Recent advances in the applications of metal-ligand cooperation via dearomatization and aromatization of pincer complexes

Metal-ligand cooperation (MLC) has played an important role in the development of new green homogeneous catalytic reactions. In the past we have discovered a new mode of MLC which is based on the dearomatization and aromatization of pincer complexes and have utilized it to uncover new modes of bond activation and new catalytic reactions that are atom-economic, environmentally benign and sustainable. Building upon our earlier discoveries which have been well-reviewed in the past, this chapter discusses recent progresses on the application of the concept of MLC via dearomatization and aromatization of pincer complexes. Bond activation of greenhouse gases such as CO2 and N2O and their applications in the development of catalytic reactions have been discussed in detail. Additionally, the new concept of template catalysis where catalytic transformation occurs mainly on the pincer ligand and the metal centre acts as an “anchor” has also been discussed. Template catalysis utilizes the tool of MLC via dearomatization/aromatization to perform Michael reactions forming new C–C, C–O and C–N bonds catalysed by ruthenium, rhenium and manganese pincer complexes. © 2020, Springer Nature Switzerland AG

Pedunculopontine cell loss and protein aggregation direct microglia activation in parkinsonian rats

We previously reported a loss of cholinergic neurons within the pedunculopontine tegmental nucleus (PPTg) in rats that had been intra-nigrally lesioned with the proteasomal inhibitor lactacystin, with levels of neuronal loss corresponding to that seen in the post-mortem pedunculopontine nucleus (PPN) of advanced Parkinson’s disease (PD) patients. Here we reveal lower expression values of the acetylcholine synthesising enzyme, choline acetyltransferase, within the remaining PPTg cholinergic neurons of lesioned rats compared to sham controls. We further characterise this animal model entailing dopaminergic- and non-dopaminergic neurodegeneration by reporting on stereological counts of non-cholinergic neurons, to determine whether the toxin is neuro-type specific. Cell counts between lesioned and sham-lesioned rats were analysed in terms of the topological distribution pattern across the rostro-caudal extent of the PPTg. The study also reports somatic hypotrophy in the remaining non-cholinergic neurons, particularly on the side closest to the nigral lesion. The cytotoxicity affecting the PPTg in this rat model of PD involves overexpression and accumulation of alpha-synuclein (αSYN), affecting cholinergic and non-cholinergic neurons as well as microglia on the lesioned hemispheric side. We ascertained that microglia within the PPTg become fully activated due to the extensive neuronal damage and neuronal death resulting from a lactacystin nigral lesion, displaying a distinct rostro-caudal distribution profile which correlates with PPTg neuronal loss, with the added implication that lactacystin-induced αSYN aggregation might trigger neuronophagia for promoting PPTg cell loss. The data provide critical insights into the mechanisms underlying the lactacystin rat model of PD, for studying the PPTg in health and when modelling neurodegenerative disease

Search for R-parity violating supersymmetry using like-sign dielectrons in p(p)over-bar collisions at root s=1.8 TeV

We present a search for like-sign dielectron plus multijet events using 107 pb(-1) of data in p (p) over bar collisions at root s = 1.8 TeV collected in 1992-1995 by the CDF experiment. Finding no events that pass our selection, we set sigma x BR limits on two supersymmetric processes that can produce this experimental signature: gluino-gluino or squark-antisquark production with R-parity violating decays of the charm squark or lightest neutralino via a nonzero lambda'(121) coupling. We compare our results to the next-to-leading order calculations for gluino and squark production cross sections and set lower limits on M((g) over tilde), M((t) over tilde(1)), and M((q) over tilde)