Effects of doping in 25-atom bimetallic nanocluster catalysts for carbon–carbon coupling reaction of iodoanisole and phenylacetylene

A trio of thiolate-protected atomically precise gold nanoclusters, [Au_(23)(S-c-C_6H_(11))_(16)]~–, Au24(SCH_2pH~tBu)_(20)and [Au_(25)(SCH_2CH_2pH)_~(18)]~–, are utilized as catalysts for 4-nitrophenol(4-NP) reduction to 4-aminophenol(4-AP).Despite nearly identical sizes(~1 nm), the three nanoclusters possess distinctly different atomic packing structures and surface ligand binding modes, which contribute to different catalytic performance. The [Au_(23)(Sc-C_6H_(11))_(16)]~–nanocluster shows the highest activity with a kinetic rate constant of 0.0370 s~(-1), which is higher than those of Au24(SCH_2pH~tBu)_(20)(0.0090 s~(-1)) and [Au_(25)(SCH_2CH_2pH)_~(18)]~–(0.0242 s~(-1)). Such a trio of gold nanoclusters indicate that the atomic packing mode and electronic structure play a crucial role in determining their catalytic performance.     

BMP2 activity, although dispensable for bone formation, is required for the initiation of fracture healing

Adult bones have a notable regenerative capacity. Over 40 years ago, an intrinsic activity capable of initiating this reparative response was found to reside within bone itself, and the term bone morphogenetic protein (BMP) was coined to describe the molecules responsible for it. A family of BMP proteins was subsequently identified, but no individual BMP has been shown to be the initiator of the endogenous bone repair response. Here we demonstrate that BMP2 is a necessary component of the signaling cascade that governs fracture repair. Mice lacking the ability to produce BMP2 in their limb bones have spontaneous fractures that do not resolve with time. In fact, in bones lacking BMP2, the earliest steps of fracture healing seem to be blocked. Although other osteogenic stimuli are still present in the limb skeleton of BMP2-deficient mice, they cannot compensate for the absence of BMP2. Collectively, our results identify BMP2 as an endogenous mediator necessary for fracture repair.     

Behavior of fluxed lime iron oxide pellets in hot metal bath during melting and refining

Lump lime as a flux material in a basic oxygen furnace (BOF) often creates problems in operation due to its high melting point, poor dissolution property, hygroscopic nature, and fines generation tendency. To alleviate these problems, fluxed lime iron oxide pellets (FLIP) containing 30% CaO were developed in this study using waste iron oxide fines and lime. The suitable handling strengths of the pellet (crushing strength: 300 N; drop strength: 130 times) of FLIP were developed by treating with CO₂ or industrial waste gas at room temperature, while no separate binders were used. When the pellet was added into hot metal bath (carbon-containing molten iron), it was decomposed, melted, and transformed to produce low melting oxidizing slag, because it is a combination of main CaO and Fe₂O₃. This slag is suitable for facilitating P and C removal in refining. Furthermore, the pellet enhances waste utilization and use of CO₂ in waste gas. In this article, emphasis is given on studying the behavior of these pellets in hot metal bath during melting and refining along with thermodynamics and kinetics analysis. The observed behaviors of the pellet in hot metal bath confirm that it is suitable and beneficial for use in BOF and replaces lump lime.     

Enhanced gravi- and phototropism in plant mdr mutants mislocalizing the auxin efflux protein PIN1

Many aspects of plant growth and development are dependent on the flow of the hormone auxin down the plant from the growing shoot tip where it is synthesized. The direction of auxin transport in stems is believed to result from the basal localization within cells of the PIN1 membrane protein, which controls the efflux of the auxin anion. Mutations in two genes homologous to those encoding the P-glycoprotein ABC transporters that are especially abundant in multidrug-resistant tumour cells in animals were recently shown to block polar auxin transport in the hypocotyls of Arabidopsis seedlings. Here we show that the mdr mutants display faster and greater gravitropism and enhanced phototropism instead of the impaired curvature development expected in mutants lacking polar auxin transport. We find that these phenotypes result from a disruption of the normal accumulation of PIN1 protein along the basal end of hypocotyl cells associated with basipetal auxin flow. Lateral auxin conductance becomes relatively larger as a result, enhancing the growth differentials responsible for tropic responses.