Sentence examples for persistent proliferation from inspiring English sources

The following parameters are important for the design of chronic toxicity studies, and for the prediction of severe chronic effects: lung retention of inhaled materials for assessing the accumulation of particles, persistent inflammation in lungs, persistent proliferation of epithelial lung cells, progressive fibrogenicity, and genotoxicity in the lung cells.

Hence, especially the detection of DCX+/Mcm2+ cells is a relatively strong indicator of persistent proliferation of DCX+ cells (Fig. 8M) — however, in our samples, not beyond the age of 65.

CK5 and p63, both breast stem cell markers, were prominently overexpressed in CTBE cell mounds, indicative of persistent proliferation.

Neonatal treatment of female mice with diethystilbestrol (DES) is known to induce ovary-independent persistent proliferation and cornification of vaginal epithelium.

Indeed, activation of β-catenin within the basal epithelial cells results in premature differentiation of the luminal epithelium during pregnancy and persistent proliferation resulting in tumors.

Therefore, because a transient activation of ERK1/ERK2 is sufficient to trigger persistent proliferation, the inhibition of EGFR or other intermediate signaling components may not necessarily lead to the intended anti-proliferative effect.

This transition offers the opportunity to test a) the circuit of redox signaling based upon mitochondria and, b) a mechanistic of low H2O2 yield for persistent cell proliferation.

Thus, in contrast to what is observed with a M2 frame shift mutant virus, we have observed that the infection of animals with those viruses does not result in the induction of persistent uncontrolled proliferation of infected GC B cells.

We report a lady with a benign clinical course over 10 years and persistent CD8+/CD3-/CD57+/CD16+ LGL proliferation with presence of Howell-Jolly bodies (functional hyposplenism), an association not previously described.

Collectively, these results suggest the presence of a common mechanism for overlapping functional redundancy in IGF and insulin signaling pathways and may explain our observation of persistent increased proliferation in growth plate chondrocytes from mice lacking IR.

Moreover, considering the stability of the HTLV-1 proviral sequence, it was hypothesized that maintaining a high PVL is achieved by persistent clonal proliferation of infected cells in vivo[ 25].