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A further point of comparison relates to the sequence of branch activation, which we originally assumed to be acropetal.
This means that the auxin concentration (c) does not drop below the threshold level for branch activation so readily.
We found strongly increased branch activation at the base of gametophores (number of branching gametophores: WT, 4/60; ppccd8 mutant, 29/60).
As a control, GSK (1 μM) was used to also inhibit PERK branch activation by thapsigargin (Tg; 100 nM; lane 3).
The blue hexagons in Figure 3F represent the ratio between the auxin concentration (c) and the threshold for branch activation (T).
The biological reason that branches initiate at the base is that auxin decay reduces the auxin concentration (calculated in each simulation step) below the threshold level of branch activation.
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Computations with four values of the chain-branching activation energy are performed both in narrow and wide channels.
As the chain-branching activation energy increases, cells take a shorter time to form, and the ratio cell length over width decreases.
Increasing the chain-branching activation energy shortens the ZND reaction length and leads to more unstable detonations, according to the stability analysis.
Suggested reasons for insufficient hypertrophy after successful PVE are recanalization of the embolized portal branches, activation of underlying liver disease, and the presence of major portal hypertension with portosystemic shunting [ 31].
Further, with relevance for AD and other tauopathies, PERK branch UPR activation is also known to contribute to the phosphorylation of tau which is central to pathology in these diseases both in vitro and in vivo [ 14, 20, 39].
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