中国省域旅游业碳中和时空分异与模拟

旅游业碳中和的实现对于旅游业的绿色高质量发展和可持续发展至关重要。基于全国尺度以30个省份为分析单元,在承接团队前期关于旅游业碳达峰研究成果的基础上,借助土地利用数据、碳吸收系数和灰色预测模型分别测算与模拟了近20年和未来40年各省旅游业碳汇,通过旅游业碳中和指数反映旅游业碳排放和旅游业碳汇之间的动态变化,并利用空间自相关探索旅游业碳中和指数的时空差异。结果表明：（1）未来40年,我国省域旅游业碳汇总体呈现出"南北高,中间低"的空间分布特征,大多数省份的旅游业碳汇不断增长。东北部地区和长江流域以南各地区的旅游业碳汇较为富余,华东地区的山东、江苏和上海等省份的旅游业碳汇则相对匮乏。（2）不同情景中,低碳情景下的旅游业碳中和实现情况最好,有云南、四川和青海等7个省份在2060年之前实现了旅游业碳中和,而中等情景和基准情景下均仅有黑龙江和云南2个省份能够如期或提前实现。其中,西部和北部沿边省份的旅游业碳中和实现情况都要优于其它地区。（3）各省旅游业碳中和指数在未来40年的等级分区大致呈现出从Ⅰ级区逐步向Ⅴ级区转变的趋势,我国总体旅游业碳赤字率由2030年的96.67%逐渐降至2060年的76.67%。（4）未来40年,我国省域旅游业碳中和指数在空间上总体处于集聚态势,热点和冷点的空间分布特征较为明显,且演化趋势较为稳定。其中,热点区和次热点区主要分布在西北、西南、华南和东北地区,冷点区和次冷点区集中分布在华北、华中和华东地区。研究有效探讨了旅游业碳中和研究的理论与范式,并为中国旅游业碳中和的实现提供了一定的现实参考。     

钱江源国家公园森林物种组成和群落结构

全面了解以国家公园为主体的自然保护地体系木本植物物种组成,特别是珍稀濒危物种,分析其区系特征及不同植被类型群落结构现状,对国家公园物种保护和不同植被类型恢复具有重要指导意义。基于对钱江源国家公园全域的木本植物调查,详细分析了不同胸径大小级森林植被类型的物种组成、区系特征、种-个体曲线分析和结构特征。调查涵盖313个木本物种,温带分布的科多于热带分布的科(22/35),热带分布的属略少于温带分布的属(28/31);中国特有属7个,特有种101个,中国珍稀保护物种10个,世界自然保护联盟(IUCN)红色名录的近危、易危和濒危物种17个。在同等取样水平下,物种多样性在常绿阔叶林最高,天然针叶林次之,杉木林最低;全域所有个体及各林型的径级分布总体呈现明显的倒"J"形,群落总体上更新良好。研究发现钱江源国家公园物种丰富,但由于包含较多次生林等植被类型,整体温带多于热带区系成分,亟待采取措施恢复至典型中亚热带常绿阔叶林植被;研究对钱江源国家公园木本植物物种的多样性及其更新情况等科学和保护实践急需解决的基本问题做出了回答,也为未来钱江源国家公园生物多样性保护和恢复提供了科学依据。     

亚热带森林转换对土壤无脊椎动物群落结构的影响

受人类活动干扰的增加,亚热带森林频繁转换为次生林和人工林,可能显著影响土壤无脊椎动物群落结构及其生态功能,但当前的认识并不一致。因此,于2022年7月调查了亚热带天然常绿阔叶林转换为次生林、米槠人工林、杉木人工林后土壤无脊椎动物群落结构特征。共捕获土壤无脊椎动物659只,丰度为26540只/m²,隶属1门6纲13目59科,其中蚁科和球角 虫 兆 科为优势类群。森林转换改变了土壤无脊椎动物群落组成和多样性。天然林向米槠人工林和杉木人工林转换后,土壤无脊椎动物丰度和类群均明显降低,其中大型土壤无脊椎动物丰度的响应更为敏感,在2种林型中分别显著降低了33.58%和36.53%。尽管林型转换对土壤无脊椎动物群落多样性指数无显著影响,但改变了土壤无脊椎动物群落组成,其中天然林与杉木人工林群落组成极不相似(J ＜ 0.25),等节 虫 兆 科为杉木人工林优势类群,占比达到59.84%。冗余分析显示,土壤湿度、凋落物现存量和凋落物磷含量是影响土壤无脊椎动物群落的主要因子,对土壤无脊椎动物群落的解释率为69.30%。可见,林型转换可能通过改变土壤理化性质和凋落物质量,调控土壤无脊椎动物群落结构。     

一株兔源A型多杀性巴氏杆菌的分离鉴定和全基因组测序及分析

【背景】多杀性巴氏杆菌可导致猪肺疫、牛出血性败血症和兔出血性败血症等多种疾病,严重威胁多种动物畜牧养殖业的健康发展。【目的】重庆某兔场送检一批病死兔,为研究其病原和治疗方法,对病原进行了微生物分离和全基因组测序分析。【方法】从2022年重庆某兔场送检兔病料中进行细菌分离纯化、生化试验、16S rRNA基因鉴定、荚膜血清型分型、药敏试验和毒力基因检测,同时通过全基因组测序结果进行毒力、耐药基因注释和遗传进化等分子生物学信息分析。【结果】该菌为兔源A:ST74多杀性巴氏杆菌,命名为LXSS001,基因组序列上传到NCBI数据库(登录号为CP119523.1),药敏试验显示该菌对四环素、杆菌肽、复方新诺明和磺胺异恶唑耐药,对头孢噻肟、头孢哌酮和丁胺卡那等药物敏感。全基因组长度为2 480 671 bp,并注释到了58个毒力基因和9类药物的靶向抗药基因。通过联合建树表明其与3480株一致性最高。【结论】本研究完成了一株A型多杀性巴氏杆菌的分离鉴定和全基因组测序,并揭示了其与国内外其他分离株的进化关系,为多杀性巴氏杆菌的后续研究提供了参考依据。     

中国禾本科植物内生真菌研究4.Epichlo(e) yangzii的人工杂交

作者首先研究Epichloe yangzii植株上的人工杂交,明确了供试菌株的交配型.然后将分离自无子座鹅观草属植物的23株"Neotvphodium属"真菌孢子分别与E.yangzii的子座杂交,其中发现有21株与E yangzii(mat-1,mat-2)杂交不亲和,有2株与E yangzii(mat-1)杂交亲和.利用tubB基因片段对8株"Neotyphodium属"真菌菌株进行系统发育分析,结果表明与E yangzii杂交亲和的2个菌株和E.yangzii聚为一枝,而其它6个菌株形成独立的分枝,进一步证实了这2个菌株足有时在宿主植物上不形成子座的Eyangzii.这说明了在宿主植物上的人工杂交是区别有时不产子座的E yangzii和Neotyphodium属真菌的有效手段.     

DNASE1L3 inhibits proliferation,invasion and metastasis of hepatocellular carcinoma by interacting with β‐catenin to promote its ubiquitin degradation pathway

As a member of the deoxyribonuclease 1 family, DNASE1L3 plays a significant role both inside and outside the cell. However, the role of DNASE1L3 in hepatocellular carcinoma (HCC) and its molecular basis remains to be further investigated. In this study, we report that DNASE1L3 is downregulated in clinical HCC samples and evaluate the relationship between its expression and HCC clinical features. In vivo and in vitro experiments showed that DNASE1L3 negatively regulates the proliferation, invasion and metastasis of HCC cells. Mechanistic studies showed that DNASE1L3 recruits components of the cytoplasmic β‐catenin destruction complex (GSK‐3β and Axin), promotes the ubiquitination degradation of β‐catenin, and inhibits its nuclear transfer, thus, decreasing c‐Myc, P21 and P27 level. Ultimately, cell cycle and EMT signals are restrained. In general, this study provides new insight into the mechanism for HCC and suggests that DNASE1L3 can become a considerable target for HCC.

Decreased expression of DNASE1L3 is associated with poor prognosis in patients with HCC DNASE1L3 inhibits the proliferation and cell cycle of HCC cells in vitro and promotes the invasion and metastasis of HCC cells DNASE1L3 inhibits the tumorigenicity and metastasis of HCC cells in vivo DNASE1L3 interacts with β‐catenin and promotes its binding to the β‐catenin destroying complex DNASE1L3 interacts with P21 and stabilizes P21 by mediating the deubiquitin activity     

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.