经典阻尼系统响应求解的分离变换辛解法

阐明经典阻尼系统响应直接辛解法的困难所在,提出一种将经典阻尼系统分离为等价的无阻尼系统,以用辛解法求解经典阻尼系统响应的方法,进一步对无阻尼系统的辛解法进行详细分析.数值算例的结果表明,所提方法有效、可行.     

齿轮发展研究综述

笔者对齿轮从古代到现在的发展历程进行了综述,并对各过程的齿轮（从材料和齿形两方面）特点、应用情况进行了详细介绍,指出现有齿轮存在的问题,最后综述这些缺点,提出了错联齿轮,以解决各种齿轮的不足。     

气流扰动下单液滴撞击单根干燥扁网丝特性数值研究

丝网分离器在工业中有着广泛地应用。本文针对液滴撞击网丝的动态过程,采用CLSVOF方法对单个液滴撞击干燥网丝的问题进行数值模拟,经过合理的简化,建立了气流扰动下单液滴撞击干燥扁网丝面的二维数学模型,分析了液滴撞击角和撞击位置对液滴撞击行为特性的影响。数值计算的结果表明:液滴撞击到干燥网丝上分为铺展和飞溅2个过程,撞击角越小,上铺展半径越大,下铺展半径越小,分离的二次液滴体积越大;液滴撞击网丝的位置离网丝边缘越近,越容易产生二次液滴,二次液滴的总体积越多。     

SRSF3 and HNRNPH1 Regulate Radiation-Induced Alternative Splicing of Protein Arginine Methyltransferase 5 in Hepatocellular Carcinoma

Protein arginine methyltransferase 5 (PRMT5) is an epigenetic regulator which has been proven to be a potential target for cancer therapy. We observed that PRMT5 underwent alternative splicing (AS) and generated a spliced isoform PRMT5-ISO5 in hepatocellular carcinoma (HCC) patients after radiotherapy. However, the regulatory mechanism and the clinical implications of IR-induced PRMT5 AS are unclear. This work revealed that serine and arginine rich splicing factor 3 (SRSF3) silencing increased PRMT5-ISO5 level, whereas heterogeneous nuclear ribonucleoprotein H 1 (HNRNPH1) silencing reduced it. Then, we found that SRSF3 and HNRNPH1 competitively combined with PRMT5 pre-mRNA located at the region around the 3′- splicing site on intron 2 and the alternative 3′- splicing site on exon 4. IR-induced SRSF3 downregulation led to an elevated level of PRMT5-ISO5, and exogenous expression of PRMT5-ISO5 enhanced cell radiosensitivity. Finally, we confirmed in vivo that IR induced the increased level of PRMT5-ISO5 which in turn enhanced tumor killing and regression, and liver-specific Prmt5 depletion reduced hepatic steatosis and delayed tumor progression of spontaneous HCC. In conclusion, our data uncover the competitive antagonistic interaction of SRSF3 and HNRNPH1 in regulating PRMT5 splicing induced by IR, providing potentially effective radiotherapy by modulating PRMT5 splicing against HCC.     

Inflammatory Mechanism of Brucella Infection in Placental Trophoblast Cells

Brucellosis is a severe zoonotic infectious disease caused by the infection of the Brucella, which is widespread and causes considerable economic losses in underdeveloped areas. Brucella is a facultative intracellular bacteria whose main target cells for infection are macrophages, placental trophoblast cells and dendritic cells. The main clinical signs of Brucella infection in livestock are reproductive disorders and abortion. At present, the pathogenesis of placentitis or abortion caused by Brucella in livestock is not fully understood, and further research on the effect of Brucella on placental development is still necessary. This review will mainly introduce the research progress of Brucella infection of placental trophoblast cells as well as the inflammatory response caused by it, explaining the molecular regulation mechanism of Brucella leading to reproductive system disorders and abortion, and also to provide the scientific basis for revealing the pathogenesis and infection mechanism of Brucella.     

A Novel Antithrombocytopenia Agent,Rhizoma cibotii,Promotes Megakaryopoiesis and Thrombopoiesis through the PI3K/AKT,MEK/ERK,and JAK2/STAT3 Signaling Pathways

Background: Cibotii rhizoma (CR) is a famous traditional Chinese medicine (TCM) used to treat bleeding, rheumatism, lumbago, etc. However, its therapeutic effects and mechanism against thrombocytopenia are still unknown so far. In the study, we investigated the effects of aqueous extracts of Cibotii rhizoma (AECRs) against thrombocytopenia and its molecular mechanism.Methods: Giemsa staining, phalloidin staining, and flow cytometry were performed to measure the effect of AECRs on the megakaryocyte differentiation in K562 and Meg-01 cells. A radiation-induced thrombocytopenia mouse model was constructed to assess the therapeutic actions of AECRs on thrombocytopenia. Network pharmacology and experimental verification were carried out to clarify its mechanism against thrombocytopenia. Results: AECRs promoted megakaryocyte differentiation in K562 and Meg-01 cells and accelerated platelet recovery and megakaryopoiesis with no systemic toxicity in radiation-induced thrombocytopenia mice. The PI3K/AKT, MEK/ERK, and JAK2/STAT3 signaling pathways contributed to AECR-induced megakaryocyte differentiation. The suppression of the above signaling pathways by their inhibitors blocked AERC-induced megakaryocyte differentiation. Conclusions: AECRs can promote megakaryopoiesis and thrombopoiesis through activating PI3K/AKT, MEK/ERK, and JAK2/STAT3 signaling pathways, which has the potential to treat radiation-induced thrombocytopenia in the clinic.     

EPLIN,a Putative Tumour Suppressor in Colorectal Cancer,Implications in Drug Resistance

Colorectal cancer is a serious threat to human health. Poor prognosis and frequently reported drug resistance urges research into novel biomarkers and mechanisms to aid in the understanding of the development and progression of colorectal cancer and to optimise therapeutic strategies. In the current study, we investigated the roles of a putative tumour suppressor, EPLIN, in colorectal cancer. Our clinical colorectal cancer cohort and online databases revealed a downregulation of EPLIN in colorectal cancer tissues compared with normal tissues. The reduced expression of EPLIN was associated with poor clinical outcomes of patients. In vitro cellular function assays showed that EPLIN elicited an inhibitory effect on cellular growth, adhesion, migration and invasion. Utilising a protein microarray on protein samples from normal and tumour patient tissues suggested HSP60, Her2 and other signalling events were novel potential interacting partners of EPLIN. It was further revealed that EPLIN and HSP60 were negative regulators of Her2 in colorectal cancer cells. The clinical cohort also demonstrated that expression of HSP60 and Her2 affected clinical outcomes, but most interestingly the combination of EPLIN, HSP60 and Her2 was able to identify patients with the most unfavourable clinical outcome by independently predicting patient overall survival and disease free survival. Furthermore, EPLIN and HSP60 exhibited potential to regulate cellular response to chemotherapeutic and EGFR/Her2 targeted therapeutic agents. In conclusion, EPLIN is an important prognostic factor for patients with colon cancer and reduced EPLIN in CRC contributes to aggressive traits of CRC cells and their responses to chemotherapeutic drugs. Collectively, EPLIN is a pivotal factor for the development and progression of colorectal cancer and has important clinical and therapeutic values in this cancer type.     

旋转扫描结构光的三维检测系统及其标定

针对传统平移扫描检测系统的缺陷,提出了一种基于旋转扫描线结构光的三维检测与重构系统及对应的系统参数标定方法,建立了点云数据获取模型。被测物体通过旋转实现与线结构光间的相对运动,得到被测物体的外表面二维图像。系统标定获得图像坐标与世界坐标间的转换关系,得到被测物体的三维坐标信息及数字模型。由实验可知,相机的标定精度为0.2 mm,原理样机进行物体测量的精度为0.1 mm。实验证明该系统检测精度高,具有可行性。     

低收缩耐热耐油聚氯乙烯/氮化硼复合材料的制备及其性能研究

首先使用退火处理的方法使六方氮化硼(hBN)带上羟基,并与硅烷偶联剂混合,得到表面处理后的氮化硼(BN).然后用熔融共混的方式制备出不同浓度的聚氯乙烯/氮化硼(PVC/BN)及聚氯乙烯/氮化硼/聚酰胺(PVC/BN/PA)复合材料.通过维卡软化点温度测定仪,动态力学分析仪和游标卡尺、耐油性能测试对复合材料的性能进行测试...