Sentence examples for a subsequent suppression from inspiring English sources

Some patients contributed a subsequent suppression episode (after a first viral rebound) but did not have a first suppression episode measured using acceptable assays.

A dose- and time-dependent induction of autophagy observed in tumor cells following cisplatin treatment is evidenced by up-regulation Beclin-1 and cisplatin-triggered activation of AMPK pathway leading to a subsequent suppression of mTOR activity [ 28].

In first suppression episodes, 19%% of 785 rebounds were preceded by a blip; in subsequent suppression episodes, 22%% of 695 rebounds were preceded by a blip.

Therefore, neuronal atrophy and reduction of cell size are likely associated with a hyperactivation of AMPK and subsequent suppression of protein synsthesis.

Importantly, depletion of PMN slowed the kinetics of (but did not prevent) rejection mediated by Tm and created a window of opportunity that allowed subsequent suppression of rejection by Treg.

This has led to speculation that FOXP3 induction and subsequent suppression might be a default pathway in the activation of all human T-cells (Pillai and Karandikar, 2007); however, debate continues over the suppressive qualities of transiently FOXP3+ T-cells (Allan et al., 2007).

In the vagal fibers, this enzymatic inhibition results in a decrease of central nervous system sympathetic activity, whereas in the kidneys it leads to a reduction of renal sodium reabsorption, with subsequent suppression of the RAAS.

Midbrain values returned to normal immediately after the cessation of nicotine exposure and then showed a subsequent, transient suppression of activity.

Acquisition of a sex-determining locus (SRY) transformed the ancestral autosomes to the proto-X/Y [ 3] and a subsequent stepwise suppression of meiotic recombination between X and Y led to a male-specific region on the Y-chr (MSY) [ 3, 4].

The intensity maximum was ascribed to an increase in the molecular weight and subsequent suppression of the concentration fluctuations, which was qualitatively reproduced by the Flory–Huggins free energy formula.

In conclusion, these findings suggest that the antiproliferative effects of 2-undecylsulfonyl-DMNQ on PDGF-stimulated VSMCs are due to the blockade of receptor dimerization and autophosphorylation on specific tyrosine residues of PDGF-Rβ, which resulted in the subsequent suppression of signaling cascades and a cell cycle arrest.