桔小实蝇国内研究概况

本综述了桔小实蝇的研究概况,包括桔小实蝇的分布、寄主、为害情况、种类、生物学、生态学、生理生化、经济重要性评价、综合防治等方面。     

大黄鱼源溶藻弧菌的鉴定及其菌蜕制备

【背景】菌蜕是诱导Phi X174噬菌体裂解基因E(Lysis E)在革兰氏阴性菌中表达后所获得无细胞内容物的细菌空壳。菌蜕生物安全性高,能以类似活菌方式诱导机体产生良好的系统和黏膜免疫应答。【目的】对分离自患溃疡病大黄鱼肝脏中的病原菌株16-3进行种属鉴定,利用温控调节表达系统控制Phi X174噬菌体裂解基因E在该菌株中的表达来制备菌蜕,为防控鱼类溶藻弧菌感染提供有效手段。【方法】采用形态特征观察、生理生化特性测定及16S r RNA基因序列分析等方法对菌株16-3进行鉴定;构建温控裂解质粒p BV220-Lysis E,并将其电转至溶藻弧菌菌株16-3,形成重组溶藻弧菌菌株16-3(p BV220-Lysis E);将不同起始浓度的重组溶藻弧菌培养物同时进行42°C升温诱导,比较其溶菌动力曲线和裂解效率的差异;在最佳条件下制备溶藻弧菌菌株16-3菌蜕,电镜观察其形态与结构,采用倾注平板法测定冻干菌蜕中的活菌数。【结果】综合菌株16-3在形态、生理生化及16S r RNA基因系统发育等方面的特性,确定其为溶藻弧菌;构建了温控裂解质粒p BV220-Lysis E和重组溶藻弧菌菌株16-3(p BV220-Lysis E);溶藻弧菌菌株16-3菌蜕制备的最佳条件是选择起始浓度OD600为0.3的菌液进行诱导,诱导3 h后即可收获菌蜕,其裂解效率为96.9%,但经冻干处理后的菌蜕无活菌残留;电镜观察发现菌株16-3菌蜕保持原细胞的基本形态,但细胞表面有明显的溶菌孔道,且由于细胞内容流失而使细胞表面发生皱缩。【结论】制备出溶藻弧菌菌株16-3菌蜕,为其作为疫苗或疫苗递送载体奠定了基础。     

Genetic studies to re-affiliate Edwardsiella tarda fish isolates to Edwardsiella piscicida and Edwardsiella anguillarum species

Until 2012, the genus Edwardsiella was composed by three species Edwardsiella tarda, Edwardsiella hoshinae and Edwardsiella ictaluri. In 2013, Edwardsiella piscicida, compiling fish pathogenic strains previously identified as E. tarda was described, and more recently a new species isolated from diseased eel was reported, namely Edwardsiella anguillarum.The incorporation of these species into the genus makes necessary a revision of the taxonomic position of the isolates previously identified as E. tarda. Using AFLP technique, MLSA studies and in silico DNA–DNA hybridization, 46 of 49 E. tarda isolates were re-assigned as E. piscicida and 2 as E. anguillarum, whereas it was confirmed previous classification of the Edwardsiella types and reference strains used. The study of the taxonomic resolution of the genes 16S rRNA, adk, atpD, dnaJ, glnA, hsp60, tuf as well as the possible combinations among housekeeping genes, showed that the gene dnaJ was the more resolutive. In conclusion, the use of molecular techniques is necessary to accurately identify Edwardsiella isolates, especially when differentiating new species from E. tarda.     

Effects of Litter Inputs on N<Subscript>2</Subscript>O Emissions from a Tropical Rainforest in Southwest China

Litter inputs are expected to have a strong impact on soil N₂O efflux. This study aimed to assess the effects of the litter decomposition process and nutrient efflux from litter to soil on soil N₂O efflux in a tropical rainforest. A paired study with a control (L) treatment and a litter-removed (NL) treatment was followed for 2 years, continuously monitoring the effects of these treatments on soil N₂O efflux, fresh litter input, decomposed litter carbon (LCI) and nitrogen (LNI), soil nitrate (NO₃ ^?–N), ammonium (NH₄ ⁺–N), dissolved organic carbon (DOC), and dissolved nitrogen (DN). Soil N₂O flux was 0.48 and 0.32 kg N₂O–N ha^?1 year^?1 for the L and NL treatments, respectively. Removing the litter caused a decrease in the annual soil N₂O emission by 33%. The flux values from the litter layer were higher in the rainy season as compared to the dry season (2.10 ± 0.28 vs. 1.44 ± 0.35 μg N m^?2 h^?1). The N₂O fluxes were significantly correlated with the soil NO₃ ^?–N contents (P < 0.05), indicating that the N₂O emission was derived mainly from denitrification as well as other NO₃ ^? reduction processes. Suitable soil temperature and moisture sustained by rainfall were jointly attributed to the higher soil N₂O fluxes of both treatments in the rainy season. The N₂O fluxes from the L were mainly regulated by LCI, whereas those from the NL were dominated jointly by soil NO₃ ^? content and temperature. The effects of LCI and LNI on the soil N₂O fluxes were the greatest in the 2 months after litter decomposition. Our results show that litter may affect not only the variability in the quantity of N₂O emitted, but also the mechanisms that govern N₂O production. However, further studies are still required to elucidate the impacting mechanisms of litter decomposition on N₂O emission from tropical forests.     

Differences between migrasome,a ‘new organelle’, and exosome

The migrasome is a new organelle discovered by Professor Yu Li in 2015. When cells migrate, the membranous organelles that appear at the end of the retraction fibres are migrasomes. With the migration of cells, the retraction fibres which connect migrasomes and cells finally break. The migrasomes detach from the cell and are released into the extracellular space or directly absorbed by the recipient cell. The cytoplasmic contents are first transported to the migrasome and then released from the cell through the migrasome. This release mechanism, which depends on cell migration, is named ‘migracytosis’. The main components of the migrasome are extracellular vesicles after they leave the cell, which are easy to remind people of the current hot topic of exosomes. Exosomes are extracellular vesicles wrapped by the lipid bimolecular layer. With extensive research, exosomes have solved many disease problems. This review summarizes the differences between migrasomes and exosomes in size, composition, property and function, extraction method and regulation mechanism for generation and release. At the same time, it also prospects for the current hotspot of migrasomes, hoping to provide literature support for further research on the generation and release mechanism of migrasomes and their clinical application in the future.     

Glacier as a source of novel polyethylene terephthalate hydrolases

Polyethylene terephthalate (PET) is a major component of microplastic contamination globally, which is now detected in pristine environments including Polar and mountain glaciers. As a carbon-rich molecule, PET could be a carbon source for microorganisms dwelling in glacier habitats. Thus, glacial microorganisms may be potential PET degraders with novel PET hydrolases. Here, we obtained 414 putative PET hydrolase sequences by searching a global glacier metagenome dataset. Metagenomes from the Alps and Tibetan glaciers exhibited a higher relative abundance of putative PET hydrolases than those from the Arctic and Antarctic. Twelve putative PET hydrolase sequences were cloned and expressed, with one sequence (designated as GlacPETase) proven to degrade amorphous PET film with a similar performance as IsPETase, but with a higher thermostability. GlacPETase exhibited only 30% sequence identity to known active PET hydrolases with a novel disulphide bridge location and, therefore may represent a novel PET hydrolases class. The present work suggests that extreme carbon-poor environments may harbour a diverse range of known and novel PET hydrolases for carbon acquisition as an environmental adaptation mechanism.     

2011年、2013年和2016年医院内获得性血流感染常见病原菌分布及其耐药性分析

动态监测2011年、2013年和2016年我国不同地区医院内获得性血流感染病原菌分布及耐药进展趋势。从全国10个城市回顾性收集血流感染病原菌非重复性株,采用琼脂稀释法或微量肉汤稀释法进行药物敏感性试验,采用Whonet 5.6软件对药敏试验结果进行分析。收集的2 248株血流感染病原菌中革兰阴性杆菌为1 657株 (占73.7%),革兰阳性球菌为591株 (占26.3%)。分离率排名前五的病原菌依次为大肠埃希菌 (32.6%,733株/2 248株)、肺炎克雷伯菌 (14.5%,327株/2 248株)、金黄色葡萄球菌 (10.0%,225株/2 248株)、鲍曼不动杆菌 (8.7%,196株/ 2 248株) 和铜绿假单胞菌 (6.2%,140株/2 248株)。血流感染分离的革兰阴性杆菌对抗菌药物体外敏感率较高的抗菌药物依次为粘菌素 (96.5%,1 525株/1 581株,不包括天然耐药菌株)、替加环素 (95.6%,1 375株/1 438株,不包括天然耐药菌株)、头孢他啶/克拉维酸 (89.2%,1 112株/1 246株)、阿米卡星 (86.4%,1 382株/1 599株) 和美罗培南 (85.7%,1 376株/1 605株);革兰阳性球菌对抗菌药物体外敏感率较高的抗菌药物依次为替加环素、替考拉宁和达托霉素 (敏感率均为100.0%)、万古霉素和利奈唑胺 (敏感率均为99.7%)。2011年、2013年和2016年产超广谱β-内酰胺酶肠杆菌科细菌分离率分别为50.6% (206株/407株)、49.8% (136株/273株) 和38.9% (167株/429株);碳青霉烯不敏感肠杆菌科细菌分离率分别为2.2% (9株/408株)、4.0% (16株/402株) 和3.9% (17株/ 439株);多重耐药鲍曼不动杆菌分离率分别为76.4% (55株/72株)、82.7% (43株/52株) 和87.5% (63株/72株),多重耐药铜绿假单胞菌分离率分别为9.8% (5株/51株)、20.0% (7株/35株) 和13.0% (7株/54株);甲氧西林耐药金黄色葡萄球菌的分离率分别为51.9% (41株/79株)、29.7% (19株/64株) 和31.7% (26株/82株)。屎肠球菌和粪肠球菌中高水平庆大霉素耐药株分离率分别为43.2% (48株/111株) 和40.9% (27株/66株)。碳青霉烯不敏感肠杆菌科细菌中肺炎克雷伯菌居首位,占57.1% (24株/42株) 。肠杆菌科细菌中分离出30株替加环素不敏感株,其中肺炎克雷伯菌占76.7% (23株/30株);分离出粘菌素耐药肠杆菌科细菌39株,其中大肠埃希菌、阴沟肠杆菌和肺炎克雷伯菌分别占43.6% (17株/39株)、35.9% (14株/39株) 和15.4% (6株/39株)。医院获得性血流感染病原菌主要为革兰阴性杆菌 (以大肠埃希菌和肺炎克雷伯菌为主),其对替加环素、粘菌素和碳青霉烯类药物的敏感率较高;革兰阳性球菌中分离率最高的为金黄色葡萄球菌,其次为屎肠球菌,这两种细菌对替加环素、达托霉素、利奈唑胺、万古霉素和替考拉宁的敏感率较高。粘菌素耐药肠杆菌科细菌、替加环素不敏感肠杆菌科细菌、利奈唑胺或万古霉素不敏感革兰阳性球菌的分离,警示临床高度关注,仍需动态监测耐药进展趋势。     

新早期胃癌标志物PRDX4通过清除ROS促进胃癌的发生发展

胃癌是全球第四大最常见的癌症,也是全球癌症中引起死亡的第二大原因。为了降低胃癌的死亡率,目前亟需解决的问题是发现新的早期胃癌特异性的标志物,提高早期胃癌的检出率,从而从根本上解决胃癌死亡率高的问题。实验室前期研究发现过氧化物酶4 (Peroxiredoxin 4,PRDX4)具有早期胃癌标志物的潜能,文中通过建立恶性转化模型及转化细胞过表达等方法,研究PRDX4在转化细胞中的作用。结果显示PRDX4通过减少转化细胞中活性氧(Reactive oxygen species,ROS)含量,使细胞处在利于生长增殖的微环境中,从而促进细胞发生恶性转化,即PRDX4通过清除ROS促进胃癌的发生发展。