Bioaugmentation accelerates the shift of bacterial community structure against shock load: a case study of coking wastewater treatment by zeolite-sequencing batch reactor

Bioaugmentation with degrading bacteria is an effective method to improve the treatment of refractory industrial wastewater; nevertheless there were controversial opinions about the fate of inoculated bacteria and microbial community dynamics. In this study, two lab-scale sequencing batch reactors filled with modified zeolite were used to treat a coking wastewater with pyridine and quinoline shock load, and a bacterial consortium containing three degrading strains was added in one reactor for bioaugmentation. During 120-day operation, the bioaugmented reactor removed over 99 % pyridine, 99 % quinoline, 85 % TOC, 65 % COD, and 95 % NO₃ ^?-N with higher resistance to the shock load than the non-bioaugmented reactor. Based on the terminal restriction fragment length polymorphism of 16S rDNA, bacterial community diversity increased in the bioaugmented reactor. Principal component analysis revealed that, to cope with the shock load, the indigenous bacterial community recovered to the initial structure by acclimatizing itself constantly to the inhospitable environment; but bioaugmentation accelerated the shift of whole bacterial community, resulting in a far different structure from the initial one. Canonical correspondence analysis indicated that the environmental parameters of pyridine, quinoline, TOC, and NO₃ ^?-N had close negative correlations with bioaugmentation; and NH₃-N and COD were the main parameters to impact on the bacterial community changes and treatment efficiency.     

Effects of Nickel Chloride on the Erythrocytes and Erythrocyte Immune Adherence Function in Broilers

This study was conducted to investigate the immune adherence function of erythrocytes and erythrocyte induced by dietary nickel chloride (NiCl₂) in broilers fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg NiCl₂ for 42 days. Blood samples were collected from five broilers in each group at 14, 28, and 42 days of age. Changes of erythrocyte parameters showed that total erythrocyte count (TEC), hemoglobin (Hb) contents, and packed cell volume (PCV) were significantly lower (p?p?p?p?+/K⁺-ATPase) and calcium adenosine triphosphatase (Ca²⁺-ATPase) activities were significantly decreased (p?p?2-treated groups. The results of erythrocyte immune adherence function indicated that erythrocyte C_3b receptor rosette rate (E-C_3bRR) was significantly decreased (p?p?p?p?2 in excess of 300 mg/kg caused anemia and impaired the erythrocytic integrity, erythrocytic ability to transport oxygen, and erythrocyte immune adherence function in broilers. Impairment of the erythrocytes and erythrocyte immune adherence function was one of main effect mechanisms of NiCl₂ on the blood function.     

Proteomic Analysis of Kunitz-Type Trypsin Inhibitor Deleted Soybean

Russian Journal of Plant Physiology - To explore proteomic characters of Kunitz-type trypsin inhibitors (KTIs) deleted soybean (Glycine max (L.) Merr.), seeds without KTIs and its female parent...     

Oxidative Modification of Cysteine 111 Promotes Disulfide Bond-Independent Aggregation of SOD1

Converging evidence indicates that SOD1 aggregation is a common feature of mutant SOD1-linked fALS, and seems to be directly related to the gain-of-function toxic property. However, the mechanism inducing the aggregation is not understood. To study the contribution of oxidative modification of cysteine residues in SOD1 aggregation, we systematically examined the redox state of SOD1 cysteine residues in the G37R transgenic mouse model at different stages of the disease and under oxidative stress induced by H₂O₂. Our data suggest that under normal circumstance, cysteine 111 residue in SOD1 is free; however, under oxidative stress, it is prone to oxidative modification by providing the thiolate anion (S−). With the progression of the disease, increased levels of oxidative insults facilitated the oxidation of thiol groups of cysteine residues; human mutant SOD1 could generate an upper shift band in reducing SDS-PAGE, which turned out to be a Cys111-peroxidized SOD1 species. We also detected the formation of SOD1 multimers at different stages of the disease, and found that accumulated oxidative stress facilitated the formation of aggregates, which were not mediated by disulfide bond. This oxidative modification of cysteine 111 therefore promotes the formation of disulfide bond-independent aggregation of SOD1.     

外源突变基因AGM3过表达对烟草开花的抑制和花器官发育的影响

为了解AGM3基因在异源植物中对开花及花器官发育的影响,采用农杆菌介导法将dominant negative mutation(DNM)结构基因35S-AGM3-E9导入烟草(Nicotiana tabacum),经PCR和Southern检测获得了一批阳性转化植株.荧光定量分析结果显示,AGM3在各个转基因株系中均有...     

An NF-kappaB-sensitive micro RNA-146a-mediated inflammatory circuit in Alzheimer disease and in stressed human brain cells

Human brains retain discrete populations of micro RNA (miRNA) species that support homeostatic brain gene expression functions; however, specific miRNA abundance is significantly altered in neurological disorders such as Alzheimer disease (AD) when compared with age-matched controls. Here we provide evidence in AD brains of a specific up-regulation of an NF-kappaB-sensitive miRNA-146a highly complementary to the 3'-untranslated region of complement factor H (CFH), an important repressor of the inflammatory response of the brain. Up-regulation of miRNA-146a coupled to down-regulation of CFH was observed in AD brain and in interleukin-1beta, Abeta42, and/or oxidatively stressed human neural (HN) cells in primary culture. Transfection of HN cells using an NF-kappaB-containing pre-miRNA-146a promoter-luciferase reporter construct in stressed HN cells showed significant up-regulation of luciferase activity that paralleled decreases in CFH gene expression. Treatment of stressed HN cells with the NF-kappaB inhibitor pyrollidine dithiocarbamate or the resveratrol analog CAY10512 abrogated this response. Incubation of an antisense oligonucleotide to miRNA-146a (anti-miRNA-146a; AM-146a) was found to restore CFH expression levels. These data indicate that NF-kappaB-sensitive miRNA-146a-mediated modulation of CFH gene expression may in part regulate an inflammatory response in AD brain and in stressed HN cell models of AD and illustrate the potential for anti-miRNAs as an effective therapeutic strategy against pathogenic inflammatory signaling.