A facile surfactant-free synthesis of Rh flower-like nanostructures constructed from ultrathin nanosheets and their enhanced catalytic properties

Rh is an important catalyst that is widely used in a variety of organic reactions. In recent years, many efforts have focused on improving its catalytic efficiency by fabricating catalyst nanoparticles with controlled size and morphology. However, the frequently employed synthesis route using organic compounds either as the reaction medium or capping agent often results in residual molecules on the catalyst surface, which in turn drastically diminishes the catalytic performance. Herein, we report a facile, aqueous, surfactant-free synthesis of a novel Rh flower- like structure obtained via hydrothermal reduction of Rh（acac）3 by formaldehyde. The unique Rh nanoflowers were constructed from ultrathin nanosheets, whose basal surfaces comprised {111} facets with an average thickness of -1.1 nm. The specific surface area measured by CO stripping was 79.3 m2-g-1, which was much larger than that of commercial Rh black. More importantly, the Rh nanoflower catalyst exhibited excellent catalytic performance in the catalytic hydrogenation of phenol and cyclohexene, in contrast to the commercial Rh black and polyvinyl pyrrolidone （PVP）-capped Rh nanosheets exposed by similar {111} basal surfaces.

Surfactant dependent evolution of Au-Pd alloy nanocrystals from trisoctahedron to excavated rhombic dodecahedron and multipod： a matter of crystal growth kinetics

In wet chemical syntheses of noble metal nanocrystals,surfactants play crucial roles in regulating their morphology.To date,more attention has been paid to the effect of the surfactant on the surface energy of crystal facets,while less attention has been paid to its effect on the growth kinetics.In this paper,using the growth of Au-Pd alloy nanocrystals as an example,we demonstrate that different concentration of surfactant hexadecyltrimethyl ammonium chloride(CTAC)may cause the different packing density of CTA+bilayers on different sites(face,edge or vertex)of crystallite surface,which would change the crystal growth kinetics and result in preferential crystal growth along the edge or vertex of crystallites.The unique shape evolution from trisoctahedron to excavated rhombic dodecahedron and multipod structure for Au-Pd alloy nanocrystals was successfully achieved by simply adjusting the concentration of CTAC.These results help to understand the effect of surfactants on the shape evolution of nanocrystals and open up avenues to the rational synthesis of nanocrystals with the thermodynamically unfavorable morphologies.

Origin of symmetry breaking in the seed-mediated growth of bi-metal nano-heterostructures

Seed-mediated growth is the most general way to controllably synthesize bimetal nano-heterostructures.Despite successful instances through trial and error were reported, the way for second metal depositing on the seed, namely whether the symmetry of resulted nano-heterostructure follows the original crystal symmetry of seed metal, remains an unpredictable issue to date. In this work, we propose that the thermodynamic factor, i.e., the difference of equilibrium electrochemical potentials(corresponding to their Fermi levels) of two metals in the growth solution, plays a key role for the symmetry breaking of bimetal nano-heterostructures during the seed-mediated growth. As a proof-of-principle experiment, by reversing the relative position of Fermi levels of the Pd nanocube seeds and the second metal Au with changing the concentration of reductant(L-ascorbic acid) in the growth solution, the structure of as-prepared products successfully evolved from centrosymmetric Pd@Au core-shell trisoctahedra to asymmetric Pd-Au hetero-dimers. The idea was further demonstrated by the growth of Ag on the Pd seeds. The present work intends to reveal the origin of symmetry breaking in the seed-mediated growth of nano-heterostructures from the viewpoint of thermodynamics, and these new insights will in turn help to achieve rational construction of bimetal nano-heterostructures with specific functions.

Impaired SERCA2a phosphorylation causes diabetic cardiomyopathy through impinging on cardiac contractility and precursor protein processing

Diabetic cardiomyopathy(DCM)is currently a progressive and nonstoppable complication in type 2 diabetic patients.Metabolic insults and insulin resistance are involved in its pathogenesis;however,the underlying mechanisms are still not clearly understood.Here we show that calcium dysregulation can be both a cause and a consequence of cardiac insulin resistance that leads to DCM.A western diet induces the development of DCM through at least three phases in mice,among which an early phase depends on impaired Thr^(484)-phosphorylation of sarcoplasmic/endoplasmic reticulum calcium ATPase 2a(SERCA2a)elicited by insulin resistance.Mutation of SERCA2a-Thr^(484) to a nonphosphorylatable alanine delays calcium re-uptake into the sarcoplasmic reticulum in the cardiomyocytes and decreases cardiac function at the baseline.Importantly,this mutation blunts the early phase of DCM,but has no effect on disease progression in the following phases.Interestingly,impairment of sarcoplasmic reticulum calcium re-uptake caused by the SERCA2a-Thr^(484) mutation inhibited processing of insulin receptor precursor through FURIN convertase,resulting in cardiac insulin resistance.Collectively,these data reveal a bidirectional relationship between insulin resistance and impairment of calcium homeostasis,which may underlie the early pathogenesis of DCM.Our findings have therapeutic implications for early intervention of DCM.

TBC1D1 is an energy-responsive polarization regulator of macrophages via governing ROS production in obesity

Energy status is linked to the production of reactive oxygen species(ROS)in macrophages,which is elevated in obesity.However,it is unclear how ROS production is upregulated in macrophages in response to energy overload for mediating the development of obesity.Here,we show that the Rab-GTPase activating protein(Rab GAP)TBC1D1,a substrate of the energy sensor AMP-activated protein kinase(AMPK),is a critical regulator of macrophage ROS production and consequent adipose inflammation for obesity development.TBC1D1 deletion decreases,whereas an energy overload-mimetic non-phosphorylatable TBC1D1^(S231A)Amutation increases,ROS production and M1-like polarization in macrophages.Mechanistically,TBC1D1 and its downstream target Rab8a form an energy-responsive complex with NOX2 for ROS generation.Transplantation of TBC1D1^(S231A)bone marrow aggravates diet-induced obesity whereas treatment with an ultra-stable Tt SOD for removal of ROS selectively in macrophages alleviates both TBC1D1~(S231A)mutation-and diet-induced obesity.Our findings therefore have implications for drug discovery to combat obesity.