Isochronal superpositioning of the caged dynamics, the α, and the Johari-Goldstein ß relaxations in metallic glasses.

The superposition of the frequency dispersions of the structural α relaxation determined at different combinations of temperature T and pressure P while maintaining its relaxation time τα(T, P) constant (i.e., isochronal superpositioning) has been well established in molecular and polymeric glass-formers. Not known is whether the frequency dispersion or time dependence of the faster processes including the caged molecule dynamics and the Johari-Goldstein (JG) ß relaxation possesses the same property. Experimental investigation of this issue is hindered by the lack of an instrument that can cover all three processes. Herein, we report the results from the study of the problem utilizing molecular dynamics simulations of two different glass-forming metallic alloys. The mean square displacement 〈Δr2t〉, the non-Gaussian parameter α2t, and the self-intermediate scattering function Fsq,t at various combinations of T and P were obtained over broad time range covering the three processes. Isochronal superpositioning of 〈Δr2t〉, α2t, and Fsq,t was observed over the entire time range, verifying that the property holds not only for the α relaxation but also for the caged dynamics and the JG ß relaxation. Moreover, we successfully performed density ρ scaling of the time τα2,maxT,P at the peak of α2t and the diffusion coefficient D(T, P) to show both are functions of ργ/T with the same γ. It follows that the JG ß relaxation time τß(T, P) is also a function of ργ/T since τα2,maxT,P corresponds to τß(T, P).

[Effects of human mesenchymal stem cells on airway inflammation in allergic asthma mice and the underlying mechanism].

Objectives: To investigate the effects of human umbilical cord mesenchymal stem cells (hUC-MSCs) on airway inflammation in an ovalbumin (OVA) induced asthma mouse model and the underlying mechanism. Methods: Twenty-four BALB/c mice were randomly divided into four equal groups: normal control group, OVA-induced asthmatic model group, hUC-MSCs treated group (50 µl of hUC-MSCs was transplanted into the trachea of asthmatic mice ) and hUC-MSCs control group (50 µl of hUC-MSCs was transplanted into the trachea of control mice). Human umbilical cord mesenchymal stem cells from umbilical cord of healthy new born babies were used as the source of hUC-MSCs for this study. The asthmatic conditions of the airways and the lungs were assessed by examining: (1) histopathological changes of the airways and the lungs; (2) expression of cytokines IL-6 and TGF-ß mRNA by real-time PCR; (3) total leukocytes and mast cell count in bronchoalveolar lavage fluid (BALF) and number of IL-17-expressing CD4(+) cells (Th17 cells) in the lung tissue using flow cytometry. Results: Typical histopathological changes of asthma were confirmed in the asthmatic model group. These changes included intensive inflammatory cell infiltration around the airways and patchy airway occlusion by hyperviscous mucus. The number of total leukocytes and mast cells in BALF were significantly increased in the asthmatic mice when compared with the control group (P<0.05). Mice in the asthmatic model group had significantly higher percentage of Th17 cells in lung tissues when compared with the control group (2.90% vs 0.76%, P<0.05). In contrast, in the asthmatic mice treated with hUC-MSCs, the inflammatory cell infiltration was significantly reduced compared with asthmatic mice, as observed by significantly lower leukocytes and mast cells in BALF (P<0.05) and significant reduction in the percentage of Th17 cells in the lung of OVA-challenged mice following hUC-MSCs treatment (percentage of Th17 cells: 0.24% vs 2.90%, P<0.05). The expression of mRNA for IL-6 and TGF-ß was significantly suppressed in the hUC-MSCs treatment group (0.23 vs 2.30 and 0.56 vs 6.60, both P<0.01). No asthmatic pathological changes in both normal and hUC-MSCs control groups were observed. Conclusions: hUC-MSCs significantly inhibit the airway inflammation in OVA-induced asthmatic mice. This inhibition is associated with the suppression of Th17 cells and the down-regulation of inflammatory factors such as IL-6 and TGF-ß in the lungs.

[A clinical study on the effect of nattokinase on carotid artery atherosclerosis and hyperlipidaemia].

Objective: To evaluate the efficacy of oral nattokinase (NK) in the reduction of common carotid artery intimal medial thickness (CCA-IMT) and carotid artery plaque size and in lowering blood lipids, and to explore the underlying mechanism of actions of NK and its potential clinical use. Methods: All enrolled patients were from the Out-Patient Clinic of the Department of TCM at the 3(rd) Affiliated Hospital of Sun Yat-sen University. Using randomised picking method, all patients were randomly assigned to one of two groups, NK and Statin (ST) group. NK Group-patients were given NK at a daily dose of 6 000 FU and ST Group-patients were treated with statin (simvastatin 20 mg) daily. The treatment course was 26 weeks. CCA-IMT, carotid plaque size and blood lipid profile of the patients were measured before and after treatment. Results: A total of 82 patients were enrolled in the study and 76 patients (NK 39, ST 37) completed the study. Following the treatments for 26 weeks, there was a significant reduction in CCA-IMT and carotid plaque size in both groups compared with the baseline before treatment. The carotid plaque size and CCA-IMT reduced from(0.25±0.12)cm(2) to (0.16±0.10)cm(2) and from (1.13±0.12)mm to (1.01±0.11)mm, repectively. The reduction in the NK group was significantly profound (P<0.01, 36.6% reduction in plaque size in NK group versus 11.5% change in ST group). Both treatments reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG). While the reduction in both groups was shown to be statistically significant (P<0.01), the reduction of TC, LDL-C and TG in ST group was significantly greater (P<0.05). In addition, NK significantly increased the level of high-density lipoprotein cholesterol (HDL-C) (P<0.05), in contrast, HDL-C in the ST group did not change. The lipid lowering effect observed in the NK group was not correlated to the reduction of CCA-IMT and carotid artery plaque size (r=0.35, P=0.09). Conclusions: Our findings from this pioneer clinical study suggests that daily NK supplementation is an effective way to manage the progression of atherosclerosis and potentially may be a better alternative to statins which are commonly used to reduce atherosclerosis and further to prevent cardiovascular attack and stroke in patients. The mechanism underlying the reduction of carotid atherosclerosis by NK may be independent from its lipid-lowering effect, which is different from that of statins.