Intubating conditions following rapid sequence induction with three doses of succinylcholine

Background: The aim of this prospective, randomized, double-blind study was to compare tracheal intubating conditions and the duration of apnoea following administration of 0.4, 0.6 and 1.0 mg/kg of succinylcholine during simulated rapid sequence induction of anaesthesia. Methods: Anaesthesia was induced with fentanyl 2 μg/kg and propofol 2 mg/kg followed by application of cricoid pressure. Patients were randomly allocated to three groups according to the dose of succinylcholine administered (0.4, 0.6 or 1.0 mg/kg). Intubating conditions were assessed at 60 s after succinylcholine administration. Time to first diaphragmatic contraction (apnoea time) and time to resumption of regular spontaneous breathing were noted. Results: Excellent intubating conditions were obtained in 52.4%, 95.7% and 100% of the patients after 0.4, 0.6 and 1.0 mg/kg succinylcholine, respectively; P<0.001. Acceptable intubating conditions (excellent and good grade combined) were obtained in 66.7%, 100% and 100% of the patients after 0.4, 0.6 and 1.0 mg/ kg succinylcholine, respectively; P<0.001. Apnoea time and resumption of regular spontaneous breathing were dose-dependent. Apnoea time was 3.8±1.1 min, 4.3±0.9 min and 8.2±3.4 min in groups 0.4, 0.6 and 1.0 mg/kg, respectively; P<0.001. Time to regular spontaneous breathing was 5.3±1.2 min, 5.5±1.1 min and 8.9±3.5 min in groups 0.4, 0.6 and 1.0 mg/kg, respectively; P<0.001. Conclusion: A dose of 0.6 mg/kg succinylcholine can be used for rapid sequence induction of anaesthesia as it provides acceptable intubating conditions with a shorter apnoea time compared with a dose of 1 mg/kg

KAP1 Protein: An Enigmatic Master Regulator of the Genome*

In mammalian cells, multiple cellular processes, including gene silencing, cell growth and differentiation, pluripotency, neoplastic transformation, apoptosis, DNA repair, and maintenance of genomic integrity, converge on the evolutionarily conserved protein KAP1, which is thought to regulate the dynamic organization of chromatin structure via its ability to influence epigenetic patterns and chromatin compaction. In this minireview, we discuss how KAP1 might execute such pleiotropic effects, focusing on genomic targeting mechanisms, protein-protein interactions, specific post-translational modifications of both KAP1 and associated histones, and transcriptome analyses of cells deficient in KAP1