基于多Agent仿真解析处理剩余污泥的微生物电解池种群互作关系

【背景】微生物电化学系统耦合了电化学反应和厌氧消化过程,在处理剩余污泥同时实现能源回收,成为具有应用前景的技术之一。揭示电活性生物膜和活性污泥种群互作机制,有助于进一步调控和强化系统性能。高通量核酸测序技术研究微生物群落具有投入大、耗时长和不可预测的缺点,开展微生物群落动态仿真可以更有效地预测群落结构与功能。【目的】研究厌氧消化和生物电化学系统的微生物种间热力学与动力学的演化规律。在考虑电子供体、电子受体、温度、pH值等生态条件下,分析底物的电子流向及微生物群落结构的动态变化。【方法】通过对剩余污泥处理的微生物电解池(Microbial electrolytic cell,MEC)建立一个多Agent仿真(Multi-agent-based simulation,MAS)模型,评估MEC对底物氧化电子转移的能量效率和传质效率,模拟微生物群落结构实时变化,同时耦合动力学和热力学分析;揭示影响MES运行的电子流向决定性因素及相应的微生物种群,为复杂污染物生物处理系统中种间互作和动力学研究提供基础依据。【结果】通过MAS模拟,确定MEC污泥处理工艺的最佳能量传递效率与传质效率为η=0.2,ε=0.5,MAS结合热力学与动力学参数模拟微生物的群落动态与实验组有较高的吻合性。在长期的运行中,微生物电化学系统中丙酮酸没有积累。【结论】证实了MAS结合热力学与动力学参数可以预测微生物的群落动态,并进行实时监测。研究表明多Agent仿真为微生物群落结构动态变化提供了一种新的研究方法,该方法与高通量核酸测序技术进行校验和联用,为人工和自然生态系统中微生物种群预测与评估研究提供一个新的手段。     

狭域还是广域：杂色山雀和 大山雀行为特征比较

动物行为是个体与社群适应内外环境变化（刺激）所作出的动态反应。动物的行为特征对其适合度以及进化有着重要意义,但关于鸟类行为特征对扩散以及分布的研究还较少,本文以杂色山雀（Sittiparus varius）和大山雀（Parus cinereus）这两种生活史策略相似、分布范围差异显著的雀形目鸟类为例,采用经典新环境测试法对两物种探索性、活跃性、冒险性三种行为进行比较。Mann-Whitney U-test结果显示,大山雀的探索性（Z =﹣2.582,P < 0.01）、活跃性（Z =﹣5.148,P < 0.001）、冒险性（Z =﹣2.046,P < 0.05）得分均显著高于杂色山雀,证明广域分布的大山雀探索性、活跃性及冒险性明显强于狭域分布的杂色山雀。我们由此猜想鸟类行为特征可能会与种群的分布范围相关;通过对鸟类行为特征的探究或许可以间接预测种群未来的发展方向,为种群的保护提供指导。     

Effects of starvation on death‐feigning in adult Eucryptorrhynchus brandti (Coleoptera: Curculionidae)

In insects, death‐feigning is an effective defence strategy. Eucryptorrhynchus brandti, a major borer pest in China, has a weak flight ability and exhibits obvious death‐feigning behaviour when disturbed. Despite a large number of studies of its biological and ecological properties as well as control methods, the death‐feigning behaviour has not been specifically described. In laboratory conditions, we recorded the survival rate under starvation and feeding conditions and evaluated the effect of starvation on the duration and occurrence of death‐feigning. In a continuous experiment, we examined variation in the death‐feigning duration every day over 7 day. Then, we evaluated the effects of starvation for 3, 6 and 9 day in a non‐continuous experiment and further observed variation in the death‐feigning intensity. We found that starvation significantly affected the survival rate. Survival time was significantly longer in the starvation group than in the feeding group, and females had longer survival times than males (female: 14 day, male: 8 day). In the continuous experiment, starved E. brandti had the longest duration of death‐feigning at 2 day, followed by a significant decrease. In the non‐continuous experiment, the duration and proportion of death‐feigning decreased significantly as the duration of starvation increased and were significantly lower than feeding. These observations suggest that starvation is a non‐negligible factor in the death‐feigning behaviour of E. brandti adults, facilitating the interpretation of future ecological and behavioural data of thanatosis.     

PKM2-regulated STAT3 promotes esophageal squamous cell carcinoma progression via TGF-β1-induced EMT

Recent studies have demonstrated pleiotropic roles of pyruvate kinase isoenzyme type M2 (PKM2) in tumor progression. However, the precise mechanisms underlying the effects of PKM2 on esophageal squamous cell carcinoma (ESCC) metastasis and transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) remain to be established. In this study, we observed upregulation of PKM2 in ESCC tissues that was markedly associated with lymph node metastasis and poor prognosis. High PKM2 expression in tumor tissues frequently coincided with the high pSTAT3Tyr705 expression and low E-cadherin expression. Furthermore, altered PKM2 expression was significantly associated with proliferation, migration, and invasion of ESCC cells, in addition to expression patterns of EMT markers (Snail, E-cadherin, and vimentin) and pSTAT3^Tyr705/STAT3 ratio. Overexpression of STAT3 significantly attenuated the effects of PKM2 knockdown on cell proliferation and motility as well as expression of pSTAT3 ^Tyr705 and EMT markers. Consistently, stable short hairpin RNA (shRNA)-mediated silencing of PKM2 reversed the effects of TGF-β1 treatment, specifically, upregulation of PKM2, phosphorylation of STAT3 at Tyr705, and increased EMT, migration, and invasion. We propose that PKM2 regulates cell proliferation, migration, and invasion via phosphorylation of STAT3 through TGF-β1-induced EMT. Our findings collectively provide mechanistic insights into the tumor-promoting role of PKM2, supporting its prognostic value and the therapeutic utility of PKM2 inhibitors as potential antitumor agents in ESCC.     

Betulinic acid inhibits cell proliferation,migration, and inflammatory response in rheumatoid arthritis fibroblast-like synoviocytes

Betulinic acid (BA), a pentacyclic triterpene derived from the bark of the white birch tree, has been reported to have a variety of pharmacological effects, including antioxidant, anti-inflammatory, antitumor, immunomodulatory, and antiarthritis properties. However, the role of BA in rheumatoid arthritis (RA) remains unclear. Thus, the objective of this study was to examine the effects of BA on RA fibroblast-like synoviocytes (RA-FLS) proliferation, migration, and inflammatory response, and further explore the potential underlying mechanisms. Our results showed that BA inhibited the proliferation, migration, and invasion of RA-FLSs. BA also attenuated tumor necrosis factor-α (TNF-α), enhanced matrix metalloproteinases (MMPs) expression, and inflammatory cytokines production in RA-FLS. Furthermore, BA prevented the activation of Akt/NF-κB pathway in RA-FLS exposed to TNF-α. In conclusion, these findings indicated that BA inhibits cell proliferation, migration, and inflammatory response in RA-FLS; and the Akt/NF-κB signaling pathway was involved in the protective effect of BA on RA-FLS. Thus, BA might be a potential therapeutic agent for the treatment of RA.     

Isofraxidin attenuates IL-1β-induced inflammatory response in human nucleus pulposus cells

Inflammation has been demonstrated to be the key factor for intervertebral disc degeneration (IVD), which remains a major public health problem. Isofraxidin is a coumarin compound that possesses strong anti-inflammatory activity. However, the role of isofraxidin in IVD remains unclear. The aim of this study was to evaluate the effects of isofraxidin on inflammatory response in human nucleus pulposus cells (NPCs) exposed to interleukin-1β (IL-1β). The results proved that isofraxidin attenuated the IL-1β-induced significant increases in inflammatory mediators and cytokines including nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), and IL-6. Besides, isofraxidin also inhibited the induction effect of IL-1β on matrix metalloproteinases (MMP)-3 and MMP-13. Moreover, the NF-κB activation caused by IL-1β was significantly inhibited by isofraxidin treatment. These findings suggested that isofraxidin alleviates IL-1β-induced inflammation in NPCs. Our work provided an idea that isofraxidin might act as a novel preventive role in IVD.     

NEAT1 contributes to ox-LDL-induced inflammation and oxidative stress in macrophages through inhibiting miR-128

Long noncoding RNAs (lncRNA) have been recognized as significant regulators in the progression of atherosclerosis (AS). Oxidized low-density lipoprotein (ox-LDL) can induce macrophage inflammation and oxidative stress, that serves important roles in AS. However, the exact function of lncRNA NEAT1 and its possible molecular mechanism in AS remain unclear. Here, we concentrated on the roles and molecular mechanisms of NEAT1 in AS development. In our current study, we observed that NEAT1 was elevated by ox-LDL in a dose-dependent and time-dependent manner. RAW264.7 cell survival was greatly enhanced, and cell apoptosis was significantly inhibited by LV-shNEAT1 transfection. In addition, knockdown of NEAT1 in RAW264.7 cells repressed CD36 expression and foam cell formation while NEAT1 overexpression shown an opposite process. Moreover, NEAT1 downregulation inhibited inflammation molecules including IL-6, IL-1β, and TNF-α. Meanwhile, silencing of NEAT1 can also suppress reactive oxygen species (ROS) and malondialdehyde (MDA) levels with an enhancement of superoxide dismutase (SOD) activity in RAW264.7 cells. MicroRNAs are some short RNAs, and they can regulate multiple biological functions in many diseases including AS. Here, we found that miR-128 expression was remarkably decreased in ox-LDL-incubated RAW264.7 cells. Interestingly, miR-128 mimics was able to reverse AS-correlated events induced by overexpression of NEAT1. By using bioinformatics analysis, miR-128 was predicted as a target of NEAT1 and the correlation between them was validated in our study. Taken these together, it was implied that NEAT1 participated in ox-LDL-induced inflammation and oxidative stress in AS development through sponging miR-128.