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The intriguing studies by Nern et al. [ 31] using the Cre/Lox transgenic mouse model system observed that hematopoietic genetic contribution to Purkinje cells could occur.
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Using Human Papillomavirus virus-like particles (VLPs) spiked in 10% fetal bovine serum as a model system, we observed a limit of detection of 1.5 nM in simple (buffer only) or complex (10% serum) sample matrices.
In our model system, we observed clear differential regulation of the EGF receptors.
With this model system, we observed an enhanced ability of TGF-β to activate specifically p38 MAPK, but not Smad2, in a manner correlating with increasing metastatic potential.
In our current model system, we observed an up-regulation of both pro and anti-inflammatory cytokines released from primary and BV2 microglial cells.
In our in vitro model system we observed no significant reduction of Smad2 protein expression as the cells progress through the HKc/GFI and HKc/DR stages.
Several processes are responsible for these adverse changes including impaired calcium cycling, myocardial insulin resistance, increased lipid uptake, glucotoxicity, and activation of the renin-angiotensin-aldosterone system observed in mouse models of dilated cardiomyopathy (Table 2) (20).
In our model system we observe, that MoS2 layers do not grow on the HOPG terraces but are more likely to grow at HOPG edges, one-dimensional defects, which obviously acts as growth seeds.
In the same way, Avida-ED is a model system for observing evolution in action in the laboratory and classroom.
Furthermore, our method may serve as a model system for observing seedling development and physiological and molecular studies of mycoheterotrophic plants.
A very distinct mode of interaction with the two model systems was observed.
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