Characteristics of the bioreactor landfill system using an anaerobic-aerobic process for nitrogen removal

A sequential upflow anaerobic sludge blanket (UASB) and air-lift loop sludge blanket (ALSB) treatment was introduced into leachate recirculation to remove organic matter and ammonia from leachate in a lab-scale bioreactor landfill. The results showed that the sequential anaerobic-aerobic process might remove above 90% of COD and near to 100% of NH4+ -N from leachate under the optimum organic loading rate (OLR). The total COD removal efficiency was over 98% as the OLR increased to 6.8-7.7 g/l d, but the effluent COD concentration increased to 2.9-4.8 g/l in the UASB reactor, which inhibited the activity of nitrifying bacteria in the subsequent ALSB reactor. The NO3- -N concentration in recycled leachate reached 270 mg/l after treatment by the sequential anaerobic-aerobic process, but the landfill reactor could efficiently denitrify the nitrate. After 56 days operation, the leachate TN and NH4+ -N concentrations decreased to less than 200 mg/l in the bioreactor landfill system. The COD concentration was about 200 mg/l with less than 8 mg/l BOD in recycled leachate at the late stage. In addition, it was found that nitrate in recycled leachate had a negative effect on waste decomposition.     

VPS13D bridges the ER to mitochondria and peroxisomes via Miro

Mitochondria, which are excluded from the secretory pathway, depend on lipid transport proteins for their lipid supply from the ER, where most lipids are synthesized. In yeast, the outer mitochondrial membrane GTPase Gem1 is an accessory factor of ERMES, an ER–mitochondria tethering complex that contains lipid transport domains and that functions, partially redundantly with Vps13, in lipid transfer between the two organelles. In metazoa, where VPS13, but not ERMES, is present, the Gem1 orthologue Miro was linked to mitochondrial dynamics but not to lipid transport. Here we show that Miro, including its peroxisome-enriched splice variant, recruits the lipid transport protein VPS13D, which in turn binds the ER in a VAP-dependent way and thus could provide a lipid conduit between the ER and mitochondria. These findings reveal a so far missing link between function(s) of Gem1/Miro in yeast and higher eukaryotes, where Miro is a Parkin substrate, with potential implications for Parkinson’s disease pathogenesis.     

MV-mimicking micelles loaded with PEG-serine-ACP nanoparticles to achieve biomimetic intra/extra fibrillar mineralization of collagen in vitro

Since their discovery, matrix vesicles (MVs) containing minerals have received considerable attention for their role in the mineralization of bone, dentin and calcified cartilage. Additionally, MVs' association with collagen fibrils, which serve as the scaffold for calcification in the organic matrix, has been repeatedly highlighted. The primary purpose of the present study was to establish a MVs–mimicking model (PEG-S-ACP/micelle) in vitro for studying the exact mechanism of MVs-mediated extra/intra fibrillar mineralization of collagen in vivo. In this study, high-concentration serine was used to stabilize the amorphous calcium phosphate (S-ACP), which was subsequently mixed with polyethylene glycol (PEG) to form PEG-S-ACP nanoparticles. The nanoparticles were loaded in the polysorbate 80 micelle through a micelle self-assembly process in an aqueous environment. This MVs–mimicking model is referred to as the PEG-S-ACP/micelle model. By adjusting the pH and surface tension of the PEG-S-ACP/micelle, two forms of minerals (crystalline mineral nodules and ACP nanoparticles) were released to achieve the extrafibrillar and intrafibrillar mineralization, respectively. This in vitro mineralization process reproduced the mineral nodules mediating in vivo extrafibrillar mineralization and provided key insights into a possible mechanism of biomineralization by which in vivo intrafibrillar mineralization could be induced by ACP nanoparticles released from MVs. Also, the PEG-S-ACP/micelle model provides a promising methodology to prepare mineralized collagen scaffolds for repairing bone defects in bone tissue engineering.     

Frequentist estimation of coalescence times from nucleotide sequence data using a tree-based partition

This article proposes a method of estimating the time to the most recent common ancestor (TMRCA) of a sample of DNA sequences. The method is based on the molecular clock hypothesis, but avoids assumptions about population structure. Simulations show that in a wide range of situations, the point estimate has small bias and the confidence interval has at least the nominal coverage probability. We discuss conditions that can lead to biased estimates. Performance of this estimator is compared with existing methods based on the coalescence theory. The method is applied to sequences of Y chromosomes and mtDNAs to estimate the coalescent times of human male and female populations.     

水平基因转移

简要介绍了水平基因转移（horizontal gene transfer,HGT）的基本概念以及进行转移的主要方式：由质粒或病毒等介导的水平基因转移和基因的“直接”水平转移。并结合基因组序列分析,重点阐述远缘生物之间发生的广泛的基因交流,以及其与进化、系统发育和基因工程生物安全性问题的探讨。 Abstract:In this paper the conception of horizontal gene transfer (HGT) was introduced,and main mode of HGT was also enumerated as follows:HGT by medium such as plasmid and virus etc.and the HGT without any medium.The transfer of genes from one species to another especially between remote species was emphasized by the information from genome sequencing.The problems about evolution phylogenies and safety of GEMs (gene engineered microorganisms) for HGT were discussed.     

Inactivation of Numb and Numblike in embryonic dorsal forebrain impairs neurogenesis and disrupts cortical morphogenesis

Numb and Numblike, conserved homologs of Drosophila Numb, have been implicated in cortical neurogenesis; however, analysis of their involvement in later stages of cortical development has been hampered by early lethality of double mutants in previous studies. Using Emx1(IREScre) to induce more restricted inactivation of Numb in the dorsal forebrain of numblike null mice beginning at E9.5, we have generated viable double mutants that displayed striking brain defects. It was thus possible to examine neurogenesis during the later peak phase (E12.5-E16.5). Loss of Numb and Numblike in dorsal forebrain resulted in neural progenitor hyperproliferation, delayed cell cycle exit, impaired neuronal differentiation, and concomitant defects in cortical morphogenesis. These findings reveal novel and essential function of Numb and Numblike during the peak period of cortical neurogenesis. Further, these double mutant mice provide an unprecedented viable animal model for severe brain malformations due to defects in neural progenitor cells.     

Inhibition of ROS-Activated p38MAPK Pathway is Involved in the Protective Effect of H2S Against Chemical Hypoxia-Induced Inflammation in PC12 Cells

We have demonstrated the neuroprotection of hydrogen sulfide (H₂S) against chemical hypoxia-induced injury by inhibiting p38MAPK pathway. The present study attempts to evaluate the effect of H₂S on chemical hypoxia-induced inflammation responses and its mechanisms in PC12 cells. We found that treatment of PC12 cells with cobalt chloride (CoCl₂, a hypoxia mimetic agent) enhanced IL-6 secretion, nitric oxide (NO) generation and expression levels of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS). L-canavanine, a selective iNOS inhibitor, partly blocked CoCl₂-induced cytotoxicity, apoptosis and mitochondrial insult. In addition, 7-Nitroindazole (7-NI), an inhibitor of nNOS, also partly attenuated the CoCl₂-induced cytotoxicity. The inhibition of p38MAPK by SB203580 (a selective p38MAPK inhibitor) or genetic silencing of p38MAPK by RNAi (Si-p38) depressed not only CoCl₂-induced iNOS expression, NO production, but also IL-6 secretion. In addition, N-acetyl-l-cysteine, a reactive oxygen species (ROS) scavenger, conferred a similar protective effect of SB203580 or Si-p38 against CoCl₂-induced inflammatory responses. Importantly, pretreatment of PC12 cells with exogenous application of sodium hydrosulfide (a H₂S donor, 400 μmol/l) for 30 min before exposure to CoCl₂ markedly attenuated chemical hypoxia-stimulated iNOS and nNOS expression, NO generation and IL-6 secretion as well as p38MAPK phosphorylation in PC12 cells. Taken together, we demonstrated that p38MAPK-iNOS pathway contributes to chemical hypoxia-induced inflammation and that H₂S produces an anti-inflammatory effect in chemical hypoxia-stimulated PC12 cells, which may be partly due to inhibition of ROS-activated p38MAPK-iNOS pathway.     

豹蛙核酸酶与斑蝥酸钠对肺腺癌细胞增殖的协同抑制作用

豹蛙核酸酶(onconase,Onc)是从美洲北方豹蛙卵母细胞中提取的一种核糖核酸酶,对许多肿瘤细胞都具有杀伤作用。斑蝥素(cantharidin)是存在于芫青科昆虫斑蝥体内的一种天然防御性毒素,斑蝥酸钠(sodium cantharidate,SCA)是斑蝥素半合成衍生物。鉴于Onc与SCA对非小细胞肺癌都具有杀伤作用,采用MTT法测定Onc与SCA单独与联合作用于两株肺腺癌细胞的IC50值,运用联合作用指数(combination index,CI)和等效线分析评价两者联合作用的效果。结果表明,Onc与SCA联合作用时,CI值均小于0.7,等效线分析图显示,代表Onc与SCA联合作用的点均位于加成线下方,Onc与SCA对肺腺癌SPC-A-1、A549细胞株增殖的抑制作用具有协同效应。用流式细胞仪进行的凋亡细胞检测结果也支持上述"Onc/SCA联合使用具有协同抗癌作用"的结论。     

茎瘤固氮根瘤菌ORS571鞭毛马达基因fliN与fliM的功能分析

【目的】考察茎瘤固氮根瘤菌ORS571中鞭毛马达蛋白FliN、FliM的编码基因分别缺失的突变体表型,初步探究其功能机理。【方法】本研究采用同源重组和三亲本接合转移的方法构建突变体,测定野生型及突变株的生长曲线、趋化性、胞外多糖的分泌、生物膜的形成及细胞絮凝等表型。【结果】三种菌株的生长速率基本无差,与野生型菌株相比突变株鞭毛结构丧失,趋化能力、分泌的胞外多糖和生物膜形成能力均下降,但相同时间内细胞絮凝程度比野生型明显。【结论】实验表明,鞭毛基因fliN、fliM对茎瘤固氮根瘤菌ORS571鞭毛的形成、趋化运动、胞外多糖的分泌、生物膜的形成及细胞絮凝能力等均有调控作用。