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We present an analysis of the genetic architecture of normal adult skin from 470 genetically unique mice, demonstrating the effect of germline variants, skin tissue location, and perturbation by exogenous inflammation or tumorigenesis on gene signaling pathways.
pHEMA scaffolds seeded and pre-cultured with tumorigenic M12 cells prior to implantation generated tumors in athymic nude mice, demonstrating the ability of the scaffolds to be used as a synthetic vehicle for xenograft generation.
Tumor drug accumulation was significantly enhanced by folate-PEGylated PMA-PAMAM nanoparticles, and such observation corresponded to their strong inhibition of tumor growth in tumor-bearing mice, demonstrating the success of the multifunctional targeting delivery.
Serum taken immediately from biotin-injected mice failed to label cells of untreated mice, demonstrating the rapid clearance of biotin from circulation (Fig. 1A).
Mstn−/− mice carrying a follistatin transgene had about four times the muscle mass of wild type mice, demonstrating the existence of other regulators of muscle mass with similar activity to myostatin.
The model has provided examples of modifying loci (called modifiers of Min, Mom) in mice, demonstrating the principle of genetic modulation of disease severity represented by, in these cases, intestinal adenoma multiplicity.
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The in vivo studies on B16F1 melanoma bearing C57BL/6 mice demonstrated the superior antitumor activity of P L-SS-PTX) over both free P L-SS-PTXL-P L-SS-PTX
The results in tumour model in nude mice demonstrate the possibility to deliver paclitaxel by oral route and the prospect of such formulations in increasing response to anticancer drug therapy.
A further study using anti-EpCAM CART cells for local treatment of peritoneal carcinomatosis in xenograft mice demonstrated the possibility of this approach for the clinical treatment of gastrointestinal and gynecologic malignancies (Ang et al., 2017).
These results from mice demonstrate the presence of differential electrophysiological properties between Purkinje neurons from different regions of the WT mouse cerebellum and altered intrinsic membrane properties in the absence of dystrophin.
Administration of the enzyme to mice demonstrated the PEG AP to have a 67-fold increased plasma half-life compared to the native enzyme, 65.1±2.9 h versus 57.8±1.1 min, respectively.
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