鸿雁迁徙对停歇地的选择特征

建立合理的湿地水鸟保护地是缓解水鸟栖息地丧失和种群下降的重要手段。以往的保护地设计中,由于越冬地和和繁殖地水鸟停留时间长、种群数量大,受到较多的关注。分析湿地水鸟对停歇地的选择偏好,掌握停歇地的自然条件和人类活动特征可为水鸟保护网络优化和保护地管理提供决策依据。而在水鸟迁徙过程中,停歇地作为保护网络的重要节点也发挥了重要作用。因此选择鸿雁为伞护种,获取了29只鸿雁项圈追踪数据,分析蒙古国Khukh湖-中国东北鸭绿江口秋季迁徙路线对停歇地生境选择偏好,识别了鸿雁在湿地周边不同距离梯度下的活动频率变化。根据鸿雁停歇数据共识别停歇地63处,以此为基础分析停歇的自然条件和人类活动因素特征。结果表明,鸿雁除选择湖泊和沼泽为停歇地外,周边250m内的裸地和草地也是重要栖息地;当鸿雁停歇地人类活动较少时,鸿雁倾向于选择土壤肥沃、食物丰富区,而人类活动强度加大时,栖息地植被条件提高能够为鸿雁提供遮避条件,也吸引了更多鸿雁停歇。研究建议,在水鸟迁徙重要廊道区应增加水鸟停歇地保护区,保护区的设计应根据关键保护对象活动频率加强对湿地周边的栖息地保护,减少水滨人类活动对鸿雁停歇的负面影响;在人类活动强度较大的地区设立水鸟保护地,还应加强对植被的保护,在水鸟利用频率较高的停歇地周边进行植被修复。     

CircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR‐30a‐3p and promoting PON2

Osteoarthritis (OA) is a common joint disease featured by the deterioration of articular cartilage and chondrocyte death. Emerging evidence has indicated that circular RNAs (circRNAs) play an essential role in OA progress. Here, we found that the expression of circHIPK3 was significantly decreased in human and mouse OA cartilage. Knocking down circHIPK3 increased apoptosis and intracellular ROS level in HC‐a chondrocytes. We performed proteomic studies and identified that circHIPK3 regulated chondrocyte apoptosis through the mitochondrial pathway. Results of JC‐1 staining and western blot further confirmed that mitochondrial outer membrane permeabilization was promoted in HC‐a chondrocytes transfected by circHIPK3 siRNA. In terms of mechanism, we showed that PON2 functioned as a potential target of circHIPK3 to regulate chondrocyte apoptosis. Moreover, we revealed that circHIPK3 interacted with miR‐30a‐3p to regulate PON2 expression in chondrocytes. Taken together, our findings suggested that circHIPK3 regulated chondrocyte apoptosis by mitochondrial pathway, and targeting the circHIPK3/miR‐30a‐3p/PON2 axis might be a potential strategy for OA treatment.

The current study revealed the important role of circHIPK3 in regulating chondrocyte apoptosis and maintaining extracellular matrix (ECM) homeostasis. Mechanistically, circHIIPK3 might serve as a sponge of miR‐30a‐3p to regulate PON2 expression. The downregulation of circHIIPK3 resulted in the increased expression of miR‐30a‐3p and decreased expression of PON2, thus leading to mitochondrial pathway apoptosis and ECM destruction.     

Thioredoxin 1 supports colorectal cancer cell survival and promotes migration and invasion under glucose deprivation through interaction with G6PD

Overcoming energy stress is a critical step for cells in solid tumors. Under this stress microenvironment, cancer cells significantly alter their energy metabolism to maintain cell survival and even metastasis. Our previous studies have shown that thioredoxin-1 (Trx-1) expression is increased in colorectal cancer (CRC) and promotes cell proliferation. However, the exact role and mechanism of how Trx-1 is involved in energy stress are still unknown. Here, we observed that glucose deprivation of CRC cells led to cell death and promoted the migration and invasion, accompanied by upregulation of Trx-1. Increased Trx-1 supported CRC cell survival under glucose deprivation. Whereas knockdown of Trx-1 sensitized CRC cells to glucose deprivation-induced cell death and reversed glucose deprivation-induced migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, we identified glucose-6-phosphate dehydrogenase (G6PD) interacting with Trx-1 by HuPortTM human protein chip, co-IP and co-localization. Trx-1 promoted G6PD protein expression and activity under glucose deprivation, thereby increasing nicotinamide adenine dinucleotide phosphate (NADPH) generation. Moreover, G6PD knockdown sensitized CRC cells to glucose deprivation-induced cell death and suppressed glucose deprivation-induced migration, invasion, and EMT. Inhibition of Trx-1 and G6PD, together with inhibition of glycolysis using 2-deoxy-D-glucose (2DG), resulted in significant anti-tumor effects in CRC xenografts in vivo. These findings demonstrate a novel mechanism and may represent a new effective therapeutic regimen for CRC.     

Parasite reliance on its host gut microbiota for nutrition and survival

Studying the microbial symbionts of eukaryotic hosts has revealed a range of interactions that benefit host biology. Most eukaryotes are also infected by parasites that adversely affect host biology for their own benefit. However, it is largely unclear whether the ability of parasites to develop in hosts also depends on host-associated symbionts, e.g., the gut microbiota. Here, we studied the parasitic wasp Leptopilina boulardi (Lb) and its host Drosophila melanogaster. Results showed that Lb successfully develops in conventional hosts (CN) with a gut microbiota but fails to develop in axenic hosts (AX) without a gut microbiota. We determined that developing Lb larvae consume fat body cells that store lipids. We also determined that much larger amounts of lipid accumulate in fat body cells of parasitized CN hosts than parasitized AX hosts. CN hosts parasitized by Lb exhibited large increases in the abundance of the bacterium Acetobacter pomorum in the gut, but did not affect the abundance of Lactobacillus fructivorans which is another common member of the host gut microbiota. However, AX hosts inoculated with A. pomorum and/or L. fructivorans did not rescue development of Lb. In contrast, AX larvae inoculated with A. pomorum plus other identified gut community members including a Bacillus sp. substantially rescued Lb development. Rescue was further associated with increased lipid accumulation in host fat body cells. Insulin-like peptides increased in brain neurosecretory cells of parasitized CN larvae. Lipid accumulation in the fat body of CN hosts was further associated with reduced Bmm lipase activity mediated by insulin/insulin-like growth factor signaling (IIS). Altogether, our results identify a previously unknown role for the gut microbiota in defining host permissiveness for a parasite. Our findings also identify a new paradigm for parasite manipulation of host metabolism that depends on insulin signaling and the gut microbiota.Subject terms: Animal physiology, Microbial ecology     

大熊猫国家公园四川片区自然保护地空间关系对大熊猫分布的影响

理清自然保护地的空间关系与分布格局是加强空间管控、整合优化自然保护地体系的基础。以大熊猫国家公园四川片区内的自然保护地为案例,基于ArcGIS空间数据的处理、分析与可视化表达等功能,结合韦恩(Venn)图在空间层面上量化分析了公园范围内各类自然保护地的空间关系,并进一步揭示了不同保护情景下大熊猫(Ailuropoda melanoleuca)的分布格局。研究结果表明:(1)研究区内含有6类自然保护地,占研究区总面积的75.13%,其中40.68%为交叉重叠区域。(2)各类自然保护地皆存在大面积的交叉重叠。自然保护区为研究区面积最大的自然保护地类型,占自然保护地总面积的72.53%,其中45.89%为交叉重叠区域;其他类自然保护地占自然保护地总面积的60.87%,其中66.48%为交叉重叠区域。(3)猫点密度与自然保护地的交叉重叠程度呈现逆向增长趋势,区域的重叠水平越高,猫点密度越低。(4)自然保护地整体非重叠区的猫点密度高于重叠区。自然保护区是整体猫点密度最高的自然保护地类型,其非重叠区密度明显高于重叠区;森林公园非重叠区与水利风景区重叠区呈现较高的猫点密度。(5)与自然保护区交叉重叠...     

基于生态系统服务供求评价的空间分异特征与生态格局划分——以长三角城市群为例

生态系统服务供给与需求能力存在显著的空间异质性与空间失衡,对区域经济发展与环境保护产生巨大影响。以长三角城市群区县为研究单元,分别核算其生态系统服务供给与需求值,引入梯度分析,分析生态系统服务供给与需求的空间特征,并基于供求分析提出长三角城市群生态格局分区方案,且针对性地提出相应片区的发展策略,为长三角城市群土地利用规划、区域协调发展提供科学依据。研究结果表明:(1)长三角城市群生态系统服务供给能力与土地利用类型密切相关,呈现从北到南逐渐升高趋势;(2)长三角城市群生态系统服务需求能力与社会经济发展联系紧密,在长江入海口附近形成生态系统服务需求高值区,然后向外围递减;(3)沪宁杭庐发展梯度带上,生态系统服务供需大致呈现负相关趋势;(4)基于生态系统服务供需关系构建,得到长三角城市群生态格局四大分区:生态保育区(高供给-高需求),生态修复区(低供给-高需求),生态重塑区(低供给-低需求),生态开发区(高供给-低需求)。     

三峡库区多年高水位运行对消落带狗牙根生长恢复的影响

为深入了解三峡库区多年高水位运行对消落带优势植物生长恢复的影响,分别于2008年和2017年定量调研了库区长寿段消落带狗牙根(Cynodon dactylon)种群的变化,探讨了库区高水位运行对消落带狗牙根萌发、生长和物质分配的影响。结果表明,多年的高水位运行导致不定芽形成和萌发显著被促进,形成更多的分株;高水位运行导致狗牙根分株的株高、茎宽和叶片数被显著抑制,而叶长和种群的总叶片数被显著促进,且随着消落带水位的降低叶长呈降低趋势,而叶宽和总叶片数呈增加趋势;高水位运行导致狗牙根种群匍匐茎和地下茎的茎长、茎节数和总茎长均被显著促进,且随着消落带水位降低匍匐茎茎长和茎节数呈显著的降低趋势,而地下茎茎长和茎节数呈增加趋势;高水位运行导致狗牙根地下茎储存的干质量呈增加趋势,而分株和匍匐茎的干质量呈降低趋势,而且在种群物质分配中地下茎所占的比例呈增大趋势,低水位狗牙根种群的分株和高水位种群的匍匐茎所占的比例也呈增加趋势。因此,狗牙根不仅具有很强的耐淹和生长恢复能力,也具有很强的拓殖能力,可以作为库区中低位消落带恢复和重建的主要原生物种。     

Galectin-3 critically mediates the hepatoprotection conferred by M2-like macrophages in ACLF by inhibiting pyroptosis but not necroptosis signalling

We previously documented that M2-like macrophages exert a hepatoprotective effect in acute-on-chronic liver failure (ACLF) by inhibiting necroptosis signalling. Nevertheless, the molecular mechanism behind this hepatoprotection still needs to be further dissected. Galectin-3 (GAL3) has been reported to be critically involved in the pathogenesis of multiple liver diseases, whereas the potential role of GAL3 in ACLF remains to be explored. Herein, we hypothesised that GAL3 plays a pivotal role in the hepatoprotection conferred by M2-like macrophages in ACLF by inhibiting necroptosis. To test this hypothesis, we first assessed the expression of GAL3 in control and fibrotic mice with or without acute insult. Second, loss- and gain-of-function experiments of GAL3 were performed. Third, the correlation between GAL3 and M2-like macrophage activation was analysed, and the potential role of GAL3 in M2-like macrophage-conferred hepatoprotection was confirmed. Finally, the molecular mechanism underlying GAL3-mediated hepatoprotection was dissected. GAL3 was found to be obviously upregulated in fibrotic mice with or without acute insult but not in acutely injured mice. Depletion of GAL3 aggravated hepatic damage in fibrotic mice upon insult. Conversely, adoptive transfer of GAL3 provided normal mice enhanced resistance against acute insult. The expression of GAL3 is closely correlated with M2-like macrophage activation. Through adoptive transfer and depletion experiments, M2-like macrophages were verified to act as a major source of GAL3. Importantly, GAL3 was confirmed to hold a pivotal place in the hepatoprotection conferred by M2-like macrophages through loss- and gain-of-function experiments. Unexpectedly, the depletion and adoptive transfer of GAL3 resulted in significant differences in the expression levels of pyroptosis but not necroptosis signalling molecules. Taken together, GAL3 plays a pivotal role in the hepatoprotection conferred by M2-like macrophages in ACLF by inhibiting pyroptosis but not necroptosis signalling. Our findings provide novel insights into the pathogenesis and therapy of ACLF.Subject terms: Inflammasome, Necroptosis     

Resveratrol induces AMPK and mTOR signaling inhibition-mediated autophagy and apoptosis in multiple myeloma cells

Resveratrol,a natural compound extracted from the skins of grapes,berries,or other fruits,has been shown to have anti-tumor effects against multiple myeloma(MM)...