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Sökning: swepub > (1990-1994)

  • Resultat 22621-22630 av 30759
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22621.
  • Andersson, Christer, et al. (författare)
  • Acute-phase proteins in response to tumor growth.
  • 1993
  • Ingår i: The Journal of surgical research. - : Elsevier BV. - 0022-4804. ; 55:6, s. 607-14
  • Tidskriftsartikel (refereegranskat)abstract
    • This study has evaluated the relationship between tumor growth and induction of acute-phase proteins. It has also determined whether an intact cellular immunity is obligatory for a fully expressed acute-phase plasma protein response in the presence of a highly antigenic tumor. Quantitatively, acute-phase responses (protein synthesis, plasma concentrations, hepatic RNA content, anorexia) were proportional to tumor burden. Anti-inflammatory drugs (indomethacin 1 micrograms/g body wt, dexamethasone 0.5 micrograms/g body wt) had no direct effect on the attenuation of the systemic acute-phase responses, but did affect them indirectly by decreasing tumor growth. Immune suppression (cyclosporine A at 20 or 60 micrograms/g body wt) had no effect on either acute-phase reactions or local tumor growth. In endotoxin-stimulated (lipopolysaccharide) normal mice, immune suppression aggravated anorexia and caused high mortality, while dexamethasone partly reversed these effects in endotoxin-stimulated mice. Plasma levels of acute-phase proteins correlated to circulating levels of IL-6 in untreated tumor-bearing mice, but this relationship was not obvious in either drug-treated tumor-bearing or endotoxin-stimulated mice. Tumor tissue induced the synthesis of different acute-phase proteins compared to endotoxin. However, disintegrated normal liver tissue induced the synthesis of serum amyloid protein to the same extent as the growing tumor. This effect was primarily associated with the mitochondrial/lysosomal and microsomal liver cell fractions. In conclusion, the overall acute-phase protein response is not a modulating factor of tumor growth.(ABSTRACT TRUNCATED AT 250 WORDS)
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22622.
  • Andersson, Curt, 1940 (författare)
  • Att utveckla ledare.
  • 1992
  • Licentiatavhandling (övrigt vetenskapligt/konstnärligt)
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22623.
  • Andersson, Christer, et al. (författare)
  • Identification of tissue sites for increased albumin degradation in sarcoma-bearing mice.
  • 1991
  • Ingår i: The Journal of surgical research. - 0022-4804. ; 50:2, s. 156-62
  • Tidskriftsartikel (refereegranskat)abstract
    • Plasma albumin concentration declines in both experimental and clinical cancer. Previous investigations have demonstrated that this is partly explained by increased breakdown of albumin. The present study has identified the tissue sites for increased albumin degradation in a nonmetastasizing sarcoma mouse (C57/BL6J) model. Results have been compared to nontumor-bearing animals either freely fed or food restricted (pair-weighed) so that their body composition was similar to tumor-bearing animals. Tumor-bearing mice had increased albumin degradation (0.13 +/- 0.02 mg/hr/g bw) compared to both freely fed (0.09 +/- 0.007) and pair-weighed control animals (0.05 +/- 0.008). Radioactivity from circulating [3H]raffine aldehyde labeled albumin appeared with maximum peak values in lysosomes isolated from both tumor and nontumor tissues at 48 hr following iv injection. The intralysosomal accumulation of radioactivity was two- to threefold higher in tumor tissue compared to liver tissue, although the specific activity of protease(s) for albumin degradation measured in vitro was not higher in tumor tissue (30.4 +/- 3.6 mg/hr/g tissue) compared to normal liver tissue (36.9 +/- 1.7). Accounting for the entire tumor the proteolytic capacity for albumin breakdown was however much larger in the tumor (161.6 +/- 32.6 mg/organ) compared to both normal liver (37.5 +/- 2.3) and tumor-host liver (56.4 +/- 2.8). Pepstatin inhibited 78 +/- 6% of the proteolytic activity in the tumor measured by 125I-labeled undenatured mouse albumin as the substrate. Leupeptin inhibited 49 +/- 6%. There was a significantly decreased breakdown of albumin in both skeletal muscles and the gastrointestinal tract from tumor-bearing animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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22624.
  • Andersson, Christer, et al. (författare)
  • Isolation of radiopure plasma and hepatic albumin in acute phase conditions.
  • 1994
  • Ingår i: Clinical nutrition (Edinburgh, Scotland). - 0261-5614. ; 13:1, s. 35-41
  • Tidskriftsartikel (refereegranskat)abstract
    • It is essential to obtain biochemically and radioactively pure albumin in studies on albumin metabolism and kinetics in stress and nutrition related conditions. However, published work on albumin metabolism, in both animals and man with acute phase reactions has usually been based on inadequate chemical methods for isolation of homogeneous albumin free from acute phase proteins and other contaminants. Applications of conventional antibody precipitating techniques was usually either not sufficient to give radiopure albumin, or did not allow determination of the true specific radioactivity during in vivo experiments. Thus, the lack of applicable methods to achieve radiopure albumin from small plasma and tissue samples for subsequent analyses and determination of the true specific radioactivity in albumin initiated the present method development. The combination of HPLC ionchromatography (DEAE-sepharose), affinity chromatography (Blue sepharose CL-6B, Con A sepharose) and HPLC based size exclusion chromatography (Protein PAK 300 SW, Waters) was applied. By this procedure we obtained radiopure albumin from both plasma and hepatic samples from individual mice with acute phase response as confirmed by two-dimensional electrophoresis and immune precipitation.
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22625.
  • Andersson Gäre, Boel, et al. (författare)
  • Epidemiology of juvenile chronic arthritis in southwestern Sweden: a 5-year prospective population study.
  • 1992
  • Ingår i: Pediatrics. - 0031-4005. ; 90:6, s. 950-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous epidemiological studies of juvenile chronic arthritis (JCA) report divergent results owing to differences in diagnostic criteria, patient retrieval, and study designs. To investigate incidence and prevalence of JCA in a total population, this prospective survey was performed in southwestern Sweden between 1984 and 1988. Cases were identified using the European League Against Rheumatism criteria for JCA and were reported annually from eight pediatric departments and local pediatricians in the studied area. During the 5 years, 213 new cases of JCA were found, corresponding to an incidence of 54.6 per 100,000 children younger than 16 years of age. The average annual incidence was 10.9 per 100,000. The peak incidence rate, 18.3 per 100,000 was found in girls 0 through 3 years old. The lowest incidence rate, 6.4 per 100,000, was found among boys 12 through 15 years old. In December 1988, 334 cases of JCA were recorded, giving a prevalence of 86.3 per 100,000. When patients in remission were omitted the prevalence was 64.1 per 100,000. The monoarticular+pauciarticular onset type constituted 68.3% of the prevalence cases, while 21.9 were polyarticular and 6.6% had systemic onset. To avoid underestimation of incidence and prevalence, and to get a correct picture of disease patterns, epidemiological surveys of JCA should be population-based rather than referral center-based. Further descriptive studies of JCA in different well-defined geographic areas are important to make valid comparisons. Such comparisons could give clues to etiological factors, both genetic and environmental.
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