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Small-molecule drugs that help to fold and process proteins correct type 2 diabetes in a mouse model, providing a new lead for the treatment of human diabetes.
Taken together, our results confirm the important role for TLR2 signaling in diet and/or bacteria enhanced atherosclerosis in an ApoE+/− mouse model, providing a link between innate immunity, inflammation and atherosclerosis.
Time-lapse dynamics of oocyte chromatin organisation during meiotic resumption was observed in a mouse model, providing a pathway of transition from the GV to the MII stage oocyte (M. Belli et al).
In addition to this mouse model providing a convenient method of following the progression of the systemic atherosclerotic process, it provides potential for a thorough and rapid evaluation of methods to arrest or reverse kidney alterations.
Several laboratories have demonstrated that hESC-derived endocrine cells can regulate blood glucose in a diabetic mouse model, providing proof of principle for future clinical application (for example, see studies by Kroon et al. [ 2] and Jiang et al. [ 3] and a review by van Hoof et al. [ 4]).
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Altogether, the proposed ER+/ERαKD tumor-bearing mouse model provides a promising preclinical platform to investigate novel ER-specific therapies using PET imaging.
In summary, this mouse model provides important insights into CLC development and suggests inhibition of phosphatidylinositol 3-kinase (PI3K) signaling as a potential therapeutic strategy for targeting CLC.
Although 10-fold greater quantities of antibody are required to observe significant effects in mouse, compared to our previous studies in rats, the present mouse model provides a convenient paradigm for investigating catalytic and non-catalytic antibodies.
The mouse model provides the most relevant setting to study and molecularly dissect the process of metastasis in vivo.
Collectively, these findings suggest that our mouse model provides an important experimental platform for probing the underlying mechanisms responsible for this unique disease.
In conclusion, this study demonstrates that bioluminescent N. meningitidis strains together with the CD46 transgenic mouse model provide a potent tool for in vivo investigations of meningococcal disease.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com