Influence of Sepiolite and Lignin as Potential Synergists on Flame Retardant Systems in Polylactide (PLA) and Polyurethane Elastomer (PUE).

A comparison of the influence of sepiolite and lignin as potential synergists for fire retardant (FR) systems based on ammonium polyphosphate (APP) has been carried out in polyurethane elastomer and polylactide. Different ratios of kraft lignin and sepiolite were tested in combination with APP in both polymers. The thermal stability and the fire behavior of the corresponding composites were evaluated using Thermogravimetric Analysis (TGA), a Pyrolysis Combustion Flow Calorimeter (PCFC) and Cone Calorimeter (CC).

Orexin A and orexin receptor 1 axonal traffic in dorsal roots at the CNS/PNS interface.

Hypothalamic orexin/hypocretin neurons send long axonal projections through the dorsal spinal cord in lamina I-II of the dorsal horn (DH) at the interface with the peripheral nervous system (PNS). We show that in the DH OXA fibers colocalize with substance P (SP) positive afferents of dorsal root ganglia (DRG) neurons known to mediate sensory processing. Further, OR1 is expressed in p75(NTR) and SP positive DRG neurons, suggesting a potential signaling pathway between orexin and DRG neurons.

A functional dynein-microtubule network is required for NGF signaling through the Rap1/MAPK pathway.

Rap1 transduces nerve growth factor (NGF)/tyrosine receptor kinase A (TrkA) signaling in early endosomes, leading to sustained activation of the p44/p42 mitogen-activated protein kinases (MAPK1/2). However, the mechanisms by which NGF, TrkA and Rap1 are trafficked to early endosomes are poorly defined. We investigated trafficking and signaling of NGF, TrkA and Rap1 in PC12 cells and in cultured rat dorsal root ganglion (DRG) neurons.

Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.

Degeneration of basal forebrain cholinergic neurons (BFCNs) contributes to cognitive dysfunction in Alzheimer's disease (AD) and Down's syndrome (DS). We used Ts65Dn and Ts1Cje mouse models of DS to show that the increased dose of the amyloid precursor protein gene, App, acts to markedly decrease NGF retrograde transport and cause degeneration of BFCNs. NGF transport was also decreased in mice expressing wild-type human APP or a familial AD-linked mutant APP; while significant, the decreases were less marked and there was no evident degeneration of BFCNs.

Alzheimer's disease and NGF signaling.

Age-related degeneration of basal forebrain cholinergic neurons (BFCNs) occurs early and contributes significantly to cognitive decline in Alzheimer's disease (AD). Proper function and morphology of BFCNs depends on the supply of nerve growth factor (NGF) from the cortex and the hippocampus. A large number of experiments have shown that decreased supply of NGF at the level of BFCN cell bodies leads to loss of neuronal markers and shrinkage, mimicking what is observed in AD.