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To further define the molecular mechanism, we compared the effects of NS1 188-Ala or 188-Val protein on the phosphorylation of IRF3, TBK1, and IKKε (Fig. 4a d).
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.
To investigate this mechanism, we compared the ability of wild-type and missense mutant CLDN14 to form tight junctions.
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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For the single agent mechanism we compare the quadratic, spherical and logarithmic scoring rules with a parametric family of scoring rules.
Instead, to better demonstrate the effectiveness of our mechanism, we compare it with a typical signal strength-based algorithm proposed in [15].
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.
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.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com