江苏菜豆同工凝集素的分离纯化及性质研究

江苏菜豆经酸水(PH2.0)抽提,硫酸铵分级沉淀,分离植物血球凝集素(PHA-P),分子量为128000的糖蛋白,活性回收率在80％以上,PHA-P经SP-sephadexc-50离子交换层析,分成L_4,L_3E_1,L_2E_2,L_1E_3,和E_4同工凝集素。 L_4和E_4等电点为5.4和6.5。亚基分子量分别是31000和33000,并有类似的氨基酸组成。PAGE分析为单一蛋白带。红细胞凝集活性随电泳迁移速度的加快而增强,促淋性细胞分裂活性则减弱。E_4血凝活性受CalNAc,EDTA抑制和Zn~(++)的促进。     

Prostaglandin production in the umbilical and uterine circulations in pregnant sheep at 129-136 days gestation.

Prostaglandins circulating in the maternal and foetal blood have been implicated in important physiological systems. These functions include foetal adrenal function, maintenance of patency of the ductus arteriosus, regulation of uterine and umbilical circulations, and labor and delivery type myometrial contractions. The placenta is a major site of prostaglandin production in pregnancy. Limited data are available which combine measurements of veno-arterial differences across the uterine and umbilical circulations with blood flow in these circulations to enable calculation of umbilical-placental and utero-placental production rates for the prostaglandins. In chronically instrumented pregnant ewes, between 129 and 136 days of gestation, prostaglandin F2 alpha(PGF2 alpha), 13, 14 dihydro-15-keto prostaglandin F2 alpha (PGFM), prostaglandin E2 (PGE2) were measured in the maternal carotid artery and uterine vein. Foetal PGE2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (the major metabolite of prostacyclin) were measured in umbilical venous and foetal descending aorta arterial plasma. Umbilical and uterine blood flow were measured using the diffusion-equilibrium technique. Uterine blood flow was 1693 +/- 137 ml.min-1 (mean +/- SEM); uterine production rates were 480 +/- 88 ng.min-1 for PGF2 alpha, 517 +/- 144 ng.min-1 for PGFM, and 165 +/- 27 ng.min-1 for PGE2. Umbilical blood flow was 147 +/- 17 ml.min-1.kg-1 foetal body weight. Umbilical production rates into the foetal circulation were 11 +/- 2 ng.min-1.kg-1 for PGE2 and 6 +/- 2 ng. ng.min-1.kg-1 foetal body weight for PGI2.     

植被类型变化对土壤微生物碳利用效率的影响研究进展

植被类型变化强烈影响着土壤碳循环。土壤微生物碳利用效率（CUE）是微生物将从环境中获取的碳分配给自身生长的比例,是土壤碳循环的综合指标。研究植被类型变化对CUE的影响有助于从微生物视角理解该过程中的土壤碳动态,可以为评估植被类型变化对土壤质量及生态系统碳循环的影响提供基础,具有重要的理论及实际价值。通过系统查阅相关文献,综述了植被类型变化导致的CUE变化情况,以及该过程中影响CUE的因子与机制。目前,相关研究主要涉及以林地、草地和农业用地为起点或终点的植被变化类型。天然林（原生林、次生林）变化为人工林、林地变化为草地后CUE普遍下降,随终点植被的发展CUE可能恢复至起点水平。植被成熟度越高,发生转变时CUE变化越剧烈。植被类型变化以农业用地为起点或终点时,CUE变化方向的不确定性及幅度的变异性均增加。植被类型变化导致的CUE变化主要受到植被、土壤、微生物因子及其交互作用的驱动,指示CUE的指标、采样季节和土层也会一定程度上影响CUE的变化。今后相关研究应采用直接的CUE测定方法,拓宽研究气候区及植被变化类型,关注植被变化过程中CUE变化的土层差异及动态监测,深入对植被类型变化导致的生态环境因子变化与CUE的关系及作用机制的研究。     

尺度整合视角下伊犁河谷地区生态安全格局构建——以昭苏县为例

构建生态安全格局是一种协调区域生态保护与经济发展关系的有效途径。由于生态系统服务供需差异,不同等级的行政区在生态安全格局构建中出现了空间结构错位脱节的问题。从整合视角出发,尝试整合伊犁河谷地区州级和县级两级尺度构建昭苏县生态安全格局。首先基于生态系统服务评价确定生态源地,再构建综合阻力面并采用电路理论模型识别生态廊道。研究结果显示,整合州级和县级两级尺度昭苏县共确定了24个生态源地,面积2504.47km²,主要分布于昭苏中部盆地以及北部、南部山区,土地利用类型主要为耕地、草地和林地;识别生态廊道50条,总长度200.17km。与单一尺度下生态安全格局构建相比,整合不同尺度构建生态安全格局能显著改善区域生境破碎化的问题,提高区域景观连通性。本研究提供了一种整合不同尺度下生态安全格局构建的技术框架,研究结果可为伊犁河谷地区国土空间格局优化提供有效参考。     

基于自然-经济综合视角的碳排放强度与生态盈亏多情景模拟研究——以淮海经济区为例

生态盈亏与碳排放强度是衡量生态环境质量与经济发展水平的重要指标,分析两者时空关联并预测未来演进方向对提升区域生态环境质量健康水平具有指导作用。以淮海经济区为研究对象,以2000年、2010年和2020年3期土地利用数据为基础,运用PLUS模型、双变量自相关、耦合协调度及面板计量回归模型等方法,预测并分析淮海经济区2000—2036年3种情景下碳排放强度、生态盈亏的演化特征及时空关联。结果表明：(1)常规发展情景下,淮海经济区生态性呈下降趋势,强耕地保护情景下生态性微有下降,强生态保护情景下,生态性有所上升,自然要素是主导。(2)常规发展情景下,淮海经济区碳排放量逐渐加大,强耕地保护及强生态保护情景下,则呈下降趋势;三种状态下,碳排放强度均呈下降趋势,时间轴2010—2020年降幅较大,空间序河流水系地区碳排放强度降幅较大。(3)淮海经济区碳排放强度与生态盈亏呈负相关关系,低低和低高聚类主要分布在城镇建设用地周边,高低和高高聚类分布在人类干扰较少的自然区域;高高聚类主要位于河流水系交汇区,表明水域有效降低碳排放强度的功能。(4)淮海经济区的碳排放强度与生态盈亏之间的耦合协调度呈东西高、中...     

基于分布式水文模型的水源涵养不同功能评估方法——以渭河涵养区为例

为了实现水源涵养量计算和不同功能的综合评估,基于分布式水文模型(WEP-L)提出了一种新方法,即利用WEP-L模型计算次降水过程中降水量和地表产流、冠层截留量的差值作为水源涵养量,并分别评估削洪(地表径流量)、补枯(地下径流量)、维持植被生态系统用水(植被蒸腾量)等不同水源涵养功能的评估方法。为了验证该方法的合理性,以渭河流域咸阳站以上区域为例,对比了该方法和InVEST模型方法的计算结果,由于两种方法在评估内容和使用模型上都存在差异,为了保证计算结果的可比性,先对比了基于相同评价内容的WEP-L模型法I和InVEST模型方法,再对比了基于不同评价内容的WEP-L模型法I和WEP-L模型法II,结论如下:基于相同评价内容的WEP模型法I和InVEST模型法计算结果数值接近,研究区2000-2018年水源涵养量年均值分别为12.43 mm(5.76亿m³)和12.08 mm(5.6亿m³),两种方法所得结果空间分布特征相似,稍有差异之处与InVEST模型的参数没有经过本地化处理有关;基于不同评价内容的WEP-L模型法Ⅰ和WEP-L模型法II计算结果数值相差较大,研究区2000-2018年水源涵养量均值分别为12.43 mm和432.57 mm,空间分布特征上有差异的地方分布于研究区的北部、东部及东北部,主要与两种方法评价时是否考虑蒸散发有关。WEP-L模型法II评估结果中削洪、补枯、维持植被生态系统用水等功能多年变化趋势分别为:2006-2010年期间增加、2012年以后下降以及增加。2012年后补枯功能和维持植被生态系统用水功能之间可能存在权衡关系。通过不同方法计算结果差异原因分析,证明了基于WEP-L模型的不同涵养功能评估方法的合理性,其结果也可为渭河涵养区水资源和生态保护策略的制定提供更多依据。     

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     

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.