盐节木同化枝的腋芽丛生与快速繁殖

本文通过同化枝腋芽丛生方式建立了盐生植物盐节木的快速繁殖体系。以在MS附加200 mmol·L-1 Na Cl的培养基上无菌种子萌发、生长共计4~5个月、高约3~4 cm的盐节木小苗为材料,从上截取0.5 cm长的同化枝小段为外植体,培养在MS附加不同浓度的6-BA与NAA的培养基中。结果表明:同化枝腋芽诱导与增殖最佳培养基均为MS+0.05 mg·L-1 6-BA+1mg·L-1 NAA或MS+1 mg·L-1 6-BA,初代培养30 d后,腋芽诱导率达97.5%,平均芽增殖系数为2.50;继代增殖培养时,将同化枝切成1 cm长的小段芽增殖系数提高到4.92;一次性芽苗伸长与生根培养基为MS+0.05 mg·L-1 IBA,生根率达99%;小苗经炼苗后移栽到沙子、营养土和蛭石体积比为1:1:1的基质中,成活率可达91%。     

肠系膜上动脉栓塞临床表现及影像特征研究

目的:探讨肠系膜上动脉栓塞(superior mesenteric artery embolism,SMA embolism)临床及影像特征,以及时准确诊断从而改善病人预后。方法:搜集我院2011年7月至2014年8月临床诊断为SMA栓塞的患者24例,回顾性分析其临床及影像资料。结果:24例SMA栓塞发病年龄51~84岁,平均71.9±8.1岁;临床均表现为突发腹痛(24/24,100%),腹痛多持续不缓解(18/24,75%),少有放射痛(1/24,4.17%),多伴有恶心呕吐(16/24,66.67%)、腹泻便血(15/24,62.5%),体格检查多有肠鸣音亢进(19/24,79.17%),少有腹膜刺激征(2/24,8.33%)。多合并高血压(18/24,75%)、房颤(16/24,66.67%)、冠心病(14/24,58.33%)、心脏瓣膜病变(6/24,25%)及其他周围动脉栓塞(9/24,37.5%)。临床上符合SMA栓塞三联征中至少两项特征20例(83.33%),具备典型三联征13例(54.17%)。MSCTA或DSA均表现为SMA主干截断或充盈缺损(24/24,100%),栓塞位置多位于第1空肠动脉起始至回结肠动脉起始水平段(18/24,75%),栓塞远端分支血管多显影不良(23/24,95.83%),少有侧枝循环形成(3/24,12.5%)。MSCTA显示栓塞段血管密度多有增高(12/17,70.59%),少有管径增粗(3/17,17.65%)及脂肪间隙模糊(2/17,11.76%)。肠管多有缺血改变(15/17,88.24%),肠系膜多增粗模糊(15/17,88.24%),腹水少见(1/17,5.82%)。结论:SMA栓塞临床和影像具有一定的特征性,临床怀疑SMA栓塞应及早行MSCTA或DSA明确诊断。     

Chemical space navigation in lead discovery

The number of new chemical entities has remained rather constant (averaging 37 per year) in the past decade, despite the multiple-fold increase in the number of compounds that are being made and tested. Chemical space requires novel methods that can handle the increasing number of potentially accessible molecules. Neighborhood behavior, as an approach to similarity, and chemical property space navigation are some of the recent advances that are discussed, in the context of lead discovery and appropriate pharmacokinetic properties.     

Ill nature: Disease hotspots as threats to biodiversity

Diseases are part of the natural world, but human activities may affect and disrupt the natural dynamics of diseases, threatening wildlife species and human welfare. We listed the number of species threatened by diseases and compiled their distributional ranges. Based on such data we identify global disease hotspots, regions where disrupted disease dynamics threaten to decimate several species into extinction. The number of species threatened by disease may increase, and climate change may act synergistically increasing the severity of disease incidence in the hotspots, and drive the emergence of new disease hotspots. Until now diseases were thought to play a secondary role in the biodiversity extinction crisis, but the global threat scenario is so dynamic that if we do not bring diseases to the forefront of conservation actions and policies, they may not only bring species into extinction but they may also affect human populations as well.     

Effects of dimethylsulfoxide on the ultrastructure of fixed cells

It has been reported that the use of dimethylsulfoxide (DMSO) as a solvent for fixatives enhances preservation of cellular ultrastructure. By contrast, we have shown that DMSO alters the ultrastructural integrity of glutaraldehyde fixed cells. The cell membrane, nuclear envelope, endoplasmic reticulum, ribosomes, microtubules and intracytoplasmic organelles are most susceptible to the action of DMSO. We hypothesize that DMSO exerts intracellular alterations via its interaction with remnant interfacial water in fixed cells. DMSO-induced alterations of these and related cellular components may result in the formation of artefactual structures and networks. Thus, it appears that DMSO containing glutaraldehyde neither accelerates fixation nor enhances stabilization of cellular ultrastructure. For these reasons, addition of DMSO to fixatives is not recommended.