基于生态系统服务的山水林田湖草生态保护修复研究——以南太行地区鹤山区为例

开展山水林田湖草生态保护修复是生态文明建设的重要内容,将生态系统服务评价成果与山水林田湖草生态保护修复工程相结合,以国家第三批山水林田湖草生态保护修复试点-河南省南太行地区鹤山区为例,探究生态系统服务评价成果在区域山水林田湖草生态保护修复中的应用。结果表明,近年来鹤山区生态系统服务价值整体呈下降趋势且生态环境破坏严重。其中,2014-2017年鹤山区各土地类型二级服务ESV减少了303.95万元。研究期内,水资源供给、气体调节功能、气候调节、净化环境、水文调节、土壤保持、生物多样性和美学景观等8项生态服务价值都出现不同程度的下降;在鹤山区生态保护修复工作中需要重点关注生态系统的水文调节、净化环境、土壤保持和生物多样性等服务功能,相应的生态保护修复工程应集中在河道生态修复与湿地保护、矿山生态环境修复与土地整治、森林及生物多样性保护修复;鹤山区山水林田湖草生态保护修复工程能够提升区域生态服务价值。其中,工程实施后的生态系统服务价值总量预计能达到36407.95万元,比2017年增加7741.96万元,增长率为27%且各项生态服务价值均有提升。研究结果对鹤山区山水林田湖草生态保护修复工程的实施有一定的指导性作用。     

长白山温带森林生态系统关键要素耦合及演替过程动态模拟

认识生态系统内和生态系统间耦合机制,揭示复合生态系统功能规律,对促进我国山水林田湖草沙项目一体化修复和保护实践具有重要的意义。针对目前修复和保护工程中出现的缺乏系统性、连续性等问题,以拥有丰富生态资源的长白山温带森林生态系统为研究区域,对其关键要素"水土气生"进行耦合建模。通过分析模型的运行机理,探究重要子模块之间的相互作用以及子模块内部生态关键要素的耦合机制,并以长白山温带落叶阔叶林的组成树种和环境因素为对象构建模型参数,通过运行林窗模型1000次,得出长白山温带森林的动态演替过程。结果表明:在森林生态系统的演替过程中,"水土气生"体现为模型中有效积温、干旱天数(低于土壤凋萎点的天数)、土壤可利用氮以及可利用光,这些关键要素之间相互影响,综合决定着每棵树木的更新、生长、死亡过程。模拟结果显示在长白山温带针阔混交林的动态演替过程中0-70 a,70-170 a,170-280 a,280-400 a四个阶段分别有不同的树种组成特征,与真实演替过程比较发现模拟林具有明显的阶段性。白桦、山杨为演替先锋树种,0-70 a期间生物量共占比为55%,70 a后生物量减少最后消失;紫椴、蒙古栎、水曲柳等为过渡树种,这些树种进一步改变了生长环境。红松在170 a前生物量占比仅为3%左右,随演替的发展生物量持续增加,170-280 a期间生物量占比15%,280 a之后红松生物量占总林分的50%。该结果模拟森林动态过程符合演替规律,充分说明多关键要素"水土气生"耦合机制的合理性,对于促进生态系统尺度上多生态要素耦合的相关研究提供了科学理论基础以及方法技术。     

Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex

Long noncoding RNAs (lncRNAs) play important roles in the spatial and temporal regulation of muscle development and regeneration. Nevertheless, the determination of their biological functions and mechanisms underlying muscle regeneration remains challenging. Here, we identified a lncRNA named lncMREF (lncRNA muscle regeneration enhancement factor) as a conserved positive regulator of muscle regeneration among mice, pigs and humans. Functional studies demonstrated that lncMREF, which is mainly expressed in differentiated muscle satellite cells, promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin accessibility when muscle satellite cells are activated and start to differentiate, thereby facilitating genomic binding of p300/CBP/H3K27ac to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a novel temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration.     

An insight into planarian regeneration

BackgroundPlanarian has attracted increasing attentions in the regeneration field for its usefulness as an important biological model organism attributing to its strong regeneration ability. Both the complexity of multiple regulatory networks and their coordinate functions contribute to the maintenance of normal cellular homeostasis and the process of regeneration in planarian. The polarity, size, location and number of regeneration tissues are regulated by diverse mechanisms. In this review we summarize the recent advances about the importance genetic and molecular mechanisms for regeneration control on various tissues in planarian.MethodsA comprehensive literature search of original articles published in recent years was performed in regards to the molecular mechanism of each cell types during the planarian regeneration, including neoblast, nerve system, eye spot, excretory system and epidermal.ResultsAvailable molecular mechanisms gave us an overview of regeneration process in every tissue. The sense of injuries and initiation of regeneration is regulated by diverse genes like follistatin and ERK signaling. The Neoblasts differentiate into tissue progenitors under the regulation of genes such as egfr‐3. The regeneration polarity is controlled by Wnt pathway, BMP pathway and bioelectric signals. The neoblast within the blastema differentiate into desired cell types and regenerate the missing tissues. Those tissue specific genes regulate the tissue progenitor cells to differentiate into desired cell types to complete the regeneration process.ConclusionAll tissue types in planarian participate in the regeneration process regulated by distinct molecular factors and cellular signaling pathways. The neoblasts play vital roles in tissue regeneration and morphology maintenance. These studies provide new insights into the molecular mechanisms for regulating planarian regeneration.

Genetic and molecular mechanisms for regeneration control on various tissues in planarian.     

Effects of highly selective sensory/motor nerve injury on bone metabolism and bone remodeling in rats

Objectives:This work aimed to investigate the mechanism of selective sensory/motor nerve injury in affecting bone metabolism and remodeling.Methods:The selective sensory/motor nerve injury rat model was constructed through posterior rhizotomy (PRG), anterior rhizotomy (ARG), or anterior combined with posterior rhizotomy (APRG) at the L_4-6 sensory/motor nerves on the right side of rats. Sham-operated (SOG) rats served as control. At 8 weeks after surgery, the sciatic nerves, spinal cord segments L₅ and tibial tissues were collected for analysis.Results:the integrity of trabecular bone was damaged, the number of trabecular bone was decreased and the number of osteoclasts were increased in ARG group. ARG activated NF-κβ and PPAR-γ pathways, and inhibited Wnt/β-catenin pathway. ARG group exhibited high turnover bone metabolism. In PRG group, the trabecular bone morphology became thinner, and the number of osteoclasts was increased. NF-κβ pathway was activated and OPG/RANKL ratio was decreased in PRG group. The activated osteoclasts, reduced osteoblasts activity and lower turnover bone metabolism were observed in PRG group. Additionally, the bone metabolism in APRG group was similar to ARG group.Conclusion:The posterior rhizotomy and anterior rhizotomy induced the different degree of osteoporosis in rats, which may attribute to regulate Wnt/β-catenin, NF-κβ and PPAR-γ signalling pathways.     

A comparative study of the ability of recombinant oncolytic adenovirus,doxorubicin and tamoxifen to inhibit the proliferation of breast cancer cells

In this study, we compared the inhibitory effects of recombinant oncolytic adenovirus (Ad‐apoptin‐hTERTp‐E1a, Ad‐VT) with that of doxorubicin (DOX), a first‐line chemotherapy drug, and tamoxifen (TAM), an endocrine therapy drug, on the proliferation of breast cancer cells. We found that Ad‐VT could effectively inhibit the proliferation of breast cancer cells (p < 0.01); the inhibition rate of Ad‐VT on normal mammary epithelial MCF‐10A cells was less than 20%. DOX can effectively inhibit the proliferation of breast cancer cells and also has a strong inhibitory effect on MCF‐10A cells (p < 0.01). TAM also has a strong inhibitory effect on breast cancer cells, among which the oestrogen‐dependent MCF‐7 cell inhibition was stronger (p < 0.01), At higher concentrations, TAM also had a high rate of inhibition (>70%) on the proliferation of MCF‐10A cells. We also found that both recombinant adenovirus and both drugs could successfully induce tumour cell apoptosis. Further Western blot results showed that the recombinant adenovirus killed breast cancer cells through the endogenous apoptotic pathway. Analysis of the nude mouse subcutaneous breast cancer model showed that Ad‐VT significantly inhibited tumour growth (the luminescence rate of cancer cells was reduced by more than 90%) and improved the survival rate of tumour‐bearing mice (p < 0.01). Compared with DOX and TAM, Ad‐VT has a significant inhibitory effect on breast cancer cells, but almost no inhibitory effect on normal breast epithelial cells, and this inhibitory effect is mainly through the endogenous apoptotic pathway. These results indicate that Ad‐VT has significant potential as a drug for the treatment of breast cancer.