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Träfflista för sökning "AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Reumatologi och inflammation) srt2:(1990-1999)"

Sökning: AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Reumatologi och inflammation) > (1990-1999)

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1.
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2.
  • Norgren, Lars, et al. (författare)
  • Immune response to collagen impregnated Dacron double velour grafts for aortic and aorto-femoral reconstructions
  • 1990
  • Ingår i: European Journal of Vascular Surgery. - 0950-821X. ; 4:4, s. 379-384
  • Tidskriftsartikel (refereegranskat)abstract
    • This study presents 20 patients, randomised to receive either a collagen-treated or an ordinary Dacron graft for aortic reconstructions, and the results of a skin-prick test, blood parameters and ELISA for anti-collagen antibodies as well as NMR pictures during a 6 week follow-up period. Forty per cent (4/11) of those receiving a collagen impregnated graft had a significantly increased titre of antibodies and NMR revealed in two out of 11 patients either a slightly increased amount of fluid or fibrosis around the graft, both collagen impregnated. No differences were found between the graft groups concerning body temperature and leucocyte or platelet counts. The skin-prick test for collagen was negative in all cases.
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3.
  • Ohlsson, Bodil, et al. (författare)
  • Time-course of the pancreatic changes following long-term stimulation or inhibition of the CCK-A receptor
  • 1995
  • Ingår i: International Journal of Pancreatology. - 0169-4197. ; 18:1, s. 59-66
  • Tidskriftsartikel (refereegranskat)abstract
    • Cholecystokinin (CCK) reportedly induces both hyperplastic and hypertrophic changes in the pancreas. Blockade of the CCK receptor results in decreased pancreatic secretion and atrophy. The aim of this study was to evaluate the time-course of the effects of stimulation and inhibition of the CCK-A receptor in the rat exocrine pancreas. Male rats had infusion of sulfated CCK-8, the CCK-A receptor antagonist devazepide, or sodium chloride by osmotic minipumps. After 36 h, 3, 7, or 28 d the rats had ip injections of thymidine, and 1 h later they were sacrificed. The pancreas was excised, weighed, and its content of protein, DNA, water, and enzymes was analyzed. Histologic samples were prepared for autoradiography. Pancreatic weight, protein, and DNA were increased at 36 h after the start of CCK infusion and throughout the study period. CCK stimulation also increased the content of trypsin at days 3 and 28. The labeling index of pancreatic acinar cells was increased at 36 h. Blockade of endogenous CCK by the receptor antagonist devazepide led to decreased pancreatic weight from the third day of infusion, whereas the protein content was decreased from the seventh day. At day 28, the DNA content was decreased by devazepide. However, the labeling index of acinar cells decreased transiently already at 36 h. Neither CCK nor devazepide caused any changes of protein content:DNA content ratio during the study. Continuous infusion of CCK caused pancreatic hyperplasia already after 36 h. Stimulation up to 28 d did not cause any further effects. The adverse changes found after blockade of the CCK-A receptor showed much of the same time-course.
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4.
  • Dahlqvist, Solbritt Rantapää, et al. (författare)
  • Acetylator phenotypes in primary Sjögren's syndrome
  • 1994
  • Ingår i: British Journal of Rheumatology. - : Oxford University Press (OUP). - 0263-7103 .- 1460-2172. ; 33:4, s. 405-406
  • Tidskriftsartikel (refereegranskat)
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5.
  • Dahlqvist, Solbritt Rantapää, et al. (författare)
  • Cell-cycle effects of the antirheumatic agent cph82
  • 1994
  • Ingår i: British Journal of Rheumatology. - : Oxford University Press (OUP). - 0263-7103 .- 1460-2172. ; 33:4, s. 327-331
  • Tidskriftsartikel (refereegranskat)abstract
    • The benzylidated podophyllotoxin glycoside CPH82, a potentially useful drug for treatment of RA, was tested in vitro on nine human haematopoietic cell lines for cell kinetic effects. Previous studies have shown CPH82 to behave like a colchinetype ‘metaphase’ blocker.The distribution of cells within different cell cycle compartments (G1, S, G2 and M) was analysed by a novel method using dual parameter flow cytometric analysis of stage specific antigens (proliferating cell nuclear antigen and Ki-67). With CPH82 concentrations chosen to mimic clinical conditions, eight out of nine lines showed an accumulation of cells in the G2 phase of the cell cycle. In many lines a delayed progress through S seemed to occur. Three lines were blocked in both G1 and G2, whereas the major effect on one line (HL-60) was an accumulation of cells in the G1 phase. Progression of M cells seemed only slightly delayed for some cell lines. In comparison with two related ‘metaphase’ blocking agents (podophyllotoxin and taxol), CPH82 had a different and dose-dependent pattern of cell cycle retardation. It is speculated that the cell kinetic action of CPH82 might give insight into the question why it, unlike other ‘metaphase’ blockers, has proved valuable in the treatment of RA.
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6.
  • Dahlqvist, Solbritt Rantapää, et al. (författare)
  • Chromosomal changes in rheumatoid arthritis patients treated with CPH82
  • 1996
  • Ingår i: Clinical Rheumatology. - 0770-3198 .- 1434-9949. ; 15:6, s. 584-589
  • Tidskriftsartikel (refereegranskat)abstract
    • Chromosomal changes were assessed in 19 patients with rheumatoid arthritis (RA) treated with CPH82, a benzylidated podophyllotoxin glycoside, for up to one ve:lr. The frequency of chromosomal aberrations (CA) and sister chromatid exchanges (SCE) in peripheral lymphocytes increased significantly after 12 weeks of treatment and remained elevated after 48 weeks treatment in peripheral lymphocytes. The number of CA and SCE were significantly increased in CPH82 treated patients compared with the RA patients treated with other disease modifying anti-rheumatic drugs (sulphasalazine, gold, D-penicillamine, azathioprine, methotrexate, cyclophosphamide). Only two patients treated with cyclophosphamide and azathioprine had changes of comparable levels, The results of this study suggest a mutagenic potential of CPH82 similar to that described for other immunosuppressive drugs and the newer podophyllotoxin derivatives, etoposide and teniposide.
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7.
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8.
  • Månsson, Bengt (författare)
  • Molecular and clinical studies of cartilage and bone macromolecules in arthritis
  • 1999
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The pathogenesis of inflammatory arthritides include synovial inflammation and joint tissue destruction. Tissue destruction has traditionally been regarded a consequence of inflammation, but recent observations indicate that the processes are not always closely linked and may proceed uncoupled. The ultimate target organs for the destructive process are articular cartilage and bone. This thesis focuses on the pathophysiological changes in these tissues in arthritis patients differently prone to joint damage. Proteins or fragments of proteins released into synovial fluid and blood, so called molecular markers, were studied, as indicators of ongoing processes. Groups representing destructive rheumatoid arthritis (RA), non-destructive RA and psoriatic arthritis, were studied. In RA, high serum levels of the cartilage component COMP and low levels of the 846 epitope of aggrecan, correlate to joint damage. High synovial fluid aggrecan levels correlate to cartilage destruction. The pattern in psoriatic arthritis resembles in this respect that in non-destructive RA. Most changes occur early in the disease course, indicating a critical period for long-term joint damage. The findings will be useful to prognosticate future joint damage and facilitate the selection of patients likely to benefit from tissue-protective therapy. The observations indicate involvement of different pathogenic mechanisms in destructive and non-destructive arthritis. In a project aimed at exploring the turnover of a putatively regulatory cartilage protein with molecular marker potential, chondroadherin, I have studied its release from cartilage and interactions with other cartilage matrix components. Cartilage destruction in arthritis is accomplished by matrix metalloproteases. Chondroadherin was released from cartilage when treated with APMA, known to be an activator of latent metalloproteases. The released protein appeared to be intact and associated to monomeric collagen type II, a major structural element in cartilage. The interaction between chondroadherin and collagen II was characterised by electron microscopy and surface plasmon resonance assays. Future work aims at defining the interacting sites on collagen and chondroadherin, respectively, and to study the functional consequences of chondroadherin for collagen assembly into fibrils.
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9.
  • Petersson, Ingemar (författare)
  • Developing knee joint osteoarthritis: Clinical, radiographical and biochemical features.
  • 1997
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The aim of this project was to study clinical, radiographical and biochemical features of developing, symptomatic knee osteoarthritis (OA) prospectively in individuals aged 35-54 from the general population. A questionnaire to a random sample of 2 000 individuals in the district of Laholm, Sweden, identified 279 individuals (15% of the population) with chronic (>3 months) knee pain. Of these, 204 accepted to participate in baseline examinations. The minimum prevalence of symptomatic tibiofemoral OA for the general population was 1.5 % according to the Kellgren and Lawrence radiographic system and 1.1 % according to the Ahlbäck system. The health status measured by SF-36 (Short Form 36) was impaired in individuals with symptomatic tibiofemoral OA compared both to those without radiographic changes (p at least <0.05) and to the general population in corresponding age groups (p at least <0.01). Clinical signs as measured by two independent rheumatologists showed a low interobserver agreement and a low association with radiographical signs of OA. The ratios between concentrations of aggrecan and COMP (cartilage oligomeric matrix protein) were higher in knee joint synovial lavage fluid of individuals with tibiofemoral OA than in those without OA (p<0.001). The serum levels of COMP were higher in those with bone scan abnormalities (p<0.01) and the serum concentrations of COMP increased (p<0.001) over a 3-year period in the individuals with radiographic OA after 3 years, but remained unchanged in the individuals with normal radiographs at follow up. Similar changes were found for serum BSP (bone sialoprotein) in relation to bone scan abnormalities (p<0.05) and the levels increased over the 3-year period in the group with radiographic OA at follow-up (p< 0.001). Radiographic knee OA and knee pain with impaired health status is frequently found in middle-aged individuals. Prospective monitoring of the individuals in this project including synovial fluid and serum measurements of tissue markers should add important information regarding pathogenetic features, prognostic markers and features of importance for development of therapy of knee OA.
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