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