23 research outputs found

    Acute enlargement and subsequent rupture of an abdominal aortic aneurysm in a patient receiving chemotherapy for pancreatic carcinoma

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    AbstractWe report a case of ruptured abdominal aortic aneurysm (AAA) in a patient receiving chemotherapy for pancreatic cancer. We reviewed the literature on the effects of corticosteroids and chemotherapy on aaa formation and discuss possible mechanisms for drug action to promote aneurysm expansion and rupture. If cancer and AAA coincide and curative chemotherapy is possible, a potential impact of chemotherapy on AAA expansion should be considered. (J Vasc Surg 2000;32:197-200.

    Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis

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    Rheumatoid arthritis (RA) is characterized by the recruitment of leukocytes and the accumulation of inflammatory mediators within the synovial compartment. Release of the chemokine CCL18 has been widely attributed to antigen-presenting cells, including macrophages and dendritic cells. This study investigates the production of CCL18 in polymorphonuclear neutrophils (PMN), the predominant cell type recruited into synovial fluid (SF). Microarray analysis, semiquantitative and quantitative reverse transcriptase polymerase chain reaction identified SF PMN from patients with RA as a novel source for CCL18 in diseased joints. Highly upregulated expression of other chemokine genes was observed for CCL3, CXCL8 and CXCL10, whereas CCL21 was downregulated. The chemokine receptor genes were differentially expressed, with upregulation of CXCR4, CCRL2 and CCR5 and downregulation of CXCR1 and CXCR2. In cell culture experiments, expression of CCL18 mRNA in blood PMN was induced by tumor necrosis factor α, whereas synthesis of CCL18 protein required additional stimulation with a combination of IL-10 and vitamin D3. In comparison, recruited SF PMN from patients with RA were sensitized for CCL18 production, because IL-10 alone was sufficient to induce CCL18 release. These results suggest a release of the T cell-attracting CCL18 by PMN when recruited to diseased joints. However, its production is tightly regulated at the levels of mRNA expression and protein synthesis

    Abstracts from the 8th International Conference on cGMP Generators, Effectors and Therapeutic Implications

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    This work was supported by a restricted research grant of Bayer AG

    Sepsis Diagnostics in the Era of “Omics” Technologies

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    Sepsis is a multifactorial clinical syndrome with an extremely dynamic clinical course and with high diverse clinical phenotype. Early diagnosis is crucial for the final clinical outcome. Previous studies have not identified a biomarker for the diagnosis of sepsis which would have sufficient sensitivity and specificity. Identification of the infectious agents or the use of molecular biology, next gene sequencing, has not brought significant benefit for the patient in terms of early diagnosis. Therefore, we are currently searching for biomarkers, through “omics” technologies with sufficient diagnostic specificity and sensitivity, able to predict the clinical course of the disease and the patient response to therapy. Current progress in the use of systems biology technologies brings us hope that by using big data from clinical trials such biomarkers will be found

    Semiquantitative and quantitative RT-PCR analysis of CCL18 mRNA in polymorphonuclear neutrophils

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis"</p><p>http://arthritis-research.com/content/9/5/R94</p><p>Arthritis Research & Therapy 2007;9(5):R94-R94.</p><p>Published online 17 Sep 2007</p><p>PMCID:PMC2212580.</p><p></p> Total RNA from synovial fluid polymorphonuclear neutrophils (SF PMN) of rheumatoid arthritis (RA) patients nos 1, 2, 7 and 8 and from blood PMN from healthy donor no. 2 was amplified by semiquantitative RT-PCR with primers for CCL18, CXCL10 and actin and subjected to agarose gel electrophoresis. PCR was repeated twice. Total RNA from blood and SF PMN from patients with RA (= 9) and from blood PMN from healthy donors (= 4) were subjected to quantitative RT-PCR with primers for CCL18 and HPRT. CCL18 transcript levels are presented as relative expression ratios. Bars represent median expression between RNA samples

    Microarray analysis of chemokine gene expression in synovial fluid polymorphonuclear neutrophils

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    <p><b>Copyright information:</b></p><p>Taken from "Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis"</p><p>http://arthritis-research.com/content/9/5/R94</p><p>Arthritis Research & Therapy 2007;9(5):R94-R94.</p><p>Published online 17 Sep 2007</p><p>PMCID:PMC2212580.</p><p></p> RNA of SF synovial fluid polymorphonuclear neutrophils (SF PMN) from nine patients with rheumatoid arthritis (RA) was analyzed for the expression of CC chemokines and CXC, C and CX3C chemokines . Data obtained by Gene Pix™ Analysis Software were normalized, transformed and denoted as -fold regulation versus the expression of blood PMN from healthy donors. Bars represent the median expression between nine RNA samples. Genes with median expression ratios less than -1 or more than +1 were significantly regulated. SF PMN from one representative patient with RA (no. 2) were subjected to flow cytometry with fluorescein isothiocyanate-conjugated anti-CD66b, allophycocyanin (APC)-conjugated anti-CD56, phycoerythrin (PE)-conjugated anti-CD3, anti-CD19-APC and anti-CD14-APC antibodies
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