Sentence examples for proliferation delay from inspiring English sources

The results demonstrate that the combination of GO with PVA reduces both the proliferation delay and the internal cell complexity alterations induced by GO on human osteoblasts.

However, non-calcined matrices induce on fibroblasts a significant proliferation delay with morphological alterations and dose-dependent increases in fibroblast size, internal complexity, and intracellular calcium content but without cell lysis and apoptosis.

Determining the early transcriptional indicators of prolonged S-G2 phases that coincided with cell proliferation delay, or an anticipated subsequent auxin increase, accelerated cell differentiation or death, was used to link IR-regulated hallmark functions and tissue phenotypes after IR.

As repair rate and proliferation delay carry a higher degree of uncertainty than the α/ β quotient, results are also reported for BEDs disregarding the effects of overall treatment time in Tables 5a and 5b.

If the overall treatment time is shorter than the proliferation delay T k, the term would be negative and has therefore to be set to 0 in these cases (the case for 5-day overall treatment time).

The proliferation delay T k, set to 7 days (Colorectal Cancer Collaborative Group, 2001), is subtracted from the overall treatment time T, which means that, after a delay of 7 days, repair mechanisms become relevant that lead to a loss of tumour-damaging effects at a magnitude of 0.6 Gy per day.

SWNHs inhibited proliferation, delayed mitotic entry, and promoted apoptosis of mice microglia cells.

In particular, RPL11 dysfunction results in abnormal erythrocyte development, markedly decreased progenitor cell proliferation, delayed erythroid differentiation, and markedly increased apoptosis [ 25].

In contrast, RPL11 mutations lead to a dramatic decrease in progenitor cell proliferation, delayed erythroid differentiation, with a marked increase in apoptosis and G0/G1 cell cycle arrest, and activation of the p53 pathway [ 11].

In marked contrast, in patients with RPL11 mutation or following RPL11 depletion by specific shRNA, we identified a more pronounced phenotype: a greater extent of decrease in cell proliferation, delayed erythroid differentiation and marked increase in apoptosis.

Collectively, these results imply that TGFBI plays a suppressive role in the development of mesothelioma and breast cancer cells, possibly through inhibitions of cell proliferation, delaying of G1-S phase transition, and induction of senescence.