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The mechanisms behind this increase in response variability are not known but we do know that during typical development, neural responses to sensory stimulation decrease in variability (Little, Thomas, & Letterman, 1999).
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After intervention by 0.15 ng/mL, 1.5 ng/mL, and 15 ng/mL IL-1β, the level of ERK1/2 phosphorylation induced by 1.38mM glucose stimulation decreased in a dose-dependent manner, and the insulin level correspondingly decreased.
The MFI of MitoAP-1 following fMLP stimulation decreased significantly in a dose-dependent manner (Fig. 2c).
Consequently, β-adrenergic stimulation decreases Ca buffering in PLN-KO cells and, conversely, increases it in cells missing the normal adult PKA phosphorylatable form of cardiac TnI.
In 1992, Schwarz et al. reported a correlation of V1max stimulation and decrease in critical closing pressure (Pcrit) in 18 decerebrate felines.
Upon mitogenic stimulation, the decrease in CFSE as it is portioned into daughter cells is indicative of cellular division.
The stimulation dependent decrease in FRET is compatible with a model in which the autofluorescent proteins of the non-phosphorylated form of the probe have a relative distance or orientation which allows FRET, whereas the phosphorylated form of the probe assumes a conformation less compatible with FRET.
However, during epicardial stimulation, the decrease in manifest APD from endo to epi due to intrinsic APD heterogeneity was still present (Fig. 6).
Using a model of intrahepatic biliary epithelial cells, Zhao and co-authors have shown that in response to LPS stimulation a decrease in E-cadherin expression was observed whereas expression of the mesenchymal markers (S100A and α-SMA) increased by more than 12-fold.
The degree of GluA1 endocytosis was determined by analysing the first 1 3 min after NMDA stimulation (max decrease in signal) and the rate of GluA1 recycling was determined by fitting a linear curve to the time after max internalization and calculating the time point at which 50% of fluorescence recovered.
Here, we found BCR stimulation decreased Bcl6 expression; in contrast, Bcl6 remained stable during LPS activation.
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