Nitrate supply affects root growth differentially in two rice cultivars differing in nitrogen use efficiency

Peatland soils contain large amounts of nitrogen (N) in the soil and mineralization can contribute substantially to the annual mineral N supply of grasslands. We investigated the contribution of N mineralization from peat with respect to the total annual N uptake on grasslands with anthropogenic A horizons and submerged tile drains. The study included i) a pot experiment to determine potential N mineralization from the topsoil and the subsoil, ii) a 1-year field experiment to study herbage yields and N uptake under fertilized and non-fertilized conditions and iii) a 3-year field study where herbage yield and N uptake from the top 30 cm and the entire soil profile were monitored. The 3-year field study yielded an average N uptake of 342 kg?ha^?1 under non-fertilized conditions but the contribution of subsoil peat N mineralization to the total N uptake was found to be negligible. Our calculations demonstrate that peat N mineralization contributed only 10% to 30% to the total N-uptake, mainly coming from the top 30 cm. Most of the N uptake under unfertilized conditions appears to be largely the result of mineralization from long-term inputs of dung, ditch sludge, farmyard manure, cow slurry and non-harvested herbage.     

典型煤层水微生物产甲烷潜力及其群落结构研究

内蒙古自治区二连盆地、海拉尔盆地是我国重要的煤层气产区,其中生物成因煤层气是煤层气的重要来源,但复杂物质转化产甲烷相关微生物群落结构及功能尚不清楚。【目的】研究煤层水中的微生物代谢挥发性脂肪酸产甲烷的生理特征及群落特征。【方法】以内蒙古自治区二连盆地和海拉尔盆地的四口煤层气井水作为接种物,分别添加乙酸钠、丙酸钠和丁酸钠厌氧培养;定期监测挥发性脂肪酸降解过程中甲烷和底物的变化趋势,应用高通量测序技术,分析原始煤层气井水及稳定期产甲烷菌液的微生物群落结构。【结果】除海拉尔盆地H303煤层气井微生物不能代谢丙酸外,其他样品均具备代谢乙酸、丙酸和丁酸产生甲烷的能力,其生理生态参数存在显著差异,产甲烷延滞期依次是乙酸<丁酸<丙酸;最大比产甲烷速率和底物转化效率依次是丙酸<乙酸<丁酸。富集培养后,古菌群落结构与煤层气井水的来源显著相关,二连盆地优势古菌为氢营养型产甲烷古菌Methanocalculus (相对丰度13.5%–63.4%)和复合营养型产甲烷古菌Methanosarcina (7.9%–51.3%),海拉尔盆地的优势古菌为氢营养型产甲烷古菌Methanobact...     

Influenza Virus Directly Infects Human Natural Killer Cells and Induces Cell Apoptosis

Influenza is an acute respiratory viral disease that is transmitted in the first few days of infection. Evasion of host innate immune defenses, including natural killer (NK) cells, is important for the virus''s success as a pathogen of humans and other animals. NK cells encounter influenza viruses within the microenvironment of infected cells and are important for host innate immunity during influenza virus infection. It is therefore important to investigate the direct effects of influenza virus on NK cells. In this study, we demonstrated for the first time that influenza virus directly infects and replicates in primary human NK cells. Viral entry into NK cells was mediated by both clathrin- and caveolin-dependent endocytosis rather than through macropinocytosis and was dependent on the sialic acids on cell surfaces. In addition, influenza virus infection induced a marked apoptosis of NK cells. Our findings suggest that influenza virus can directly target and kill NK cells, a potential novel strategy of influenza virus to evade the NK cell innate immune defense that is likely to facilitate viral transmission and may also contribute to virus pathogenesis.Influenza is an acute respiratory virus infection that continues to pose endemic, zoonotic, and pandemic threats to human health, with significant morbidity and mortality (17). At the early phase of viral infection, innate immunity plays important roles in host defense by limiting viral replication and helping to initiate an adaptive immune response. Natural killer (NK) cells are key effector cells in innate immunity and play a critical role in the first line of host defense against acute viral infections by directly destroying infected cells without the need for prior antigen stimulation (7, 20). As influenza illness and virus transmission usually occur in the first few days of infection, the virus has to devise strategies to evade host innate immune responses, including NK cell immunity (15, 21).NK cells can recognize and kill influenza virus-infected cells (2, 10, 23); to counteract this killing, however, influenza virus has developed an escape strategy that inhibits NK cell cytotoxicity by increasing the binding of two inhibitory receptors to the infected cells after infection (1). The individuals with complete NK cell deficiency developed life-threatening varicella zoster virus and cytomegalovirus infection, but no severe influenza virus infection occurred (30, 40). Indeed, the interaction between human NK cells and influenza virus remains poorly understood. After influenza virus infection, respiratory epithelial cells release inflammatory chemokines that recruit NK cells to the site of infection (12). As a lytic virus, numerous influenza virus particles are released from the infected epithelia and macrophages (5, 9, 33). In the infected microenvironment, NK cells undoubtedly encounter these infective virus particles. It is therefore important to investigate the direct interaction of NK cells with influenza virus. Patients with severe influenza virus infection were shown to have diminished NK cells in peripheral blood and an almost complete absence of pulmonary NK cells, together with marked apoptosis (13, 42). During influenza virus infection in mice, a transient increase of NK cytotoxicity is followed by a marked decrease in NK cell activity, with a virus dose-dependent effect (8, 28). These data suggest that influenza virus may directly target NK cells as part of its immunoevasion strategies. However, no reports of the direct effects of influenza virus on human NK cells have so far been available.In this study, we demonstrated that influenza virus infects and replicates in primary human NK cells. Viral infection was dependent on sialic acids on the cells. The entry was mediated by both clathrin- and caveolin-dependent endocytosis rather than macropinocytosis. Influenza virus infection induced a marked apoptosis of NK cells, which contributed to reduced NK cell cytotoxicity. This, to the best of our knowledge, is the first paper to demonstrate that influenza virus can directly infect NK cells and induce cell apoptosis. These findings suggest that influenza virus may have developed a novel strategy to evade NK cell innate immune defenses, which is likely to facilitate viral transmission and may also contribute to virus pathogenesis.     

Acute effect of hemodialysis on serum levels of the proinflammatory cytokines

Chronic inflammation is a common feature of end-stage renal disease, which carries a heightened risk of atherosclerosis and other co-morbid conditions. Dialysis treatment per se can bring additional risk factors for inflammation, such as increased risk of local graft and fistula infections, impure dialysate or bio-incompatible membranes. Our study was designed to determine whether a hemodialysis session leads to an acute substantial alteration in the plasma levels of the proinflammatory cytokines interleukin (IL)-6, IL-1beta and tumor necrosis factor (TNF)-alpha, the T-lymphocyte activation factor soluble IL-2 receptor (sIL-2R), and an inflammation mediator and chemotactic granulocyte factor, IL-8, in end-stage renal disease patients receiving chronic intermittent HD. In this study, 21 (12 male/nine female) patients undergoing chronic hemodialysis were enrolled. The acute effect of a hemodialysis session on serum cytokine concentrations was assessed by comparison of pre-hemodialysis and post-hemodialysis determinations. Serum IL-1beta, sIL-2R, IL-6, IL-8 and TNF-alpha levels were determined with chemiluminescence enzyme immunometric assays. A significant difference was not observed for IL-1beta, IL-6, TNF-alpha, and sIL-2R concentrations in pre-hemodialysis and post-hemodialysis specimens (p>0.05). Serum median (25th-75th percentiles) IL-8 concentration was 69.4 (34.9-110.3) pg/ml before hemodialysis, and decreased to 31.5 (18.0-78.8) pg/ml following hemodialysis (p: 0.006). Clearance of IL-8 increased by 0.47+/-0.08 pg/ml for each unit increase in pre-dialysis IL-8 (p<0.001) and decreased by 5.63+/-2.59 pg/ml for each unit increase in pre-dialysis urea mmol/l (p<0.05). In conclusion, the results of our study demonstrate that a hemodialysis session markedly decreases IL-8 concentration, which is significantly affected by pre-dialysis concentrations, indicating that removal of IL-8 is a concentration gradient-dependent action, but does not change the serum levels of IL-1beta, sIL-2R, IL-6, and TNF-alpha, underlining importance of the structural characteristics of the molecules.     

A study on the immune receptors for polysaccharides from the roots of Astragalus membranaceus, a Chinese medicinal herb

The immunopotentiating effect of the roots of Astragalus membranaceus, a medicinal herb, has been associated with its polysaccharide fractions (Astragalus polysaccharides, APS). We herein demonstrate that APS activates mouse B cells and macrophages, but not T cells, in terms of proliferation or cytokine production. Fluorescence-labeled APS (fl-APS) was able to selectively stain murine B cells, macrophages and a also human tumor cell line, THP-1, as determined in flow cytometric analysis and confocal laser scanning microscopy. The specific binding of APS to B cells and macrophages was competitively inhibited by bacterial lipopolysaccharides. Rabbit-anti-mouse immunoglobulin (Ig) antibody was able to inhibit APS-induced proliferation of, and APS binding to, mouse B cells. Additionally, APS effectively stimulated the proliferation of splenic B cells from C3H/HeJ mice that have a mutated TLR4 molecule incapable of signal transduction. These results indicate that APS activates B cells via membrane Ig in a TLR4-independent manner. Interestingly, macrophages from C3H/HeJ mice were unable to respond to APS stimulation, suggesting a positive involvement of the TLR4 molecule in APS-mediated macrophage activation. Monoclonal Ab against mouse TLR4 partially inhibited APS binding with macrophages, implying direct interaction between APS and TLR4 on cell surface. These results may have important implications for our understanding on the molecular mechanisms of immunopotentiating polysaccharides from medicinal herbs.     

Antigenic properties of T cell antigen-specific receptors isolated from the surface of rabbit and mouse spleen and lymph node cells

The presence ofa allotypic determinants was tested in fractions obtained by gel filtration of antigen-specific receptors isolated by immunoadsorption from lymphoid cells of antigen-stimulateda3-3 rabbits. This technique, as well as the inhibition of the reaction of isolated receptors with anti-T cell receptor antisera (anti R) by anti-a3 antibodies failed to demonstrate the presence of a allotypie determinants. The inhibitory effect of antigen-specific receptors isolated from the lymphoid cells of stimulated A/J mice on the cytotoxic effect of anti-Ia antibodies on mouse spleen cells in the presence of rabbit complement was tested. All preparations inhibited the cytotoxic reaction with the average effectivity of 60%. In order to confirm the presence of Ia determinants on the rabbit and mouse T cell receptor molecules it was shown that the reactions of three anti-R antisera with 12 different receptor preparations were inhibited by anti-la antibodies. SDS-PAGE analyses of¹²⁵I-labelled mouse specific receptors and the precipitate obtained by anti-R antisera showed that T cell receptors were present in fractions with molar mass 100 and 85 kg/mol. The molar mass of the former fraction after reduction and alkylation was 45 kg/mol.     

微分脉冲伏安法测定沙苑子中鼠李柠檬素类黄酮含量

在 0 .0 5 m ol/ L 硫酸铵溶液中 ,采用微分脉冲伏安法 ,测定沙苑子中鼠李柠檬素类黄酮含量。灵敏度达 10 - 6mol/ L,在 6 .10× 10 - 6～ 3.0 5× 10 - 5m ol/ L 浓度范围内峰电流与沙苑子苷浓度成线性关系 (r=0 .995 9) ,回收率达96 .9%～ 10 3.0 % (RSD=2 .5 4 % ,n=6 )。结果表明 ,可不经分离直接测定沙苑子提取液中鼠李柠檬素类黄酮的含量