Sentence examples for lethal lesion from inspiring English sources

Here, a lethal lesion is defined as the local modification of DNA generated from the direct and indirect action of ionisation radiation (i.e. a double-strand break).

Here, (langle N_{{text{NP}}} (C,D) rangle) encompasses the lethal lesion generated from direct photon interaction with NPs, secondary electron generated from photon cellular medium interaction collisions with NPs, and secondary electron/photons generated from photon NP interactions collision with other NPs.

H2AX is phosphorylated by ATM kinase in response to DNA double-strand breaks (DSBs; the most lethal lesion); this event results in the recruitment of downstream repair factors into a microscopically visible focus [ 48, 49].

This analysis shows that the presence of GdBN induces an increase of directly lethal lesions and a decrease of sub-lethal lesions.

The enhancement of directly lethal lesions is attributed to the amplification of complex molecular damage as shown elsewhere [23].

end{aligned} (3)Within each cell under photon irradiation, lethal lesions are generated inhomogeneously and the probability of their creation is a direct function of local dose deposition.

Second, that cell "inactivation", e.g. cell death, can be attributed to the creation of a number of lethal lesions within a sensitive small sub-cellular volume such as the cell nucleus (Scholz and Kraft 1996, 2004).

Using these assumptions, it is possible to describe the survival fraction for a cell under photon irradiation in terms of the mean number of lethal lesions ((langle N (D) rangle)): begin{aligned}{text{SF}}[D] = exp (-langle N (D) rangle ) end{aligned} (2)and inversely: begin{aligned} displaystyle langle N (D) rangle = -log ({text{SF}}[D]).

If the spatial distribution of NP uptake within the cell line remains approximately constant with concentration, then from a mechanistic perspective the mean number of lethal lesions generated from these effects can be scaled with average NP density up to a critical saturation threshold (McKinnon et al. 2016).

It has been suggested that these ring-open products block DNA polymerases and create potentially lethal lesions [44].

Ionising radiation (IR) also kills cancer cells; DNA double-strand breaks (DSBs) are the lethal lesions.