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Studies of genetically modified mice and of molecular pathways in activated glia are beginning to shed light on this issue.
It also serves as a complementary platform for studies in genetically modified mice and as a model to evaluate pharmaceutical therapeutic approaches for impaired wound healing.
The availability of regulatory sequences directing tissue-specific expression of transgenes in genetically modified mice and large animals is a prerequisite for the development of adequate models for human diseases.
In recent years molecular mechanisms of fracture repair are investigated mainly in genetically modified mice and also in rats using biomimetic agents to accelerate fracture repair, but translation to clinical use is not yet available.
Besides genetically modified mice and ex vivo heart explants, ESCs provide a cellular model to study the early steps of valve development and might constitute a human therapeutic cell source for decellularized tissue-engineered valves.
In this review we compile several studies on using genetic modified mice and humanized mice to study function of transcriptional factors in lymphopoiesis, including T lymphocyte and Natural killer (NK) cell development.
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Until now, functions of spastin and mutated spastin have been identified in vitro, by over- or underexpression in human and animal cell lines, and in genetically modified mouse and Drosophila models.
However, experiments requiring major surgery frequently lead to serious postoperative complications and death, particularly if genetically modified mice with anatomical and physiological abnormalities undergo extensive interventions such as transmitter implantation.
These data permit the design of novel tests assessing behavioural changes, memory and learning in normal and genetically modified mice, both in the laboratory and in naturalistic settings.
Experimental models range from large animal models designed to mimic the human clinical situation, to gene modified mice, isolated hearts and cell cultures.
In genetically modified mice, enhanced bone mass and enhanced stiffness, strength and mineral concentration of the cortical bone matrix are generally associated with reduced TGF-β signaling [ 3, 20, 23].
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