Platelet‐rich plasma inhibits osteoblast apoptosis and actin cytoskeleton disruption induced by gingipains through upregulating integrin β1

The aim of this study was to explore the effects of platelet‐rich plasma on gingipain‐caused changes in cell morphology and apoptosis of osteoblasts. Mouse osteoblasts MC3T3‐E1 cells were treated with gingipain extracts from Porphyromonas gingivalis in the presence or absence of platelet‐rich plasma. Apoptosis was detected with terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling staining. F‐actin was determined by phalloidin‐fluorescent staining and observed under confocal microscopy. Western blot analysis was used to detect integrin β1, F‐actin, and G‐actin protein expressions. A knocking down approach was used to determine the role of integrin β1. The platelet‐rich plasma protected osteoblasts from gingipain‐induced apoptosis in a dose‐dependent manner, accompanied by upregulation of integrin β1. Platelet‐rich plasma reversed the loss of F‐actin integrity and decrease of F‐actin/G‐actin ratio in osteoblasts in the presence of gingipains. By contrast, the effects of platelet‐rich plasma were abrogated by knockdown of integrin β1. The platelet‐rich plasma failed to reduce cell apoptosis and reorganize the cytoskeleton after knockdown of integrin β1. In conclusion, platelet‐rich plasma inhibits gingipain‐induced osteoblast apoptosis and actin cytoskeleton disruption by upregulating integrin β1 expression.     

Ring‐opening of azetidiniums by nucleophiles. Synthesis of polysubstituted linear amines

This microreview focuses on the nucleophilic ring‐opening of azetidiniums presenting various substitution patterns at C2, C3, and C4. In most cases, the nucleophilic ring‐opening occurred in a stereoselective and regioselective fashion producing functionalized linear amines. Experimental selectivities associated with Density Functional Theory (DFT) calculations have allowed a better understanding of the parameters governing the regioselectivities.     

气候变化下生物交互作用对树线生态过程的影响

树线交错带是具有强烈生物交互作用的高寒生态过渡带,生物互作与树线生态过程密切相关。本研究系统综述了气候变化下植物间、动植物间和微生物与植物间互作因子对树线生态过程的影响。植物间互利或竞争作用的强度调控变暖背景下树线生态过程的变化,目前尚缺少树轮生态学证据,且亟待检验高阶互作的适用性;动物采食活动、微生物与植物间互作可通过影响土壤状况、改变树木生长和更新等生态过程动态,增强或削弱树线与气候间耦合关系。迄今为止,地下与地上过程联系如何影响气候变暖下的树线动态尚不明晰,而营养级间互作可能调制树线生态过程对气候响应。青藏高原等高寒区具有开展此类研究的优势与潜力。     

闽东南地区马尾松古树对气候变化和虫灾的生态弹性

马尾松是我国南方地区广泛分布的先锋造林树种。在全球变暖、气候干旱化和虫灾频发的趋势下,研究马尾松对环境干扰的生态弹性对森林管理有重要意义。本文对福建省仙游县百松村的马尾松古树进行树木年轮样品采集,建立区域首个马尾松树轮宽度标准年表(1865—2014年)。结果表明: 当年7—9月低相对湿度和5—9月极端高温是树木生长的主要限制因素。根据树轮极端窄年确定1869、1889、1986、1991和1993是极端事件年。时序叠加分析发现,极端事件发生前两年的持续低值加剧了极端事件的影响。干旱年份更容易引发虫灾。1889年是受虫灾影响最严重的年份,1986和1991年受到虫灾和干旱气候的双重影响,其余极端年主要受干旱气候的影响。树木对虫灾的抵抗力弱于对干旱事件的抵抗力;除1991年外,树木对虫灾的相对弹性力高于对干旱事件的相对弹性力。1889年的相对弹性力最高,1991年受到连续极端事件的影响,相对弹性力最低。2000年以来研究区干旱化趋势加强,马尾松古树遭受干旱和虫灾的干扰加强,部分树木死亡。     

呼伦贝尔沙地樟子松径向生长特征的VS模型模拟分析

利用Vaganov-Shashkin模型对呼伦贝尔地区4个样点的沙地樟子松标准化宽度年表进行模拟研究,在2000年以前时段拟合度较好,而2000年以后时段拟合度较差。进而选取2000年以前的模拟结果进行径向生长过程分析。结果表明: 呼伦贝尔沙地樟子松主要的生长季为每年的5—9月,温度对每年樟子松生长初期与末期具有显著影响,而在树木生长季旺盛期,土壤湿度的不足是制约树木生长的主要因素。极端窄年树木径向生长速率受土壤湿度的影响较极端宽年明显,生长季中期7—8月树木径向生长速率在宽窄年份均呈降低趋势,表明该时期沙地樟子松生长均受到不同程度的干旱胁迫。研究结果与我国半干旱地区树木年轮生理模型分析特征相符,模型对呼伦贝尔沙地樟子松径向生长模拟具有一定的适用性。     

High-altitude tree growth responses to climate change across the Hindu Kush Himalaya

兴都库什喜马拉雅地区高海拔树木生长对气候变化的响应 高海拔地区快速升温可能导致树木对温度响应更为敏感,而限制高海拔地区树木生长的关键气候因子以及气候变化对树木生长产生多大程度的影响尚不清楚。本研究在兴都库什喜马拉雅地区收集了73 个样点的树轮数据,包括3个优势属的树种(Abies属、Juniperus属和Picea属),样点海拔均在3000 m以上。 将时间动态规整(dynamic time warping)的方法用于建立亚区域年表,以考虑不同站点年表之间变化的同步 性。同时,定量分析了气候因子对树木生长的贡献以及树木生长与气候因子关系的时空动态。研究结果发现,73个站点年表可以聚为3类,且与其所处的生物气候区相对应,即西喜马拉雅地区,中东喜马拉雅地区和藏东南地区。在干旱的西喜马拉雅地区,树木生长与冬、春两季的降水呈正相关关系,而在湿润的藏东南地区,树木生长与冬季温度和春季降水呈正相关关系。树木生长受最低温度的影响最大,特别是冬季温度,其重要性从西到东呈现递增趋势。滑动窗口相关分析表明,在中西喜马拉雅地区,影响树木生长的冬季温度信号在减弱,然而在藏东南地区该信号随着1980年以来的快速升温而增强。本研究结果表明,若该地区升温持续,在西喜马拉雅地区可能会因变暖引起的水分亏缺而造成森林衰退,而在藏东南地区因树木生长得益于变暖而使得森林扩张。     

MoSep3 and MoExo70 are needed for MoCK2 ring assembly essential for appressorium function in the rice blast fungus,Magnaporthe oryzae

Polar growth during appressorium formation is vital for the penetration peg formation in the rice blast fungus, Magnaporthe oryzae. Previous research has shown that the Sln1-septin-exocyst complex, localized at the base of the appressorium in contact with the leaf surface, forms a ring structure that influences growth polarity and affects penetration peg formation, and is necessary for pathogenicity. Our previous research showed CK2 proteins assemble another ring structure positioned perpendicular to the Sln1-septin-exocyst complex. Our research showed that the CK2 ring needs to become correctly assembled for penetration peg function and subsequent plant infection. In the present study, we found that the ring structures of CK2 are absent in the appressorium of ΔMoSep3 septin deletion mutants lacking the septin ring of the Sln1-septin-exocyst complex. Sln1 affects the septin proteins that recruit the exocyst complex that localizes as another ring at the appressorium's bottom. Destruction of the exocyst complex by mutation also causes incorrect localization of the CK2 ring structure. In conclusion, CK2 probably takes part in reestablishing the appressorium' spolarity growth necessary for penetration peg formation. We can also conclude that the correct localization and assembly of one or more CK2 ring structures in the appressorium depend on the initial assembly of the Sln1-septin-exocyst complex two rings at the base of the appressorium.     

A microstructurally informed model for the mechanical response of three-dimensional actin networks

We propose a class of microstructurally informed models for the linear elastic mechanical behaviour of cross-linked polymer networks such as the actin cytoskeleton. Salient features of the models include the possibility to represent anisotropic mechanical behaviour resulting from anisotropic filament distributions, and a power law scaling of the mechanical properties with the filament density. Mechanical models within the class are parameterized by seven different constants. We demonstrate a procedure for determining these constants using finite element models of three-dimensional actin networks. Actin filaments and cross-links were modelled as elastic rods, and the networks were constructed at physiological volume fractions and at the scale of an image voxel. We show the performance of the model in estimating the mechanical behaviour of the networks over a wide range of filament densities and degrees of anisotropy.     

An affine micro-sphere-based constitutive model,accounting for junctional sliding,can capture F-actin network mechanics

Actin filaments are a major component of the cytoskeleton and play a crucial role in cell mechanotransduction. F-actin networks can be reconstituted in vitro and their mechanical behaviour has been studied experimentally. Constitutive models that assume an idealised network structure, in combination with a non-affine network deformation, have been successful in capturing the elastic response of the network. In this study, an affine network deformation is assumed, in which we propose an alternative 3D finite strain constitutive model. The model makes use of a micro-sphere to calculate the strain energy density of the network, which is represented as a continuous distribution of filament orientations in space. By incorporating a simplified sliding mechanism at the filament-to-filament junctions, premature filament locking, inherent to affine network deformation, could be avoided. The model could successfully fit experimental shear data for a specific cross-linked F-actin network, demonstrating the potential of the novel model.     

The Influences of A Nitrogen Atom Position in Dinucleoside 2-,3-,4-Pyridylphosphonates on Fragmentation Patterns in Electrospray Ionization Multistage Tandem Mass Spectra

2-,3-,4-Pyridylphosphonates and their phosphonothioate congeners were analyzed by electrospray ionization multistage tandem mass spectrometry (ESI-MSⁿ). It was found that the fragmentation pathways of these compounds were not influenced to any detectable extent by the stereochemistry at the phosphorus centers but were sensitive to the position of a nitrogen atom in the pyridine ring of these compounds. Possible mechanisms for fragmentations of the investigated compounds are discussed in detail.