Methods: Multicenter retrospective cohort study of cardiac arrest patients who underwent TTM between July 2007 and December 2012. We examined the association between BMI and the time from initiation of cooling to attainment of target temperature (32-34 degrees C).

Results: Of 236 patients treated with TTM, 184 were included in the study. Mean age was 57.8 +/- 17.0 years; 78/184 (42%) were female and 48/184 (26%) had VF/VT as the initial rhythm. Median time to reach target temperature from ROSC was 6.4 (4.1, 9.8) h and median time from initiation of TTM to target temperature was

3.4 (2.1, 5.8) h. Cooling duration was a median of 24.0 (23.0, 24.0) h and median rewarming time was 12.0 (9.5, 18.0) h. Overall, 104/184 (56.5%) achieved target temperature within 4 h and 128/184 (69.6%) within 6 h. Increased BMI was associated with a longer time to

achieve target temperature Selleck PU-H71 from initiation of TTM (p = 0.01). check details There was no significant difference across BMI groups in time to achieve target temperature from ROSC (0.07), skin breakdown (p = 0.35), survival (p = 0.21), nor rate of good neurologic outcome (p = 0.32).

Conclusions: Target temperature was frequently achieved within 4-6 h; as BMI increased, the time to reach target temperature from initiation of TTM was prolonged. There was no significant difference across BMI groups for survival or good neurologic outcome. (C) 2013 Published by Elsevier Ireland Ltd.”
“Memory

is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced. We now report on the effects of enhanced training on retention after temporary inactivation of cerebral nuclei known to be involved in memory, namely the substantia nigra (SN), striatum (STR), and amygdala (AMY). When training was conducted with a relatively low intensity of foot shock ( 1.0 mA), post-training infusion of lido caine into the SN, STR, or AMY produced a marked memory deficit. Increasing Emricasan Apoptosis inhibitor the aversive stimulation to 2.0 mA protected memory from the amnesic effect of intranigral lidocaine, but there was still a deficit after its infusion into the STR and AMY. Administration of lidocaine into each of these nuclei, in the groups that had been trained with 3.0 mA, was completely ineffective in producing alterations in memory consolidation. Simultaneous infusion of lidocaine into STR + SN, AMY + SN, or AMY + STR was also ineffective in altering memory formation when the highest foot shock intensity was used for training.