不同生境条件下滨海芦苇湿地C、N、P化学计量特征

为阐明不同生境对黄河三角洲滨海芦苇湿地土壤和植物碳(C)氮(N)磷(P)含量及生态化学计量特征的影响,选取新生湿地和退耕湿地两种湿地类型为研究对象,对土壤和植物体C、N、P含量及其化学计量特征进行研究。研究表明:1)退耕芦苇湿地土壤TC、TN的含量明显增加,TP的含量变化不大。2)新生湿地和退耕湿地土壤R_(C、N、P)分别为42.6:1.6:1、71.2:2.0:1,R_(NP)低于全球平均水平(13.1)和我国平均水平(5.2),土壤表现为N限制。新生湿地土壤剖面中,R_(CN)和R_(CP)变化剧烈;R_(NP)值随深度的增加而减小;退耕湿地土壤R_(C、N、P)值规律性较好,R_(CN)随深度的增加而变大,R_(CP)和R_(NP)值随深度的增加而减小。3)新生湿地和退耕湿地中芦苇整株R_(CN)、R_(CP)和R_(NP)平均值分别为78.2、1753、22.4;67.0、1539、23.0。开垦活动可以降低芦苇植物体R_(CN)和R_(CP)值,但由于芦苇植物体本身对R_(NP)的约束性较高,对R_(NP)值的影响不大,芦苇植株R_(NP)约为23。以上结论可以为黄河三角洲国家级自然保护区正在进行的湿地保护与恢复工作提供借鉴和参考。     

DNA甲基转移酶的表达调控及主要生物学功能

DNA甲基化是表观遗传学的重要部分, 同组蛋白修饰相互作用, 通过改变染色质结构, 调控基因表达。在哺乳类细胞或人体细胞中, DNA甲基化与细胞的增殖、衰老、癌变等生命现象有着重大关系。对催化DNA甲基化的DNA甲基转移酶(DNA methyltransferase, Dnmt)的研究可以揭示DNA甲基化对基因表达调控的机制, 从而研究与之相关的重要生命活动。文章以DNA甲基转移酶作为切入点, 探讨DNA甲基转移酶在基因表达调控中发挥的作用及其主要生物学功能。     

COX-2 is required to mediate crosstalk of ROS-dependent activation of MAPK/NF-κB signaling with pro-inflammatory response and defense-related NO enhancement during challenge of macrophage-like cell line with Giardia duodenalis

Giardia duodenalis, the causative agent of giardiasis, is among the most important causes of waterborne diarrheal diseases around the world. Giardia infection may persist over extended periods with intestinal inflammation, although minimal. Cyclooxygenase (COX)-2 is well known as an important inducer of inflammatory response, while the role it played in noninvasive Giardia infection remains elusive. Here we investigated the regulatory function of COX-2 in Giardia-induced pro-inflammatory response and defense-related nitric oxide (NO) generation in macrophage-like cell line, and identified the potential regulators. We initially found that Giardia challenge induced up-regulation of IL-1β, IL-6, TNF-α, prostaglandin (PG) E2, and COX-2 in macrophages, and pretreatment of the cells with COX-2 inhibitor NS398 reduced expressions of those pro-inflammatory factors. It was also observed that COX-2 inhibition could attenuate the up-regulated NO release and inducible NO synthase (iNOS) expression induced by Giardia. We further confirmed that Giardia-induced COX-2 up-regulation was mediated by the phosphorylation of p38 and ERK1/2 MAPKs and NF-κB. In addition, inhibition of reactive oxygen species (ROS) by NAC was shown to repress Giardia-induced activation of MAPK/NF-κB signaling, up-regulation of COX-2 and iNOS, increased levels of PGE2 and NO release, and up-expressions of IL-1β, IL-6, and TNF-α. Collectively, in this study, we revealed a critical role of COX-2 in modulating pro-inflammatory response and defense-related NO production in Giardia-macrophage interactions, and this process was evident to be controlled by ROS-dependent activation of MAPK/NF-κB signaling. The results can deepen our knowledge of anti-Giardia inflammatory response and host defense mechanisms.     

Biohydrodynamics and Ecology of Life Forms of Pelagial

The relation between inertial forces and frictional forces characterizing the pattern of movement of plankton and nekton organisms, respectively, and expressed by the Reynolds number Re may be used as a base for classifying the life forms of the pelagial. The upper limit for the existence of euplanktic forms connected with devices for increasing the hydrodynamic resistance and ensuring passive floating with the least expenditure of energy corresponds to Re values ≦5,0 · 10⁵. The upper boundary of the nektoplankton is in correspondance to Re ≦2,0 · 10⁷. The organization of nekton organisms capable of active directed horizontal movement and with devices for reducing the hydrodynamic resistance is in accordance with Re >5,0 · 10³, as a rule is in accordance with Re > 10⁵.     

Sodium butyrate inhibits aerobic glycolysis of hepatocellular carcinoma cells via the c‐myc/hexokinase 2 pathway

Aerobic glycolysis is a well‐known hallmark of hepatocellular carcinoma (HCC). Hence, targeting the key enzymes of this pathway is considered a novel approach to HCC treatment. The effects of sodium butyrate (NaBu), a sodium salt of the short‐chain fatty acid butyrate, on aerobic glycolysis in HCC cells and the underlying mechanism are unknown. In the present study, data obtained from cell lines with mouse xenograft model revealed that NaBu inhibited aerobic glycolysis in the HCC cells in vivo and in vitro. NaBu induced apoptosis while inhibiting the proliferation of the HCC cells in vivo and in vitro. Furthermore, the compound inhibited the release of lactate and glucose consumption in the HCC cells in vitro and inhibited the production of lactate in vivo. The modulatory effects of NaBu on glycolysis, proliferation and apoptosis were related to its modulation of hexokinase 2 (HK2). NaBu downregulated HK2 expression via c‐myc signalling. The upregulation of glycolysis in the HCC cells induced by sorafenib was impeded by NaBu, thereby enhancing the anti‐HCC effect of sorafenib in vitro and in vivo. Thus, NaBu inhibits the expression of HK2 to downregulate aerobic glycolysis and the proliferation of HCC cells and induces their apoptosis via the c‐myc pathway.     

Targeting UPR branches,a potential strategy for enhancing efficacy of cancer chemotherapy

Cancer cells are often exposed to cell intrinsic stresses and environmental perturbations that may lead to accumulation of unfolded and/or misfolded proteins in...