Activation of HERV-K(HML-2) disrupts cortical patterning and neuronal differentiation by increasing NTRK3.

The biological function and disease association of human endogenous retroviruses (HERVs) are largely elusive. HERV-K(HML-2) has been associated with neurotoxicity, but there is no clear understanding of its role or mechanistic basis. We addressed the physiological functions of HERV-K(HML-2) in neuronal differentiation using CRISPR engineering to activate or repress its expression levels in a human-pluripotent-stem-cell-based system.

[An aggregation method for determination of parameters of mathematical models].

Two mathematical models for calculation of the probability of post-radiation complications in normal tissues are considered. The first model provides calculation of the probability of post-radiation complications within the entire dose and tissue volume range. The second model is approximative.