Brought to life more than half a century ago and successfully applied for high-value petrochemical intermediates production, nickel-catalyzed olefin oligomerization is still a very dynamic topic, ...with many fundamental questions to address and industrial challenges to overcome. The unique and versatile reactivity of nickel enables the oligomerization of ethylene, propylene, and butenes into a wide range of oligomers that are highly sought-after in numerous fields to be controlled. Interestingly, both homogeneous and heterogeneous nickel catalysts have been scrutinized and employed to do this. This rare specificity encouraged us to interlink them in this review so as to open up opportunities for further catalyst development and innovation. An in-depth understanding of the reaction mechanisms in play is essential to being able to fine-tune the selectivity and achieve efficiency in the rational design of novel catalytic systems. This review thus provides a complete overview of the subject, compiling the main fundamental/industrial milestones and remaining challenges facing homogeneous/heterogeneous approaches as well as emerging catalytic concepts, with a focus on the last 10 years.
Alzheimer's disease and NGF signaling Salehi, A; Delcroix, J-D; Swaab, D F
Journal of Neural Transmission,
03/2004, Volume:
111, Issue:
3
Journal Article
Peer reviewed
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. The delivery of sufficient amounts of NGF signal to BFCN cell bodies depends on the effective participation of several factors including sufficient synthesis and release of NGF, adequate synthesis and expression of NGF receptors by BFCNs, normal signaling and retrograde transport of NGF-receptor complex, and finally effective induction of gene expression by NGF. In the past few years it has become clear that decreased amounts of NGF at the level of BFCN cell bodies is largely due to failed retrograde transport rather than decreased synthesis, binding or expression of NGF receptors in the BFCN terminals. We will discuss in vivo evidence supporting decreased retrograde transport of NGF in a mouse model with BFCN degeneration, and will attempt to match these findings with our studies in postmortem human AD brain. We will speculate about the possible mechanisms of failed NGF retrograde transport and its relationship to AD pathology.
Age-related degeneration of basal forebrain cholinergic neurons (BFCNs) contributes to cognitive decline in Alzheimer's disease and Down's syndrome. With aging, the partial trisomy 16 (Ts65Dn) mouse ...model of Down's syndrome exhibited reductions in BFCN size and number and regressive changes in the hippocampal terminal fields of these neurons with respect to diploid controls. The changes were associated with significantly impaired retrograde transport of nerve growth factor (NGF) from the hippocampus to the basal forebrain. Intracerebroventricular NGF infusion reversed well established abnormalities in BFCN size and number and restored the deficit in cholinergic innervation. The findings are evidence that even BFCNs chronically deprived of endogenous NGF respond to an intervention that compensates for defective retrograde transport. We suggest that age-related cholinergic neurodegeneration may be a treatable disorder of failed retrograde NGF signaling.
The objective was to determine whether stress‐activated protein kinases (SAPKs) mediated the transfer of diabetes‐induced stress signals from the periphery to somata of sensory neurons. Thus, we ...characterized axonal transport of SAPKs in peripheral nerve, studied any alteration in streptozotocin (STZ)‐diabetic rats and examined effects of neurotrophin‐3 (NT‐3) on diabetes‐induced events. We demonstrate that c‐jun N‐terminal kinase (JNK) and p38 are bidirectionally axonally transported at fast rates in sciatic nerve. In STZ‐diabetic rats the relative levels of retrograde axonal transport of phosphorylated (activated) JNK and p38 were raised compared with age‐matched controls (all data are in arbitrary units and expressed as fold increase over control: JNK 54–56 kDa isoforms, control 1.0 ± 0.19, diabetic 2.5 ± 0.26; p38, control 1.0 ± 0.09, diabetic 2.9 ± 0.52; both P < 0.05). Transport of total enzyme levels of JNK and p38 and phosphorylated extracellular signal‐regulated kinase (ERK) was not significantly altered and anterograde axonal transport of phosphorylated JNK and p38 was unaffected by diabetes. The transcription factor ATF‐2, which is phosphorylated and activated by JNK and p38, also exhibited elevated retrograde axonal transport in STZ‐diabetic animals (control 1.0 ± 0.07, diabetic 3.0 ± 0.41; P < 0.05). Treatment of STZ‐diabetic animals with 5 mg/kg human recombinant NT‐3 prevented activation of JNK and p38 in sciatic nerve (phosphorylated JNK, control 1.0 ± 0.09, diabetic 1.95 ± 0.35, diabetic + NT‐3 1.09 ± 0.12; P < 0.05 diabetic versus others; phosphorylated p38, control 1.0 ± 0.16, diabetic 4.7 ± 0.9, diabetic + NT‐3 1.19 ± 0.18; P < 0.05 diabetic versus others). The results show that JNK and p38 are transported axonally and may mediate the transfer of diabetes‐related stress signals, possibly triggered by loss of neurotrophic support, from the periphery to the neuronal soma.
A reconfigurable parasitic patch array is designed to provide polarization and pattern diversities. The performance of the device is predicted using a commercial simulator including a pin diode ...modelling and an optimization procedure of the switched loads based on an equivalent flow graph. Measurements of the correlation factor and the diversity gain in an indoor environment are performed with a dedicated platform for two orientations of the antenna.
Target-derived NGF promotes the phenotypic maintenance of mature dorsal root ganglion (DRG) nociceptive neurons. Here, we provide in vivo and in vitro evidence for the presence within DRG neurons of ...endosomes containing NGF, activated TrkA, and signaling proteins of the Rap1/Erk1/2, p38MAPK, and PI3K/Akt pathways. Signaling endosomes were shown to be retrogradely transported in the isolated sciatic nerve in vitro. NGF injection in the peripheral target of DRG neurons increased the retrograde transport of p-Erk1/2, p-p38, and pAkt in these membranes. Conversely, NGF antibody injections decreased the retrograde transport of p-Erk1/2 and p-p38. Our results are evidence that signaling endosomes, with the characteristics of early endosomes, convey NGF signals from the target of nociceptive neurons to their cell bodies.
Effects of delivery of nerve growth factor, from a catheterized osmotic mini-pump to the proximal stump of a transected sciatic nerve, were compared with the effects of normal saline. A pilot ...measured retrograde axonal transport of nerve growth factor to determine a pump concentration which raised axonal transport ipsilaterally, but not contralaterally. The effects of this delivery over 12
days were then determined on expression of growth-associated protein-43, trkA, p75
NTR and preprotachykinin A ipsilateral and contralateral to the pump in dorsal root ganglia at L
4 and L
5 (pooled). Ganglionic expression was measured both as messenger RNA and protein. Axotomy (saline pumps) increased growth-associated protein-43 messenger RNA (318±14%: all changes are percent of contralateral, non-axotomized ganglia with saline pumps) and immunoreactivity (431±43%). The increase was significantly less (
P<0.001) ipsilateral to nerve growth factor pumps (191±45%). Axotomy reduced expression of p75
NTR (messenger RNA: 52±17%,
P<0.01; immunoreactivity: 74±3%,
P<0.05). These decreases were converted to increases by nerve growth factor delivery (respectively 143±40% and 281±67%; both
P<0.01). With trkA, axotomy decreased the expression of the messenger RNA (68±40%,
P<0.01) and of the primary translation product—110,000 mol. wt protein (55±12%,
P<0.01)—but not the fully glycosylated trkA protein (mol. wt 145,000). Nerve growth factor delivery did not affect trkA expression. Axotomy reduced messenger RNA for the substance P precursor, preprotachykinin A, to 42±17% (
P<0.01) and this reduction was prevented by nerve growth factor treatment.
We suggest that the primary effect of nerve growth factor on axotomized C-fibres is not to promote regeneration, although that may be its secondary effect via an action on Schwann cells. It is possible that reduced neuronal sensitivity to nerve growth factor during regeneration is advantageous in suppressing nociception.
The hydrogenolysis reaction of biomass-derived xylitol to glycols and glycerol has been carried out in different water/organic solvent mixtures over a bifunctional Ru/MnO/C catalyst under ...alkaline-free conditions at 60 bar H2 and 200 °C. In pure water, the retro-aldol reaction takes place. However, decarbonylation and epimerization are the dominant reactions and produce C4 and C5 alditols, which limits the overall selectivity to glycols and glycerol (30%). When 90:10 vol % water/1,4-dioxane and water/2-PrOH solutions are used as solvents, the product distribution is very similar to the one in water. Meanwhile, in 90:10 vol % water/primary alcohol (ROH with R = Me, Et, nPr, nBu), the overall selectivity to glycols and glycerol is greatly enhanced (up to 70%), whereas the selectivity to C4 and C5 alditols is reduced. In a solution with a higher MeOH proportion of 20 vol %, the glycols are detected with even higher selectivity; however, some deactivation of the catalyst is observed. TGA analysis of the used catalysts shows that during the process some coke is deposited on the catalyst via a dehydrogenation step of ROH. The coke selectively inhibits the Ru sites that are active for the undesired reactions of decarbonylation and epimerization.
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