4,4-Dihydrodithienosilole (DTSH2) was isolated from a mixture of 3,3′-dibromobithiophene, n-BuLi, and H2SiCl2 and was fully characterized. The reaction of DTSH2 with a Pt(0) complex, prepared in situ from [Pt(PCy3)2] and DPPE (1,2-bis(diphenylphosphino)ethane), produced a bis(silyl)platinum complex [Pt(DTSH)2(dppe)] (1) with two hydrodithienosilole ligands. DTSH2 undergoes cyclodimerization accompanied by skeletal rearrangement to afford a cis-fused bicyclic compound (2) upon heating the solution in the presence of a catalytic amount of 1 or [Ni(PPh3)4]. The product has a Si–Si bond that bridges two Si atoms, separated by 2.309(1) Å. Bicyclic disilane 2 forms the Pt complex (3) with two Si ligands and retaining the 10-membered macrocycle ligand via the Si–Si bond cleavage.
Since the advent of the nanotechnology era, the environmental sink has been continuouslyreceiving engineered nanomaterials as well as their derivatives. Our current understanding of the potential impact of nanomaterials on invertebrate immunity is limited to only a handful of initial studies including those on earthworms. Recently, we reported selective accumulation of silver nanoparticles in the amoebocyte population of Eisenia fetida coelomocytes in vitro. In this review, we give an overview of available literature on the life-history impacts on earthworms, and what we have learnt of the immune responses to nanoparticles with references to other invertebrate species and vertebrate counterparts. We discuss the significant contribution of amoebocytes as nanoparticle scavengers and suggest a possibility of studying inter-cellular communications in coelomocytes. Implications from the leading researches in vertebrate models tell us that study of the nanoparticle recognition involved in cellular uptake as well as sub- and inter-cellular events may uncover further intriguing insights into earthworm’s immunity in the nanomaterial world.
Localized insulin-derived amyloid masses occasionally form at the site of repeated insulin injections in patients with insulin-dependent diabetes and cause subcutaneous insulin resistance. Various kinds of insulin including porcine insulin, human insulin, and insulin analogues reportedly formed amyloid fibrils in vitro and in vivo, but the impact of the amino acid replacement in insulin molecules on amyloidogenicity is largely unknown. In the present study, we demonstrated the difference in amyloid fibril formation kinetics of human insulin and insulin analogues, which suggests an important role of the C-terminal domain of the insulin B chain in nuclear formation of amyloid fibrils. Furthermore, we determined that cyclodextrins, which are widely used as drug carriers in the pharmaceutical field, had an inhibitory effect on the nuclear formation of insulin amyloid fibrils. These findings have significant implications for the mechanism underlying insulin amyloid fibril formation and for developing optimal additives to prevent this subcutaneous adverse effect.
ABSTRACT Nanoparticles can acquire a biomolecular corona with a species-specific biological identity. However, “non-self” incompatibility of recipient biological systems is often not considered, for example, when rodents are used as a model organism for preclinical studies of biomolecule-inspired nanomedicines. Using zebrafish embryos as an emerging model for nano-bioimaging, here we unraveled the in vivo fate of intravenously injected 70 nm SiO 2 nanoparticles with a protein corona pre-formed from fetal bovine serum (FBS), representing a non-self biological identity. Strikingly rapid sequestration and endolysosomal acidification of nanoparticles with the pre-formed FBS corona were observed in scavenger endothelial cells within minutes after injection. This led to loss of blood vessel integrity and inflammatory activation of macrophages over the course of several hours. As unmodified nanoparticles or the equivalent dose of FBS proteins alone failed to induce the observed pathophysiology, this signifies how the corona enriched with a differential repertoire of proteins can determine the fate of the nanoparticles in vivo . Our findings thus reveal the adverse outcome triggered by incompatible protein coronas and indicate a potential pitfall in the use of mismatched species combinations during nanomedicine development.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Nanoparticles can acquire a biomolecular corona with a species-specific biological identity. However, "non-self" incompatibility of recipient biological systems is often not considered, for example, when rodents are used as a model organism for preclinical studies of biomolecule-inspired nanomedicines. Using zebrafish embryos as an emerging model for nanobioimaging, here we unravel the in vivo fate of intravenously injected 70 nm SiO2 nanoparticles with a protein corona preformed from fetal bovine serum (FBS), representing a non-self biological identity. Strikingly rapid sequestration and endolysosomal acidification of nanoparticles with the preformed FBS corona were observed in scavenger endothelial cells within minutes after injection. This led to loss of blood vessel integrity and to inflammatory activation of macrophages over the course of several hours. As unmodified nanoparticles or the equivalent dose of FBS proteins alone failed to induce the observed pathophysiology, this signifies how the corona enriched with a differential repertoire of proteins can determine the fate of the nanoparticles in vivo. Our findings thus reveal the adverse outcome triggered by incompatible protein coronas and indicate a potential pitfall in the use of mismatched species combinations during nanomedicine development.
Diiron(II) complex with a new dinucleating ligand containing terminal amino group, 2,6bis[bis( 6-pivalamido-2-pyridylmethyl)aminomethyl]-4-aminophenol (tppap) (1), [F~(tppap )(C~5COOht (2), was synthesized.The self-assembled monolayer (SAM) of 2, 21 Au, was prepared by the coupling reaction between 2 and activated ester-modified Au electrode.The redox behavior of 2/ Au was observed in aqueous solution at room temperattrre, which suggests that 2 on Au surface has been stabilized as compared with 2 in homogeneous solution.In addition, the redox potentials of 2/ Au assignable to Fe 2 (11,11)/(III,III) and F~(II,IIIIIII,III) shifted to negative direction by bubbling of molecular dioxygen, which returned to the original potential by Ar bubbling.These behaviors were reversible, suggesting that 2/Au can reversibly bind/release molecular dioxygen in aqueous solution at room temperature.
