2001-2019年中国自然保护区生态环境质量时空变化特征及其驱动力

自然保护区对维护生物多样性,改善生态环境质量具有重要作用。然而,我国自然保护区生态环境质量变化及其对自然因素与人类活动的响应规律还不清晰,理解这些规律对我国的生态文明建设以及生物多样性的保护具有重要意义。基于2001—2019年中国历史高分辨率生态环境质量数据CHEQ数据集以及自然因素,利用Theil-Sen Median趋势分析、Mann-Kendall检验以及多元回归残差分析等方法,探究了2001—2019年中国自然保护区的生态环境质量时空变化特征及其对自然因素与人类活动驱动因素的响应。结果表明：(1)我国自然保护区的CHEQ指数呈现多阶段波动变化,总体呈小幅度下降趋势,平均趋势率为-0.54×10^-3/a;在空间上,中国自然保护区CHEQ变化趋势值呈“南高北低,东高西低”的分布格局;(2)自然因素与人类活动的共同作用是我国自然保护区生态环境质量恶化的主要原因,且恶化区域主要分布在自然保护区的实验区和缓冲区。其中自然因素对我国自然保护区生态环境质量变化的影响在-3×10^-3/a—0/a之间,人类活动的影响在-1×10^-3     

铁线蕨中间纤维的研究及某些植物类角蛋白的比较分析

应用整装电镜制样技术,结合选择性抽提方法在铁线蕨（ＡｄｉａｎｔｕｍｐｈｉｌｉｐｐｅｎｓｅＬ．）叶细胞中观察到直径１０ｎｍ的纤维网络结构。免疫印迹结果显示：经选择性抽提得到的纤维蛋白与动物角蛋白抗体有免疫交叉反应,间接免疫荧光标记也得到类似结果,而且此类蛋白能在体外自组装为１０ｎｍ或更粗的纤维。说明蕨类植物细胞中存在类角蛋白中间纤维网络。免疫印迹结果表明,螺旋藻（ＳｐｉｒｕｌｉｎａｓｕｂｔｉｌｌｉｓｉｎａＫｕｔｚ．）细胞,地钱（ＭａｒｃｈａｎｔｉａｐｏｌｙｍｏｒｐｈａＬ．）叶状体,铁线蕨（Ａ．ｐｈｉｌｉｐｐｅｎｓｅＬ．）、银杏（ＧｉｎｋｇｏｂｉｌｏｂａＬ．）、白菜（ＢｒａｓｉｃａｐｅｋｉｎｅｎｓｉｓＲｕｐｒ．）的叶组织经选择性抽提后得到的蛋白均与动物角蛋白抗体有免疫交叉反应。其中,螺旋藻仅含有两种类酸性角蛋白,而其余４种植物材料均含有３种类酸性角蛋白及３种类碱性角蛋白。结合以往实验结果,我们认为类角蛋白在植物细胞中是普遍存在的。     

Expression of BMP2/4/7 during the odontogenesis of deciduous molars in miniature pig embryos

Bone morphogenetic proteins (BMPs) play important roles in tooth development. However, their expression has not been studied in miniature pigs, which have many anatomical similarities in oral and maxillofacial region compared to human. This study investigated BMP2/4/7 expression patterns during deciduous molar development in miniature pigs on embryonic days (E) 40, 50, and 60. The mandibles were fixed, decalcified, and embedded before sectioning. H&E staining, immunohistochemistry, in situ hybridization using specific radionuclide-labeled cRNA probes, and real-time PCR were used to detect the BMP expression patterns during morphogenesis of the third deciduous molar. H&E staining showed that for the deciduous third molar, E40 represented the cap stage, E50 represented the early bell stage, and E60 represented the late bell stage or secretory stage. BMP2 was expressed in both the enamel organ and in the dental mesenchyme on E40 and E50 and was expressed mainly in pre-odontoblasts on E60. BMP7 expression was similar to BMP2 expression, but BMP7 was also expressed in the inner enamel epithelium on E60. On E40, BMP4 was expressed mainly in the epithelium, with some weak expression in the mesenchyme. On E50, BMP4 expression was stronger in the mesenchyme but weaker in the epithelium. On E60, BMP4 was expressed mainly in the mesenchyme. These data indicated that BMP2/4/7 showed differential spatial and temporal expression during the morphogenesis and odontogenesis of deciduous molars, suggesting that these molecules were associated with tooth morphogenesis and cell differentiation.     

Applications of functional gene microarrays for profiling microbial communities

Functional gene arrays (FGAs) have been considered as a specific, sensitive, quantitative, and high throughput metagenomic tool to detect, monitor and characterize microbial communities. Especially GeoChips, the most comprehensive FGAs have been applied to analyze the functional diversity, composition, structure, and metabolic potential or activity of a variety of microbial communities from different habitats, such as aquatic ecosystems, soils, contaminated sites, extreme environments, and bioreactors. FGAs are able to address fundamental questions related to global change, bioremediation, land use, human health, and ecological theories, and link the microbial community structure to environmental properties and ecosystem functioning. This review focuses on applications of FGA technology for profiling microbial communities, including target preparation, hybridization and data processing, and data analysis. We also discuss challenges and future directions of FGA applications.     

Omentin protects against LPS-induced ARDS through suppressing pulmonary inflammation and promoting endothelial barrier via an Akt/eNOS-dependent mechanism

Acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary inflammation and endothelial barrier permeability. Omentin has been shown to benefit obesity-related systemic vascular diseases; however, its effects on ARDS are unknown. In the present study, the level of circulating omentin in patients with ARDS was assessed to appraise its clinical significance in ARDS. Mice were subjected to systemic administration of adenoviral vector expressing omentin (Ad-omentin) and one-shot treatment of recombinant human omentin (rh-omentin) to examine omentin''s effects on lipopolysaccharide (LPS)-induced ARDS. Pulmonary endothelial cells (ECs) were treated with rh-omentin to further investigate its underlying mechanism. We found that a decreased level of circulating omentin negatively correlated with white blood cells and procalcitonin in patients with ARDS. Ad-omentin protected against LPS-induced ARDS by alleviating the pulmonary inflammatory response and endothelial barrier injury in mice, accompanied by Akt/eNOS pathway activation. Treatment of pulmonary ECs with rh-omentin attenuated inflammatory response and restored adherens junctions (AJs), and cytoskeleton organization promoted endothelial barrier after LPS insult. Moreover, the omentin-mediated enhancement of EC survival and differentiation was blocked by the Akt/eNOS pathway inactivation. Therapeutic rh-omentin treatment also effectively protected against LPS-induced ARDS via the Akt/eNOS pathway. Collectively, these data indicated that omentin protects against LPS-induced ARDS by suppressing inflammation and promoting the pulmonary endothelial barrier, at least partially, through an Akt/eNOS-dependent mechanism. Therapeutic strategies aiming to restore omentin levels may be valuable for the prevention or treatment of ARDS.Acute respiratory distress syndrome (ARDS) is a devastating condition with a 30–60% mortality rate.^{1, 2} Although the pathogenesis of ARDS is complex, the inflammatory response and endothelial barrier disruption play important roles in the development of ARDS.^{3, 4, 5} Therefore, in addition to conventional anti-inflammatory treatments, therapeutic strategies aim to restore pulmonary endothelial barrier integrity and function through regulating inter-endothelial AJs and the endothelial cytoskeleton to minimize protein leakage and leukocyte infiltration under ARDS conditions.^{6, 7}Obesity, especially visceral obesity, has clearly been shown to impair systemic vasculature and to lead to the initiation and progression of vascular disorders.^{8, 9, 10} Although different from the well-documented impacts of obesity on cardiovascular disease, the relationships between obesity and ARDS have not been well elucidated. Clinical and experimental data focused on pertinent physiological changes in obesity indicate that the obesity may alter ARDS pathogenesis by ‘priming'' the pulmonary endothelial barrier for insult and amplifying the early inflammatory response, thus lowering the threshold to initiate ARDS.^{11, 12} Contrary to conventional dogma, adipose tissue is now appreciated as an important endocrine tissue that secretes various bioactive molecules called adipokines, which contribute to the progression of diverse vascular diseases, including hypertension, cardiovascular disease and atherosclerosis.^{13, 14, 15, 16} Although ARDS is not a classified pulmonary vascular disease, it is a severe inflammatory lung condition with widespread pulmonary endothelial breakdown. Clinical evidence has indicated that the obesity might be an emerging risk factor for ARDS and that circulating adipokines levels are associated with the initiation and progression of ARDS.^{11, 12, 17, 18} Moreover, experimental studies have suggested that some anti-inflammatory adipokines, such as adiponectin and apelin, exert beneficial actions on ARDS.^{19, 20, 21}Omentin is an anti-inflammatory adipokine that is abundant in human visceral fat tissue.^{22, 23} Paradoxically, higher circulating omentin-1 levels are present in lean and healthy individuals compared with the obese and diabetic patients. Moreover, as a novel biomarker of endothelial dysfunction, reduced circulating omentin levels are related to the pathological mechanism of obesity-linked vascular disorders, including type 2 diabetes, atherosclerosis, hypertension and cardiovascular disease.^{24, 25, 26, 27, 28} Furthermore, experimental studies have found that omentin stimulates vasodilation in isolated blood vessels and suppresses cytokine-stimulated inflammation in endothelial cells (ECs).^{29, 30, 31} Thus, these data suggest that omentin may protect against obesity-related vascular complications through its anti-inflammatory and vascular-protective properties; however, little is known regarding its role in lung tissue. It was reported that decreased circulating omentin-1 levels could be regarded as an independent predictive marker for the obstructive sleep apnea syndrome and that omentin protects against pulmonary arterial hypertension through inhibiting vascular structure remodeling and abnormal contractile reactivity.^{32, 33, 34} However, to our knowledge, no study has assessed the impact of omentin on ARDS.Akt-related signaling pathways function as an endogenous negative feedback mechanism in response to the injurious stimulus. Our prior studies have demonstrated that Akt-related signaling contributes to protection against ARDS.^{35, 36} Moreover, omentin has been reported to exert anti-inflammatory, pro-survival and pro-angiogenic functions in various cells via an Akt-dependent mechanism.^{30, 31, 37, 38, 39, 40, 41, 42}Collectively, given that ARDS is ultimately an obesity-related disorder of vascular function and that omentin is a favorable pleiotropic adipokine capable of anti-inflammatory, pro-angiogenic and anti-apoptotic abilities; omentin may exert beneficial effects on ARDS. In the present study, we first aimed to appraise the clinical significance of omentin in ARDS and then specifically evaluated its impact on inflammation and the endothelial barrier. Furthermore, we mechanistically investigated the role of Akt-related signaling pathways in these effects induced by omentin in vivo and in vitro.     

Programmed cell death and aerenchyma formation in roots

Lysigenous aerenchyma contributes to the ability of plants to tolerate low-oxygen soil environments, by providing an internal aeration system for the transfer of oxygen from the shoot. However, aerenchyma formation requires the death of cells in the root cortex. In maize, hypoxia stimulates ethylene production, which in turn activates a signal transduction pathway involving phosphoinositides and Ca2+. Death occurs in a predictable pattern, is regulated by a hormone (ethylene) and provides an example of programmed cell death.     

p47(phox) PX domain of NADPH oxidase targets cell membrane via moesin-mediated association with the actin cytoskeleton

Activation of phagocytic NADPH oxidase requires association of its cytosolic subunits with the membrane-bound flavocytochrome. Extensive phosphorylation of the p47(phox) subunit of NADPH oxidase marks the initiation of this activation process. The p47(phox) subunit then translocates to the plasma membrane, bringing the p67(phox) subunit to cytochrome b558 to form the active NADPH oxidase complex. However, the detailed mechanism for targeting the p47(phox) subunit to the cell membrane during activation still remains unclear. Here, we show that the p47(phox) PX domain is responsible for translocating the p47(phox) subunit to the plasma membrane for subsequent activation of NADPH oxidase. We also demonstrate that translocation of the p47(phox) PX domain to the plasma membrane is not due to interactions with phospholipids but rather to association with the actin cytoskeleton. This association is mediated by direct interaction between the p47(phox) PX domain and moesin.     

Synthesis and biological evaluation of 9-fluorenone derivatives for SPECT imaging of α7-nicotinic acetylcholine receptor

The α7-nicotinic acetylcholine receptor (α7-nAChR) subtype, is found to have a connection with the pathogenesis of a variety of psychiatric and neurological disorders. Herein, we report the development of radioiodinated 9-fluorenone derivatives as single-photon emission computed tomography (SPECT) imaging tracers for α7-nAChRs. Among the derivatives, the best member of the series 10 (Ki = 2.23 nM) were radiolabeled with ¹²⁵I for in vitro and in vivo studies. The radiotracer [¹²⁵I]10 exhibited robust brain uptake and specifically labeled α7-nAChRs with a peak uptake value of 9.49 ± 0.87%ID/g in brain. Blocking studies demonstrated that the tracer was highly specific toward α7-nAChR. Furthermore, ex vivo autoradiography and micro-SPECT/CT dynamic imaging in mice confirmed the excellent imaging properties. In addition, molecular docking was also performed to rationalize the potency of the chosen compounds towards α7-nAChRs. To conclude, compound 10 could serve as a promising radiotracer for the α7-nAChRs.     

槭属的系统演化与地理分布

槭属（Acer L．）属槭树科（Aceraceae）,200种,分布于亚、欧、北美和非洲北缘。本文研究了槭属的系统演化、地理分布、起源与扩散。认为：（1）槭树科与无患于科关系密切,槭属是槭树科2属中较进化的类群。（2）在原始而典型的槭属植物的基础上,槭属沿花的各部减少,有的器官甚至向完全退化的方向演化,但也有少数向增加数目的方向特化。（3）讨论了槭属4亚属23组的演化趋势,并绘制出其系统演化图。（4）槭属起源于侏罗纪的中国四川东部、湖北、湖南及其邻近地区,并向西、东北和南方扩散而进入西亚、欧洲、非洲北缘、北美洲和马来半岛至印尼。