In situ strengths of matrix in a composite

A major obstacle to achieving reasonable strength prediction of a composite only from its constituent information is in the determination of in situ strengths of the matrix. One can measure only the original strengths of the pure matrix, on the basis of which the predicted transverse strengths of a unidirectional (UD) composite are far from reality. It is impossible to reliably measure matrix in situ strengths. This paper focuses on the correlation between in situ and original strengths. Stress concentrations in a matrix owing to the introduction of fibers are attributed to the strength variation. Once stress concentration factors (SCFs) are obtained, the matrix in situ strengths are assigned as the original counterparts divided by them. Such an SCF cannot be defined following a classical approach. All of the relevant issues associated with determining it are systematically addressed in this paper. Analytical expressions for SCFs under transverse tension, transverse compression, and transverse shear are derived. Closed-form and compact formulas for all of the uniaxial strengths of a UD composite are first presented in this paper. Their application to strength predictions of a number of typical UD composites demonstrates the correctness of these formulas.

Assessment of composite failure and ultimate strength without experiment on composite

This paper attempts to estimate the ultimate strength of a laminated composite only based on its con- stituent properties measured independently. Three important issues involved have been systematically addressed, i.e., stress calculation for the constituent fiber and matrix materials, failure detection for the lamina and laminate upon the internal stresses in their constituents, and input data determination of the constituents from monolithic measurements. There are three important factors to influence the accuracy of the strength prediction. One is the stress concentration factor （SCF） in the matrix. Another is matrix plasticity. The third is thermal residual stresses in the constituents. It is these three factors, however, that have not been sufficiently well realized in the composite community. One can easily find out the elastic and strength parameters of a great many laminae and laminates in the current literature. Unfortunately, necessary information to determine the SCF, the matrix plasticity, and the thermal residual stresses of the composites is rare or incomplete. A useful design methodology is demonstrated in the paper.

In Silico Molecular Docking Study of Repensine and Bentysrepinine against HBV DNA Polymerase

Bentysrepinine （Y101 ）, a derivative of repensine, is a novel di-peptide structure isolated from Dichondra repens. In vitro and in vivo tests exhibited that bentysrepinine markedly inhibited DNA-HBV and cccDNA activities. The binding mode of Y101 and repensine with DNA polymerase was driven by hydrophobic interactions. This might provide novel recognition of inhibitory effect of Y1 01 against HBV, though its inhibition mechanism needs to be validated by bio-assay at cellular level and of polymerase activity. Preliminary docking study suggested that Y101 might be able to inhibit HIV inverse transcriptase, also have the potential to interact with DNA polymerase and HCV NS5B polymerase.

Total Flavonoids from Flowers of Abelmoschus manihot for Amelioration of α-naphthylisothiocyanate-induced Cholestasis by Regulating Expression of Transporters

Objective To explore the molecular mechanisms of the total flavonoids extracted from the flowers of Abelmoschus manihot（TFA） against α-naphthylisothiocyanate（ANIT）-induced cholestasis. Methods The hepatoprotective activities of TFA（125, 250 and 500 mg/kg） were investigated on ANIT-induced cholestatic liver injury in rats. Serum levels of alanine aminotransferase（ALT）, aspartate aminotransferase（AST）, total bilirubin（TBIL）, total bile acid（TBA）, and bile flow were measured to evaluate the protective effect of TFA. Furthermore, the hepatic m RNA and protein levels of transports, multidrug resistance-associated protein 2（MRP2）, bile salt export pump（BSEP）, and Na＋-taurocholate cotransporting polypeptide（NTCP） were investigated to elucidate the protective mechanisms of TFA against ANIT-induced cholestasis. Results Pretreatment of TFA significantly and dose-dependently decreased the ANIT-induced elevation of serum ALT, AST, TBIL, and TBA levels and increased the ANIT-induced suppression of bile flow. Moreover, TFA was found to increase the expression of liver MRP2, BSEP, and NTCP in both protein and m RNA levels in ANIT-induced liver injury in rats with cholestasis. Conclusion TFA exerts a therapeutic effect on ANIT-induced liver injury in rats with cholestasis, possibly through regulating the expressions of hepatic transporters.