01785nas a2200229   4500008004100000022001400041245009100055210006900146260007500215300001200290490000600302520098700308653001501295653001301310653002401323653001401347653002001361100001901381700001701400700001901417856011901436       2016                        eng d  a1867-388000aCompounds with low-valent p-block elements for small molecule activation and catalysis0 aCompounds with lowvalent pblock elements for small molecule acti  aPOSTFACH 101161, 69451 WEINHEIM, GERMANYbWILEY-V C H VERLAG GMBHcFEB  a486-5010 v83 a<p>The past decade has witnessed staggering progress in the chemistry of compounds with low-valent main-group elements. Although these discoveries are mostly fundamental by nature, these compounds show promising reactivity towards small molecule activation. The reactivity of these compounds stems from the modest HOMO-LUMO energy gap; a characteristic known for the transition metals. The journey began in 2005 with the facile activation of dihydrogen by an alkyne analog of germanium [ArGeGeAr; Ar=2,6-Trip(2)-C6H3 (Trip=2,4,6-iPr(3)-C6H2)]. Subsequently, tremendous progress has been achieved in understanding and elucidating the potential of these compounds to activate small molecules as well as to use them in a variety of stoichiometric and catalytic transformations. In this review, we focus on developments in the activation of H-2, NH3, CO, and CO2 by compounds with multiply bound or open shell main-group elements. Emphasis will be given to their catalytic activity.</p>10aactivation10acarbenes10amain-group elements10asilylenes10asmall molecules1 aYadav, Sandeep1 aSaha, Sumana1 aSen, Sakya, S.  uhttps://library.ncl.res.in/content/compounds-low-valent-p-block-elements-small-molecule-activation-and-catalysis-103043nas a2200253   4500008004100000245008900041210006900130260000900199300000700208490000700215520224100222653001002463653001502473653002402488653001402512653001402526653002202540653001802562653001402580100001602594700002802610700003602638856011502674       2020                        eng d00aPhagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia0 aPhagocytosis of fulllength Tau oligomers by Actinremodeling of a  cJAN   a100 v173 a<p>Background Alzheimer's disease is associated with the accumulation of intracellular Tau tangles within neurons and extracellular amyloid-beta plaques in the brain parenchyma, which altogether results in synaptic loss and neurodegeneration. Extracellular concentrations of oligomers and aggregated proteins initiate microglial activation and convert their state of synaptic surveillance into a destructive inflammatory state. Although Tau oligomers have fleeting nature, they were shown to mediate neurotoxicity and microglial pro-inflammation. Due to the instability of oligomers, in vitro experiments become challenging, and hence, the stability of the full-length Tau oligomers is a major concern. Methods In this study, we have prepared and stabilized hTau40(WT) oligomers, which were purified by size-exclusion chromatography. The formation of the oligomers was confirmed by western blot, thioflavin-S, 8-anilinonaphthaalene-1-sulfonic acid fluorescence, and circular dichroism spectroscopy, which determine the intermolecular cross-beta sheet structure and hydrophobicity. The efficiency of N9 microglial cells to phagocytose hTau40(WT) oligomer and subsequent microglial activation was studied by immunofluorescence microscopy with apotome. The one-way ANOVA was performed for the statistical analysis of fluorometric assay and microscopic analysis. Results Full-length Tau oligomers were detected in heterogeneous globular structures ranging from 5 to 50 nm as observed by high-resolution transmission electron microscopy, which was further characterized by oligomer-specific A11 antibody. Immunocytochemistry studies for oligomer treatment were evidenced with A11(+) Iba1(high) microglia, suggesting that the phagocytosis of extracellular Tau oligomers leads to microglial activation. Also, the microglia were observed with remodeled filopodia-like actin structures upon the exposure of oligomers and aggregated Tau. Conclusion The peri-membrane polymerization of actin filament and co-localization of Iba1 relate to the microglial movements for phagocytosis. Here, these findings suggest that microglia modified actin cytoskeleton for phagocytosis and rapid clearance of Tau oligomers in Alzheimer's disease condition.</p>
10aActin10aactivation10aAlzheimer's disease10amicroglia10amigration10aneurodegeneration10aTau Oligomers10aTauopathy1 aDas, Rashmi1 aBalmik, Abhishek, Ankur1 aChinnathambi, Subashchandrabose  uhttps://library.ncl.res.in/content/phagocytosis-full-length-tau-oligomers-actin-remodeling-activated-microglia00708nas a2200205   4500008004100000022001400041245010500055210006900160260000900229300001400238490000700252653001500259653001300274653001400287100001700301700002000318700001900338700001900357856012600376       2024                        eng d  a0276-733300aSaturated NHC-stabilized borenium, boronium, hydride-bridged boron cations, and a bora-acyl chloride0 aSaturated NHCstabilized borenium boronium hydridebridged boron c  cJUN   a1355-13610 v4310aactivation10aBORINIUM10aChemistry1 aKundu, Gargi1 aAmrutha, P., R.1 aTothadi, Srinu1 aSen, Sakya, S.  uhttps://library.ncl.res.in/content/saturated-nhc-stabilized-borenium-boronium-hydride-bridged-boron-cations-and-bora-acyl