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To this end, we have designed, synthesized and evaluated a panel of new RAD51 inhibitors, denoted IBR compounds.
We evaluated a panel of cytokines and chemokines to determine whether NAP plus SAL work through a cytokine/chemokine-mediated pathway in preventing these alterations.
We evaluated a panel of humoral immune responses in the largest published group of superinfected individuals (n = 21), compared to a set of 3 1 matched singly infected controls from the same cohort.
Using recombinant HBV antigens (Ags) and HBV-specific antibodies (Abs), we designed and evaluated a panel of enzyme-linked immunosorbent assays (ELISAs) detecting the main hepatitis B-related viral markers, namely HBV surface Ag (HBsAg), HBV e Ag (HBeAg), Abs to HBsAg (anti-HBs), Abs to HBV core Ag (anti-HBc) and Abs to HBeAg (anti-HBe), in blood serum.
To rule out a possible off-target effect, we evaluated a panel of GLI1 shRNA targeting sequences in the ESFT cell line TC71.
We have evaluated a panel of 48 SNPs (derived from a published set of 52) and presented a method for two multiplex PCR/LDR assays for those SNPs.
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Here, we synthesize and evaluate a panel of cationic polymers for gene delivery to both cultured and primary human T cells.
The same cell line was used to evaluate a panel of erythromycin-derived agonists and provided EC50 values for receptor activation that agree closely with data obtained in contractility assays.
Our goal in this work is to evaluate a panel of mAbs for their inhibitory and extraction abilities, thus optimizing assay sensitivity with all BoNT/A subtypes.
Here, we evaluate a panel of 16 monoclonal anti-BoNT/A mAbs for their ability to inhibit the in vitro activity of the complex form of BoNT/A1, /A2, and /A3 as well as the recombinantly produced BoNT/A1 LC.
In order to accomplish this, we used qMSP to evaluate a panel of 19 TSGs among true SGT malignancies (ACC, MEC, SDC), one benign SGT type (PA), as well as in normal salivary tissue.
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