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1 re in a biological sample (e.g., DNA damage, reproductive cell death).
2 omosomal instability correlated with delayed reproductive cell death.
3 enetic pathways required for protection from reproductive cell death.
4  by UCN-01 do not necessarily correlate with reproductive cell death.
5 s of the biological end points of persistent reproductive cell death and apoptosis were consistent, s
6 g-held tenet that DNA damage is the cause of reproductive cell death and further validating this mode
7 ing delayed HR showed no evidence of delayed reproductive cell death, and there was no correlation be
8        These results suggest that persistent reproductive cell death can, in part, be explained by th
9 lones for sister chromatid exchange, delayed reproductive cell death, delayed mutation, mismatch repa
10      For example, after 9.5 Gy, which causes reproductive cell death in 99% of both types of cells, t
11 med that cell death in this model represents reproductive cell death in isolation from apoptotic cell
12 hway of EGFR is critical for protection from reproductive cell death in Radelegans.
13 eveloped a tissue model of radiation-induced reproductive cell death in the nematode Caenorhabditis e
14                                              Reproductive cell death is the primary mode of death in
15  Caenorhabditis elegans of radiation-induced reproductive cell death ("Radelegans") in isolation of a
16       Chromosomal instability and persistent reproductive cell death show a significant correlation a
17 nse pathway is necessary for protection from reproductive cell death, supporting the long-held tenet
18 romosomal instability (P < 0.1), and delayed reproductive cell death (the persistent reduction in pla
19 he EGFR signaling pathway in protection from reproductive cell death, the primary form of tumor stem
20 the possible role of apoptosis in persistent reproductive cell death, we analyzed subsets of chromoso