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By contrast, in both cell models, only a small set of 14 genes was identified as being deregulated in common by both glitazones and glitazars, while only 11 and 60 genes were deregulated in common by glitazones and glitazars, respectively.
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Integration in intergenic regions was favored in active or resting CD4+ cell models only.
In cancer stem cell models, only a small persistent population of cells accrue the necessary mutations and are responsible for relapse and metastasis through a stem-cell-like process of differentiation and self-renewal [ 13].
Several genes were specifically altered by glitazone treatment in one liver cell model only.
In the hierarchical cancer stem cell model, only a small group of undifferentiated or poorly differentiated cells, representing less than 5% of the total tumour mass, can repopulate.
While ex vivo data demonstrated an upregulation of Progranulin by H. pylori, in the AGS cell model, only the concentration of Progranulin in the supernatant was strongly induced, whereas the cellular expression, analyzed in the lysate, was decreased.
While γδ T cell cytokine production is observed in both models, only mycobacterial challenge induces γδ T cell cytotoxicity [ 12, 13, 28].
These results are also the basic solution for any fuel cell model because only losses have to be specified in detail.
The estimation problem can be regarded as equivalent to the accurate reconstruction of ionic current kinetics and amplitudes in an excitable cell model, given only action potential experimental data.
Nevertheless, both that work as well as our own were performed in relatively simple epithelial cell models that mimic only a small aspect of the complex interactions occurring between host cells and intestinal pathogens or commensals.
In an immortalized murine cell culture model, only claudin-12 mRNA levels were down-regulated under conditions mimicking hyperammonemia.
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