陕北黄土高原柠条灌丛穿透雨特征与影响因素

穿透雨是降雨再分配的主要组分,对干旱半干旱区的土壤水分补给和植被生长具有关键作用。灌丛穿透雨的影响机制特别是植被特征对穿透雨的影响需要进一步的定量研究,且目前对穿透雨空间异质性与聚集效应的研究相对较少。以陕北黄土高原典型灌丛—柠条为研究对象,于2016年对六道沟小流域柠条冠层下8个方位的穿透雨以及降雨和植被因子进行系统观测,分析穿透雨量、穿透雨率、穿透雨空间变异和聚集效应的变化特征,辨识影响穿透雨的主要降雨和植被因子,并建立相应的定量关系。结果表明:次降雨下柠条的穿透雨量、穿透雨率和空间变异系数平均值分别为11.88 mm、75.71%和21.80%。穿透雨量主要由降雨量决定,随降雨量增加而线性增加(R~2=0.99)。穿透雨率和空间变异系数主要受降雨量和降雨强度影响,穿透雨率随降雨量和I_30增加而呈对数增加(R~2=0.71和0.54),渐进值约为95%,而穿透雨空间变异系数则随降雨量和I_30增加而呈幂函数递减(R~2=0.71和0.60),稳定值约为10%。冠层厚度和枝倾角是影响穿透雨的主要植被因子,并分别呈显著的线性负相关和正相关(P0.05)。柠条穿透雨具有一定的聚集效应,平均发生频率为8.53%,且聚集效应在大雨量、高雨强和长历时降雨事件中更加明显。     

Substoichiometric Hsp104 regulates the genesis and persistence of self-replicable amyloid seeds of Sup35 prion domain

Prion-like self-perpetuating conformational conversion of proteins is involved in both transmissible neurodegenerative diseases in mammals and non-Mendelian inheritance in yeast. The transmissibility of amyloid-like aggregates is dependent on the stoichiometry of chaperones such as heat shock proteins (Hsps), including disaggregases. To provide the mechanistic underpinnings of the formation and persistence of prefibrillar amyloid seeds, we investigated the role of substoichiometric Hsp104 on the in vitro amyloid aggregation of the prion domain (NM-domain) of Saccharomyces cerevisiae Sup35. At low substoichiometric concentrations, we show Hsp104 exhibits a dual role: it considerably accelerates the formation of prefibrillar species by shortening the lag phase but also prolongs their persistence by introducing unusual kinetic halts and delaying their conversion into mature amyloid fibers. Additionally, Hsp104-modulated amyloid species displayed a better seeding capability compared to NM-only amyloids. Using biochemical and biophysical tools coupled with site-specific dynamic readouts, we characterized the distinct structural and dynamical signatures of these amyloids. We reveal that Hsp104-remodeled amyloidogenic species are compositionally diverse in prefibrillar aggregates and are packed in a more ordered fashion compared to NM-only amyloids. Finally, we show these Hsp104-remodeled, conformationally distinct NM aggregates display an enhanced autocatalytic self-templating ability that might be crucial for phenotypic outcomes. Taken together, our results demonstrate that substoichiometric Hsp104 promotes compositional diversity and conformational modulations during amyloid formation, yielding effective prefibrillar seeds that are capable of driving prion-like Sup35 propagation. Our findings underscore the key functional and pathological roles of substoichiometric chaperones in prion-like propagation.     

Structural biology of ex vivo mammalian prions

The structures of prion protein (PrP)–based mammalian prions have long been elusive. However, cryo-EM has begun to reveal the near-atomic resolution structures of fully infectious ex vivo mammalian prion fibrils as well as relatively innocuous synthetic PrP amyloids. Comparisons of these various types of PrP fibrils are now providing initial clues to structural features that correlate with pathogenicity. As first indicated by electron paramagnetic resonance and solid-state NMR studies of synthetic amyloids, all sufficiently resolved PrP fibrils of any sort (n > 10) have parallel in-register intermolecular β-stack architectures. Cryo-EM has shown that infectious brain-derived prion fibrils of the rodent-adapted 263K and RML scrapie strains have much larger ordered cores than the synthetic fibrils. These bona fide prion strains share major structural motifs, but the conformational details and the overall shape of the fibril cross sections differ markedly. Such motif variations, as well as differences in sequence within the ordered polypeptide cores, likely contribute to strain-dependent templating. When present, N-linked glycans and glycophosphatidylinositol (GPI) anchors project outward from the fibril surface. For the mouse RML strain, these posttranslational modifications have little effect on the core structure. In the GPI-anchored prion structures, a linear array of GPI anchors along the twisting fibril axis appears likely to bind membranes in vivo, and as such, may account for pathognomonic membrane distortions seen in prion diseases. In this review, we focus on these infectious prion structures and their implications regarding prion replication mechanisms, strains, transmission barriers, and molecular pathogenesis.     

尺度变换的正确率分析

采用优势规则和随机规则为基础的尺度分析方法．对分类的TM数据(景观类型图,包含8类型)进行了尺度变换分析。随着尺度的增加。优势规则分析方法使景观中优势景观类型的面积增加,相反．面积较小的非优势景观类型的面积减少。随机规则使各景观类型的面积基本上保持不变。随着尺度的增加．随机Kappa指数、位置Kappa指数和标准Kappa指数减少。在优势规则分析法中数量Kappa指数减少,但在随机规则为基础的处理中它保持100％。优势规则处理中的正确率大于随机规则处理的。由景观类型的面积百分比引起的数量正确率在优势规则处理中增加．但在随机规则处理中保持9．64％不变;相反数量错误在优势规则处理中明显增加。但在随机规则处理中少量增加。偶然正确率保持12．50％不变。位置正确率减少,相反位置错误明显增加。层和亚层水平上的位置正确率和错误的变化不明显．而网格水平上的位置正确率和错误大幅度减少。网格水平上的位置正确率和错误率决定了整个位置正确率和错误率．同时位置正确率和错误率基本上决定了整个正确率和错误率。标准Kappa指数大于等于70％作为选择依据．认为210m是优势规则处理法的尺度阈值,150m是随机规则处理法的尺度阈值。欲提高尺度阈值,必须改变研究范围或分类系统。     

西藏飞蝗虫粪粗提物的成分分析及其活性测定

西藏飞蝗作为青藏高原独有的飞蝗亚种,近年来发生危害严重,对其聚集机制的研究是西藏飞蝗生态治理的基础.采用自制Y型嗅觉仪、气质联用(GC-MS)和触角电位反应(EAG)等方法对西藏飞蝗虫粪粗提物进行了活性测定和成分分析.结果表明:乙醇浸提法是提取西藏飞蝗虫粪粗提物的较好方法.西藏飞蝗虫粪粗提物活性随虫龄增加,并且群居型成虫虫粪粗提物的活性最强.散居型蝗虫对蝗蝻虫粪粗提物的趋向性高于同虫态群居型蝗虫对蝗蝻虫粪粗提物的趋向性.不同虫态的西藏飞蝗虫粪粗提物所含化合物种类及含量有所差别,部分化合物与东亚飞蝗聚集信息素成分相同.西藏飞蝗对人工合成化合物的电生理反应变化趋势可分为三类:2μL/mL浓度下触角电位反应值最高;不同虫态西藏飞蝗对同一化合物的电生理反应变化趋势不一致;随浓度增加电生理反应显著增加.     

黄野螟群体大小对幼虫个体生存和发育的影响

幼虫聚集取食是一些鳞翅目昆虫提高幼虫生长和存活的手段。通过对聚集取食的黄野螟Heortia vitessoides Moore幼虫在室内条件下进行饲养,探究黄野螟幼虫的群体数量大小(分别为30、60、90头幼虫)对幼虫体长、发育速度、达末龄(5龄)时的存活率的影响。分析发现在排除天敌捕食和食物缺乏的前提下,从3龄开始,大群体(90头)的体长显著大于小群体(30头),大群体的幼虫发育速度显著快于小群体,大群体对幼虫前4个龄期时的成活率没有显著提高,尽管大群体的存活率在均值上高于小群体,但是幼虫总体存活率在不同群体中差异不显著。黄野螟幼虫的聚集取食对幼虫的生长的促进作用明显,显著促进了幼虫的生长,加快了幼虫的发育。     

短尾蝮蛇毒磷脂酶A2的分离纯化及抗血小板聚集作用

目的研究短尾蝮蛇毒磷脂酶A2的分离纯化及其抗血小板聚集作用。方法磷脂酶A2的分离纯化采用CM-SephadexC-25、DEAE-SepharoseCL-6B、SephacrylS-200、SephadexG-75柱层析法,用SDS-聚丙烯酰胺凝胶电泳测定其蛋白分子质量,以磷脂酶Az测定方法测定其酶活性,用比浊法测定其对二磷酸腺苷（ADP）引起的血小板聚集的影响。结果从短尾蝮蛇毒中纯化所得磷脂酶A2的相对分子质量为16．0×10^3（非还原）、17．6×10^3（还原）,它具有磷脂酶A2活性,能明显抑制ADP引起的血小板聚集并呈剂量-效应关系。结论此方法成功地从短尾蝮蛇毒中分离纯化出磷脂酶A2,并能抑制血小板聚集。     

Nanoimaging for protein misfolding and related diseases

Misfolding and aggregation of proteins is a common thread linking a number of important human health problems. The misfolded and aggregated proteins are inducers of cellular stress and activators of immunity in neurodegenerative diseases. They might possess clear cytotoxic properties, being responsible for the dysfunction and loss of cells in the affected organs. Despite the crucial importance of protein misfolding and abnormal interactions, very little is currently known about the molecular mechanism underlying these processes. Factors that lead to protein misfolding and aggregation in vitro are poorly understood, not to mention the complexities involved in the formation of protein nanoparticles with different morphologies (e.g., the nanopores) in vivo. A better understanding of the molecular mechanisms of misfolding and aggregation might facilitate development of the rational approaches to prevent pathologies mediated by protein misfolding. The conventional tools currently available to researchers can only provide an averaged picture of a living system, whereas much of the subtle or short-lived information is lost. We believe that the existing and emerging nanotools might help solving these problems by opening the entirely novel pathways for the development of early diagnostic and therapeutic approaches. This article summarizes recent advances of the nanoscience in detection and characterization of misfolded protein conformations. Based on these findings, we outline our view on the nanoscience development towards identification intracellular nanomachines and/or multicomponent complexes critically involved in protein misfolding.     

神经退行性疾病中的TDP-43蛋白聚集和相变

随着全球老龄化人口的急剧增加,神经退行性变已经成为危害公共健康的主要疾病.在神经退行性疾病(肌萎缩侧索硬化症(ALS)、额颞叶变性病(FTLD)和阿尔茨海默病(AD)等)患者脑组织中均能观察到蛋白质聚集形成的包涵体,其中TAR DNA结合蛋白43 (TDP-43)是主要成分之一.目前已发现多个TDP-43基因突变与家族...     

Wortmannin对凝血酶诱导的人血小板聚集和磷脂酰肌醇三磷酸累积的影响

 Ｗ ｏｒｔｍ ａｎｎｉｎ 是肌醇磷脂 ３ 激酶的不可逆抑制剂．用比浊法分析血小板聚集;肌醇磷脂用３２ Ｐ 磷酸钠标记,用氯仿和甲醇抽提,用 Ｔ Ｌ Ｃ和放射自显影分析,研究了 Ｗ ｏｒｔｍ ａｎｎｉｎ 对凝血酶诱导的人血小板聚集和磷脂酰肌醇三磷酸（ Ｐ Ｉ Ｐ３）累积的影响．结果显示, Ｗ ｏｒｔｍ ａｎｎｉｎ 对凝血酶（５００ Ｕ／ Ｌ）诱导的人血小板聚集有抑制作用,这种抑制作用在一定范围内呈剂量依赖关系（２０～８０μｍ ｏｌ／ Ｌ）．凝血酶（５００ Ｕ／ Ｌ）诱导人血小板 Ｐ Ｉ Ｐ３ 的累积, Ｗ ｏｒｔｍ ａｎｎｉｎ 对此累积有抑制作用,这种抑制作用在一定范围内呈剂量依赖关系（４０～１６０ μｍ ｏｌ／ Ｌ）．结果提示： Ｗ ｏｒｔｍ ａｎｎｉｎ 可能是潜在的抗血小板药物,抑制凝血酶诱导的人血小板聚集主要与其抑制 Ｐ Ｉ Ｐ３ 的累积有关．结果也提示,肌醇磷脂 ３ 激酶在血小板活化中起重要作用．