北京通州平原生态林空间结构特征

林分空间结构直接反映林木间资源竞争情况和生长空间分配状况,对掌握生态林生长状况、制定林分结构调控措施,提升森林质量和生态服务具有重要作用。本文以北京市通州区油松林、白蜡林、旱柳林、毛白杨林、国槐林、刺槐林和垂柳林7种平原生态林为对象,采用聚集度、角尺度、大小比数、开敞度、树冠指数、竞争指数、边缘效益和空间结构综合指数评价了平原生态林的空间结构特征。结果表明: 研究区林分水平分布格局良好,聚集度处于0.32～1.41,角尺度都分布在0.4左右,大小比数主要分布在0.5附近。林分垂直分布格局有待改善,开敞度介于0.19～0.52,大部分树冠指数在0.7左右,竞争指数均大于50,整体居于高位状态。除刺槐林空间结构综合评价指数为Ⅲ级外,其他6种林分均为Ⅱ级,林分开阔程度较低,生活力一般,各林分空间结构综合评价指数从大到小为刺槐林>垂柳林>油松林>旱柳林>白蜡林>国槐林>毛白杨林。     

2001—2020年川西北高原归一化植被指数演变特征及其对极端气候的响应

川西北高原是典型的生态气候敏感区,其植被状况与气候变化密切相关。本研究基于2001—2020年MODIS-NDVI数据集和气象数据,采用最大值合成、地理探测器模型、线性趋势分析、相关分析等方法,研究川西北高原生长季归一化植被指数(NDVI)的变化趋势及其对气候因子的响应机制。结果表明: 研究期间,川西北高原植被覆盖度整体状况良好,86.8%的区域植被稳定,12.6%的区域NDVI呈弱持续性上升趋势,0.6%的区域NDVI呈下降趋势,全区生态环境呈稳中向好的发展趋势。研究区植被覆盖度空间差异大,总体呈由西南向东北上升的趋势,并有显著的立体变化。海拔1350 m以下,NDVI随海拔升高而上升;海拔1350～3650 m,NDVI无显著变化;海拔3650～5900 m,NDVI随海拔升高而下降,在4750～5900 m快速下降;海拔5900 m以上,几乎无植被。川西北高原的NDVI受多种自然因子交互作用影响,热量因子(月最高气温极大值、月最低气温极小值、植物生长期、年均温、生长期均温)是主导气候因子,除月最高气温极大值外,其余温度因子对NDVI均以正贡献为主。NDVI对气温指数的响应高于降水指数。在气候变暖背景下,极端气温暖指数对川西北高原植被生长尤其是高海拔地区植被生长及改善以促进作用为主。     

一种基于数码相机图像和群落冠层结构调查的草地地上生物量估算方法

草地地上生物量是影响其生态系统功能最重要的因素之一, 也是草地生态学研究中不可或缺的监测指标。草地地上生物量监测多采用收割法进行, 但这种破坏性取样方法会对研究区域带来巨大干扰, 尤其是面积较小的长期定位监测或者控制实验研究样地, 从而使得地上生物量监测的频次受到很大限制。因此, 通过获取某些原位易测变量, 建立地上生物量的估算方法具有重要意义。该研究依托内蒙古典型草地刈割控制实验平台, 通过数码照片获取不同土地利用方式下的植被覆盖度, 并对样方内的叶面积指数、植被高度、物种多样性等参数进行了测定, 最后利用一元回归模型、逐步回归模型和随机森林模型对地上生物量进行估算。结果表明, 植被覆盖度、叶面积指数、植被平均高度、植被最大高度和物种丰富度是影响地上生物量的主要驱动因素。通过构建适宜于本地的逐步回归模型, 可以实现草地地上生物量的准确预测。在该研究区域中, 预测模型的决定系数(R²) = 0.91, 均方根误差(RMSE) = 35.60 g·m^-2。该研究提供了一种快速、准确且非破坏性测定草地地上生物量的方法, 可作为传统收割法的有效补充。     

水淹频率变化对鄱阳湖增强型植被指数的影响

水淹状况是湿地植被动态的重要影响因素。该研究基于谷歌地球引擎(GEE)平台, 利用2000-03-01至2020-02-29所有覆盖研究区域的MODIS遥感影像数据, 分析20年间水淹频率(IF)、增强型植被指数(EVI)的时空变化以及湿地植被对IF变化的响应, 得出以下结论: (1) 20年来鄱阳湖水文节律发生了明显改变, 高IF (IF > 75%)水域面积呈现下降趋势, 从2000年1 435.3 km²下降至2019年的510.25 km², 降幅为64.45%; (2)区域平均EVI呈显著上升趋势, 植被扩张主要集中在中部IF下降区域; (3)分析不同总水淹频率区域中平均EVI年际变化, 发现EVI与水淹状况的变化趋势相似, 2009年之后鄱阳湖水域面积萎缩趋势缓解, EVI增长速度出现下降; (4)鄱阳湖湿地植被主要沿水域面积萎缩方向扩张, 基于像元统计20年间IF与EVI的变化趋势, 发现它们在空间分布上高度吻合, 这种空间异质性进一步证实水淹状况起到调节植被动态变化的作用。     

研究报告：鳗弧菌（Vibrio anguillarum）核酸适配体的筛选及其结合蛋白的分离鉴定

目的鳗弧菌（Vibrio anguillarum）是水产养殖中的重要条件致病菌,每年给水产养殖业造成巨大的经济损失,研究其致病机制、对其进行快速的检测鉴定是其病害防治的前提和基础。核酸适配体因其高亲和力、高特异性等多种优点,在微生物的靶标分析、检测鉴定以及致病机制等多个领域都呈现出较好的应用潜力。因此,筛选鳗弧菌的核酸适配体,利用核酸适配体对鳗弧菌相关位点进行分析鉴定,不仅能为鳗弧菌的检测鉴定提供一个新的手段,对于探索鳗弧菌相关位点在其病害防治中的作用也具有重要意义。方法以鳗弧菌为靶目标,采用每轮测序的SELEX筛选方法,从高频序列中筛选鳗弧菌的核酸适配体;采用单链DNA浓度法测定核酸适配体的亲和力,研究核酸适配体对鳗弧菌的亲和特异性;采用Origin软件、选择反比例函数（Hyperbola函数）进行非线性拟合,获得核酸适配体的亲和常数（K_d）和最大亲和力（A_m）;采用磁分离技术和聚丙烯酰胺凝胶电泳分离纯化出核酸适配体H5的结合蛋白,通过质谱对该蛋白质进行分析鉴定,并利用Prabi、Phyre2、Psortb 3.0等在线网站分析该结合蛋白的...     

In love and war: The morphometric and phylogenetic basis of ornamentation,and the evolution of male display behavior,in the livebearer genus Poecilia

Exaggerated male traits under sexual selection are often used for both competition and courtship, raising the question of whether ornaments evolved simultaneously for both functions, or if use in one context preceded use in another. Here, we apply a phylogenetic approach to study the evolution of ornamental dorsal fins in male poeciliid fish of the subgenera Mollienesia and Limia, which exhibit convergent development of an enlarged dorsal fin, and often direct erect‐fin displays to male and female conspecifics. Unlike prior categorical assessments of poeciliid adornments, we measure dorsal fin exaggeration with a continuous index of ornamentation. Phylogenetic logistic and generalized least squares regression analyses indicate that high index values are significantly associated with the use of two component postures of courtship and aggressive displays, dorsal fin erection and body curvature, but not with the presence of sexual dichromatism. Male displays initially evolved for male–male aggression in the common ancestor of Mollienesia and Limia, suggesting that this signal originated for competition, then became co‐opted for courtship. These results support the armament‐ornament hypothesis for evolution of exaggerated male traits, and are consistent with an evolutionary shift in the predominant mechanisms of sexual selection from intra‐ to intersexual.     

Autophagy protects against redox-active trace metal-induced cell death in rabbit synovial fibroblasts through Toll-like receptor 4 activation

Reactive oxygen species (ROS) are implicated to play a role in initiating rheumatoid arthritis (RA) pathogenesis. We have investigated the mechanism(s) by which essential redox-active trace metals (RATM) may induce cell proliferation and cell death in rabbit synovial fibroblasts. These fibroblast-like synovial (FLS) cells, which express Toll-like receptor 4 (TLR4), were used as a model system that plays a role in potentially initiating RA through oxidative stress. Potassium peroxychromate (PPC, [Cr⁵⁺]), ferrous chloride (FeCl₂, [Fe²⁺]), and cuprous chloride (CuCl, [Cu⁺]) in the indicated valency states were used as exogenous pro-oxidants that can induce oxidative stress through TLR4 coupled activation that also causes HMGB1 release. We measured the proliferation index (PI) of FLS, and examined the effect of RATM oxidants on apoptosis and autophagy by fluorescence cell-sorting flow cytometry (FC). Cell cycle was analysed by FC and autophagy-related protein expression levels were measured by western blot. Our data showed that as RATM as prooxidants increased intracellular ROS (iROS) that can induce oxidative stress. Whereas iROS increased PI in FLS, these reactive species also protected cells against apoptosis by inducing autophagy. Our results indicate that ROS/TLR4-coupled activation may contribute to the pathogenesis of RA in FLS by induction of autophagy. The signalling pathway by which inflammation and its tissue destructive sequel may occur in RA underlies the need for developing therapeutic agents that can inhibit release of tissue-damaging high mobility group box 1 (HMGB1), cytokines, and possess both trace metal chelating capacity and oxidant scavenging properties in a directed combinatorial therapy for RA.     

Mutual regulation between IGF-1R and IGFBP-3 in human corneal epithelial cells

The insulin-like growth factor type 1 receptor (IGF-1R) is part of the receptor tyrosine kinase superfamily. The activation of IGF-1R regulates several key signaling pathways responsible for maintaining cellular homeostasis, including survival, growth, and proliferation. In addition to mediating signal transduction at the plasma membrane, in serum-based models, IGF-1R undergoes SUMOylation by SUMO 1 and translocates to the nucleus in response to IGF-1. In corneal epithelial cells grown in serum-free culture, however, IGF-1R has been shown to accumulate in the nucleus independent of IGF-1. In this study, we report that the insulin-like growth factor binding protein-3 (IGFBP-3) mediates nuclear translocation of IGF-1R in response to growth factor withdrawal. This occurs via SUMOylation by SUMO 2/3. Further, IGF-1R and IGFBP-3 undergo reciprocal regulation independent of PI3k/Akt signaling. Thus, under healthy growth conditions, IGFBP-3 functions as a gatekeeper to arrest the cell cycle in G0/G1, but does not alter mitochondrial respiration in cultured cells. When stressed, IGFBP-3 functions as a caretaker to maintain levels of IGF-1R in the nucleus. These results demonstrate mutual regulation between IGF-1R and IGFBP-3 to maintain cell survival under stress. This is the first study to show a direct relationship between IGF-1R and IGFBP-3 in the maintenance of corneal epithelial homeostasis.     

RNA-binding protein,human antigen R regulates hypoxia-induced autophagy by targeting ATG7/ATG16L1 expressions and autophagosome formation

Autophagy, a prosurvival mechanism offers a protective role during acute kidney injury. We show novel findings on the functional role of RNA binding protein, HuR during hypoxia-induced autophagy in renal proximal tubular cells-2 (HK-2). HK-2 cells showed upregulated expressions of HuR and autophagy-related proteins such as autophagy related 7 (ATG7), autophagy related 16 like 1 (ATG16L1), and LC3II under hypoxia. Increased autophagosome formation was visualized as LC3 puncta in hypoxic cells. Further, short hairpin-RNA-mediated loss of HuR function in HK-2 cells significantly decreased ATG7 and ATG16L1 protein expressions. Bioinformatics prediction revealed HuR motif binding on the coding region of ATG7 and AU-rich element at 3′UTR ATG16L1 messnger RNA (mRNA). The RNA immunoprecipitation study showed that HuR was predominantly associated with ATG7 and ATG16L1 mRNAs under hypoxia. In addition, HuR enhanced autophagosome formation by regulating LC3II expressions. These results show that HuR regulates ATG7 and ATG16L1 expressions and thereby mediate autophagy in HK-2 cells. Importantly, HuR knockdown cells underwent apoptosis during hypoxia as observed through the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Collectively, these findings show the crucial role of HuR under hypoxia by regulating autophagy and suppressing apoptosis in renal tubular cells.     

IGFBP-2 stimulates calcium/calmodulin-dependent protein kinase kinase 2 activation leading to AMP-activated protein kinase induction which is required for osteoblast differentiation

Insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins-2 (IGFBP-2) function coordinately to stimulate osteoblast differentiation. Induction of AMP-activated protein kinase (AMPK) is required for differentiation and is stimulated by these two factors. These studies were undertaken to determine how these two peptides lead to activation of AMPK. Enzymatic inhibitors and small interfering RNA were utilized to attenuate calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) activity in osteoblasts, and both manipulations resulted in failure to activate AMPK, thereby resulting in inhibition of osteoblast differentiation. IGFBP-2 and IGF-I stimulated an increase in CaMKK2, and inhibition of IGFBP-2 binding its receptor resulted in failure to induce CaMKK2 and AMPK activation. Injection of a peptide that contained the IGFBP-2 receptor-binding domain into IGFBP-2^−/− mice activated CaMKK2 and injection of a CaMKK2 inhibitor into normal mice inhibited both CamKK2 and AMPK activation in osteoblasts. We conclude that induction of CaMKK2 by IGFBP-2 and IGF-I in osteoblasts is an important signaling event that occurs early in differentiation and is responsible for activation of AMPK, which is required for optimal osteoblast differentiation.