In conclusion, we propose that the regular patterns, which comprise the majority of spikes in PC SS trains, can control the amplitude of subsequent timing signals by modulating the amplitude of rebound spikes in downstream DCN neurons. Only one previous multifactorial intervention study has exclusively recruited participants with dementia. Interventions were based upon those used in successful trials in people without dementia, and the study did not show a significant reduction in falls or number of fallers. The retinoblastoma susceptibility gene encodes a nuclear phosphoprotein RB with tumor suppression function. Inheritance of germline RB1 mutation causes retinoblastoma with 90% penetrance in children; the tumor cells exhibit loss of heterozygosity at the RB1 locus with the invariable loss the normal RB1 allele. The bi-alleleic inactivation of the RB1 gene has also been detected in sporadic human cancers of a variety of tissue origins at an average frequency of approximately 10%. The current knowledge suggests that RB suppresses tumor development by inhibiting cell proliferation and promoting terminal differentiation. The anti-proliferation function of RB is dependent on its interaction with the cellular E2F-family transcription factors, which are heterodimers consisting of E2F and DP subunits. RB directly interacts with several members of the E2F family to inhibit E2F-dependent transcription. The E2F transcription factors AMN107 regulate genes required for cell proliferation and apoptosis. By inhibiting E2F-dependent transcription, RB negatively regulates cell proliferation and apoptosis. Previous studies have demonstrated that RB-dependent growth arrest is protective against apoptosis. Fibroblasts derived from Rbnull embryos are defective in DNA damage-induced G1, S and G2 arrest and exhibit increased apoptotic response to genotoxins. The ectopic expression of RB in SAOS-2 osteosarcoma cells induces G1 arrest and protects from apoptosis induced by ionizing radiation. Induced expression of a constitutively active RB that lacks nine phosphorylate sites interfered with doxorubicin-induced activation of caspase-3 as a consequence of G1arrest. The apoptosis resistance of G1-arrested cells is likely to involve RB-dependent transcriptional repression of E2F-regulated pro-apoptotic genes. Therefore, the anti-apoptotic activity of RB has mostly been considered as a secondary effect of its growth suppression function. In this study, we show that RB and RB-KN can inhibit apoptosis without causing cell cycle arrest. We have demonstrated that RB-KN is a separation of function mutant, which is useful in further studies of the anti-apoptotic function of RB. To screen for genes that regulate lipid processing and organ development in zebrafish, we developed an assay to study zebrafish larvae at stages before the mouth opens and swallowing begins. BODIPY-C12 fatty acid was injected into the yolk and three day old embryos harvested for lipid extraction.