The Specificity of Human Capital and Risk Management of the College Counselor from the Perspective of Internationalization

Shifting the concept of human resource to the concept of human capital is an inevitable tendency in developing human resource of college counselor. It is because the college counselor has its own specificity that it is hardly possible to avoid the risks of entry and exit which brings in completely. The paper listed the priority of psychological capital, human capital and social capital of the college counselor from the perspective of in-system in the order to attempt to discuss their inner logical relationship based on the basic theory of risk management. Key words: College counsellor; The specificity of human capital; Risk management; In-system Résumé: Déplacer le concept de ressources humaines pour le concept de capital humain est une tendance inévitable dans le développement des ressources humaines de conseiller du collège. C'est parce que le conseiller collège a sa propre spécificité qu'il n'est guère possible d'éviter les risques d'entrée et de sortie qui amène à fond. Le document énumère les priorités du capital psychologique, le capital humain et le capital social de la conseillère collège dans la perspective d'en-système dans l'ordre pour tenter de discuter de leur relation logique interne basé sur la théorie de base de gestion des risques. Mots clés: Université de conseiller; La spécificité du capital humain; La gestion des risques; Et du systèm

S100A6 promotes proliferation and migration of HepG2 cells via increased ubiquitin-dependent degradation of p53

S100A6 protein (calcyclin), a small calcium-binding protein of the S100 family, is often upregulated in various types of cancers, including hepatocellular carcinoma (HCC). The aim of this study was to illustrate the molecular mechanism of S100A6 in regulating the proliferation and migration of HCC cells

Interfacial engineering of nickel/vanadium based two-dimensional layered double hydroxide for solid-state hydrogen storage in MgH₂

As a high-density solid-state hydrogen storage material, magnesium hydride (MgH2) is promising for hydrogen transportation and storage. Yet, its stable thermodynamics and sluggish kinetics are unfavorable for that required for commercial application. Herein, nickel/vanadium trioxide (Ni/V2O3) nanoparticles with heterostructures were successfully prepared via hydrogenating the NiV-based two-dimensional layered double hydroxide (NiV-LDH). MgH2 + 7 wt% Ni/V2O3 presented more superior hydrogen absorption and desorption performances than pure MgH2 and MgH2 + 7 wt% NiV-LDH. The initial discharging temperature of MgH2 was significantly reduced to 190 °C after adding 7 wt% Ni/V2O3, which was 22 and 128 °C lower than that of 7 wt% NiV-LDH modified MgH2 and additive-free MgH2, respectively. The completely dehydrogenated MgH2 + 7 wt% Ni/V2O3 charged 5.25 wt% H2 in 20 min at 125 °C, while the hydrogen absorption capacity of pure MgH2 only amounted to 4.82 wt% H2 at a higher temperature of 200 °C for a longer time of 60 min. Moreover, compared with MgH2 + 7 wt% NiV-LDH, MgH2 + 7 wt% Ni/V2O3 shows better cycling performance. The microstructure analysis indicated the heterostructural Ni/V2O3 nanoparticles were uniformly distributed. Mg2Ni/Mg2NiH4 and metallic V were formed in-situ during cycling, which synergistically tuned the hydrogen storage process in MgH2. Our work presents a facile interfacial engineering method to enhance the catalytic activity by constructing a heterostructure, which may provide the mentality of designing efficient catalysts for hydrogen storage.The authors appreciatively acknowledge the financial supports from the National Natural Science Foundation of China (Grant No. 51801078)

Effect of iron deficiency on c-kit⁺ cardiac stem cells in vitro.

AimIron deficiency is a common comorbidity in chronic heart failure (CHF) which may exacerbate CHF. The c-kit⁺ cardiac stem cells (CSCs) play a vital role in cardiac function repair. However, much is unknown regarding the role of iron deficiency in regulating c-kit⁺ CSCs function. In this study, we investigated whether iron deficiency regulates c-kit⁺ CSCs proliferation, migration, apoptosis, and differentiation in vitro.MethodAll c-kit⁺ CSCs were isolated from adult C57BL/6 mice. The c-kit⁺ CSCs were cultured with deferoxamine (DFO, an iron chelator), mimosine (MIM, another iron chelator), or a complex of DFO and iron (Fe(III)), respectively. Cell migration was assayed using a 48-well chamber system. Proliferation, cell cycle, and apoptosis of c-kit⁺ CSCs were analyzed with BrdU labeling, population doubling time assay, CCK-8 assay, and flow cytometry. Caspase-3 protein level and activity were examined with Western blotting and spectrophotometric detection. The changes in the expression of cardiac-specific proteins (GATA-4,TNI, and β-MHC) and cell cycle-related proteins (cyclin D1, RB, and pRB) were detected with Western blotting.ResultDFO and MIM suppressed c-kit⁺ CSCs proliferation and differentiation. They also modulated cell cycle and cardiac-specific protein expression. Iron chelators down-regulated the expression and phosphorylation of cell cycle-related proteins. Iron reversed those suppressive effects of DFO. DFO and MIM didn't affect c-kit⁺ CSCs migration and apoptosis.ConclusionIron deficiency suppressed proliferation and differentiation of c-kit⁺ CSCs. This may partly explain how iron deficiency affects CHF prognosis

Autophagy Is Involved in the Cardioprotection Effect of Remote Limb Ischemic Postconditioning on Myocardial Ischemia/Reperfusion Injury in Normal Mice, but Not Diabetic Mice

<div><p>Background</p><p>Recent animal study and clinical trial data suggested that remote limb ischemic postconditioning (RIPostC) can invoke potent cardioprotection. However, during ischemia reperfusion injury (IR), the effect and mechanism of RIPostC on myocardium in subjects with or without diabetes mellitus (DM) are poorly understood. Autophagy plays a crucial role in alleviating myocardial IR injury. The aim of this study was to determine the effect of RIPostC on mice myocardial IR injury model with or without DM, and investigate the role of autophagy in this process.</p><p>Methodology and Results</p><p>Streptozocin (STZ) induced DM mice model and myocardial IR model were established. Using a noninvasive technique, RIPostC was induced in normal mice (ND) and DM mice by three cycles of ischemia (5 min) and reperfusion (5 min) in the left hindlimb. In ND group, RIPostC significantly reduced infarct size (32.6±3.0% in ND-RIPostC vs. 50.6±2.4% in ND-IR, <i>p</i><0.05) and improved cardiac ejection fraction (49.70±3.46% in ND-RIPostC vs. 31.30±3.95% in ND-IR, <i>p</i><0.05). However, in DM group, no RIPostC mediated cardioprotetion effect was observed. To analyze the role of autophagy, western blot and immunohistochemistry was performed. Our data showed that a decreased sequestosome 1 (SQSTM1/p62) level, an increased Beclin-1 level, and higher ratio of LC3-II/LC3-I were observed in ND RIPostC group, but not DM RIPostC group.</p><p>Conclusions</p><p>The current study suggested that RIPostC exerts cardioprotection effect on IR in normal mice, but not DM mice, and this difference is via, at least in part, the up-regulation of autophagy.</p></div

Transmission electron microscopy images to show the ultrastructural changes.

<p>A: ND-sh, normal morphology without ultrastructural changes; B: ND-IR, a classic early autophagic vacuole (AV) with double limiting membrane (incompletely closure) containing mitochondria. C: ND-RIPostC, RIPostC-induced autophagosomes (arrows) formation with the characteristic morphology of autophagy and swelling mitochondria. D: ND-3MA, fewer autophagosome. E: DM-sh, normal morphology without ultrastructural changes. F: DM-IR, many autophagosomes contain mitochondria (m). G: DM-RIPostC, few autophagosomes. H: DM-3MA, few autophagosomes with double membrane (arrows) and mitochondrial swelling. Figures are representative images of five different heart samples. Data were presented as means ± SEM, n = 5 per group. *<i>P</i><0.05 vs. the sh group; ^#<i>P</i><0.05 vs. ND-IR and DM-RIPostC. Scale bar = 1 µm.</p

Isolation and identification of c-kit⁺ CSCs.

<p>(A) The c-kit⁺ CSCs isolated by immunomagnetic microbeads were almost small, round, phase-bright on the first day. (B) Three days later, c-kit⁺ CSCs gradually attached to the plate, proliferated, and clustered. (C) Quantitative analysis of surface markers of cells expanded in culture by FACS. (D) The expression of c-kit was examined with western blotting in the isolated cells (CSC) and cardiac myocytes (CM). (E) Immunostaining of isolated cells. All experiments were repeated 5 times.</p

Immunohistochemical analysis of autophagy markers after RIPostC.

<p>(A) immunohistochemical analysis was performed after 3 hours of reperfusion to test the expression of autophagic markers. (B–C) Bar graph showed the quantification of the autophagy markers. In the ND groups, RIPostC treatment markedly enhanced the expression of LC3 and Beclin-1, and decreased the level of SQSTM1/p62 compared with IR. (C) No significant difference was observed between DM-RIPostC and DM-IR. Original magnification: ×200. Figures are representative images of at least 4 experiments in each group.</p

Autophagy was upregulated during myocardial IR.

<p>(A) Western blot was performed to test the expression of Beclin-1, LC3, and SQSTM1. (B–D) Bar graph showing the quantification of the immunoreactive band obtained as above. The ratio of LC3-II/LC3-I and the expression of Beclin-1 gradually increased and the SQSTM1 expression gradually decreased. A significant difference of these autophagy markers was detected after 3 hours of postreperfusion in ND group and DM group. Figures are representative images of 5 different heart samples, and each experiment was repeated three times. For ND and DM group, *<i>P</i><0.05 vs. the Sham group, ^#<i>P</i><0.05 (ND-IR3h vs. DM-IR3 h).</p

Effect of iron deficiency on c-kit⁺ CSCs differentiation (A–F) and migration (G).

<p>Dexamethasone (10⁻⁸ M) was used to induce differentiation. Cellular morphology and cardiac-specific proteins were assayed. Cells were treated with dexamethasone (A), dexamethasone+DFO (B), dexamethasone+DFO+Fe (C), or dexamethasone+MIM (D). No obvious change in cellular morphology was observed in these groups. The expression levels of cardiac-specific proteins (β-MHC, TNI, and GATA-4) were down-regulated under iron deficiency condition (E, F). (G) Cell migration was assessed. Cells treated with culture medium alone were defined as control group. After c-kit⁺ CSCs were pre-incubated with DFO, MIM, or the complex of DFO and Fe(III) for 24 h, migrated cells were measured by quantitative analysis. Compared with control, c-kit⁺ CSCs migration was not affected by DFO, MIM, or the complex of DFO and Fe(III) (p>0.05). * p<0.05, $ p<0.01 (compared with cells treated with Dexamethasone alone). All experiments were repeated 5 times.</p