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Träfflista för sökning "WFRF:(Jonsson Anders) srt2:(1995-1999)"

Sökning: WFRF:(Jonsson Anders) > (1995-1999)

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  • Toksvig-Larsen, Søren, et al. (författare)
  • The Porous-Coated Anatomic Total Knee Experience. Special Emphasis on Complications and Wear
  • 1996
  • Ingår i: Journal of Arthroplasty. - 0883-5403. ; 1:11, s. 11-17
  • Tidskriftsartikel (refereegranskat)abstract
    • One hundred sixty knees in 141 patients with the Primary Porous-Coated Anatomic prosthesis (Howmedica, Rutherford, NJ) were evaluated after a follow-up period of 5.6 years (range, 1–10 years). One hundred six knees were in the latest follow-up evaluation, including clinical examination and a defined standing radiograph with a follow-up period of 6.3 years (range, 3–10 years). Survivorship analysis regarding the cumulative revision rate (including completion with a patellar component) was 0.88 at the 8-year and 0.84 at the 10-year follow-up examination. The clinical result was satisfying/good, with a mean Hospital for Special Surgery score of 83 (range, 39–97). Five percent had thinning greater than 30% of the tibial component. The wear was calculated to be 1.0 mm (range, 0–9 mm), including three revised tibial components with heavy wear. Excluding the revised cases, the wear was 0.7 mm.
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  • Frost, Anders, et al. (författare)
  • Interleukin-13 inhibits cell proliferation and stimulates interleukin-6 formation in isolated human osteoblasts.
  • 1998
  • Ingår i: The Journal of clinical endocrinology and metabolism. - 0021-972X. ; 83:9, s. 3285-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Interleukin-13 (IL-13) is a recently identified cytokine that is secreted by activated T cells and regulates inflammatory responses. We have investigated the effects of IL-13 on isolated human osteoblast-like cells (hOB). IL-13 dose-dependently (1-100 pmol/L) reduced the incorporation rate of [3H]thymidine in hOB cells by more than 50%. Using a cell metabolic assay as well as direct cell counting, we found that treatment with IL-13 lead to a decrease in hOB cell number. The effect was both time and dose dependent, and after 12 days of culture, treatment with IL-13 (0.1 nmol/L) caused a 70% decrease in the number of cells. Also, IL-13 increased the levels of IL-6 messenger ribonucleic acid in hOBs, as measured by ribonuclease protection assay, and stimulated secretion of IL-6 into culture supernatants. In conclusion, IL-13 inhibits cell proliferation and increases IL-6 formation in human osteoblasts. Our findings suggest that IL-13 may cause bone loss due to impaired osteoblastic growth and IL-6-induced osteoclast recruitment.
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  • Huh, C, et al. (författare)
  • Decreased metastatic spread in mice homozygous for a null allele of the cystatin C protease inhibitor gene
  • 1999
  • Ingår i: Molecular Pathology. - 1366-8714. ; 52:6, s. 332-340
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: Increased or altered activities of cysteine proteases have been implicated in serious human disorders such as cancer, rheumatoid arthritis, sepsis, and osteoporosis. To improve the current knowledge of the regulatory role of a major mammalian cysteine protease inhibitor, cystatin C, in such disease processes, a cystatin C deficient mouse was generated and characterized. METHODS: The mouse cystatin C gene was inactivated by insertion of a bacterial neo gene through homologous recombination in 129/Sv embryonic stem cells. Embryonic stem cell clones were injected into C57BL/6J blastocysts followed by injection of the blastocysts into pseudopregnant female mice. F1 offspring with agouti coat colour after mating of chimaeric males with C57BL/6J females were examined by DNA analysis, and mice carrying the targeted mutation were intercrossed to obtain homozygous cystatin C deficient (CysC-/-) mice. To study the role of cysteine proteases and their inhibitors in metastasis, the spread of B16-F10 melanoma cells in CysC-/- and wild-type mice was compared. Analysis of the formation of remote metastases was carried out by intravenous injection of beta-galactosidase transfected B16-F10 cells and subsequent determination of cancer cell colonies in the lungs. RESULTS: Cystatin C deficient mice were fertile and showed no gross pathological abnormality up to 6 months of age. Compared with wild-type mice, seven times fewer large metastatic colonies were counted by means of a dissecting microscope in CysC-/- mice two weeks after tail vein injection of B16-F10 cells. At all of eight time points from 15 minutes to two weeks after intravenous injection of tumour cells, the CysC-/- mice had significantly fewer lung metastases. The observed differences were smaller when beta-galactosidase transfected cells were used to allow counting of small colonies. Subcutaneous and intracerebral tumour growth was not different in the CysC-/- mice. CONCLUSIONS: Cystatin C concentrations in vivo might influence metastasis in some tissues. The decreased metastatic spread of B16-F10 cells in CysC-/- mice is the result of both reduced seeding and reduced growth of tumour cells in their lungs.
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