青藏高原气候变化对农牧民开垦的影响

自1980年代后期以来,青藏高原持续变暖趋势明显,且增温幅度高于我国其他地区。基于遥感数据和种植适宜性模型的一些研究表明,该地区足够的农业热量资源增加了适宜耕种土地的面积,为农牧民的开垦行为创造了有利的条件。然而,对农牧民是否开垦以及开垦原因的实证研究,以及农牧民如何平衡气候变化带来的开垦机遇、风险和人口压力,仍然缺少认识。以青藏高原的3个典型产粮区域("一江两河"地区、河湟谷地、壤塘县)为研究区,利用605户农户家庭调研数据,分析了影响农牧民开垦行为的影响因素。计量结果表明,农牧民感知冬季持续时间的整体变化趋势、家庭总人口、抚养比与农牧民开垦行为呈显著正相关关系;农牧民感知降水的整体变化趋势、人均打工年收入、户主受教育水平、是否借贷、居住地距集镇距离与农牧民开垦行为呈显著负相关关系。随着城镇化的不断加快,农牧民对非农工作的认可度越来越高,加之政府的管制,使得开垦现象并不普遍。由于农牧民的开垦对青藏高原的生态环境极有可能造成不可逆的负面影响,应该提供更多的非农就业机会,促进农业集约化,加强监管,以降低开垦的可能性。     

泌桐高速公路生态护坡不同草灌混播10a后的植被群落特征

稳定的边坡群落是公路边坡生态防护的目标,为探究高速公路生态护坡工程10 a演替后群落特征,该研究以泌桐高速公路为依托,布设自然恢复、单一狗牙根播种和5个不同播种密度的草灌混播生态防护措施,分析不同恢复方式对边坡群落组成、生活型和物种多样性的影响。结果表明:(1)调查样方内共有52种植物,分属于17科49属。禾本科、菊科和豆科植物共26属29种,占种总数的55.77%,表明这三大科植物在边坡群落演替过程中起着重要作用。(2) 10 a演替后不同恢复方式下群落中多年生植物比例高于一年生草本植物。(3)在草灌混播样地中,群落物种多样性指数随着播种密度的增加呈先增加后降低的单峰变化趋势,在播种密度为每平方米500株时达到最大。(4)草灌混播的生态恢复效果优于纯草本种植和自然恢复方式。(5)播种密度对草灌混播群落类型,地上生物量和物种多样性指数没有显著影响。从植物的生长效果及成本方面考虑,初播密度每平方米为500~600株的草灌混播可构建较为稳定的边坡植物群落,实现最佳的边坡恢复效果,可应用于类似区域边坡生态恢复工程。     

环状RNA在胃癌中的研究现状与策略

环状RNA (circRNA)是一种共价闭合的非编码RNA,可以调节真核生物中的基因表达.最近应用高通量RNA测序和生物信息学方法揭示人类细胞中存在大量circRNA.许多circRNA具有一定的组织和时序特异性,且与生理发育和各种肿瘤等疾病密切相关. circRNA被证明在细胞质中富集和稳定,表明其具有作为肿瘤生物标志物的潜力.胃癌(gastric carcinoma,GC)是一种常见的恶性肿瘤,在全球癌症相关死亡原因中排第3位.尽管该疾病在诊断和治疗方面取得了许多进展,但GC患者的预后仍然很差,大多数国家的5年总生存率低于30%.因此,寻找能调节GC发生发展和评估预后的新分子机制和治疗靶标至关重要.近年来circRNA在胃癌中的研究不断增多,其在胃癌的发生发展、诊断、治疗及预后过程中扮演重要角色.本文就circRNA产生机制及一般特征、生物学功能、在胃癌中的研究进展及研究中存在的问题作一综述.     

Dexamethasone suppresses osteogenesis of osteoblast via the PI3K/Akt signaling pathway in vitro and in vivo

The hypofunction of osteoblasts induced by glucocorticoids (GCs) has been identified as a major contributing factor for GC-induced osteoporosis (GIO). However, the biological mechanism underlying the effect of GC in osteoblasts are not fully elucidated. Recent studies implicated an important role of phosphoinositide 3-kinase (PI3K)/protein kinase B(Akt) signaling pathway in the regulation of bone growth. We propose that the PI3K/Akt signaling may be implicated in the process of GC-induced osteogenic inhibition in osteoblasts. In this study, primary osteoblasts were used in vitro and in rats in vivo to evaluate the biological significance of the PI3K/Akt pathway in GC-induced bone loss. In vivo, dexamethasone (Dex)-treated rats had low bone mineral density and decreased expression levels of alkaline phosphatase (ALP), osteocalcin (OCN), and phosphorylated Akt (p-Akt) in bone tissue. In vitro study shows that Dex over the dose of 10^–8 M remarkably inhibited cellular osteogenesis, as represented by decreased cell viability, lessened ALP activity, and suppressed osteogenic protein expressions including ALP and OCN. Meanwhile, a dramatic downregulation in the PI3K/Akt pathway phosphorylation was also observed in Dex-treated osteoblasts. These changes were marked rescued by treatment with a PI3K agonist 740Y-P. Moreover, downregulation of ALP and OCN expressions by LY294002 can mimic the suppressive effects of Dex. These data together reveal that the suppressed PI3K/Akt pathway is involved in the regulatory action of Dex on osteogenesis.     

Soluble CXCL16 promotes TNF‐α‐induced apoptosis in DLBCL via the AMAD10‐NF‐κB regulatory feedback loop

We had previously identified that the co‐expression of transmembrane CXCL16 (TM‐CXCL16) and its receptor CXCR6 is an independent risk factor for poor survival in patients with diffuse large B‐cell lymphoma (DLBCL). However, the impact of the soluble form of CXCL16 (sCXCL16) on the pathogenesis of DLBCL remains unknown. In the present study, the synergistic effect of sCXCL16 and tumor necrosis factor α (TNF‐α) on apoptosis in DLBCL cell lines (OCI‐LY8 and OCI‐LY10) was investigated in vitro. sCXCL16 reinforced TNF‐α‐mediated inhibition of DLBCL cell proliferation, as determined by the cell counting kit‐8 assay. The results of annexin V staining showed that sCXCL16 enhanced TNF‐α‐induced apoptosis in OCI‐LY8 and OCI‐LY10 cells through a death receptor‐caspase signaling pathway. The results of gene microarray suggested a significant upregulation of differentially expressed genes in the TNF signaling pathway. sCXCL16 increased the concentration of extracellular TNF‐α by binding to CXCR6 to activate the nuclear factor‐κB (NF‐κB) signaling pathway. TNF‐α also induced the secretion of sCXCL16 by increasing the expression of ADAM10, which is known to cleave TM‐CXCL16 to yield sCXCL16. Moreover, bioinformatics analysis revealed that elevated TNF‐α and ADAM10 expression levels in tumor tissues predicted better survival in patients with DLBCL. Thus, our study suggests that sCXCL16 enhances TNF‐α‐induced apoptosis of DLBCL cells, which may involve a positive feedback loop consisting of TNF‐α, ADAM10, sCXCL16, and members of the NF‐κB pathway. sCXCL16 and TNF‐α may be used as prognostic markers in the clinic, and their combinational use is a promising approach in the context of DLBCL therapy.     

SubCellBarCode: Proteome-wide Mapping of Protein Localization and Relocalization

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Resolving Cell Fate Decisions during Somatic Cell Reprogramming by Single-Cell RNA-Seq

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