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Among these 12 miRNAs only let-7b-5p has been previously described as being modulated by ionizing radiations in primary or cancer cells [ 34].
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We conducted epi-allelic hypomorphic analysis using selected p53-targeting shRNAs to determine the threshold of p53-dependent responses to ionizing radiation in primary human endothelial cells.
Since apoptosis is not efficiently induced by radiation in primary fibroblasts, the up-regulation of pro-apoptotic genes by direct radiation does not appear to be sufficient to tip the overall balance toward programmed cell death in this cell type.
With six new bird mitochondrial genomes (hummingbird, swift, kagu, rail, flamingo and grebe) we test the proposed Metaves/Coronaves division within Neoaves and the parallel radiations in this primary avian clade.
Absorbed radiation doses in primary target organs, compared for 64Cu-MM-302 and approved molecular imaging agents.
Here we investigate effects of SU9518, a PDGFR inhibitor combined with ionizing radiation in human primary fibroblasts and endothelial cells in vitro, with a view on utilizing RTKI for antifibrotic therapy.
Our previous studies have demonstrated that salivary acinar cells are sensitive to γ-radiation-induced apoptosis in primary cultures in vitro and in vivo [12] [14].
In this study we show direct evidence for the production of a radiation-induced bystander response in primary human fibroblasts.
Maximum changes occurred in mid latency (auditory) EPs suggesting that maximum changes occur in the corresponding neural generators in the thalamus, thalamic radiations, and primary auditory cortical areas.
Previous studies have addressed metabolic changes in primary brain tumors occurring after radiation therapy [ 14- 16].
TP53 mutations in primary melanoma tumors induced by UVB radiation have been described previously by Zerp et al [ 16].
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