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The observed reduction in the expression of multiple clock genes by up-regulation of TOC1 could not be described by our previous model, where only LHY and CCA1 were affected by TOC1 [ 2, 3].
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The R Package, e1071 [ 62], was applied to build the support vector machine models using the same training data and test data as used by our previous modeling approaches.
Here we address this fundamental issue by focusing on the interplay between the catabolism of glucose and fatty acids by a generic mammalian cell, by extending our previous model of glucose catabolism within the crowded intracellular milieu of proliferating cells [16].
We begin by reviewing results from our previous model.
We modeled osmotic volume change by equation (13), similar to our previous model [8].
Here, we extend our previous model by including the repression of multiple clock genes by TOC1 and explore TOC1 effect on the clock.
This extended PBE model was developed from our previous model by adding a surfactant mass balance, including the effects of the free surfactant concentration on the interfacial tension and the surface coverage of drops and by modeling the coalescence frequency to be a function of the surfactant coverage.
We improved on our previous model by introducing a new scoring function.
In order to further understand how the defects influence the physical characteristics of the device, the P-E hysteresis loops and IDS-VGS curve for the SWCNT/BNT/HfO2-FeFET and SWCNT/BNT-FeFET were simulated by considering asymmetric charge caused by defects using our previous models [12, 28].
Our previous models were limited by a lack of quantitative measurements of cell surface receptor densities.
The model development was guided by our previous results obtained with a model that distinguished three fixed compartments between which the surface receptors were considered as partitioned [5].
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