested with purified collagenase, and a second extraction with 4M GuHCl was performed, which yielded appreciable amounts of proteoglycans. When pro‐teoglycans from second extractions were compared with those from first extractions, the following changes were observed: an increase in chondroitin sulfate; a relative decrease in keratan sulfate; a decrease in protein content; and a decrease in the ratio of chondroitin 6‐sulfate to chondroitin 4‐sulfate. The same changes were found when nonaggregating proteoglycans were compared with proteoglycan aggregates, when proteoglycans from young cartilage were compared with those from mature cartilage, when proteoglycans from knee cartilage were compared with those from hip cartilage, and when proteoglycans from upper layers of cartilage were compared with those from deeper layers. It is suggested that the differences found between first and second extractions of cartilage, between upper and lower layers of cartilage, and between knee and hip cartilage are caused by variations in the relative amount of nonaggregating proteoglycans and/or variations in proteoglycan size.
Unusual metacarpophalangeal osteoarthritis in a jackhammer operator
Authors: Fam Adel G. , Kolin Arnost 
Published: February 2007

AbstractSevere, atypical osteoarthritis of the metacarpo‐phalangeal and elbow joints in a jackhammer operator is reported. Articular tissue resected at surgery demonstrated gross fibrillation and histologic evidence of calcification of articular cartilage, and multiple, bony fragments embedded in the synovium. Operation of a pneumatic drill may accentuate a tendency toward development of osteoarthritis in workers who are predisposed to the disease and may also cause it to localize at unusual sites such as the elbow, shoulder, wrist, and metacarpophalangeal joints.
CHARACTERIZATION OF RABBIT GENES FOR SYNOVIAL CELL COLLAGENASE
Authors: Fini M. Elizabeth , Gross Robert H. , Brinckerhoff Constance E. 
Published: February 2007

AbstractTo provide tools for understanding collagenase gene expression in rheumatoid arthritis, we have isolated and characterized genomic clones for rabbit synovial cell collagenase. These clones represent 2 types of collagenase gene, at least 1 of which is transcribed in synovial fibroblasts. By examining the rabbit genome in situ, we provide evidence that there are only 2 different synovial cell collagenase genes found in a haploid genome. Amplification of these genes is not a mechanism for collagenase messenger RNA induction by phorbol esters.
IN vitro production of autoantibodies to u1 ribonucleoproteins by peripheral blood mononuclear cells from patients with connective tissue diseases
Authors: Ohosone Yasuo , Akizuki Masashi , Hirakata Michito , Satoh Minoru , Yamagata Hajime , Homma Mitsuo 
Published: February 2007

AbstractAntibodies to U1 ribonucleoproteins produced by peripheral blood mononuclear cells from patients with connective tissue diseases were measured by a sensitive enzyme‐linked immunosorbent assay and by immunoblotting. Mononuclear cells from patients with high‐titer serum antibodies spontaneously started secreting IgG anti—U1 RNP antibodies on the second day after culture. The amount of anti—U1 RNP in the culture supernatants reached maximum level on day 8. The most effective production of anti—U1 RNP by B cells was observed when they were cultured in the presence of T cells and adherent cells. Mononuclear cells from patients without anti—U1 RNP antibodies or from normal subjects did not produce a measurable amount of anti—U1 RNP. Treatment of mononuclear cells by cycloheximide resulted in complete inhibition of anti—U1 RNP secretion, which indicates that antibody in the culture supernatants reflects the active biologic phenomenon in vitro. The methods described should be useful in the study of the cellular mechanisms involved in antinu‐clear antibody production of connective tissue diseases.
Human synovial fibroblasts produce urokinase‐type plasminogen activator
Authors: Medcalf Robert L. , Hamilton John A. 
Published: February 2007

AbstractThe plasminogen activator produced by cultured human synovial fibroblasts was investigated both biochemically and immunologically. Stimulated either by all‐trans‐retinoic acid or by monocyte‐conditioned medium, these fibroblasts elaborated a plasminogen activator with electrophoretic mobility similar to that of urokinase (Mr = 52 kilodaltons), and which also had immunologic cross‐reactivity with urokinase. The plasminogen activator found in rheumatoid synovial fluids has been shown to be of the urokinase type. The findings reported here are consistent with the notion that synovial fibroblasts are a source of this proteinase.
Abnormal immunoglobulin and rheumatoid factor synthesis by blood lymphocytes in patients with primary Sjögren's syndrome
Authors: Rodriguez Martjn A. , Baroja Miren L. , Leon‐Ponte Matilde , Abadi Isaac 
Published: February 2007

AbstractPeripheral blood B lymphocytes from patients with primary Sjögren's syndrome showed significantly higher spontaneous synthesis of IgG, IgM, and IgM rheumatoid factor in vitro, compared with B lymphocytes from healthy controls. Lymphocytes from patients also showed higher IgM rheumatoid factor production after mitogen stimulation. Patients had competent suppressor activity for IgG, but not for IgM synthesis. Pre‐irradiation of T cells, but not depletion of OKT8+ cells, markedly enhanced IgG synthesis in cocultures with autologous B cells; therefore, the T lymphocyte responsible for this effect is radiosensitive and is not identified by OKT8. OKT8+ lymphocytes from patients did not suppress Ig synthesis by autologous B plus T cell cocultures. However, OKT8+ cells from normal controls down‐regulated Ig synthesis by B plus T cells from patients. The abnormal proportion of helper and suppressor cells suggests that there is altered redistribution of regulatory subpopulations in peripheral blood from Sjögren's syndrome patients.
Products of polymorphonuclear cell injury inhibit IgG enhancement of monosodium urate‐induced superoxide production
Authors: Rosen Michael S. , Baker Daniel G. , Schumacher H. Ralph , Cherian Plammoottil V. 
Published: February 2007

AbstractThe generation of polymorphonuclear cell (PMN) superoxide ion (O2−) by monosodium urate (MSU) crystals may be important in the pathogenesis of acute gout. Coating MSU crystals with IgG prior to exposure to PMN markedly augmented O2− generation. This augmentation was inhibited by supernates, termed cell lysate, derived from sonicated PMN or PMN exposed to MSU crystals for 5 hours at 37°C. Lysate was effective in inhibiting O2− production when incubated with MSU crystals prior to, during, or after MSU crystals were exposed to IgG. No IgG could be eluted from crystals exposed to both lysate and IgG. Immunoelectron microscopy showed virtually no IgG on crystal surfaces after incubation of crystals with lysate and IgG. These data suggest that products of PMN injury can modulate further PMN responses to MSU crystals. This phenomenon provides a negative feedback loop and is one possible mechanism for the self‐limitation of acute gouty attacks.
Alterations in a cartilage matrix glycoprotein in canine osteoarthritis
Authors: Fife Rose S. 
Published: February 2007

AbstractA number of biochemical abnormalities have been described in osteoarthritic (OA) cartilage, but little study has been devoted to changes in the noncollagenous, nonproteoglycan proteins of cartilage in this condition. Using a canine model of OA produced by transection of the anterior cruciate ligament of the knee, we have demonstrated that distinct alterations occur in a 550,000‐dalton cartilage matrix glycoprotein in OA canine cartilage. This protein is a major protein constituent of normal articular cartilage. Fragments which are immunologically cross‐reactive with the 550,000‐dalton protein were more abundant in OA cartilage than in normal articular cartilage. Immunofluorescence studies revealed that staining with specific antiserum to the protein was absent in OA cartilage. This was the only noncollagenous, nonproteoglycan protein noted to undergo significant changes in this model of OA.
Cyclosporin a in rheumatoid arthritis: preliminary clinical results of an open trial
Authors: Dougados Maxime , Amor Bernard 
Published: February 2007

AbstractTwelve patients with refractory rheumatoid arthritis were included in a 1–year open trial of cyclosporin A (CsA), 5 mg/kg/day. Clinical efficacy was observed 1 month after beginning treatment, was well established after 4 months of therapy, and remained stable for the remainder of the 1‐year treatment period. Among the numerous side effects observed, renal toxicity and hypertension occurred suddenly during the trial and required constant monitoring, adequate therapy, and modulation of CsA dosage. Cyclosporin A seems to be an effective treatment for active rheumatoid arthritis, but it requires close monitoring for toxicity.
Modulation of cartilage destruction by select nonsteroidal antiinflammatory drugs
Authors: Herman Jerome H. , Appel Alan M. , Hess Evelyn V. 
Published: February 2007

AbstractNon‐enzymatic factors produced by synovial tissue can potentially mediate cartilage destruction by inducing the synthesis and release of matrix‐degrading proteinases from chondrocytes. Pharmacologic control of this process is of potential clinical relevance. The in vitro effect of therapeutic concentrations of select nonsteroidal antiinflammatory drugs on the synthesis and activity of catabolism‐inducing cytokines produced by 6‐day explant cultures of osteoarthritic and rheumatoid synovial tissue was studied. Piroxicam regularly suppressed such factor synthesis by both types of tissue without significantly affecting total protein synthesis. This did not occur using sodium salicylate or indomethacin in osteoarthritis tissue cultures and was observed only occasionally in rheumatoid arthritis cultures. None of the nonsteroidal antiinflammatory drugs studied consistently blocked catabolism‐inducing activity in osteoarthritis tissue, whereas piroxicam more consistently inhibited activity produced by rheumatoid arthritis tissue. Results suggest that the catabolism‐inducing factors produced by the 2 tissue sources may differ.
Acute transverse myelopathy successfully treated with plasmapheresis and prednisone in a patient with primary sjöugren's syndrome
Authors: Konttinen Yrjöu T. , Kinnunen Esko , Bonsdorff Martin Von , Lillqvist Petra , Immonen Ilkka , Bergroth Ville , Segerberg‐Konttinen Margaretha , Friman Claes 
Published: February 2007

AbstractWe report a case of acute transverse myelopathy in a patient with primary Sjögren's syndrome of 3 years duration. Our patient's acute transverse myelopathy developed within 1 week and resulted in complete paraparesis below the mamillary level. Extensive laboratory investigation ruled out viral, bacterial, and fungal etiology, Guillain‐Barré syndrome, poliomyelitis, and multiple sclerosis. At diagnosis, treatment was initiated immediately with prednisone (80 mg/day) and plasmapheresis, which was performed as a first‐aid measure. Improvement was noted as early as 10 days after the start of therapy. Within 5½ months of the first symptoms of paralysis, the patient walked without difficulty and returned to her normal activities. A causal relationship between plasmapheresis/prednisone therapy and recovery has not been proven but merits further consideration.
The extracellular control of intracellular aspirin hydrolysis
Authors: Costello Patrick B. , Green Floyd A. 
Published: February 2007

AbstractWe have previously presented evidence that an intra‐erythrocyte arylesterase is primarily responsible for the deacetylation of aspirin to salicylate. We now report studies on extracellular control factors. The fractional acetylsaticylic acid (ASA) hydrolysis at the completion of 20‐minute incubations in suspensions of washed red blood cells (RBC) with human serum albumin (HSA) decreased sharply, from 0.6 at 0 gm/dl HSA to 0.2 at 5.0 gm/dl HSA. In RBC suspensions with oleic, linoleic, and lauric acid, ASA hydrolysis increased as fatty acid:HSA ratios increased. The addition of salicylate (SA) also resulted in an increase in the fraction hydrolyzed. In a separate, more direct, ultracentrifugation assay, unbound ASA levels were similarly affected by HSA and the other ligands. When SA and oleic acid were incubated with ASA in RBC, additive competition for binding sites was apparent at relatively low levels of the fatty acid. In the presence of increasing concentrations of sodium SA, 5‐amino SA, and 4‐amino SA, ASA hydrolysis in RBC suspensions was increased by an average of 137%, 75%, and 54%, respectively. The most reasonable explanation for these findings is that the intact ASA molecule binds to albumin and that the binding of competing ligands can modulate the levels of free ASA in the circulation. This, in turn, affects the amount of drug available as substrate for penetration into the RBC and reaction with the intracellular hydrolase which catalyzes ASA deacetylation. Such factors controlling drug availability, if validated in vivo, could be important with regard to the antiinflammatory and anti‐platelet properties of aspirin.
Infective complications of plasma exchange: a prospective study
Authors: Singer Donald R. J. , Roberts Benita , Cohen Jonathan 
Published: February 2007

AbstractWe examined the incidence and types of infective complications which occurred in 41 patients whose medical management included plasma exchange (PX) by intermittent cannulation; femoral, subclavian, or internal jugular catheter; or arteriovenous shunt. A high incidence of positive cultures from vascular access catheters was demonstrated. Of 23 patients for whom data were available, 13 had positive cultures, and results on 3 of these showed > 1 species. Gram‐positive cocci were typically found. Of the 34 patients who received drug immunosuppression with PX, 1 patient developed severe shunt‐site infection, and an additional 4 developed bacteremia. Seven patients were given PX alone, and none of these developed clinically significant infection; however, this difference in infection rate did not reach statistical significance. Clinically significant access‐related infection remains an infrequent but potentially important hazard of therapeutic PX.
Tumoral calcinosis presenting as adhesive capsulitis: case report and literature review
Authors: Croock Alan D. , Silver Richard M. 
Published: February 2007

AbstractTumoral calcinosis (TC) is an uncommon disorder characterized by large calcific soft tissue deposits, usually adjacent to large joints. In the past, the etiology was unclear, but recently, TC has been considered to be an inherited metabolic disorder, characterized by elevated serum phosphorus and 1,25‐dihydroxyvitamin D levels, normocalcemia, and calcific deposits. However, these features have been shown to vary widely, with formes frustes of TC now being recognized. We report an unusual case of TC, which presented as an adhesive capsulitis, in an elderly North American black woman. The patient's nationality, late age of presentation, and multiple sites of involvement are uncommon features of TC. The clinicopathologic features and possible etiologies of this rare condition are briefly reviewed.