绿化植物的生活型对边坡植被物种多样性及护坡性能的影响

为了探讨绿化植物生活型构成对边坡植被物种多样性及护坡性能的影响, 揭示生活型构成-群落特征-物种多样性-生态系统功能间的内在联系, 借助三物种组装实验, 分别构建以草本、灌木或乔木为主体的草本型(HHX_i)、灌木型(SSX_i)、乔木型(AAX_i)或草-灌-乔混合型(HSA)配置模式的实验小区, 对实验区内边坡植被的群落特征、护坡性能进行持续4年的生态监测。结果表明: (1)边坡植被的物种丰富度与绿化植物生活型构成有关, AAX_i的物种丰富度总体高于其他模式, 呈AAX_i > SSX_i > HSA > HHX_i趋势。(2)不同配置模式边坡植被的群落盖度不一样, 年际间差异显著: 建坪初期(2010-2011年), HHX_i的群落盖度远高于其他模式, HSA次之, AAX_i最低; 2012-2013年间, HSA的群落盖度最高, HHX_i次之, AAX_i最低。(3)边坡植被的Shannon-Wiener指数、Pielou指数与绿化植物生活型构成有关, 其变化规律与群落盖度类似: 建坪初期, HHX_i的多样性水平远高于其他模式, 呈HHX_i > HSA > SSX_i > AAX_i趋势; 之后, 呈HSA > HHX_i > SSX_i > AAX_i趋势。(4)边坡植被的护坡性能与群落内的物种多样性密切相关: 多样性水平越高, 护坡性能越强。可见, 在生态护坡过程中, 绿化植物生活型构成对提高边坡植被物种多样性、改善护坡性能至关重要。     

Elevated GAPDH expression is associated with the proliferation and invasion of lung and esophageal squamous cell carcinomas

Glyceraldehyde‐3‐phosphate dehydrogenase, is one of the most investigated housekeeping genes and widely used as an internal control in analysis of gene expression levels. The present study was designed to assess whether GAPDH is associated with cancer cell growth and progression and, therefore may not be a good internal control in cancer research. Our results from clinical tissue studies showed that the levels of GAPDH protein were significantly up‐regulated in lung squamous cell carcinoma tissues, compared with the adjacent normal lung tissues, and this was confirmed by western blotting and immunohistochemistry. GAPDH knockdown by siRNA resulted in significant reductions in proliferation, migration, and invasion of lung squamous carcinoma cells in vitro. In a nude mouse cancer xenograft model, GAPDH knockdown significantly inhibited the cell proliferation and migration/invasion in vivo. In summary, GAPDH may not be an appropriate internal control for gene expression studies, especially in cancer research. The role of GAPDH in cancer development and progression should be further examined in pre‐clinical and clinical studies.     

蛋白质复合体非变性凝胶电泳技术及其应用新进展

非变性凝胶电泳技术是研究蛋白质复合体的强有力工具。重点介绍了蓝绿温和非变性凝胶电泳(BN-PAGE)技术的原理和特点,比较了由BN-PAGE衍生的蓝色温和琼脂糖凝胶电泳、清澈温和非变性凝胶电泳(CN-PAGE)和高分辨清澈温和非变性凝胶电泳(HrCN-PAGE)技术的差异和适用范围,并概括地介绍了这些技术在植物蛋白质复合体研究中应用的新进展。     

2000-2015年中国陆地生态系统蒸散时空变化及其影响因素

准确量化区域蒸散时空格局及其影响因素对理解陆地生态系统碳水循环具有十分重要的意义。近年来中国经历了严重的空气污染及气候波动,亟须探讨蒸散的时空变化及其影响因素。基于PT-JPL（Priestly-Taylor Jet Propulsion Laboratory）模型,集成遥感数据和气象数据模拟了中国陆地生态系统2000-2015年蒸散,并分析其时空变化及影响因素。结果表明：1）参数优化后PT-JPL模型可解释蒸散年际变化的68%,优于原始模型及MODIS蒸散产品;2）中国地区多年平均蒸散为440.16 mm/a,呈东南沿海到西北内陆逐渐递减的空间格局;3）2000-2015年蒸散整体呈轻微下降趋势（slope=6.48 Gt/a,P=0.17）,但具有年代际差异,2000-2010年中国地区蒸散呈显著下降趋势（slope=21.05,P < 0.01）,占全国蒸散总量45.05%的内蒙古地区、甘新地区、黄土高原地区及青藏地区解释了61.88%的年际变化;2010-2015年呈轻微上升趋势（slope=10.48,P=0.71）,各地区均无显著变化趋势;4）辐射主导了蒸散的年代际差异,分别解释了2010年前后蒸散下降及上升趋势的51.45%、85.26%。蒸散呈显著变化趋势的内蒙古地区、黄土高原地区及青藏地区主要受辐射控制,甘新地区主要受降水和温度的影响。     

当归抗抑郁作用及配伍应用

旨在探讨当归在抑郁症治疗中发挥的作用。通过分析相关文献,结合当归的临床功效和抑郁症的疾病特点,概括当归抗抑郁作用规律。当归在抑郁症治疗中具有补血以养肝体、活血以通心脉、通便以利肠腑的作用,以其为主药的抗抑郁复方临床应用广泛。当归的抗抑郁作用值得进一步深入研究。     

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.     

Identification of the Degradation Determinants of Insulin Receptor Substrate 1 for Signaling Cullin-RING E3 Ubiquitin Ligase 7-mediated Ubiquitination

Hyperactivation of mechanistic target of rapamycin complex 1 (mTORC1) and its effector kinase S6 kinase 1 (S6K1) is known to trigger multisite seryl phosphorylation of insulin receptor substrate 1 (IRS1), leading to its ubiquitination and degradation. This negative feedback inhibition functions to restrain PI3K activity and plays critical roles in the pathogenesis of cancer and type II diabetes. Recent work has implicated a role for cullin-RING E3 ubiquitin ligase 7 (CRL7) in targeting IRS1 for mTORC1/S6K1-dependent degradation. In the present study we have employed both cell-based degradation and reconstituted ubiquitination approaches to define molecular features associated with IRS1 critical for CRL7-mediated ubiquitination and degradation. We have mapped IRS1 degradation signal sequence to its N-terminal 574 amino acid residues, of which the integrity of Ser-307/Ser-312 and Ser-527, each constituting a S6K1 phosphorylation consensus site, was indispensible for supporting CRL7-forced degradation. In vitro, S6K1 was able to support the ubiquitination of bacterially expressed IRS1 N-terminal fragment by CRL7 but at low levels. In contrast, CRL7 supported efficient ubiquitination of IRS1 N-terminal fragment in hyperphosphorylated form, which was isolated from infected insect cells, suggesting requirement of additional phosphorylation by kinases yet to be identified. Finally, removal of IRS1 amino acids 1–260 led to substantial reduction of ubiquitination efficiency, suggesting a role for this region in mediating productive interactions with CRL7. The requirement of multisite phosphorylation and the N terminus of IRS1 for its turnover may ensure that complete IRS1 degradation occurs only when mTORC1 and S6K1 reach exceedingly high levels.