三江平原七星河流域湿地植物多样性及影响因素

湿地植物多样性是生物多样性的重要组成部分,在维护湿地生态功能和湿地生态系统稳定性方面发挥着极其重要的作用。为研究七星河流域湿地植物的多样性,选择七星河流域的七星河国家级自然保护区和三环泡国家级自然保护区,分别于2016年和2017年,对该流域内湿地植物进行了实地植物样方调查,共计调查194个样方,利用TWINSPAN进行了样方群落划分,并采用广义线性模型分析了影响植物多样性的影响因素。结果表明七星河流域湿地植物共有532种,隶属于80科,212属,主要群落类型为湿苔草-隐果苔草群丛;狭叶甜茅群丛;萍蓬草-狐尾藻群丛;漂筏苔草群丛;小叶章-臌囊苔草群丛;甜茅-芦苇群丛;芦苇群丛;貉藻群丛等,狭叶甜茅群丛物种多样性较单一,芦苇群丛的物种多样性较丰富。广义线性模型分析结果得出物种多样性与植被密度密切相关,植被密度越大,物种的多样性越小。为七星河流域物种多样性研究提供了重要的基础数据。     

Responses of soil labile organic carbon and water-stable aggregates to reforestation in southern subtropical China

中国南亚热带土壤易分解有机碳和水稳性团聚体对造林的响应 造林被认为可以提高土壤碳稳定性并促进土壤碳累积。然而,实验结果差异很大,造林在提高土壤碳稳定性方面的作用仍存在争议。因此,在森林生态系统中不同土壤碳库对造林如何响应目前尚不清楚。基于此,本文对亚热带地区的尾叶桉林(Eucalyptus urophylla)、厚荚相思林(Acacia crassicarpa)、 红锥林(Castanopsis hystrix)、10树种混交林和自然恢复草坡等5种不同林型的土壤碳组分进行了研究,评估其不同土层(0–10、10–20、20–40 和40–60 cm)中的土壤易分解有机碳(容易被高锰酸钾氧化的有机碳ROC和土壤可溶性有机碳DOC)及土壤团聚体相关的碳对造林的响应。实验结果表明,造林(与自然恢复草坡比较)和林型并没有显著影响土壤ROC浓度,而自然恢复草坡土壤的DOC浓度在4个土层中均最高。0–10 cm土层中各径级的土壤团聚体其碳(C)浓度均是红锥林最高。此外,在任一土层中,林型对不同径级土壤水稳性团聚体比例的影响均不显著。但是土壤深度显著改变土壤团聚体的分布,0–20 cm土层主要为>0.25 mm粒径的团聚体,20–60 cm土层则是0.053–2 mm粒径的团聚体占主导。这些结果显示造林和林型影响土壤DOC 和团聚体C,而且它们相比于ROC对造林的响应更为敏感。研究发现,与自然恢复相比,人工林降低了土壤DOC浓度,暗示它可能会减少土壤C的淋溶损失。此外,红锥林能够通过物理保护提高表土层中土壤碳的稳定性。本研究为关注土壤碳汇功能时的中国南亚热带地区造林树种选择提供了有价值的信息。     

Functional genomics of C190T single nucleotide polymorphism in human N-acetyltransferase 2

N-acetyltransferase 2 (NAT2) catalyzes N-acetylation and O-acetylation of many drugs and environmental carcinogens. Genetic polymorphisms in the NAT2 gene have been associated with differential susceptibility to cancers and drug toxicity from these compounds. Single nucleotide polymorphisms (SNPs) have been identified in the human NAT2 coding region. A new allele, NAT2*19, possessing the C190T (R64W) exchange, was recently identified. In order to understand the effect of this new SNP, recombinant NAT2*4 (reference) and NAT2*19 were expressed in yeast (Schizosaccharomyces pombe). The C190T (R64W) SNP in NAT2*19 caused substantial reduction in the NAT2 protein level and stability, but did not cause significant reduction in transformation efficiency or mRNA level. The enzymatic activities for N-acetylation of two arylamine carcinogens (2-aminofluorene, 4-aminobiphenyl), and a sulfonamide drug (sulfamethazine) were over 100-fold lower for NAT2 19 compared to reference NAT2 4. Kinetic studies showed a reduction in Vmax but no significant change in substrate Km. In addition, the SNP caused significant reduction in the O-acetylation of the N-hydroxy-2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine. These results show that NAT2*19 possessing the C190T (R64W) SNP encodes a slow acetylator phenotype for both N- and O-acetylation, due to a reduction in the amount and stability of the NAT2 19 allozyme.     

Molecular mechanism of diapause in insect (I)

The embryonic diapause of the silkworn,Bombyx mori, is induced by the diapause hormone (DH) which is secreted from the suboesophageal ganglion of pupae. The diapause nature of bivoltine strains uses environmental stimuli as the initial signal to determine the diapause nature. The experiments showed that DH gene expreon is a direct response to the environmend stimulus, such as high incubation temperature. The cDNA from the embryonic stage wa cloned and sequenm analysis showed the cDNA encoding DH. Expmion patterns of the DH gene in embryonic stage are different ar incubation temperatures 15°C and 25°C, suggesting that the incubation tempcreturt as an environmental signal is kept within the body to control the DH gene expmion at the pupal stage, so that the embryonic diapause of next generation can be determined.     

Oxidized low-density lipoprotein induces secretion of interleukin-1β by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation

Oxidized low-density lipoprotein (ox-LDL) is a critical mediator of atherogenesis. Macrophage uptake of ox-LDL and their subsequent development into foam cells is the principal event in atherosclerosis. Interleukin-1β (IL-1β), a prototypic multifunctional cytokine involved in inflammation, has an important effect on the pathogenesis and progression of atherosclerosis. Here we show that the phagocytosis of ox-LDL can induce human macrophages to secrete IL-1β by activating the NLRP3 inflammasome, and we further show that the activation of the NLRP3 inflammasome is dependent on the generation of reactive oxygen species and is related to the cathepsin B pathway. Furthermore, ox-LDL can upregulate the expression of the pro-IL-1β protein, thus priming IL-1β secretion. Therefore, our results suggest that the role of ox-LDL in atherosclerosis-related inflammation may involve the activation of the NLRP3 inflammasome.     

Assessing the contribution of tumor mutational phenotypes to cancer progression risk

Cancer occurs via an accumulation of somatic genomic alterations in a process of clonal evolution. There has been intensive study of potential causal mutations driving cancer development and progression. However, much recent evidence suggests that tumor evolution is normally driven by a variety of mechanisms of somatic hypermutability, which act in different combinations or degrees in different cancers. These variations in mutability phenotypes are predictive of progression outcomes independent of the specific mutations they have produced to date. Here we explore the question of how and to what degree these differences in mutational phenotypes act in a cancer to predict its future progression. We develop a computational paradigm using evolutionary tree inference (tumor phylogeny) algorithms to derive features quantifying single-tumor mutational phenotypes, followed by a machine learning framework to identify key features predictive of progression. Analyses of breast invasive carcinoma and lung carcinoma demonstrate that a large fraction of the risk of future clinical outcomes of cancer progression—overall survival and disease-free survival—can be explained solely from mutational phenotype features derived from the phylogenetic analysis. We further show that mutational phenotypes have additional predictive power even after accounting for traditional clinical and driver gene-centric genomic predictors of progression. These results confirm the importance of mutational phenotypes in contributing to cancer progression risk and suggest strategies for enhancing the predictive power of conventional clinical data or driver-centric biomarkers.     

Knockdown of DIXDC1 Inhibits the Proliferation and Migration of Human Glioma Cells

DIX domain containing 1 (DIXDC1), the human homolog of coiled-coil-DIX1 (Ccd1), is a positive regulator of Wnt signaling pathway. Recently, it was found to act as a candidate oncogene in colon cancer, non-small-cell lung cancer, and gastric cancer. In this study, we aimed to investigate the clinical significance of DIXDC1 expression in human glioma and its biological function in glioma cells. Western blot and immunohistochemistry analysis showed that DIXDC1 was overexpressed in glioma tissues and glioma cell lines. The expression level of DIXDC1 was evidently linked to glioma pathological grade and Ki-67 expression. Kaplan–Meier curve showed that high expression of DIXDC1 may lead to poor outcome of glioma patients. Serum starvation and refeeding assay indicated that the expression of DIXDC1 was associated with cell cycle. To determine whether DIXDC1 could regulate the proliferation and migration of glioma cells, we transfected glioma cells with interfering RNA-targeting DIXDC1; investigated cell proliferation with Cell Counting Kit (CCK)-8, flow cytometry assays, and colony formation analyses; and investigated cell migration with wound healing assays and transwell assays. According to our data, knockdown of DIXDC1 significantly inhibited proliferation and migration of glioma cells. These data implied that DIXDC1 might participate in the development of glioma, suggesting that DIXDC1 can become a potential therapeutic strategy for glioma.     

(−)‐Epicatechin rescues the As2O3‐induced HERG K+ channel deficiency possibly through upregulating transcription factor SP1 expression

(?)‐Epicatechin (EPI) has beneficial effects on the cardiovascular disease. The human ether‐a‐go‐go‐related gene (HERG) potassium channel is crucial for repolarization of cardiac action potential. Dysfunction of the HERG channel can cause long QT syndrome type 2 (LQT2). Arsenic trioxide (As₂O₃) has shown efficacy in the treatment of acute promyelocytic leukemia. However, As₂O₃ can induce the deficiency of HERG channel and cause LQT2. In this study, we examined whether EPI could rescue the As₂O₃‐induced HERG channel deficiency. We found that 3 μM EPI obviously increased protein expression and current of HERG channel. EPI was able to recover the protein expression and current of HERG channel disrupted by As₂O₃. EPI was able to increase the expression of SP1 protein and recover the expression of SP1 protein disrupted by As₂O₃. In addition, EPI significantly shortened action potential duration prolonged by As₂O₃. Our data suggest that EPI rescues As₂O₃‐induced HERG channel deficiency through upregulating SP1 expression.