Development of Self-Healable Organic/Inorganic Hybrid Materials Containing a Biobased Copolymer via Diels-Alder Chemistry and Their Application in Electromagnetic Interference Shielding.

In this study, a novel biobased poly(ethylene brassylate)-poly(furfuryl glycidyl ether) copolymer (PEBF) copolymer was synthesized and applied as a structure-directing template to incorporate graphene and 1,1'-(methylenedi-4,1-phenylene)bismaleimide (BMI) to fabricate a series of self-healing organic/inorganic hybrid materials. This ternary material system provided different types of diene/dienophile pairs from the furan/maleimide, graphene/furan, and graphene/maleimide combinations to build a crosslinked network via multiple Diels-Alder (DA) reactions and synergistically co-assembled graphene sheets into the polymeric matrix with a uniform dispersibility. The PEBF/graphene/BMI hybrid system possessed an efficient self-repairability for healing structural defects and an electromagnetic interference shielding ability in the Ku-band frequency range. We believe that the development of the biobased self-healing hybrid system provides a promising direction for the creation of a new class of materials with the advantages of environmental friendliness as well as durability, and shows potential for use in advanced electromagnetic applications.

Effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expression of SHIP mRNA / 中国实验血液学杂志

This study was aimed to investigate the effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expressiom of SHIP mRNA. The K562 cells were cultured and treated with different concentrations of bortezomib, 5-azacytidine or their combination for 24 hours. Then, the expression of SHIP mRNA was detected by RT-PCR,the cell proliferation was analyzed by using MTT assay and flow cytometry. The results showed that 5-20 nmol/L bortezomib could effectively inhibit the proliferation of K562 and this inhibitory effect gradually enhanced along with the increase of bortezomib concentration, the group of bortezomib combined with 5-azacytidine showed more inhibitory effect on K562 cells than that of bortezomib or 5-azacytidine alone.The bortezomib could promote the apoptosis of K562 cells in a dose-dependent manner,and this apoptotic effect was higher in group of bortezomib combined with 5-azacytidine than that in group of bortezomib or 5-azacytidine alone.Bortezomib could down-regulated the expression of SHIP mRNA in a dose-dependent manner,and this down-requlated effect was higher in group of bortezomib combined with 5-azacytidine than that in group of bortezomib or 5-azacytidine alone.It is concluded that bortezomib and 5-azacytidine can induce apoptosis by inhibiting the expression of SHIP mRNA in K562 cells.The combination of bortezomib with 5-azacytidine displays a synergetic effect.

Effect of proteasome inhibitor bortezomib on proliferation, apoptosis and SHIP gene expression in K562 cells / 中国实验血液学杂志

This study was aimed to investigate the effects of proteasome inhibitor bortezomib on proliferation, apoptosis and the SHIP expression of K562 cells. K562 cells were treated with bortezomib of different concentrations. Cell proliferation was analyzed by MTT assay, cell apoptosis was detected by flow cytometry and SHIP mRNA expression was assayed by RT-PCR.The results showed that after being treated with 10, 20, 50 and 100 nmol/L bortezomib for 24 h, the inhibitory rates of K562 cells were (5.76 ± 1.47)%, (10.55 ± 1.59)%, (17.14 ± 2.05)% and (27.69 ± 3.57)% respectively, and were higher than that in control (1.30 ± 0.10); when K562 cells were treated with 20 nmol/L bortezomib for 24, 48 and 72 h, the inhibitory rates of cell proliferation were (10.55 ± 1.59)%, (16.33 ± 2.53)% and (19.78 ± 1.56)% respectively, there was statistic difference of cell proliferation rate between 24 h group and 48 h group (P < 0.05). After being treated with 10,20,50,100 nmol/L bortezomib for 24 h, the apoptotic rates of K562 cells were (12.7 ± 0.6)%, (26.9 ± 0.9)%, (32.6 ± 1.2)% and (72.5 ± 1.5)% respectively,and all higher than that in control (1.0 ± 0.5)% (P < 0.05). According to results of RT-PCR detection, the expression level of SHIP mRNA was obviously up-regulated after treatment with bortezomib, and showed statistical difference in comparison with control. It is concluded that bortezomib inhibits proliferation of K562 cells in time and concentration-dependent manner and induces apoptosis through up-regulation of SHIP gene.

Effects of ischemic postconditioning on myocardial cell during ischemia/reperfusion period in rabbits / 中华胸心血管外科杂志

Objective To investigate the effects of ischemic postconditioning (Post) on myocardial cell apoptosis and expres- sion of Bcl-2 and Bax protein during ischemia/reperfusion period in rabbits.Methods Eighteen rabbits were randomly allocated to three groups (6 in each group),sham operation (group S),ischemia/reperfusion group(group IR) and ischemic postconditioning group(group Post).Group IR and group Post were subjected to 15 minutes of left anterior descending coronary artery occlusion followed for 30 minutes of reperfusion.Ischemic postconditioning was achieved by three 30 seconds cycles of reperfusion,each followed by 30 seconds ischemia.Cardiomyocyte apoptosis were determined by in situ TDT-mediated dUTP nick end labeling (TUNEL) and DNA electrophoresis.The expression of Bcl-2 and Bax proteins in apoptotic myocardial cells were detected by immunohistochemistry sepa- rately.Results Compared with group IR,apoptotic index was significantly reduced in group Post [(28.06?2.92) % vs.(55.70? 13.96)%,P