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To study their mechanisms, we compared their kinetics of antiviral suppression with those of other classes of DAA, using the hepatitis C virus genotype 1a cell culture−infectious virus H77S.3.
Based on these mechanisms, we compared the effect of different treatments (apoptosis-inducing agents, Hydrocortisone and Adriamycin, anti-angiogenic agent, TNP-470, and immunomodulators-Levamisole and BCG) on two experimental tumours (B16 melanoma and AKR lymphoma) growing in young and old mice.
Since complement activation and intracellular killing by microbicidal molecules are events linked to proinflammatory mechanisms, we compared the ability of B. abortus and S. typhimurium to consume complement and their resistance to cationic peptides, PMN extracts and normal serum.
To determine whether the poor tumor rejection efficacy of the CD3 mAb-stimulated CTLs is due to lack of activation of cytotoxic effecter mechanisms, we compared activation of the cytotoxic pathways in the tumor-specific CTLs.
To discriminate between these two mechanisms we compared the occurrence of protein binding peaks to the distribution of the corresponding sequence motifs for CTCF, GAF and SU HW) (respectively grey and colored lines in Fig. 3a).
To examine whether the revealed disease associations reflect common causal mechanisms, we compared GO assignments of genes in the six largest disease groups.
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Focussing on the first three of these general mechanisms, we compare and contrast their hallmark characteristics, and discuss the role of various local DNA sequence features (e.g. recombination-promoting motifs, repetitive sequences and sequences capable of non-B DNA formation) in mediating the recombination events that underlie gross genomic rearrangements.
Based on this mechanism, we compared the therapeutic efficacy of two apoptosis inducers, hydrocortisone and adriamycin, on AKR lymphoma and B16 melanoma growth in young and old mice.
In order to understand the underlying mechanism we compared antibody responses between those protected and those not protected [6].
To characterize the steepness of the here discussed mechanism, we compared its response to a Hill-type reaction (see Methods).
To delineate the mechanism, we compared global gene expression changes between APC and APC Rac1 intestines by microarray.
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