With Robert Hawkins (1984) he demonstrated how cognitivist aspects of associative learning (e.g., blocking, second-order conditioning, overshadowing) could be explained cell-biologically by sequences and combinations of these basic forms implemented in higher neural anatomies.
It also helps explain cell growth and death.
Therefore, we explain cell death by the known phenomenon of Zn dissolution in the aqueous media.
Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston.
To date, the processes of mitochondrial fusion-fission have been used to investigate and explain cell death induced by different environmental stresses, such as ethanol [34], hyperosmotic [35], and acetic acid stress [36].
Existing studies of pattern formation by Rhos have focussed predominantly on explaining cell polarity.
When looking at Rho cycling in motile eukaryotic cells, Mori et al. [25] used a wave-pinning model to explain cell polarity.
One potential mechanism to explain cell and tissue vulnerability could be related to diversity in the expression of protein chaperones across different neuronal populations and different tissues.
Thus, histone acetylation levels are important for cell proliferation but do not explain cell size increases.
Future works could focus on combining all kind of regulations together to explain cell cycle control.
Several experiments on cell competition in flies indicate that trophic theories may be too simplistic to explain cell competition.
