氯化锂/丙三醇改性玉米淀粉/聚对苯二甲酸-己二酸丁二醇酯复合材料的结构与性能

为制备具有良好综合性能的淀粉(CS)/聚对苯二甲酸-己二酸丁二醇酯(PBAT)共混材料,以氯化锂(LiCl)和丙三醇(Gly)构建新型复合改性剂,提出了一步共混制备改性CS/PBAT共混材料的新方法。通过扫描电镜(SEM)、X射线衍射(XRD)、差示扫描量热分析(DSC)、力学性能测试等考察了复合改性剂中LiCl对淀粉的作用效果,探究了复合改性剂对CS/PBAT共混材料结构和性能的影响。结果表明,Gly/LiCl复合改性剂中LiCl的引入能够增强改性剂与淀粉羟基和PBAT酯基之间的电子相互作用,进一步破坏淀粉的氢键和颗粒结构,从而降低CS/PBAT的结晶度,改善淀粉与PBAT的相容性,提高共混材料的韧性、耐水性和降解性能,表现出比单纯丙三醇改性更好的作用效果。采用Gly和LiCl质量比10:1的复合改性剂,在CS和PBAT质量比为50:75时改性CS/PBAT共混材料具有优良的力学性能,其断裂伸长率从改性前的21.9%提高到了271.7%,拉伸强度从改性前的13.4 MPa变为10.8 MPa,下降不大,显示出良好的改性作用。

Influence of mycophenolate mofetil (MMF) upon thematuration and allo-stimulatory activity of cultured progenitors of dendritic cells and the effectson the tolerance induction in allograft recipients

To investigate the influence of mycophenolate mofetil (MMF) upon the maturation and the allo-stimulatory activity of cultured progenitors of dendritic cells (DCp), and to evaluate the effects of the pre-treated dentritic cells of recipients with MMF on the tolerance induction as well as its possible mechanism, GM-CSF and MMF were added to the in vitro cultured progenitor cells, and the immuno-phenotypical analysis was performed by means of flow cytometry. The secretion of IL-12 was detected by ELISA and the stimulatory activities of DCp on allogeneic T cells were observed by mixed lymphocyte reaction. Twenty-four C57BL/6 mice were divided into 3 groups (each with 8 mice), in which group A of mice accepted allografts of heart from BALB/c mice, group B of mice had received untreated DCp from donors of BALB/c mice 7 days before transplantation, and C57BL/6 mice in group C were treated by injection with MMF-treated allografts of heart from BALB/c mice 7 days before transplantation. The survival times of allografts and the changes of the cytokine levels in sera of the recipient mice were observed after transplantation. The experimental results showed that MMF could significantly inhibit the expressions of the co-stimulatory molecules CD80 and CD86 on DCs and the secretion of IL-12 and the allo-stimulatory activities of DCs were also markedly inhibited. The survival times of allografts in group B of mice were longer than those in group A, while the group C showed the longest survival times of allografts, with a marked reduction in the production of the Th1 type cytokines. It is evident that MMF has a suppressive effect on the maturation and allo-stimulatory activities of the cultured dendritic cell progenitors, thus leading to a donor specific tolerance in heart-transplanted recipients.

Deregulation of tumor suppressive ASXL1−PTEN/AKT axis in myeloid malignancies

Mutations of epigenetic regulators are pervasive in human tumors.ASXL1 is frequently mutated in myeloid malignancies.We previously found that ASXL1 forms together with BAP1 a complex that can deubiquitinylate mono-ubiquitinylated lysine 119 on histone H2A(H2AK119ub1),a Polycomb repressive mark.However,a complete mechanistic understanding of ASXL1 in transcriptional regulation and tumor suppression remains to be defined.Here,we find that depletion of Asxl1 confers murine 32D cells to IL3-independent growth at least partly due to sustained activation of PI3K/AKT signaling.Consistently,Asxl1 is critical for the transcriptional activation of Pten,a key negative regulator of AKT activity.Then we confirm that Asxl1 is specifically enriched and required for H2AK119 deubiquitylation at the Pten promoter.Interestingly,ASXL1 and PTEN expression levels are positively correlated in human blood cells and ASXL1 mutations are associated with lower expression levels of PTEN in human myeloid malignancies.Furthermore,malignant cells with ASXL1 downregulation or mutations exhibit higher sensitivity to the AKT inhibitor MK2206.Collectively,this study has linked the PTEN/AKT signaling axis to deregulated epigenetic changes in myeloid malignancies.It also provides a rationale for mechanism-based therapy for patients with ASXL1 mutations.