1Higher BAC was found in KO mice after 3 h of EtOH access.
2Methods: Basolateral amygdala samples from control and EtOH-drinking male and female monkeys were processed.
3The COC-ETOH group also attended significantly fewer medication management sessions during the 12-week trial.
4EtOH caused a dose-dependent decrease in BMD and BMC without affecting bone mineral area.
5The molecular mechanisms regulating presynaptic effects of this chronic EtOH exposure are largely unknown.
6Several QTLs overlapped with loci repeatedly linked to EtOH drinking in previous mouse studies.
7In the current study, we examined the modulation of EtOH-induced bone loss during pregnancy.
8These effects were inhibited by co-administration of EtOH and NAC.
9Conclusions: ER stress plays an important role in EtOH-induced damage to the developing brain.
10Strengths and limitations of indirectly imaging brain EtOH are discussed.
11However, cellular proliferation and number were greater for gamma irradiated films compared to EtOH soaked.
12Methods: Ferrets were exposed to moderate doses of EtOH during the brain growth spurt period.
13One of the most deleterious consequences of EtOH exposure is neuronal loss in the developing brain.
14In contrast, EtOH feeding of TgCAT mice had no effect on trabecular bone compared with PF controls.
15EtOH treatment did not affect WIN-induced catalepsy.
16Exposure to either FFAs or EtOH given separately led to steatosis which was augmented when they were combined.