Our physiological data suggest that stress engages CRF and opioid afferents to the LC, which have opposing influences on this noradrenergic system.
These data support recent transcriptomic studies suggesting that heat stress engages different responses related to apoptosis and oxidative stress in corals [9], [34], [35], [41], [42].
Similarly to lactose shift, cold stress engages numerous metabolites without connectivity in the stable network, such as leucine, oxalate, trehalose, phenylalanine or uracil.
The dynamic of initiation, activation and completion of apoptotic cascade in corals incubated with the different thermal treatments support this model whereby early thermal stress engages activation of apoptosis and the onset of a delayed protective response in corals.
ER stress engages an adaptive reaction to restore proteostasis known as the unfolded protein response (UPR).
Metabolic inhibition has been shown to be synthetically lethal to cancer cells because hyperactivation or oncogenes tends to make them 'addicted' to glucose or glutamine, but also because energetic stress engages a 'metabolic checkpoint' which cannot occur in cancer cells with certain mutations such as deficiency in p53.
Previous research has documented that, compared to women, men may be more likely to cope with stress by engaging in behaviors (i.e., smoking, alcohol consumption) which may contribute to elevated blood pressure [ 13].
Some men try to cope with this stress by engaging in unhealthy habits, such as substance abuse, escapism, and violence.
These stressors – including oxidative stress, oncogene activation, and radiation stress -- engage various intracellular signaling pathways such as the p16INK4a-retinoblastoma (Rb) pathway and the p19Arf-Mdm2-p53-p21Cip1/Waf1 pathway.
Some individuals, especially those whose consumption quantities are apparently not affected by stress, may engage in compensatory behaviors which are not reflected by the observed consumption quantities.
