TbxHo0.9−xNd0.1(Fe0.8Co0.2)1.93/epoxy (0 ⩽ x ⩽ 0.40) composites are fabricated in the presence of a magnetic field. The structural and dynamic magnetoelastic properties are investigated as a function of both magnetic bias field Hbias and frequency f at room temperature. The composites are formed as textured orientation structure of 1–3 type with 〈1 0 0〉 preferred orientation for x ⩽ 0.10 and 〈1 1 1〉-orientation for x ⩾ 0.25. The composites generally possess insignificant eddy-current losses for frequency up to 50 kHz, and their dynamic magnetoelastic properties depend greatly on Hbias. The elastic modulus (E3H and E3B) shows a maximum negative ΔE effect, along with a maximum d33, at a relatively low Hbias ~ 80 kA/m, contributed by the maximum motion of non-180° domain-wall. The 1–3 type composite for x ⩾ 0.25 shows an enhanced magnetoelastic effect in comparison with 0 to 3 type one, which can be principally ascribed to its easy magnetization direction (EMD) towards 〈1 1 1〉 axis and the formation of 〈1 1 1〉-texture-oriented structure in the composite. These attractive dynamic magnetoelastic properties, e.g., the low magnetic anisotropy and d33,max as high as 2.0 nm/A at a low Hbias ~ 80 kA/m, along with the light rare-earth Nd element existing in insulating polymer matrix, would make it a promising magnetostrictive material system.
Methicillin-resistant Staphylococcus aureus (MRSA) is a major multidrug-resistant bacterial pathogen. The evolution of MRSA is dynamic posing an ongoing threat to humans. The evolution of MRSA includes horizontal gene transfer, which is mediated by mobile genetic elements, plasmids, and bacteriophages, and also mutations. In this review, we clarify the recent trends in MRSA from the perspectives of drug-resistance transfer and uncontrollable infections, particularly those occurring in community settings. We first address the role of MRSA as a disseminator of multidrug resistance. We have studied the cell-to-cell transfer of drug resistance, in which transfer frequencies range from 10-3 to 10-8. The mechanisms of drug-resistance transfers include the self-transmission of large plasmids, the mobilization of small nonconjugative plasmids, the generalized transduction of phages, and the transfer of transposons with circular intermediates. We then discuss uncontrollable infections. Although several anti-MRSA agents have been developed, uncontrollable cases of MRSA infections are still reported. Examples include a case of uncontrollable sepsis arising from a community-associated MRSA (CA-MRSA) with the ST8/SCCmecIVl genotype, and a relapsing severe invasive infection of ST30/SCCmecIVc CA-MRSA in a student athlete. Some of these cases may be attributable to unique adhesins, superantigens, or cytolytic activities. The delayed diagnosis of highly adhesive and toxic infections in community settings may result in CA-MRSA diseases that are difficult to treat. Repeated relapse, persistent bacteremia, and infections of small-colony variants may occur. To treat MRSA infections in community settings, these unique features of MRSA must be considered to ensure that diagnostic delay is avoided.
Multi-walled carbon nanotubes/Mg-doped ZnO (MWNTs/Zn1-xMgxO) nanohybrids were prepared by co-precipitation method, and their photocatalytic activity for methyl orange (MO) was studied. Experimental results showed that Mg-doped ZnO nanoparticles were successfully deposited on the surface of MWNTs under annealing at 450 °C and 550 °C. The resultant MWNTs/Zn0.9Mg0.1O nanohybrids had better photocatalytic activity for degradation of methyl orange than pure ZnO: the rates of MO photodegradation were 100 % and 30 % for 1 h, respectively. The enhancement in the photocatalytic activity was attributed to the excellent electronic properties of MWNTs and Mg-doping.
Pathological aggregation and accumulation of α-synuclein in neurons play a core role in Parkinson’s disease (PD) while its overexpression is a common PD model. Autophagy-lysosomal pathways are general intraneural mechanisms of protein clearance. Earlier a suppressed autophagy in the brain of young transgenic mice overexpressing the А53Т-mutant human α-synuclein (mut(PD)) was revealed. Previous studies have recognized that Cystatin C displays protective activity against neurodegeneration. This cysteine protease inhibitor attracts particular attention as a potential target for PD treatment related to autophagy modulation. Here we evaluated the mRNA levels of Cst3 encoding Cystatin C in different brain structures of 5 m.o. mut(PD) mice at standard conditions and after the chronic treatment with a neuroprotective agent, ceftriaxone (100 mg/kg, 36 days). The inflammatory markers, namely, microglial activation by IBA1 expression and mRNA levels of two chitinases genes (Chit1, Chia1), were also assessed but no significant difference was found between control and transgenic mice. Cst3 mRNA levels were significantly reduced in the striatum and amygdala in the transgenic PD model. Furthermore, this was associated with autophagy decline and might be added to early signs of synucleinopathy development. We first demonstrated the modulation of mRNA levels of Cst3 and autophagy marker Becn1 in the brain by ceftriaxone treatment. Taken together, the results support the potential of autophagy modulation through Cystatin C at early stages of PD-like pathology.