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Hat three clones ZK1, ZK2 and ZK6 were obtained by limiting dilution and further characterized. Our PCR genotyping results verified these three clones, ZK1, ZK2 and ZK6 are MARCO-/- and SR-AI/ II-/--deficient (Fig. 1). These cell lines are able to grow rapidly in RPMI or DMEM complete media in the absence of exogenous M-CSF or other growth factors, and their doubling time is 12?6 h on the average
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R macrophages which was derived from brochoalveolar lavage (BAL) obtained from MS-/- mice [31]. Immortalization was conducted by infection of the primary AMs from MS/- mice with a retrovirus J2. The immortalized AMs were cloned by limiting dilution method. Three of the clones, designated as ZK-1, ZK-2 and ZK-6 were chosen for further characterization of macrophage phenotype and phagocytic function
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Lightly the uptake of fluorescent latex beads by ZK1 cells (Fig. 6B). Furthermore, to determine whether the size of dextran sulfate molecules alters the effect on ZK1 cells' uptake of latex beads, we tested different sizes of DS in the binding/phagocytosis assay. The results indicated thatonly dextran sulfate with smaller molecular weight (5-8kDa) inhibited binding, whereas larger 100-500-kDa dext
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NAlveolar macrophages play a central role in lung defense [3,36,37]. The class A scavenger receptors (SRA) MARCO and SR-AI/II are expressed on alveolar macrophages and function in innate defenses against inhaled pathogens and particles [7,8,10,11,17]. However, large number of murine alveolar macrophages with SRA deficient are rarely available for in vitro studies. To further investigate the role o
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Pacity of latex beads similar to primary AMs deficient in MARCO and SR-AI/II. All three clones showed significantly decreased uptake of fluorescent latex beads compared to the wild type primary AMs (Fig. 6A). Observed differences in phagocytic capacity between these clones and parental primary AMs from MS-/- mice may reflect the heterogeneity seen in populations of primary alveolar macrophages.ZK1
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Itada M, Kitagawa H, Igarashi K, Hirose S, Kanakubo Y: Polyamine lowered the hepatic lipid peroxide level in rats. Res Commun Chem Pathol Pharmacol 1988, 62:235-249. Merentie M, Uimari A, Pietil?M, Sinervirta R, Kein en TA, Veps nen J, Khomutov A, Grigorenko N, Herzig KH, J ne J, Alhonen L: Oxidative stress and inflammation in the pathogenesis of activated polyamine catabolism-induced acute pancr
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L antibodies made also rapidly clear to the clinicians that a reliable predictive factor for outcome was, in fact, lacking [3-7]. The introduction of K-RAS mutational status analysis allowed a reliable selection of resistant patients (i.e. those with mutated K-RAS). However not all K-RAS wildtype cases were also responders to anti-EGFR monoclonal antibodies. This observation made the need for furt
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Allele primers, amplifies a 434 bp DNA fragment from SRA-deficient ZK1, ZK2 and ZK6 cells. With primers for MARCO wild-type allele, amplifies a 500 bp DNA fragment from WT mice; with primers for MARCO mutant allele, amplifies a 850 bp DNA fragment from ZK cells. ZK1, ZK2 and ZK6 clones exhibited both MARCO and SRA-I/II-deficient. PCR products, ca.10 l/each was resolved on a 1.5 agarose gel by gel