Effect of culture condition on the growth,biochemical composition and EPA production of alkaliphilic Nitzschia plea isolated in the Southeast of China

Bioprocess and Biosystems Engineering - To overcome the contamination in open pond, microalgal strain selection should focus on species with tolerability to extreme environments. In this study, a...     

Phospho-regulated ACAP4-Ezrin Interaction Is Essential for Histamine-stimulated Parietal Cell Secretion

The ezrin-radixin-moesin proteins provide a regulated linkage between membrane proteins and the cortical cytoskeleton and also participate in signal transduction pathways. Ezrin is localized to the apical membrane of parietal cells and couples the protein kinase A activation cascade to the regulated HCl secretion. Our recent proteomic study revealed a protein complex of ezrin-ACAP4-ARF6 essential for volatile membrane remodeling (Fang, Z., Miao, Y., Ding, X., Deng, H., Liu, S., Wang, F., Zhou, R., Watson, C., Fu, C., Hu, Q., Lillard, J. W., Jr., Powell, M., Chen, Y., Forte, J. G., and Yao, X. (2006) Mol. Cell Proteomics 5, 1437–1449). However, knowledge of whether ACAP4 physically interacts with ezrin and how their interaction is integrated into membrane-cytoskeletal remodeling has remained elusive. Here we provide the first evidence that ezrin interacts with ACAP4 in a protein kinase A-mediated phosphorylation-dependent manner through the N-terminal 400 amino acids of ACAP4. ACAP4 locates in the cytoplasmic membrane in resting parietal cells but translocates to the apical plasma membrane upon histamine stimulation. ACAP4 was precipitated with ezrin from secreting but not resting parietal cell lysates, suggesting a phospho-regulated interaction. Indeed, this interaction is abolished by phosphatase treatment and validated by an in vitro reconstitution assay using phospho-mimicking ezrin^S66D. Importantly, ezrin specifies the apical distribution of ACAP4 in secreting parietal cells because either suppression of ezrin or overexpression of non-phosphorylatable ezrin prevents the apical localization of ACAP4. In addition, overexpressing GTPase-activating protein-deficient ACAP4 results in an inhibition of apical membrane-cytoskeletal remodeling and gastric acid secretion. Taken together, these results define a novel molecular mechanism linking ACAP4-ezrin interaction to polarized epithelial secretion.     

Upper limb kinematical analysis of an elite weight lifter in the squat snatch

The kinematical parameters such as translational acceleration and angular acceleration in the upper limb of a weightlifter may change regularly during different phases of squat snatch. This study aims to make this question clear. At first, the joint coordinate system (JCS) of human upper limb based on the anatomical landmarks is defined. Then a novel method for calculating the kinematical parameters was brought forward, which was based on analyzing the relative position of the JCS to world coordinate system during an instantaneous situation and the relationship among each JCS at different times during squat snatch. Motion capture system is used to gather the data of the upper limb in an elite weightlifter during squat snatch (the mass of the barbell is 20 kg) and the method mentioned before is applied to analyze the data. Finally, the law of the change of kinematical parameters in each phase of squat snatch is found.     

基于InVEST模型的疏勒河流域碳储量时空变化研究

研究区域土地利用方式与生态系统服务碳储量的关系，对于区域生态系统保护及经济社会可持续发展具有重要意义。利用InVEST模型碳储量模块和CA-Markov模型，探究并预测疏勒河流域1990-2015及2015-2040年流域生态系统碳储量时空变化特征及其与土地利用方式之间的关系。结果表明：疏勒河流域1990、1995、2000、2005、2010、2015年碳储量分别为7.994×10⁸、7.996×10⁸、7.998×10⁸、8.038×10⁸、8.064×10⁸、8.071×10⁸t，呈逐年增加趋势，累计增加7.7×10⁶t。土地利用类型变化是导致生态系统碳储量变化的主要因素，未利用地向耕地和草地转化有利于碳储量增加，而草地向耕地和未利用地的转化则导致碳储量减少。疏勒河流域碳储量存在显著的空间格局，碳储量较高区域呈现"北部点状-中部带状-南部点状片状"特征，这种分布格局与流域土地利用类型紧密联系。预测表明至2040年疏勒河流域碳储量为9.128×10⁸t，较2015年增加13.1%，主要原因是草地、耕地和林地面积较大幅度增长，提高了流域内的碳储量。     

LincRNA-p21 alleviates atherosclerosis progression through regulating the miR-221/SIRT1/Pcsk9 axis

Atherosclerosis (AS) is the main aetiology of coronary heart disease, cerebral infarction and peripheral vascular disease in humans. Long-noncoding RNA (LincRNA)-p21 has been reported to participate in the development of AS. Therefore, this study was designed to investigate the mechanism of LincRNA-p21 on suppressing the development of AS. We fed ApoE^−/− mice with a high-fat diet to induce an AS mouse model where the lesion area of AS and the extent of lipid deposition were measured. The binding of LincRNA-p21 and miR-221 or miR-221 and SIRT1 was measured using a dual luciferase reporter gene assay and RIP. Following loss- and gain- function assays, CCK8, EdU, Transwell assay and scratch test were performed to determine the biological processes of human aortic endothelial cells (HAECs). miR-221 was highly expressed while SIRT1 was poorly expressed in AS. LincRNA-p21 acted as a sponge for miR-221. miR-221 targeted and negatively regulated the expression of SIRT1. LincRNA-p21 promoted the deacetylation of Pcsk9 by SIRT1 by competitively binding to miR-221, whereby promoting HAEC proliferation, migration and tube formation. In conclusion, LincRNA-p21 acted as a molecular sponge for miR-221 to promote deacetylation of the promoter region of Pcsk9 by SIRT1, therefore preventing the development of AS.     

MicroRNA‐876‐5p inhibits cell proliferation,migration and invasion by targeting c‐Met in osteosarcoma

Recently, aberrant expression of miR‐876‐5p has been reported to participate in the progression of several human cancers. However, the expression and function of miR‐876‐5p in osteosarcoma (OS) are still unknown. Here, we found that the expression of miR‐876‐5p was significantly down‐regulated in OS tissues compared to para‐cancerous tissues. Clinical association analysis indicated that underexpression of miR‐876‐5p was positively correlated with advanced clinical stage and poor differentiation. More importantly, OS patients with low miR‐876‐5p level had a significant shorter overall survival compared to miR‐876‐5p high‐expressing patients. In addition, gain‐ and loss‐of‐function experiments demonstrated that miR‐876‐5p restoration suppressed whereas miR‐876‐5p knockdown promoted cell proliferation, migration and invasion in both U2OS and MG63 cells. In vivo studies revealed that miR‐876‐5p overexpression inhibited tumour growth of OS in mice. Mechanistically, miR‐876‐5p reduced c‐Met abundance in OS cells and inversely correlated c‐Met expression in OS tissues. Herein, c‐Met was recognized as a direct target of miR‐876‐5p using luciferase reporter assay. Notably, c‐Met restoration rescued miR‐876‐5p attenuated the proliferation, migration and invasion of OS cells. In conclusion, these findings indicate that miR‐876‐5p may be used as a potential therapeutic target and promising biomarker for the diagnosis and prognosis of OS.     

CD138免疫磁珠细胞分选的FISH技术在多发性骨髓瘤诊断中的应用

为了分析CD138免疫磁珠细胞分选的染色体荧光原位杂交(FISH)技术在提高多发性骨髓瘤(MM)细胞遗传学异常检测敏感性的作用。本研究选取我院收治的30例确诊MM的患者为研究对象,分离骨髓单个核细胞,应用探针组合,同时采用2种方法进行细胞遗传学检测:实验组采用CD138免疫磁珠分选浆细胞后行荧光原位杂交技术(MACS-FISH)检测;对照组直接荧光原位杂交技术(D-FISH)检测。结果:30例MM患者,实验组采用CD138 MACS-FISH检出率为83.3%,对照组D-FISH法细胞遗传异常检出率为46.7%,两组差异具有统计学意义(p<0.05)。研究结果表明:分析不同类型的细胞遗传异常,MACS-FISH法1q21检出率为46.7%,RB1检出率为50.0%,Ig H检出率为70.0%,P53检出率为20.0%;D-FISH法检出率分别为23.3%,30.0%、36.7%、10.0%。通过细胞核型分析,30例MM患者中,发现5例患者为异常核型,仅为16.7%,其中1例患者为单一结构异常,复杂异常核型患者为4例。我们的研究结论表明:进行CD138免疫磁珠分选浆细胞的FISH技术在多发性骨髓瘤诊断应用中可显著提高细胞遗传学异常检测敏感性,具有临床推广应用的价值。