Phase Formation, Microstructure, and Magnetic Properties of Nd14.5Fe79.3B6.2 Melt-Spun Ribbons with Different Ce and Y Substitutions.

Phase formation and microstructure of (Nd1-2xCexYx)14.5Fe79.3B6.2 (x = 0.05, 0.10, 0.15, 0.20, 0.25) alloys were studied experimentally. The results reveal that (Nd1-2xCexYx)14.5Fe79.3B6.2 annealed alloys show (NdCeY)2Fe14B phase with the tetragonal Nd2Fe14B-typed structure (space group P42/mnm) and rich-RE (α-Nd) phase, while (Nd1-2xCexYx)14.5Fe79.3B6.2 ribbons prepared by melt-spun technology are composed of (NdCeY)2Fe14B phase, α-Nd phase and α-Fe phase, except for the ribbon with x = 0.25, which consists of additional CeFe2 phase. On the other hand, magnetic properties of (Nd1-2xCexYx)14.5Fe79.3B6.2 melt-spun ribbons were measured by a vibrating sample magnetometer (VSM). The measured results show that the remanence (Br) and the coercivity (Hcj) of the melt-spun ribbons decrease with the increase of Ce and Y substitutions, while the maximum magnetic energy product ((BH)max) of the ribbons decreases and then increases. The tendency of magnetic properties of the ribbons could result from the co-substitution of Ce and Y for Nd in Nd2Fe14B phase and different phase constitutions. It was found that the Hcj of the ribbon with x = 0.20 is relatively high to be 9.01 kOe, while the (BH)max of the ribbon with x = 0.25 still reaches to be 9.06 MGOe. It suggests that magnetic properties of Nd-Fe-B ribbons with Ce and Y co-substitution could be tunable through alloy composition and phase formation to fabricate novel Nd-Fe-B magnets with low costs and high performance.

The protective effect of isosteviol sodium on cardiac function and myocardial remodelling in transverse aortic constriction rat.

Pathological hypertrophy contributes to heart failure and there is not quite effective treatment to invert this process. Isosteviol has been shown to protect the heart against ischaemia-reperfusion injury and isoproterenol-induced cardiac hypertrophy, but its effect on pressure overload-induced cardiac hypertrophy is still unknown. Pressure overload induced by transverse aortic constriction (TAC) causes cardiac hypertrophy in rats to mimic the pathological condition in human. This study examined the effects of isosteviol sodium (STVNa) on cardiac hypertrophy by the TAC model and cellular assays in vitro. Cardiac function test, electrocardiogram analysis and histological analysis were conducted. The effects of STVNa on calcium transient of the adult rat ventricular cells and the proliferation of neonatal rat cardiac fibroblasts were also studied in vitro. Cardiac hypertrophy was observed after 3-week TAC while the extensive cardiac dysfunction and electronic remodelling were observed after 9-week TAC. Both STVNa and sildenafil (positive drug) treatment reversed the two process, but STVNa appeared to be more superior in some aspects and did not change calcium transient considerably. STVNa also reversed TAC-induced cardiac fibrosis in vivo and TGF-ß1-induced fibroblast proliferation in vitro. Moreover, STVNa, but not sildenafil, reversed impairment of the autonomic nervous system induced by 9-week TAC.

Isosteviol sodium protects the cardiomyocyte response associated with the SIRT1/PGC-1α pathway.

Cardiomyocyte dysfunction is attributed to excess oxidative damage, but the molecular pathways involved in this process have not been completely elucidated. Evidence indicates that isosteviol sodium (STVNa) has cardioprotective effects. We therefore aimed to identify the effect of STVNa on cardiomyocytes, as well as the potential mechanisms involved in this process. We established two myocardial hypertrophy models by treating H9c2 cells with high glucose (HG) and isoprenaline (ISO). Our results showed that STVNa reduced H9c2 mitochondrial damage by attenuating oxidative damage and altering the morphology of mitochondria. The results also indicated that STVNa had a positive effect on HG- and ISO-induced damages via mitochondrial biogenesis. The protective effects of STVNa on cardiomyocytes were associated with the regulation of the SIRT1/PGC-1α signalling pathway. Importantly, the effects of STVNa involved different methods of regulation in the two models, which was confirmed by experiments using an inhibitor and activator of SIRT1. Together, the results provide the basis for using STVNa as a therapy for the prevention of cardiomyocyte dysfunctions.

STVNa Attenuates Isoproterenol-Induced Cardiac Hypertrophy Response through the HDAC4 and Prdx2/ROS/Trx1 Pathways.

Recent data show that cardiac hypertrophy contributes substantially to the overall heart failure burden. Mitochondrial dysfunction is a common feature of cardiac hypertrophy. Recent studies have reported that isosteviol inhibits myocardial ischemia-reperfusion injury in guinea pigs and H9c2 cells. This work investigated the protective mechanisms of isosteviol sodium (STVNa) against isoproterenol (Iso)-induced cardiac hypertrophy. We found that STVNa significantly inhibited H9c2 cell and rat primary cardiomyocyte cell surface, restored mitochondrial membrane potential (MMP) and morphological integrity, and decreased the expression of mitochondrial function-related proteins Fis1 and Drp1. Furthermore, STVNa decreased reactive oxygen species (ROS) levels and upregulated the expression of antioxidant factors, Thioredoxin 1 (Trx1) and Peroxiredoxin 2 (Prdx2). Moreover, STVNa restored the activity of histone deacetylase 4 (HDAC4) in the nucleus. Together, our data show that STVNa confers protection against Iso-induced myocardial hypertrophy primarily through the Prdx2/ROS/Trx1 signaling pathway. Thus, STVNA is a potentially effective treatment for cardiac hypertrophy in humans.

Effects of flow pattern, device and formulation on particle size distribution of nebulized aerosol.

The evaluation of particle size recommended in the pharmacopeias requires a constant flow rate, and the method for pediatric inhaled drugs is the same as for adult drugs. In this study, the aerosol concentration and particle size distribution (PSD) were measured under a realistic breathing pattern and constant flow. Two types of nebulizer (i.e., breath-enhanced nebulizer and vibrating-mesh nebulizer) and two formulations (i.e., budesonide suspension and albuterol solution) were chosen for comparison. The aerosol concentration under the realistic pattern was not constant, which was different from the result at constant flow. The changing trend of aerosol concentration varied with the operation process of each device. The aerosol concentration profile was similar between budesonide suspension and albuterol solution. As to the PSD, as inspiratory flow increased, the X50 (50% undersize) increased with all nebulizers but Omron microAir NE-U22 nebulizer. There was good agreement between X50 obtained under the realistic inhalation patterns and their equivalent average flow rates by Bland-Altman analysis, although the X50 obtained under the realistic inhalation pattern was greater than value at constant flow. The agreement of the two breath-enhanced jet nebulizers was better than that of the vibrating-mesh nebulizers. The X50 of budesonide was not equal to that of albuterol when using the same nebulizer. Interestingly, a significant difference was observed in the X50 and Span when comparing the results of PSD under adult and child breathing patterns. Furthermore, all vibrating-mesh nebulizers produced aerosol droplets having larger mean diameter and narrower size distribution than those of the air-jet nebulizers. We conclude that it will be more conducive to the evaluation of particle size to use a laser diffractometer under a realistic pattern and make up for the shortcomings of cascade impactors. The effects of flow pattern, nebulizer and formulation should be taken into account in the evaluation of the qualities of nebulizer products in pharmaceutical practice.