MgH2@Mg(BH4)2 Core-Shell-like Nanostructures: Synthesis, Hydrolysis Performance, and Promotion Mechanism.

The hydrolysis of hydrides, represented by MgH2, delivers substantial capacity and presents an appealing prospect for an on-site hydrogen supply. However, the sluggish hydrolysis kinetics and low hydrogen yield of MgH2 caused by the formation of a passivation Mg(OH)2 layer hinder its practical application. Herein, we present a dual strategy encompassing microstructural design and compounding, leading to the successful synthesis of a core-shell-like nanostructured MgH2@Mg(BH4)2 composite, which demonstrates excellent hydrolysis performance. Specifically, the optimal composite with a low Ea of 9.05 kJ mol-1 releases 2027.7 mL g-1 H2 in 60 min, and its hydrolysis rate escalates to 1356.7 mL g-1 min-1 H2 during the first minute at room temperature. The nanocoating Mg(BH4)2 plays a key role in enhancing the hydrolysis kinetics through the release of heat and the formation of local concentration of Mg2+ field after its hydrolysis. This work offers an innovative concept for the design of hydrolysis materials.

Amorphous Thickness-Dependent Strengthening-Softening Transition in Crystalline-Amorphous Nanocomposites.

Core-shell crystalline-amorphous nanocomposites, featuring nanograins surrounded by thick amorphous boundaries, are promising nanoarchitectures for achieving exceptional strength through cooperative strengthening effects. However, a comprehensive understanding of the influence of characteristic sizes, particularly the amorphous thickness, on codeformation strengthening is still lacking, limiting the attainment of the strength limit. Here, we employ molecular dynamics simulations to investigate Cu-CuTa crystalline-amorphous nanocomposites with varying grain sizes and amorphous thicknesses. Our findings demonstrate significant strengthening effects in nanocomposites, effectively suppressing the Hall-Petch breakdown observed in traditional amorphous-free nanograined Cu. Intriguingly, we observe a maximum strength followed by a strengthening-softening transition dependent on the amorphous thickness, as exemplified by a representative nanocomposite featuring a 12.5 nm grain size and a critical amorphous thickness of 4 nm. Inspired by observed shifts in atomistic mechanisms, we developed a theoretical model encompassing variations in grain size and amorphous thickness, providing valuable insights into the size-strength relationship for crystalline-amorphous nanocomposites.

Boron-Doped Spherical Hollow-Porous Silicon Local Lattice Expansion toward a High-Performance Lithium-Ion-Battery Anode.

Silicon (Si) attracts extensive attention as the advanced anode material for lithium (Li)-ion batteries (LIBs) because of its ultrahigh Li storage capacity and suitable voltage plateau. Hollow porous structure and dopant-induced lattice expansion can enhance the cycling stability and transporting kinetics of Li ions. However, it is still difficult to synthesize the Si anode possessing these structures simultaneously by a facile method. Herein, the lightly boron (B)-doped spherical hollow-porous Si (B-HPSi) anode material for LIBs is synthesized by a facile magnesiothermic reduction from B-doped silica. B-HPSi exhibits local lattice expansion located on boundaries of refined subgrains. B atoms in Si contribute to the increase of the conductivity and the expansion of lattices. On the basis of the first-principles calculations, the B dopants induce the conductivity increase and local lattice expansion. As a result, B-HPSi electrodes exhibit a high specific capacity of ∼1500 mAh g-1 at 0.84 A g-1 and maintains 93% after 150 cycles. The reversible capacities of ∼1250, ∼1000, and ∼800 mAh g-1 can be delivered at 2.1, 4.2, and 8.4 A g-1, respectively.

Neuroprotective Effects of Loganin on MPTP-Induced Parkinson's Disease Mice: Neurochemistry, Glial Reaction and Autophagy Studies.

Parkinson's disease (PD) is a progressive neurodegenerative disease, involving resting tremor and bradykinesia, for which no recognized therapies or drugs are available to halt or slow progression. In recent years, natural botanic products have been considered relatively safe, with limited side effects, and are expected to become an important source for clinical mediation of PD in the future. Our study focuses on the ability of loganin, a compound derived from fruits of cornus, to mediate neuroprotection in a mouse model of PD. Mice were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) with a dosage of 30 mg/kg daily for 5 days to establish a subacute PD model and treated with loganin. Locomotor activity was assessed by a pole test, then mice were euthanized at 1 and 3 days after the last treatment, and brain tissue was prepared for subsequent assays. Loganin rescued decrease of dopamine levels and tyrosine hydroxylase (TH) expression in the striatum, and shortened total locomotor activity (TLA) time of mice. Furthermore, loganin alleviated microglia and astrocyte activation, and suppressed TNF-α and caspase-3 expression through a c-Abl-p38-NFκB pathway. Loganin also downregulated LC3-II and Drp1 expression, and decreased the level of acidic vesicular organelles (AVOs). Loganin exerts neuroprotective effects on MPTP-induced PD mice by decreasing inflammation, autophagy, and apoptosis, suggesting that loganin could serve as a therapeutic drug to ameliorate PD. J. Cell. Biochem. 118: 3495-3510, 2017. © 2017 Wiley Periodicals, Inc.

Neuroprotective effects of Astilbin on MPTP-induced Parkinson's disease mice: Glial reaction, α-synuclein expression and oxidative stress.

Astilbin (AST), a dihydro-flavonol glycoside, is a major bioactive ingredient in Astilbe thunbergii, Engelhardia roxburghiana, Smilax corbularia and Erythroxylum gonocladum, and has been shown to have anti-inflammatory, antioxidative and neuroprotective effects, suggesting potential therapeutic value in the treatment of Parkinson's disease (PD). We explored the neuroprotective effects of AST in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease mice. Mice were administered with MPTP (30 mg/kg, i.p) daily for 5 days, to establish a subacute Parkinson's disease model, followed by daily treatment with AST or saline for 7 days. Pole and traction tests showed that AST ameliorated the impaired motor functions in MPTP-induced Parkinson's disease mice. High performance liquid chromatography analysis revealed that AST treatment prevented MPTP-induced decreases in striatal dopamine levels. Immunofluorescence assays showed that AST reduced the loss of dopaminergic neurons and the activation of microglia and astrocytes in the substantia nigra. Western blot analyses revealed that AST suppressed α-synuclein overexpression and activated PI3K/Akt in the striatum following MPTP treatment. AST also prevented the MPTP-induced reduction in total superoxide dismutase and glutathione activity in the striatum. AST exerts neuroprotective effects on MPTP-induced PD mice by suppressing gliosis, α-synuclein overexpression and oxidative stress, suggesting that AST could serve as a therapeutic drug to ameliorate PD.

Aucubin alleviates glial cell activation and preserves dopaminergic neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonian mice.

Aucubin (AUC) is a major bioactive ingredient in Eucommia ulmoides, Plantain asiatica, and Aucuba japonica, and has been shown to exert anti-inflammatory, antioxidative, and neuroprotective effects. We explore the neuroprotective effects of AUC in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonian mice. Mice were administered MPTP (30 mg/kg) daily for 5 days, followed by treatment with AUC for 7 days. Measurement of dopamine levels was performed by high-performance liquid chromatography and tyrosine hydroxylase expression was assessed by western blot. Our results showed that AUC treatment improved mobility in the pole descent test and the traction test, and reduced the loss of dopaminergic neurons in MPTP-induced parkinsonian mice. AUC treatment rescued the decreased dopamine and tyrosine hydroxylase levels in the striatum of parkinsonian mice. Furthermore, AUC treatment reduced both microglia and astrocyte activation in the substantia nigra of parkinsonian mice. These findings suggest that AUC exerts neuroprotective effects, in part by reducing inflammation and preserving dopaminergic neurons. Possible protection mechanisms involved in MPTP-induced parkinsonian mice need to be clarified further.

Dissecting the mechanism of martensitic transformation via atomic-scale observations.

Martensitic transformation plays a pivotal role in the microstructural evolution and plasticity of many engineering materials. However, so far the underlying atomic processes that accomplish the displacive transformation have been obscured by the difficulty in directly observing key microstructural signatures on atomic scale. To resolve this long-standing problem, here we examine an AISI 304 austenitic stainless steel that has a strain/microstructure-gradient induced by surface mechanical attrition, which allowed us to capture in one sample all the key interphase regions generated during the γ(fcc) → ε(hcp) → α'(bcc) transition, a prototypical case of deformation induced martensitic transformation (DIMT). High-resolution transmission electron microscopy (HRTEM) observations confirm the crucial role of partial dislocations, and reveal tell-tale features including the lattice rotation of the α' martensite inclusion, the transition lattices at the ε/α' interfaces that cater the shears, and the excess reverse shear-shuffling induced γ necks in the ε martensite plates. These direct observations verify for the first time the 50-year-old Bogers-Burgers-Olson-Cohen (BBOC) model, and enrich our understanding of DIMT mechanisms. Our findings have implications for improved microstructural control in metals and alloys.