基于长时间序列landsat数据的科尔沁沙地土地利用演变分析

以科尔沁沙地沙丘-草甸过渡带区域主要土地覆被类型为研究对象，以1987-2017年多时相Landsat TM/OLI遥感影像解译分类为基础，参考生态学植被演替研究方法，系统分析研究区30年来的土地利用/覆被动态演变规律，研究结果表明：（1）决策树法在复杂下垫面不同覆被类型的同步识别效果较好，所有影像分类精度均达到88%以上，分类效果较好，其中2017年分类精度最高为95.24%，达到了分类研究的要求；（2）研究区存在着"半灌丛-草甸地-灌丛"的植被结构特征，且整体表现为"南进北退"的变化趋势。结合土地利用动态度分析结果表明人类活动干涉下，研究区整体上遵循了半干旱区植被条件改善的一般规律，侧面反映该研究区域生态环境的持续不稳定性和脆弱性；（3）研究区覆被类型发生变化的总面积达到2623.59 hm²，总变化强度为63.76%。其中正向演替的比例为52.61%，以半灌丛面积的持续减小与沙地草甸面积的持续扩张为主要变化特征。但同时，半灌丛转为沙地的面积为184.95 hm²，表明以放牧为主的研究区同时发生着局部的逆行演变；（4）质心迁移结果反映了1987-2017年间，除人为影响较大的林地、草地以及耕地向北迁移外，其他植被类型的质心都有很明显的南迁，主要植被类型重心迁移距离依次由大到小为耕地 > 半灌丛 > 灌丛 > 沙地草甸 > 湿地草甸 > 林地。研究通过记录科尔沁沙地连续扩展的时空模式，展示了遥感-生态和时间序列影像在30 m分辨率下跟踪土地利用/覆被变化的潜力，为提高干旱半干旱区土地利用情况的动态监测效率，开展土地利用/覆被动态演变研究提供参考。     

miR‐124a inhibits the proliferation and inflammation in rheumatoid arthritis fibroblast‐like synoviocytes via targeting PIK3/NF‐κB pathway

Abnormal hyperplasia of fibroblast‐like synoviocytes (FLS) leads to the progression of rheumatoid arthritis (RA). This study aimed to investigate the role of miR‐124a in the pathogenesis of RA. The viability and cell cycle of FLS in rheumatoid arthritis (RAFLS) were evaluated by Cell Counting Kit 8 and flow cytometry assay. The expression of PIK3CA, Akt, and NF‐κB in RAFLS was examined by real‐time PCR and Western blot analysis. The production of tumour necrosis factor (TNF)‐α and interleukin (IL)‐6 was detected by ELISA. The joint swelling and inflammation in collagen‐induced arthritis (CIA) mice were examined by histological and immunohistochemical analysis. We found that miR‐124a suppressed the viability and proliferation of RAFLS and increased the percentage of cells in the G1 phase. miR‐124a suppressed PIK3CA 3'UTR luciferase reporter activity and decreased the expression of PIK3CA at mRNA and protein levels. Furthermore, miR‐124a inhibited the expression of the key components of the PIK3/Akt/NF‐κB signal pathway and inhibited the expression of pro‐inflammatory factors TNF‐α and IL‐6. Local overexpression of miR‐124a in the joints of CIA mice inhibited inflammation and promoted apoptosis in FLS by decreasing PIK3CA expression. In conclusion, miR‐124a inhibits the proliferation and inflammation in RAFLS via targeting PIK3/NF‐κB pathway. miR‐124a is a promising therapeutic target for RA.     

Genetic diversity and relationship of Fritillaria thunbergii Miq. landraces and related taxa

Genetic diversity and differentiation of four landraces of Fritillaria thunbergii Miq. and two congeners Fritillaria cirrhosa D. Don and Fritillaria anhuiensis S. C. Chen et S. F. Yin were evaluated using ISSR markers. The results showed that the genetic diversity of F. thunbergii was high at the specie level but relatively lower at the landrace level. A high level of genetic differentiation among four F. thunbergii landraces was detected based on the gene differentiation coefficient and the AMOVA, in line with the low inter-landrace gene flow. MS-tree analysis showed that the four F. thunbergii landraces were clustered on adjacent positions of the tree, and that Kuanye (Ft-KY) landrace was relatively distantly related to other landraces. In line with the MS-tree analysis, PCoA revealed that the three species of Fritillaria can be divided into two groups and three subgroups, among which there occurred a remarkable genetic differentiation.     

混交对亚热带针叶树根际土壤氮矿化和微生物特性的影响

混交阔叶树是退化红壤区针叶林改造的重要措施之一，土壤养分供应和转化是评价混交效应的重要参数，但混交后针叶树根际土壤氮矿化特征及其影响因素还不清楚。选取退化红壤区马尾松（Pinus massoniana Lamb.）纯林、湿地松（Pinus elliottii Engelmann）纯林及其补植木荷（Schima superba Gardn.et Champ.）形成的马-木混交林和湿-木混交林为研究对象，采集4种林分下针叶树根际土壤，测定速效养分含量、氮矿化速率、氮水解酶活性和微生物磷脂脂肪酸含量，探究混交对针叶树根际土壤氮供应及微生物特性的影响，分析土壤氮矿化和微生物特性间的相关性。结果表明：混交显著增加了针叶树根际土壤铵态氮，矿质氮和有效磷含量，而对硝态氮影响不显著。根际土壤氮矿化以硝化作用为主，混交后针叶树根际土壤氨化速率降低了27.0%，硝化速率增加了55.4%，而最终净氮矿化速率增加了24.1%。两个树种间，马尾松根际土壤矿质氮含量和净氮矿化速率显著高于湿地松。针叶树根际土壤真菌、丛枝菌根真菌，总微生物生物量及真菌/细菌比在混交后显著增加，且马尾松根际土壤总微生物和真菌生物量分别比湿地松高18.9%和27.0%。同时，针叶树根际土壤β-N-乙酰氨基葡萄糖苷酶活性在混交后显著增强，且根际土壤硝化速率和净氮矿化速率与微生物指标和酶活性正相关。总的来说，混交阔叶树显著提高了针叶树根际土壤氮供应，以此应对阔叶树混交后带来的养分竞争压力，而马尾松倾向于积极性的应对策略，通过增加土壤氮矿化以适应外界环境改变。     

研究报告: 组织蛋白酶B介导NLRP3小体在砷致小胶质细胞炎症激活中的作用

目的 探究组织蛋白酶B（CTSB）介导NLRP3小体在砷致小胶质细胞（BV-2）炎症激活中的作用。方法 取处于对数生长期的BV-2细胞，分别暴露于终浓度为0、2、4、8 μmol/L亚砷酸钠（NaAsO₂）溶液培养24 h，检测细胞活性，测定各组细胞内CTSB和细胞焦亡相关蛋白NLRP3、Caspase-1、IL-18、IL-1β的表达水平。流式细胞仪检测胞内溶酶体膜稳定性。基于实验结果，增设CTSB抑制剂组（5 μmol/L CA074-Me +8 μmol/L NaAsO₂、10 μmol/L CA074-Me+8 μmol/L NaAsO₂），检测两组细胞内炎症相关蛋白NLRP3、Caspase-1和IL-1β、IL-18的表达水平。结果 与对照组比较，各染砷组细胞抑制率增高，呈现剂量效应关系，溶酶体膜稳定性下降，差异有统计学意义（P<0.01），胞内CTSB、NLRP3、IL-1β、IL-18、Caspase-1表达增高，差异有统计学意义（P<0.01）；与对照组（8 μmol/L NaAsO₂）比较，抑制剂组BV-2细胞胞内CTSB、NLRP3、IL-1β、IL-18、Caspase-1水平均降低，差异有统计学差异（P<0.01）。结论 NaAsO₂通过诱导小胶质细胞内CTSB水平的上升，介导NLRP3炎症小体激活小胶质细胞，促其释放炎性因子，致神经系统损伤。     

Exosomal transfer of miR-106a-5p contributes to cisplatin resistance and tumorigenesis in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC), a subclass of cancers of the neck and head, is a predominant cause of cancer-associated death worldwide. Hence, there is a critical need for research into NPC-related treatment strategies. Cisplatin is a promising therapy option for NPCs and other cancers that is frequently utilized. Some patients acquire resistance to cisplatin therapy, which complicates the successful use of cisplatin treatment in NPCs. Although exosomal transfer of oncogenic miRNAs has been shown to improve recipient cell proliferation, metastasis and chemoresistance, the molecular mechanism behind this effect on NPC has yet to be fully understood. Exosomal microRNAs (miRNAs) from cisplatin-resistant cells were identified as significant mediators of chemoresistance in NPC cells in this investigation. Initially, we found that exosomal miR-106a-5p levels in the serum of chemoresistant and last-cycle patients were greater than in that of non-resistant and first-cycle patients. Also, exosomal miR-106a-5p enhanced the proliferative ability of NPC cells. Mechanistically, exosomal miR-106a-5p targets ARNT2, which further activates AKT phosphorylation, and thus promotes NPC cell proliferation, decreases apoptosis and in turn regulates tumorigenesis. We found similar results using in vivo NPC models, where exosomal miR-106a-5p through regulation of ARNT2 (aryl hydrocarbon receptor nuclear translocator 2) promoted tumorigenesis. Taken together, these findings indicate that exosomal miR-106a-5p could be a promising diagnostic biomarker and drug target for patients with NPC.