胡蔓藤种子发芽试验研究初探

采用胡蔓藤采摘时果皮已转褐色的成熟种子和采摘时果皮为黄绿色的刚成熟的种子,进行以素黄泥、商品粗腐质物和河沙三种作基质,在刚成熟的种子播后加盖相应的基质等试验。试验结果两种成熟种子在素黄泥上发芽率都很高,其他两种培养基均不利于发芽,三种基质作为播后覆盖均影响发芽。     

“最大持续产量”及其确定方法的探讨

我国《中药材生产质量管理规范》(ＧＡＰ)的起草工作已正式启动 ,其目的是通过规范中药材生产过程 ,以保证药材达到规定的质量标准。由于药材生产在我国品种繁多 ,且 80 %左右为野生药材 ,因此在规范中药材生产的同时 ,必须保护和发展野生中药材资源。为此 ,在草拟的《中药材生产质量管理规范 (ＧＡＰ)指导原则 (Ａ)植物药材》的文件中 ,明确提出“调控野生药材的采集强度 ,坚持最大持续产量 (ｍａｘｉｍｕｍｓｕｓｔａｉｎｅｄｙｉｅｌｄ ,ＭＳＹ)原则 ,以保护野生药材资源 ,并进一步促进药用植物种植业和动物养殖业的发展 ,保证中药资源的…     

中药硫熏法炮制工艺中存在的问题及对策

自古,我国就是中草药的发源地,我国中药产业已经完成了包括中药研发、中药种植、中药生产和中药销售的整个中药产业链的开发,而对中药材的生产和保存是中药科学的基础,本文阐述了采用硫熏对中药材进行加工的研究现状,并且探讨其存在的问题,以及解决相应问题的对策。从而为硫磺熏制加工中药材的提供科学可靠的依据。     

中药材连作障碍原因及防治途径研究

中药材连作障碍严重、产量降低、品质变劣,是中药材生产中亟待研究和解决的“瓶颈“问题.从土壤养分的亏缺、中药材化感物质的自毒作用、土传病害的加重3方面概述了中药材连作障碍的原因,并提出了连作障碍的防治途径.     

药材道地观与中药材生产

本文阐述了现代道地中药材的概念演变,道地中药材是经过千百年来的疗效认证而普遍得到人们认可的优质中药材。通过对中药材栽培历史的分析,本文认为道地中药材的优质性主要来自野生资源。多数中药栽培发展较晚,栽培生产技术与环境结合尚未达到最优化的程度。从道地中药材成因的角度分析,野生中药材在生长年限、种质、生境、性状、成份等各方面与栽培中药材都与明显的差异,其质量也一定不同,因此对栽培中药材的道地性的应有待于进一步认识。同时,通过将现代栽培技术与中药材栽培相结合,会对栽培中药材的质量稳定和提高发挥重要作用。     

南药新时代

正清代屈大均在《广东新语》的"黩货"中有曰"又戒在任官吏不得私市南药",这可能是我国"南药"一词的最早记载。1969年,国家商业部、外贸部、农垦部、林业部、卫生部、财政部六部委联合签发《关于发展南药生产问题的意见》,"南药"一词开始逐渐频繁地见诸各种文献资料和中药材生产的文件中。     

我国中药材植物保护研究70年——基于文献计量分析

建国70年来,我国在中药材植物保护研究领域取得了长足进展.笔者利用中国知网(CNKI)数据库,以国家中药材产业技术体系确定的28个“十三五”重点中药材品种为基础,检索了1949—2019年中药材植物保护研究的有关文献;并对检索文献进行分析,总结建国70年来中药材植物保护研究的发展历程和研究进展;同时对中药材植物保护研究存在的问题进行梳理并提出相应的解决思路.以期为中药材植物保护事业未来发展提供参考.     

广东省胡颓子属植物种质资源及果实利用评价

在标本查阅和野外调查的基础上,对广东省胡颓子属（Elaeagnus L．）植物资源现状进行了综合评价,并对产量高且可生产性强的部分种类的果实矿质元素及氨基酸等营养成分的含量进行了分析测定。结果表明,广东产胡颓子属植物11种1变种,其中一些种类的果实中含有丰富的矿质元素;角花胡颓子（E．gonyanthes Benth．）和密花胡颓子（E．cottferta Roxb．）果实的营养价值较高、果实较大、有明显酸味,可作为第3代果品加工的生产资源;生存环境的保护对广东省胡颓子属植物资源的保护极其重要。     

海南与市售槟榔等中药材中重金属含量比较研究

本文用石墨炉原子吸收分光光度法测定了海南与市售槟榔等六种中药材中的铅元素含量 ,用原子荧光法测定了其中砷、汞元素的含量 ;通过对海南与市售槟榔等六种中药材 (槟榔、益智仁、砂仁、巴戟天、丁香及肉豆蔻 )中铅、砷、汞含量的比较研究 ,说明海南生态环境的优良是实现中药材GAP种植 ,生产绿色中药材的最佳环境     

猛兽捕鸟大晒台

正捕鸟技术哪家强?狞猫、猞猁、薮猫等中小型猫科动物纷纷挺起胸膛。"咳咳,地球人都知道你们善捕鸟,可是,哥迷们表示,看你们捕鸟都看腻了,他们要看猛兽捕鸟,比如胡狼、狮子、老虎捕鸟!""胡狼也算猛兽?开玩笑!"狞猫吐槽道。"现在小编们拒绝人越来越没技术含量了!"猞猁翻了个转瞬即逝的白眼。小编:"要不要这么犀利……"胡狼捕沙鸡胡狼杰利最近爱上了捕沙鸡,确切地说,是爱上了捕猎沙鸡时瞬间腾空的感觉,就跟飞一样。不同于杰利的单打独斗,胡狼群中的"有才狼"甚至悟     

钩吻(Gelsemium elegans)生物碱结构类型增补探讨

根据对亚洲钩吻(Gelsemium elegans)的化学研究结果,探讨将已知5种生物碱骨架类型扩展为9种,其中新增补并命名为Geleboline-type,Gelselegine-type,Gelsemamide-type,以及首次报道在亚洲钩吻中得到的Yohimbane-type类型。     

Nematode behavior: the taste of success, the smell of danger!

Through experience, the nematode worm Caenorhabditis elegans learns to distinguish high quality bacteria--food--from low quality or toxic bacteria. Increased release of the neurotransmitter serotonin onto identified interneurons determines whether C. elegans chooses to feed or leave.     

西双版纳野生有毒植物资源调查研究

通过野外及走访调查,对西双版纳野生有毒植物资源进行了调查,同时对其科属分布、生活型组成、毒性、有毒部位进行了分析。结果显示,西双版纳野生有毒植物289种,隶属于79科214属,其中优势科集中在豆科、大戟科、天南星科、夹竹桃科、芸香科,优势属为大戟属和茄属;生活型以草本植物居多,占36.68%;有毒部位以全株或全草有毒为主,占37.37%;毒性以小毒植物占大多数,剧毒植物有5种,大毒植物有11种。通过走访调查了解到,商陆、钩吻、相思子、曼陀罗、洋金花、油桐、蓖麻等有毒植物种类在民间曾多次发生误食中毒甚至死亡事例,需要特别注意识别。今后应加强对常见有毒植物的辨识与防范科普宣传,同时加强对有毒植物的开发和应用研究。     

Glyoxalase-1 prevents mitochondrial protein modification and enhances lifespan in Caenorhabditis elegans

Studies of mutations affecting lifespan in Caenorhabditis elegans show that mitochondrial generation of reactive oxygen species (ROS) plays a major causative role in organismal aging. Here, we describe a novel mechanism for regulating mitochondrial ROS production and lifespan in C .  elegans: progressive mitochondrial protein modification by the glycolysis-derived dicarbonyl metabolite methylglyoxal (MG). We demonstrate that the activity of glyoxalase-1, an enzyme detoxifying MG, is markedly reduced with age despite unchanged levels of glyoxalase-1 mRNA. The decrease in enzymatic activity promotes accumulation of MG-derived adducts and oxidative stress markers, which cause further inhibition of glyoxalase-1 expression. Over-expression of the C .  elegans glyoxalase-1 orthologue CeGly decreases MG modifications of mitochondrial proteins and mitochondrial ROS production, and prolongs C .  elegans lifespan. In contrast, knock-down of CeGly increases MG modifications of mitochondrial proteins and mitochondrial ROS production, and decreases C .  elegans lifespan.     

Caenorhabditis elegans reproductive aging: Regulation and underlying mechanisms

Female reproductive decline is one of the first aging phenotypes in humans, manifested in increasing rates of infertility, miscarriage, and birth defects in children of mothers over 35. Recently, Caenorhabditis elegans (C. elegans) has been developed as a model to study reproductive aging, and several studies have advanced our knowledge of reproductive aging regulation in this organism. In this review, we describe our current understanding of reproductive cessation in C. elegans, including the relationship between oocyte quality, ovulation rate, progeny number, and reproductive span. We then discuss possible mechanisms of oocyte quality control, and provide an overview of the signaling pathways currently identified to be involved in reproductive span regulation in C. elegans. Finally, we extend the relevance of C. elegans reproductive aging studies to the issue of human female reproductive decline, and we discuss ideas concerning the relationship between reproductive aging and somatic longevity.     

Effects of Plagiorchis elegans (Digenea: Plagiorchiidae) infection of Biomphalaria glabrata (Pulmonata: Planorbidae) on a challenge infection with Schistosoma mansoni (Digenea: Schistosomatidae)

Prior exposure of Biomphalaria glabrata to the eggs of an incompatible digenean, Plagiorchis elegans, rendered this snail host less suitable to a compatible species, Schistosoma mansoni. Although P. elegans failed to develop patent infections in B. glabrata, it reduced the production of S. mansoni cercariae by 88%. Concomitantly, host attributes such as reproduction, growth, and survival were compromised. The effect of P. elegans infection was most severe among snails that, in addition, had developed patent schistosome infections. Although few S. mansoni cercariae were produced, egg production by B. glabrata was only 4% of control values. Furthermore, no doubly infected snails survived for more than 3 wk after patency, whereas controls experienced no mortality during the same time period. The above effects were attributable to the establishment and persistence of P. elegans sporocysts in the tissues of the incompatible snail host. Their indirect antagonistic interaction with thelarval stages of S. mansoni may be mediated, in part, through their long-term stimulation of the host's internal defense mechanisms. These findings are discussed with a view to use P. elegans and other plagiorchiid digeneans as agents in the biological control of snails and snail-borne diseases.     

MosSCI and gateway compatible plasmid toolkit for constitutive and inducible expression of transgenes in the C. elegans germline

Here we describe a toolkit for the production of fluorescently tagged proteins in the C. elegans germline and early embryo using Mos1-mediated single copy insertion (MosSCI) transformation. We have generated promoter and 3'UTR fusions to sequences of different fluorescent proteins yielding constructs for germline expression that are compatible with MosSCI MultiSite Gateway vectors. These vectors allow tagged transgene constructs to be inserted as single copies into known sites in the C. elegans genome using MosSCI. We also show that two C. elegans heat shock promoters (Phsp-16.2 and Phsp-16.41) can be used to induce transgene expression in the germline when inserted via MosSCI transformation. This flexible set of new vectors, available to the research community in a plasmid repository, should facilitate research focused on the C. elegans germline and early embryo.     

Paralysis and killing of Caenorhabditis elegans by enteropathogenic Escherichia coli requires the bacterial tryptophanase gene

Pathogenic Escherichia coli, including enteropathogenic E. coli (EPEC), enterohaemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC) and enterotoxigenic E. coli (ETEC) are major causes of food and water-borne disease. We have developed a genetically tractable model of pathogenic E. coli virulence based on our observation that these bacteria paralyse and kill the nematode Caenorhabditis elegans. Paralysis and killing of C. elegans by EPEC did not require direct contact, suggesting that a secreted toxin mediates the effect. Virulence against C. elegans required tryptophan and bacterial tryptophanase, the enzyme catalysing the production of indole and other molecules from tryptophan. Thus, lack of tryptophan in growth media or deletion of tryptophanase gene failed to paralyse or kill C. elegans. While known tryptophan metabolites failed to complement an EPEC tryptophanase mutant when presented extracellularly, complementation was achieved with the enzyme itself expressed either within the pathogen or within a cocultured K12 strains. Thus, an unknown metabolite of tryptophanase, derived from EPEC or from commensal non-pathogenic strains, appears to directly or indirectly regulate toxin production within EPEC. EPEC strains containing mutations in the locus of enterocyte effacement (LEE), a pathogenicity island required for virulence in humans, also displayed attenuated capacity to paralyse and kill nematodes. Furthermore, tryptophanase activity was required for full activation of the LEE1 promoter, and for efficient formation of actin-filled membranous protrusions (attaching and effacing lesions) that form on the surface of mammalian epithelial cells following attachment and which depends on LEE genes. Finally, several C. elegans genes, including hif-1 and egl-9, rendered C. elegans less susceptible to EPEC when mutated, suggesting their involvement in mediating toxin effects. Other genes including sek-1, mek-1, mev-1, pgp-1,3 and vhl-1, rendered C. elegans more susceptible to EPEC effects when mutated, suggesting their involvement in protecting the worms. Moreover we have found that C. elegans genes controlling lifespan (daf-2, age-1 and daf-16), also mediate susceptibility to EPEC. Together, these data suggest that this C. elegans/EPEC system will be valuable in elucidating novel factors relevant to human disease that regulate virulence in the pathogen or susceptibility to infection in the host.