The feasibility of using a two-stage autotrophic nitrogen removal process to treat sewage

The feasibility of using a two-stage autotrophic nitrogen removal process to treat sewage was examined in this study. The obtained results showed that total nitrogen (TN) could be efficiently removed by 88.38% when influent TN and chemical oxygen demand (COD) were 45.87 and 44.40 mg/L, respectively. In the first stage, nitritation was instantly achieved by the bioaugmentation strategy, and can be maintained under limited oxygen condition (below 0.2mg/L). The ratio of nitrite to ammonium in the effluent of the nitritation reactor can be controlled at approximate 1.0 by adjusting aeration rate. In the second stage, anammox was realized in the upflow anaerobic sludge blanket (UASB) reactor, where the total nitrogen removal rate was 0.40 kg Nm(-3)d(-1) under limited-substrate condition. Therefore, the organic matter in sewage can be firstly concentrated in biomass which could generate biogas (energy). Then, nitrogen in sewage could be removed in a two-stage autotrophic nitrogen removal process.     

缺氧环境下白细胞介素8通过Akt-STAT3通路提高骨髓间充质干细胞自噬和增殖能力

探讨缺氧环境下,白细胞介素8(Interleukin-8,IL-8)对人骨髓间充质干细胞(Human bone marrow mesenchymal stem cells,hBMSC)增殖和自噬能力的影响以及机制。在缺氧模型下,未进行刺激的hBMSC为缺氧对照组;以100μmol/L人IL-8蛋白刺激的MSC为IL-8组;若先添加50μmol/L MK2206(Akt蛋白抑制剂)培养30 min,然后再添加100μmol/L IL-8则为Akt抑制剂组,在正常条件下培养的MSC为正常对照组。利用Ed U细胞增殖实验、TUNEL细胞凋亡实验、Western blotting或ELISA等实验分别检测各组MSC细胞Ed U标记阳性细胞的数目、细胞凋亡、自噬蛋白(LC-3)和Akt/STAT3等蛋白的表达。相对于缺氧对照组和Akt抑制剂组,IL-8明显提高hBMSC增殖和细胞自噬,并降低hBMSC的凋亡率,IL-8组hBMSC的Akt、STAT3和VEGF等蛋白表达增高。结果表明,缺氧环境下,IL-8通过Akt-STAT3通路发挥对MSC的保护作用,对保护MSC抗缺血缺氧性损伤,促进MSC在再生医学中应用具有重要意义。     

侧脑室注射心房钠尿肽对大鼠室旁核单位放电...

We have applied microelectrode technique to record 118 spontaneously firing units from the hypothalamus in rats. Detection of the recording sites showed that 84 were in the paraventricular nucleus (PVN) and 34 were near the PVN (near-PVN). After intracerebroventricular (i.c.v.) administration of atrial natriuretic polypeptide (ANP), 91% (P less than 0.005) of the PVN neurones and 71% (P greater than 0.05) of near-PVN neurones sensitive to ANP showed a significant decrease in spontaneously firing rate. After i.c.v. administration of hypertonic NaCl solution, 64.7% (P less than 0.005) of the PVN neurones and 61.1% (P greater than 0.05) of near-PVN neurones showed a significant increase in firing rate. The results indicate that i.c.v. administration of ANP profoundly inhibits the electrical activity of the PVN neurones, but hypertonic NaCl solution markedly stimulates the PVN neurones.     

Predicting protein-protein interactions by combing various sequence- derived features into the general form of Chou's Pseudo amino acid composition

Knowledge of protein-protein interactions (PPIs) plays an important role in constructing protein interaction networks and understanding the general machineries of biological systems. In this study, a new method is proposed to predict PPIs using a comprehensive set of 930 features based only on sequence information, these features measure the interactions between residues a certain distant apart in the protein sequences from different aspects. To achieve better performance, the principal component analysis (PCA) is first employed to obtain an optimized feature subset. Then, the resulting 67-dimensional feature vectors are fed to Support Vector Machine (SVM). Experimental results on Drosophila melanogaster and Helicobater pylori datasets show that our method is very promising to predict PPIs and may at least be a useful supplement tool to existing methods.     

CHO工程细胞株低血清培养的初探

以DMEM: F12(1: 1)为基础培养基,对CHO细胞的低血清培养进行了初步探索,降低培养基中血清含量,观察了细胞在10%、5%和1%等不同浓度低血清培养条件下生长状态和外源蛋白表达活性的变化.试验结果表明:在含1%血清的F12: DMEM(1: 1)培养基中,细胞仍能保持良好的生长状态,且培养上清中的目的蛋白活性与常规血清浓度10% DMEM培养条件下的活性接近.从而达到了既可以降低生产成本,又可以降低纯化难度的目的.     

Predictive value of circulating miR-328 and miR-134 for acute myocardial infarction

MicroRNA (miRNAs) is demonstrated to be present in the blood of humans and has been increasingly suggested as a novel biomarker for various pathological processes in the heart, including myocardial infarction, myocardial remodeling and progression to heart failure. In this study, we aim to evaluate the diagnostic and prognostic value of circulating miR-328 and miR-134 in patients with acute myocardial infarction (AMI). Circulating levels of miR-328 and miR-134 were detected by quantitative real-time PCR in plasma samples from 359 AMI patients and 30 healthy volunteers. Concentrations of high-sensitivity cardiac troponin T (hs-cTnT) were measured using electrochemiluminescence-based methods. MiRNAs were assessed for discrimination of a clinical diagnosis of AMI and for association with primary clinical endpoint defined as a composite of cardiogenic death and development of heart failure within 6 months after infarction. Results showed that levels of plasma miR-328 and miR-134 were significantly higher in AMI patients than in healthy controls. Receiver operating characteristic curve analyses showed significant diagnostic value of miR-328 and miR-134 for AMI. However, neither of them was superior to hs-cTnT for the diagnosis. Additionally, increased miRNA levels were strongly associated with increased risk of mortality or heart failure within 6 months for miR-328 (OR 7.35, 95 % confidence interval 1.07–17.83, P < 0.001) and miR-134 (OR 2.28, 95 % confidence interval 1.03–11.32 P < 0.001). In conclusion, circulating miR-328 and miR-134 could be potential indicators for AMI, and the miRNA levels are associated with increased risk of mortality or development of heart failure.     

Homocysteine inhibits endothelial progenitor cells proliferation via DNMT1-mediated hypomethylation of Cyclin A

Endothelial progenitor cells (EPCs) contribute to neovasculogenesis and reendothelialization of damaged blood vessels to maintain the endothelium. Dysfunction of EPCs is implicated in the pathogenesis of vascular injury induced by homocysteine (Hcy). We aimed to investigate the role of Cyclin A in Hcy-induced EPCs dysfunction and explore its molecular mechanism. In this study, by treatment of EPCs with Hcy, we found that the expression of Cyclin A mRNA and protein were significantly downregulated in a dose-dependent manner. Knockdown of Cyclin A prominently reduced proliferation of EPCs, while over-expression of Cyclin A significantly promoted the cell proliferation, suggesting that Hcy inhibits EPCs proliferation through downregulation of Cyclin A expression. In addition, epigenetic study also demonstrated that Hcy induces DNA hypomethylation of the Cyclin A promoter in EPCs through downregulated expression of DNMT1. Moreover, we found that Hcy treatment of EPCs leads to increased SAM, SAH and MeCP2, while the ratio of SAM/SAH and MBD expression decrease. In summary, our results indicate that Hcy inhibits Cyclin A expression through hypomethylation of Cyclin A and thereby suppress EPCs proliferation. These findings demonstrate a novel mechanism of DNA methylation mediated by DNMT1 in prevention of Hcy associated cardiovascular disease.