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1.
Phys Chem Chem Phys ; 18(43): 29923-29934, 2016 Nov 21.
Article in English | MEDLINE | ID: mdl-27761534

ABSTRACT

The martensite/parent coherent interface of Mn-based shape memory alloys (SMAs) is a significant part in the research of their martensitic transformation, reversible shape memory effect and magnetic shape memory effect. In the present work, a chemical-structural model was proposed to calculate the martensite/parent coherent interfacial energy of Mn-X (X = Cu, Fe) alloys. In this model, the coherent heterophase interfacial energy consists of chemical and structural parts. Resulting from the formation process of the heterophase interface, the chemical interfacial energy is expressed as the incremental value of bond energy, while the structural part is obtained by calculating the interfacial strain energy. The results show that the structural interfacial energy plays the chief role in the total interfacial energy, and the total interfacial energy decreases as the temperature rises when the alloy composition is fixed. In addition, the preferred orientation has noteworthy influence on the total interfacial energy. Using the proposed model, interfacial energy, interfacial entropy, interfacial enthalpy and interfacial heat capacity are found to be correlated with temperature and interface preferred orientation. Furthermore, the influences of alloy composition, modulus softening, and the index of the habit plane on the results were discussed.

2.
Tissue Antigens ; 83(2): 76-81, 2014 Feb.
Article in English | MEDLINE | ID: mdl-24397461

ABSTRACT

Hepatitis B virus (HBV) infection is one of the major causes of chronic liver inflammation. Tim-3 acts as a negative regulatory molecule and plays a critical role in immune tolerance. In the current study, we investigated Tim-3 expression on peripheral monocytes and CD3+CD16/CD56+ natural killer like T (NKT-like) cells in chronic hepatitis B (CHB) patients. Peripheral blood mononuclear cells (PBMCs) were isolated from 52 CHB patients and 60 healthy controls. Tim-3+CD14+ cells and Tim-3+CD3+CD16/CD56+ cells were analyzed by flow cytometry. Results showed that expression of Tim-3 was significantly increased on both the monocytes and NKT-like cells in CHB patients than in controls (P = 0.002 and P < 0.001, respectively). Tim-3 levels on monocytes and NKT-like cells were further upregulated in patients with acute-on-chronic liver failure (ACLF). In addition, we assessed the correlation of Tim-3 expression with levels of alanine aminotransferase (ALT) and tumor necrosis factor alpha (TNF-α). Data revealed that Tim-3 expression on both monocytes and NKT-like cells was positively correlated with level of ALT (r = 0.59, P < 0.001, and r = 0.60, P < 0.001, respectively), whereas Tim-3 expression on NKT-like cells was negatively correlated with serum level of TNF-α (r = -0.54, P < 0.001) in CHB patients. Our results suggest that Tim-3 may play important roles in the pathogenesis of CHB.


Subject(s)
End Stage Liver Disease/genetics , Gene Expression , Hepatitis B, Chronic/genetics , Killer Cells, Natural/metabolism , Liver Failure, Acute/genetics , Membrane Proteins/genetics , Monocytes/metabolism , Adult , Alanine Transaminase/genetics , Alanine Transaminase/immunology , CD3 Complex/genetics , CD3 Complex/immunology , CD56 Antigen/genetics , CD56 Antigen/immunology , Case-Control Studies , End Stage Liver Disease/etiology , End Stage Liver Disease/immunology , End Stage Liver Disease/virology , Female , GPI-Linked Proteins/genetics , GPI-Linked Proteins/immunology , Hepatitis A Virus Cellular Receptor 2 , Hepatitis B virus/immunology , Hepatitis B, Chronic/complications , Hepatitis B, Chronic/immunology , Hepatitis B, Chronic/virology , Humans , Immune Tolerance , Killer Cells, Natural/virology , Liver Failure, Acute/etiology , Liver Failure, Acute/immunology , Liver Failure, Acute/virology , Male , Membrane Proteins/immunology , Monocytes/virology , Receptors, IgG/genetics , Receptors, IgG/immunology , Signal Transduction , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/immunology
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