退火遗传算法及其应用

将模拟退火方法引入遗传算法中,对非线形问题进行优化。该算法克服了ＳＧＡｓｒ 的过早收敛的问题,并解决了染色体样性要求。最后将该算法应用于解决水资源优化分配的问题中,优化结果同样具备上述特点。     

浙江菌类药资源调查及利用研究初报

本文较全面地了浙江菌类药中药资源。其内容包括开展本项目的方法,研究结果。分别对本省自然环境、野生菌类药中药资源的分布进行了重点论述,简要介绍了菌类药调查结果,重点研究种类,并对本省的菌类药现状和展望作了评述;文后列有本项目研究中公开发表的文献,使本方基本能反映本专题的研究内容。     

HDAC8 drives spindle organization during meiotic maturation of porcine oocytes

ObjectivesHistone deacetylase 8 (HDAC8) is one of the class I HDAC family proteins, which participates in the neuronal disorders, parasitic/viral infections, tumorigenesis and many other biological processes. However, its potential function during female germ cell development has not yet been fully understood.Materials and methodsHDAC8‐targeting siRNA was microinjected into GV oocytes to deplete HDAC8. PCI‐34051 was used to inhibit the enzyme activity of HDAC8. Immunostaining, immunoblotting and fluorescence intensity quantification were applied to assess the effects of HDAC8 depletion or inhibition on the oocyte meiotic maturation, spindle/chromosome structure, γ‐tubulin dynamics and acetylation level of α‐tubulin.ResultsWe observed that HDAC8 was localized in the nucleus at GV stage and then translocated to the spindle apparatus from GVBD to M II stages in porcine oocytes. Depletion of HDAC8 led to the oocyte meiotic failure by showing the reduced polar body extrusion rate. In addition, depletion of HDAC8 resulted in aberrant spindle morphologies and misaligned chromosomes due to the defective recruitment of γ‐tubulin to the spindle poles. Notably, these meiotic defects were photocopied by inhibition of HDAC8 activity using its specific inhibitor PCI‐34051. However, inhibition of HDAC8 did not affect microtubule stability as assessed by the acetylation level of α‐tubulin.ConclusionsCollectively, our findings demonstrate that HDAC8 acts as a regulator of spindle assembly during porcine oocyte meiotic maturation.     

Reconstruction of Surface Porous PEEK Decorated with Strontium-doped Calcium Phosphate Coatings for Enhancing Osteogenic Activity

The aim of this study was to reconstruct surface porous structure with hundreds of micrometers and then bio-mineralize Sr-doped Calcium Phosphate(Sr-doped CaP)o...     

四川省森林植被固碳经济价值动态

<正>确估算森林植被固碳经济价值可为森林生态系统的生态效益评价提供基础数据。利用1997年和2014年两期四川省森林资源清查数据,依据不同森林类型的生物量与蓄积量回归方程和支付意愿法,估算了四川省两个时期森林植被的固碳经济价值。结果表明,从1997年到2014年,四川省森林植被固碳经济价值由703.17亿元增长到865.75亿元,净增长162.58亿元,年均增长9.56亿元,年均增长率为1.36%;在两个时期,云冷杉林的固碳经济价值比重最大,分别占总固碳经济价值的54.82%和46.62%,表明云冷杉森林植被类型在全省森林植被固碳经济价值中占有重要的地位;四川省天然林和人工林植被的固碳经济价值均呈增加趋势,并且人工林植被固碳经济价值年均增长速率(7.42%)明显高于天然林(1.03%);四川省森林植被固碳经济价值总体上随林龄的增加而增加。研究结果说明,实施包括天然林保护工程在内的森林保护和经营管理措施对提高森林植被的固碳经济价值具有重要的作用。     

一株PCBs降解菌的降解特性及发酵条件优化

【目的】针对一株多氯联苯的高效降解菌,考察其对多氯联苯(PCBs)的降解特性,并对降解条件进行优化。【方法】以不同浓度的2,4,4′-TCB与3,3′,4,4′-TCB为唯一碳源,研究苜蓿中华根瘤菌(Sinorhizobium melilon)对不同多氯联苯的降解转化能力,并进行发酵条件优化以及共代谢试验。【结果】接入菌株转化7 d后,随着底物浓度的增加,该菌对2,4,4′-TCB的降解能力呈下降趋势。在最低浓度1.0 mg/L时降解率最高,为93.3%;而在最高浓度50.0 mg/L时为65.1%。对于较难降解的四氯联苯3,3′,4,4′-TCB,菌株在最低浓度1.0 mg/L时降解率为56.2%,最高浓度25.0 mg/L时为22.8%。在温度30°C、pH 7.0、接种量4.5 mL、装液量25 mL时,获得菌株转化10.0 mg/L 2,4,4′-TCB的最优发酵条件,7 d的降解率由原来的54.8%提高到83.6%。柠檬烯、香芹酮及甘露醇作为共代谢底物也可较好地提高菌株降解效果。【结论】苜蓿中华根瘤菌对PCBs有很好的降解效果,研究结果对PCBs的微生物降解及环境中PCBs的生物修复具有较好的意义和应用价值。     

我国苏云金杆菌研究60年

综述了我国近60年来的苏云金杆菌研究进展,包括资源收集及分类鉴定、Bt新基因的发掘及组学研究、病理学与作用机制、毒力测定、产品标准化、产业化,并就Bt生物农药存在的问题及改善途径进行了探讨。     

LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration

The adult mammalian heart is thought to be a terminally differentiated organ given the postmitotic nature of cardiomyocytes. Consequently, the potential for cardiac repair through cardiomyocyte proliferation is extremely limited. Low-density lipoprotein receptor-related protein 6 (LRP6) is a Wnt co-receptor that is required for embryonic heart development. In this study we investigated the role of LRP6 in heart repair through regulation of cardiomyocyte proliferation. Lrp6 deficiency increased cardiomyocyte cell cycle activity in neonatal, juvenile and adult mice. Cardiomyocyte-specific deletion of Lrp6 in the mouse heart induced a robust regenerative response after myocardial infarction (MI), led to reduced MI area and improvement in left ventricular systolic function. In vivo genetic lineage tracing revealed that the newly formed cardiomyocytes in Lrp6-deficient mouse hearts after MI were mainly derived from resident cardiomyocytes. Furthermore, we found that the pro-proliferative effect of Lrp6 deficiency was mediated by the ING5/P21 signaling pathway. Gene therapy using the adeno-associated virus (AAV)9 miRNAi-Lrp6 construct promoted the repair of heart injury in mice. Lrp6 deficiency also induced the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our study identifies LRP6 as a critical regulator of cardiomyocyte proliferation, which may lead to the development of a novel molecular strategy to promote myocardial regeneration and repair.Subject terms: Cell-cycle exit, Cytokinesis     

A protein–protein interaction map reveals that the Coxiella burnetii effector CirB inhibits host proteasome activity

Coxiella burnetii is the etiological agent of the zoonotic disease Q fever, which is featured by its ability to replicate in acid vacuoles resembling the lysosomal network. One key virulence determinant of C. burnetii is the Dot/Icm system that transfers more than 150 effector proteins into host cells. These effectors function to construct the lysosome-like compartment permissive for bacterial replication, but the functions of most of these effectors remain elusive. In this study, we used an affinity tag purification mass spectrometry (AP-MS) approach to generate a C. burnetii-human protein-protein interaction (PPI) map involving 53 C. burnetii effectors and 3480 host proteins. This PPI map revealed that the C. burnetii effector CBU0425 (designated CirB) interacts with most subunits of the 20S core proteasome. We found that ectopically expressed CirB inhibits hydrolytic activity of the proteasome. In addition, overexpression of CirB in C. burnetii caused dramatic inhibition of proteasome activity in host cells, while knocking down CirB expression alleviated such inhibitory effects. Moreover, we showed that a region of CirB that spans residues 91–120 binds to the proteasome subunit PSMB5 (beta 5). Finally, PSMB5 knockdown promotes C. burnetii virulence, highlighting the importance of proteasome activity modulation during the course of C. burnetii infection.