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  • 1
    Electronic Resource
    Electronic Resource
    Diminished microtubules in fibroblast cells derived from inherited dystrophic muscle explants (1979)
    [s.l.] : Nature Publishing Group
    Nature 278 (1979), S. 178-180 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Fig. 1 Cells derived from cardiac expiants obtained from 7-d-old normal (a) and dystrophic () chickens exhibit no apparent difference in morphology or distribution of cytoplasmic actin stress fibres. Actin antibody stain. Scale bar, 10 ??. Fig. 2 Cells derived from normal cardiac expiants (a) of ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/278178a0
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Cytokine and Nitric Oxide Production in the Acute Phase of Bacterial Cell Wall-Induced Arthritis (1997)
    Springer
    Inflammation 21 (1997), S. 113-131 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have investigated the temporal relationship among proinflammatory cytokine expression, nitric oxide (NO) production and joint inflammation in the acute phase of bacterial cell wall-derived peptidoglycan polysaccharide(PG/PS)-induced arthritis. Acute joint inflammation was induced in female LEW/N rats by a single intraperitoneal injection of PG/PS. Arthritis index and paw volume were quantified and joint histopathology was evaluated during acute joint inflammation (0–10 days). Tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) were determined by bioassay whereas nitric oxide (NO) was quantified by measuring serum nitrate/nitrite levels via the Griess procedure. We found that serum levels of TNF and serum IL-1 preceded the increase in IL-6 and NO production. Furthermore, the production of these proinflammatory cytokines and NO preceded bone erosion and osteoclast activity. Erosion of subchondral bone preceded pannus formation and cellular synovitis in the acute phase of PG/PS-induced arthritis. The temporal expression of TNF, IL-1, IL-6 and NO suggest a cascade of inflammatory mediators in which monocytes and macrophages respond to PG/PS with enhanced synthesis of TNF and IL-1, which may in turn promote the synthesis of IL-6 and NO. We postulate that one or more of these inflammatory events are responsible for initiating the subchondral bone erosion observed in acute joint inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027351111240
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Modulation of endothelial cell permeability by lung carcinoma cells: A potential mechanism of malignant pleural effusion formation (1994)
    Springer
    Inflammation 18 (1994), S. 407-417 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examined the hypothesis that tumor cells metastatic to the pleura secrete a soluble factor(s) that directly increases endothelial cell permeability. Nitrocellulose filters were endothelialized with bovine pulmonary artery endothelial cells and exposed to conditioned media from either human lung adenocarcinoma (Calu-3), human lung squamous cell carcinoma (SK-MES-1), or control media for 16 h. The diffusional permeability (Pd × 10−5 cm/sec) to [14C]albumin was then determined for each monolayer with Ussing-type chambers. Both adenocarcinoma conditioned media (ACCM) and squamous cell carcinoma conditioned media (SCCM) caused a two- to threefold increase in endothelial monolayer permeability. The addition of indomethacin (10 μg/ml) blocked the observed permeability increase in ACCM but not in SCCM, suggesting that the increase in permeability by ACCM was secondary to the production of prostaglandins. To confirm this, a variety of prostanoids previously shown to be produced by the Calu-3 cell line were added directly to the endothelial monolayer. Prostaglandin F2α (PGF2α) in both low (10 ng/ml) and high (100 ng/ml) concentrations for 16 h resulted in a three- to fourfold increase in permeability. Prostaglandin E2 (PGE2) resulted in a small increase in [14C]albumin permeability but only at high concentrations (100 ng/ml). PGF2α production by the two tumor cell lines was measured using radioimmunoassay. Baseline adenocarcinoma production of PGF2α was 117.5 pmol/106 cells and fell to 24.2 pmol/106 cells hours following incubation with indomethacin. The decrease in PGF2α occurred in parallel with the changes in permeability. Concomitant, reversible changes in cell shape and F-actin distribution were detected in endothelial cells exposed to ACCM. No significant production of PGF2α by the squamous cell carcinoma cell line was detected. These results suggest that both adenocarcinoma and squamous cell carcinoma secrete a soluble factor(s) that directly increases endothelial cell permeability to albumin and that in the case of adenocarcinoma this soluble factor may be a prostanoid such as PGF2α.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01534438
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    Paper (German National Licenses)
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