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The complex pathology of these diseases cannot be readily dissected in these targeted mouse models, highlighting the need to develop novel transgenic mice that can be used to assess the distinct effects of intracellular stress and ECM alterations on chondrocytes and growth plate pathology.
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A review of other otitis-prone mouse models highlights the diverse biological processes that can influence susceptibility to this condition.
The first demonstration of the therapeutical potential of iPSCs in a humanized sickle-cell anaemia mouse model, highlighting the need to resolve the problems relating to the use of retroviruses and oncogenes in reprogramming for human therapy.
Differences between human and mouse models highlight the difficulties at comparing the results obtained in these systems.
These Apc1638N compound mouse models highlight the importance of p21, but not p27, in colon cancer prevention by non-steroidal antiinflammatory drugs (NSAID) [39], [40].
Together, the estrogen receptor-α knockout and PRKO mouse models highlight the specific importance of ovarian estrogen rather than progesterone in epithelial ductal elongation in the pubescent mammary gland.
Recent studies showing the efficacy of passive administration of polyclonal anti-HCV Ig (Meuleman et al., 2011) and anti-E2 neutralizing monoclonal antibodies (Law et al., 2008) in preventing HCV infection of mouse models, highlight the value of neutralizing monoclonal antibodies for therapeutic or prophylactic purposes.
After a description of its role in normal mammary gland development and its status in the pathological gland, we will emphasize the contribution of transgenic mouse models in highlighting how crucial β1-integrin appears to be for breast cancer progression.
Research extending from cell culture into mouse models has highlighted the ability of Hippo signaling components to drive mammalian cancer development.
Recent progress in understanding Treg biology and the development of experimental mouse models has highlighted potential avenues in the translation of research-based knowledge to the clinic.
Numerous findings, ranging from epidemiological studies to molecular analyses of mouse models, have highlighted a strong contribution of chronic inflammation to tumour development [ 1, 2].
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