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Our ability to study the developing human brain has recently been dramatically advanced by the development of human 'brain organoids', three-dimensional culture systems that recapitulate selected aspects of human brain development in reductionist, yet complex, tissues in vitro.
The establishment of cell culture systems that recapitulate each stage of liver development has led to the identification of several extracellular signals that affect hepatocytic differentiation.
Our ability to dissect oncogenic events is largely dependent on the availability of model systems that recapitulate human carcinogenesis at both the pathological and molecular levels.
Our ability to dissect oncogenic events is largely dependent on the availability of model systems that recapitulate human carcinogenesis at pathological and molecular levels.
In vivo models are the gold standard for predicting the clinical biomaterial host response due to the scarcity of in vitro model systems that recapitulate physiological settings.
Understanding these mechanisms will ultimately require techniques that are capable of quantifying traction forces with high precision and accuracy in vivo or in systems that recapitulate in vivo conditions, such as microfabricated tissues and engineered substrata.
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Taken together, we have demonstrated an in vitro system that recapitulates in vivo stiffening of PDAC tumors.
Here we constructed a GFP reporter system that recapitulates the alternative splicing of SMN1 and SMN2 pre-mRNA.
To test this hypothesis and to better understand the molecular mechanisms that control these interactions, we established a three-dimensional (3D) human cell culture system that recapitulates the tumor heterogeneity observed in vivo.
Here, through the use of a physiomimetic system that recapitulates the mechanical microenvironment found within healthy and fibrotic pancreas, we show that matrices mirroring rigidities found within fibrotic pancreas activate PSCs, whilst matrices resembling healthy pancreas induce and maintain quiescence in previously activated PSCs.
First, using a reconstituted liposomal system that recapitulates basic aspects of the BCL-2-regulated MOMP pathway, we demonstrate that MCL-1 inhibits BAX permeabilizing function via a "dual-interaction" mechanism, while submicromolar concentrations of gossypol reverse MCL-1-mediated inhibition of functional BAX activation.
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CEO of Professional Science Editing for Scientists @ prosciediting.com