Mechanisms for <100> interstitial dislocation loops to diffuse in BCC iron.

The mobility of dislocation loops in materials is a principle factor in understanding the mechanical strength, and the evolution of microstructures due to deformation and radiation. In body-centered cubic (BCC) iron, the common belief is that <100> interstitial dislocation loops are immobile once formed. However, using self-adaptive accelerated molecular dynamics (SSAMD), a new diffusion mechanism has been discovered for <100> interstitial dislocation loops. The key aspect of the mechanism is the changing of the habit planes between the {100} plane and the {110} plane, which provides a path for the <100> loops to diffuse one-dimensionally. The migration behavior modeled with SSAMD is further confirmed by in-situ transmission electron microscopy (TEM) measurements, and represents a significant step for understanding the formation of <100> loop walls and the mechanical behavior of BCC Fe under irradiation.

Shock wave propagation, plasticity, and void collapse in open-cell nanoporous Ta.

We systematically investigate the wave propagation, plasticity and void collapse, as well as the effects of porosity, specific surface area and impact velocity, in a set of open-cell nanoporous Ta, during shock compression, via performing large-scale non-equilibrium molecular dynamics simulations. The shock wave propagation presents an impedance, sensitive to porosity, but not to specific surface area. Such surprising phenomena are due to the similar sensitivities in density and stress variations to porosity or specific surface area. Upon impact, shock front shapes change from ramped to steep ones, with increasing porosity, specific surface area or impact velocity, owing to the transition from the heterogeneous to homogeneous plasticity along transverse directions. This transition of plasticity arises by (i) the strong impedance on large deformation bands as porosity increases; and (ii) the transition from deformation twinning to dislocation slips, and to amorphization, as the specific surface area or impact velocity increases. Shock-induced plasticity, including their nucleation, growth and interactions, also facilitates the collapse of voids.

Surface premelting/recrystallization governing the collapse of open-cell nanoporous Cu via thermal annealing.

We systematically investigate the collapse of a set of open-cell nanoporous Cu (np-Cu) materials with the same porosity and shape but different specific surface areas, during thermal annealing, by performing large-scale molecular dynamics simulations. Two mechanisms govern the collapse of np-Cu. One is direct surface premelting, facilitating the collapse of np-Cu, when the specific surface area is less than a critical value (∼2.38 nm-1). The other is recrystallization followed by surface premelting, accelerating the sloughing of ligaments and the annihilation of voids, when the critical specific surface area is exceeded. Surface premelting results from surface reconstruction by prompting localized "disordering" and "chaos" on the surface, and the melting temperature reduces linearly with the increase of the specific surface area. Recrystallization is followed by surface premelting as the melting temperature is below the supercooling point, where a liquid is unstable and instantaneously recrystallizes.

[Analysis of Koch phenomenon of Mycobacterium tuberculosis-infected guinea pigs vaccinated with recombinant tuberculosis vaccine AEC/BC02].

OBJECTIVE: To observe the Koch phenomenon of Mycobacterium tuberculosis(MTB)-infected guinea pigs after vaccinated with killed H37Ra bacteria or tuberculosis vaccine candidate AEC/BC02. METHODS: Eighteen guinea pigs were challenged subcutaneously with 5.0×10(3) CFU MTB and after 40 days were divided into 3 groups (6 per group): NS group, AEC/BC02 group and H37Ra group, which were injected intramuscularly 3 times at 1 day interval with normal saline, AEC/BC02 vaccine and killed H37Ra bacteria respectively. Three weeks after the first vaccination, all guinea pigs were sacrificed to evaluate gross pathological scores for liver, spleen and lung, bacterial loads in lung and spleen, and lung inflammation. RESULTS: The gross pathological score in H37Ra group (48±26) was lower than that in NS group(62±15), but the difference was not significant (t=1.093, P=0.300). The AEC/BC02 group had a significantly lower gross pathological score (36±15) than NS group (t=2.980, P=0.014). No significant difference between H37Ra group and AEC/BC02 group was observed (t=1.009, P=0.337). The spleen bacterial load [(5.31±0.80) log10 CFU]in H37Ra group was slightly lower than that in NS group[(5.57±0.75) log10 CFU] but the difference was not significant (t=1.581, P=0.574). In AEC/BC02 group bacterial load in the spleen was (4.64±0.64) log10 CFU and significantly lower than NS group (t=2.306, P=0.044) and no significant difference between H37Ra group and AEC/BC02 group was observed (t=1.602, P=0.140). Meanwhile, the lung bacterial load in AEC/BC02 group was (3.71±1.01) log10 CFU and in H37Ra group was (3.82±1.25) log10 CFU. Compared to (4.15±0.69) log10 CFU in the NS group, no significant differences were found (t=0.881, P=0.399; t=0.566, P=0.584, respectively). For the lung inflammation, the inflamed areas in H37Ra group were significantly larger [(33.0±4.4%)] than those in both NS group [(14.8±8.4) %, t=4.719, P=0.001] and AEC/BC02 group [(14.8±8.4) %, t=3.616, P=0.005], and no significant differences were seen between AEC/BC02 group and NS group (t=1.041, P=0.322). CONCLUSION: The lung inflammation indicated that killed H37Ra bacteria evoked an obvious Koch reaction in the MTB-infected guinea pigs, whereas AEC/BC02 vaccine showed a low risk of causing Koch phenomenon.