区域生态文明建设水平综合评估指标

2007年中国政府提出"生态文明"建设以来,已批准了三批52个生态文明建设试点。生态系统与社会经济发展的复杂性要求科学、客观地评估区域生态文明建设,以便科学地决策和行动。区域生态文明建设是一个复合的过程,其核心在于社会-经济-自然复合生态系统各组分的和谐进步。因此,基于生态系统服务(ES)、生态足迹(EF)和人均GDP3个指标,以及这3个指标所代表的资源禀赋、人类对自然生态系统的占用、经济增长之间的线性逻辑关系,构建综合性相对指数;并以此对2010年中国大陆各省(市、直辖市)的生态文明建设水平进行了综合评估,其中,海南省的生态文明建设指数最大,为0.5091,北京市的指数最小,为0.0377;最后,分析了2010年中国大陆各省(市、区)生态文明建设的生态压力和生态效率,北京、天津和上海3个直辖市处于低资源禀赋高资源消费状况,全国大多数省(市、区)处于低消耗和低产出的阶段,经济增长尚有较大的潜力。     

一株生防圆突起链霉菌的分类鉴定

菌株SCY311是从河南省凤凰山土壤样品中分离到的对多种植物病原真菌具有拮抗活性的一株放线菌。为了明确其分类地位, 在形态特征、培养特征、生理生化特征、细胞壁组分测定等传统分类学方法的基础上, 测定和分析了菌株的16S rRNA基因序列。结果表明, 菌株SCY311在高氏一号培养基上生长良好, 基内菌丝呈褐色; 气生菌丝灰色至鼠灰色, 不产生可溶性色素, 无吸水现象; 孢子链卷曲, 末端形成闭合或开放螺旋; 孢子椭圆或圆柱状, 表面形成结节状突起; 生理生化特征和在国际链霉菌计划(ISP)培养基上的培养特     

ALKBH5/MAP3K8 axis regulates PD-L1+ macrophage infiltration and promotes hepatocellular carcinoma progression

Hepatocellular carcinoma is one of the most common malignant tumors.M6A is a novel epigenetic modification that have been emerged as vital regulators for the progression of HCC. However, the regulatory role, clinical significance and the details of the modification, such as the impact on the local tumor environment, remain largely unclear. Our study showed that ALKBH5 was highly expressed in HCC and high ALKBH5 expression predicted a worse prognosis of HCC patients. Prediction of ALKBH5 function by tissue samples and single cell sequencing Gene Set Variation Analysis. Primary CD3 + T lymphocytes and bone marrow-derived macrophages were used to evaluate the effect of ALKBH5 on immune microenvironment. The results indicated that ALKBH5 promote HCC cell proliferation, metastasis and PD-L1+macrophage recruitment. Mechanistically the results showed that ALKBH5 regulates MAP3K8 expression in a m6A dependent manner which mediates the proliferation and metastasis of HCC cells. ALKBH5 also promotes the activation of JNK and ERK pathways through upregulating MAP3K8, thus regulating the expression of IL-8 and promoting macrophage recruitment. Taken together, these data show that ALKBH5 promotes HCC growth, metastasis and macrophage recruitment through ALKBH5/MAP3K8 axis and it may serve as a potential diagnostic marker and target for treatment of HCC patients.     

斑点叉尾鮰源普通变形杆菌的分离、鉴定及药敏特性

【目的】对患病斑点叉尾鮰进行病原菌分离、鉴定及药敏实验,为斑点叉尾鮰肠道坏死病的防控提供参考。【方法】从患病斑点叉尾鮰病灶、肝、脾和肾分离纯化病原菌,经理化特性测定及16S rRNA基因序列分析对其进行鉴定,开展人工感染试验,并利用纸片扩散法进行药敏特性分析。【结果】分离菌株k1为本次引发斑点叉尾鮰病害的致病菌,其对斑点叉尾鮰的LD50为2.82×10~5 CFU/g。菌株k1理化特性与普通变形杆菌Proteus vulgaris基本一致,16S rRNA基因序列与普通变形杆菌相似性最高,综合判定分离菌株为普通变形杆菌。分离菌株k1对环丙沙星、头孢唑林及头孢拉定等12种抗生素高度敏感,对苯唑西林、阿莫西林及痢特灵等7种抗生素耐药。【结论】分离菌株k1是斑点叉尾鮰病原菌,养殖时可选用庆大霉素及氟苯尼考等药物进行防控。     

Age‐related memory vulnerability to interfering stimuli is caused by gradual loss of MAPK‐dependent protection in Drosophila

Age‐related memory impairment (AMI) is a common phenomenon across species. Vulnerability to interfering stimuli has been proposed to be an important cause of AMI. However, the molecular mechanisms underlying this vulnerability‐related AMI remain unknown. Here we show that learning‐activated MAPK signals are gradually lost with age, leading to vulnerability‐related AMI in Drosophila. Young flies (2‐ or 3‐day‐old) exhibited a significant increase in phosphorylated MAPK levels within 15 min after learning, whereas aged flies (25‐day‐old) did not. Compared to 3‐day‐old flies, significant 1 h memory impairments were observed in 15‐, 20‐, and 30‐day‐old flies, but not in 10‐day‐old flies. However, with post‐learning interfering stimuli such as cooling or electric stimuli, 10‐day‐old flies had worse memory performance at 1 h than 3‐day‐old flies, showing a premature AMI phenomenon. Increasing learning‐activated MAPK signals through acute transgene expression in mushroom body (MB) neurons restored physiological trace of 1 h memory in a pair of MB output neurons in aged flies. Decreasing such signals in young flies mimicked the impairment of 1 h memory trace in aged flies. Restoring learning‐activated MAPK signals in MB neurons in aged flies significantly suppressed AMI even with interfering stimuli. Thus, our data suggest that age‐related loss of learning‐activated neuronal MAPK signals causes memory vulnerability to interfering stimuli, thereby leading to AMI.     

The small nonstructural protein NP1 of human bocavirus 1 directly interacts with Ku70 and RPA70 and facilitates viral DNA replication

Human bocavirus 1 (HBoV1), a member of the genus Bocaparvovirus of the family Parvoviridae, causes acute respiratory tract infections in young children. Well-differentiated pseudostratified human airway epithelium cultured at an air-liquid interface (HAE-ALI) is an ideal in vitro culture model to study HBoV1 infection. Unique to other parvoviruses, bocaparvoviruses express a small nonstructured protein NP1 of ~25 kDa from an open reading frame (ORF) in the center of the viral genome. NP1 plays an important role in viral DNA replication and pre-mRNA processing. In this study, we performed an affinity purification assay to identify HBoV1 NP1-inteacting proteins. We identified that Ku70 and RPA70 directly interact with the NP1 at a high binding affinity, characterized with an equilibrium dissociation constant (K_D) of 95 nM and 122 nM, respectively. Furthermore, we mapped the key NP1-interacting domains of Ku70 at aa266-439 and of RPA70 at aa181-422. Following a dominant negative strategy, we revealed that the interactions of Ku70 and RPA70 with NP1 play a significant role in HBoV1 DNA replication not only in an in vitro viral DNA replication assay but also in HBoV1-infected HAE-ALI cultures. Collectively, our study revealed a novel mechanism by which HBoV1 NP1 enhances viral DNA replication through its direct interactions with Ku70 and RPA70.     

传染性支气管炎病毒N蛋白CTL表位与BF2*15鸡MHC I基序的相互作用

【目的】近年来鸡传染性支气管炎病毒在国内鸡群呈现流行趋势,尤其是变异毒株的出现,加剧了对鸡群的危害。鸡主要组织相容复合体蛋白(MHC I)通过特定的基序结合抗原表位多肽,进而识别感染病毒的细胞并引起免疫反应,达到清除病毒的效果。鉴定BF2*15鸡主要组织相容复合体(MHC I)的结合基序。【方法】采用同源建模、分子动力学和分子对接等计算方法,构建了传染性支气管炎病毒(IBV)N蛋白表位多肽和鸡MHC I BF2*15之间的复合物结构,来探索BF2*15识别抗原表位多肽的潜在结合基序。【结果】通过对该复合物的相互作用关系分析,鉴定出BF2*15鸡主要组织相容复合体(MHC I)的一条潜在结合基序"x-Arg-xx-x-Arg"。【结论】解释了传染性支气管炎病毒N蛋白CTL表位与BF2*15鸡MHC I基序的相互作用原理,该研究结果对了解传染性支气管炎病毒免疫机制以及基于特定基序筛选和设计通用疫苗具有借鉴意义。     

The connecting cilium inner scaffold provides a structural foundation that protects against retinal degeneration

Inherited retinal degeneration due to loss of photoreceptor cells is a leading cause of human blindness. These cells possess a photosensitive outer segment linked to the cell body through the connecting cilium (CC). While structural defects of the CC have been associated with retinal degeneration, its nanoscale molecular composition, assembly, and function are barely known. Here, using expansion microscopy and electron microscopy, we reveal the molecular architecture of the CC and demonstrate that microtubules are linked together by a CC inner scaffold containing POC5, CENTRIN, and FAM161A. Dissecting CC inner scaffold assembly during photoreceptor development in mouse revealed that it acts as a structural zipper, progressively bridging microtubule doublets and straightening the CC. Furthermore, we show that Fam161a disruption in mouse leads to specific CC inner scaffold loss and triggers microtubule doublet spreading, prior to outer segment collapse and photoreceptor degeneration, suggesting a molecular mechanism for a subtype of retinitis pigmentosa.

Inherited retinal degeneration due to loss of photoreceptor cells is a leading cause of human blindness. Ultrastructure expansion microscopy on mouse retina reveals the presence of a novel structure inside the photoreceptor connecting cilium, the inner scaffold, that protects the outer segment against degeneration.