Additionally, we suggest the utility of comparing mammosphere data to computational mammosphere simulations in elucidating the growth characteristics

of mammary (cancer) stem cells. (C) 2010 Elsevier Ltd. All rights reserved.”
“Feedback inhibition serves to modulate release when neurotransmitter levels in the synaptic cleft are elevated. The “”classical”" feedback auto-inhibition of neurotransmitter release is predominantly mediated by activation of presynaptic G-protein-coupled receptors (GPCRs) and exhibits slow kinetics. In cholinergic and glutamatergic synapses and for focal graded depolarization of the axon terminal, feedback inhibition was found to be voltage-dependent. At high depolarizations, such as the one produced by an action potential, low concentrations of neurotransmitter were insufficient ATM inhibitor to inhibit release. On the other hand, at higher neurotransmitter concentrations, feedback inhibition was observed also for action potential-evoked release. This finding suggests the presence of an additional mechanism of feedback inhibition that operates also

at large presynaptic depolarizations. Using the glutamatergic crayfish neuromuscular junction we discovered a novel, extremely fast, form of feedback inhibition which hampers action potential-evoked release. This novel mechanism is pertussis toxin-insensitive, and is activated already 1 ms after flash photolysis producing glutamate concentrations higher than the ones required to activate the classical feedback inhibition. find more This finding implies that this mechanism is recruited only when glutamate levels in the synaptic cleft are relatively high (after high-frequency activation or in pathological conditions). We show that both the classical and this novel mechanism operate under physiological conditions. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The well-known Kirschner-Panetta model for tumour-immune System interplay

[Kirschner, next D., Panetta, J.C., 1998. Modelling immunotherapy of the tumour-immune interaction. J. Math. Biol. 37(3), 235-252] reproduces a number of features of this essential interaction, but it excludes the possibility of tumour suppression by the immune system in the absence of therapy. Here we present a hybrid-stochastic version of that model. In this new framework, we show that in reality the model is also able to reproduce the suppression, through stochastic extinction after the first spike of an oscillation. (C) 2010 Elsevier Ltd. All rights reserved.”
“Several lines of evidence suggest the existence of multiple progestin receptors that may account for rapid and delayed effects of progesterone in the CNS. The delayed effects have been long attributed to activation of the classical progestin receptor (Pgr). Recent studies have discovered novel progestin signaling molecules that may be responsible for rapid effects.