Phosphorus recovery from wastewater through microbial processes

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Highlights? EBPR is a mature, effective technology to concentrate P from dilute streams. ? EBPR sludge is rich in phosphorus: it can be applied to land. ? Phosphorus in EBPR sludge can be recovered as struvite; P needs to first be solubilized. ? Solubilization of P through anaerobic digestion is attractive, but complexing with metal ions needs to be minimized.     

Pyrolytic characteristics of biomass acid hydrolysis residue rich in lignin

Pyrolytic characteristics of acid hydrolysis residue (AHR) of corncob and pinewood (CAHR, WAHR) were investigated using a thermo-gravimetric analyzer (TGA) and a self-designed pyrolysis apparatus. Gasification reactivity of CAHR char was then examined using TGA and X-ray diffractometer. Result of TGA showed that thermal degradation curves of AHR descended smoothly along with temperature increasing from 150 °C to 850 °C, while a “sharp mass loss stage” for original biomass feedstock (OBF) was observed. Char yield from AHR (42.64-30.35 wt.%) was found to be much greater than that from OBF (26.4-19.15 wt.%). In addition, gasification reactivity of CAHR char was lower than that of corncob char, and there was big difference in micro-crystallite structure. It was also found that CAHR char reactivity decreased with pyrolysis temperature, but increased with pyrolysis heating rate and gasification temperature at 850-950 °C. Furthermore, CAHR char reactivity performed better under steam atmosphere than under CO₂ atmosphere.     

Protein expression changes during cotton fiber elongation in response to low temperature stress

Low temperature stress is one of the major abiotic stresses limiting the formation of cotton (Gossypium hirsutum L.) fiber qualities, especially fiber length. To investigate the molecular adaptation mechanisms of cotton fiber elongation to low temperature stress, two cotton cultivars, Kemian 1 (low temperature-tolerant) and Sumian 15 (low temperature-sensitive), were planted in the field at two sowing dates (25 April and 10 June). The two sowing dates resulted in different growing conditions and the main environmental difference between them was temperature, particularly the mean daily minimum temperature (MDTmin). When the sowing date was delayed, the MDTmin decreased from 26.9 °C (25 April) to 20.6 °C (10 June). Low temperature stress (MDTmin of 20.6 °C) shortened the fiber length significantly in two cultivars, but the decreased extent was larger in Sumian 15 than that in Kemian 1. Proteomic analysis of three developmental stages (10, 15 and 20 days post-anthesis [DPA]) showed that 37 spots changed significantly (p < 0.05) in abundance under low temperature stress and they were identified using mass spectrometry. These proteins were involved in malate metabolism, soluble sugar metabolism, cell wall loosening, cellulose synthesis, cytoskeleton, cellular response, and redox homeostasis. The results suggest that the enhancement of osmoticum maintenance, cell wall loosening, cell wall components biosynthesis, and cytoskeleton homeostasis plays important roles in the tolerance of cotton fibers to low temperature stress. Moreover, low levels of PEPCase, expansin, and ethylene signaling proteins may potentially lead to the low temperature sensitivity of Sumian 15 at the proteomic level.     

Phylodynamics of H5N1 avian influenza virus in Indonesia

Understanding how pathogens invade and become established in novel host populations is central to the ecology and evolution of infectious disease. Influenza viruses provide unique opportunities to study these processes in nature because of their rapid evolution, extensive surveillance, large data sets and propensity to jump species boundaries. H5N1 highly pathogenic avian influenza virus (HPAIV) is a major animal pathogen and public health threat. The virus is of particular importance in Indonesia, causing severe outbreaks among poultry and sporadic human infections since 2003. However, little is known about how H5N1 HPAIV emerged and established in Indonesia. To address these questions, we analysed Indonesian H5N1 HPAIV gene sequences isolated during 2003-2007. We find that the virus originated from a single introduction into East Java between November 2002 and October 2003. This invasion was characterized by an initially rapid burst of viral genetic diversity followed by a steady rate of lineage replacement and the maintenance of genetic diversity. Several antigenic sites in the haemagglutinin gene were subject to positive selection during the early phase, suggesting that host-immune-driven selection played a role in host adaptation and expansion. Phylogeographic analyses show that after the initial invasion of H5N1, genetic variants moved both eastwards and westwards across Java, possibly involving long-distance transportation by humans. The phylodynamics we uncover share similarities with other recently studied viral invasions, thereby shedding light on the ecological and evolutionary processes that determine disease emergence in a new geographical region.     

基于地形因子的天童地区常绿树种和落叶树种共存机制研究

位于亚热带的浙江天童和古田山常绿阔叶林大样地分布有较高比例的落叶树种,那么它们与常绿树种的共存机制是什么?常绿树种和落叶树种生态习性差异较大,二者对生境的选择应有所不同,我们推测生境分化可能是两类植物实现共存的主要机制。为检验该假设,我们以天童20ha动态样地调查数据为依托,选择个体数≥20的55个常绿树种和42个落叶树种作为分析对象,用典范对应分析(CCA)研究了地形因子对二者分布的影响差异,用torus转换检验来分析常绿树种和落叶树种与各类地形生境的关联。结果如下:(1)CCA分析表明地形因子对常绿树种分布的解释量为19.2%,对落叶树种分布的解释量为7.0%。(2)torus转换检验结果表明,与沟谷成正关联的常绿树种和落叶树种的比例分别为16.4%和28.6%,成负关联的比例分别为40%和7%;与山脊成正关联的常绿树种和落叶树种的比例分别为41.8%和4.8%,成负关联的比例分别为10.9%和47.6%;与受干扰生境成正关联的常绿树种和落叶树种的比例分别为16.4%和42.9%。上述结果说明地形对常绿树种分布的影响大于落叶树种;两个植物类群对生境的选择多呈现相反格局,尤其是在沟谷生境和山脊生境,这进一步表明生境分化是常绿树种和落叶树种共存的重要机制之一,生态位理论在一定程度上能较好地解释亚热带常绿阔叶林物种多样性的维持。     

Sex-based transmural differences in cardiac repolarization and ionic-current properties in canine left ventricles

The female sex is associated with longer electrocardiographic QT intervals and increased proarrhythmic risks of QT-prolonging drugs. This study examined the hypothesis that sex differences in repolarization may be associated with differential transmural ion-current distribution. Whole cell patch-clamp and current-clamp were used to study ionic currents and action potentials (APs) in isolated canine left ventricular cells from epicardium, midmyocardium, and endocardium. No sex differences in AP duration (APD) were found in cells from epicardium versus endocardium. In midmyocardium, APD was significantly longer in female dogs (e.g., at 1 Hz, female vs. male: 288 +/- 21 vs. 237 +/- 8 ms; P < 0.05), resulting in greater transmural APD heterogeneity in females. No sex differences in inward rectifier K+ current (I(K1)) were observed. Transient outward K+ current (I(to)) densities in epicardium and midmyocardium also showed no sex differences. In endocardium, female dogs had significantly smaller I(to) (e.g., at +30 mV, female vs. male: 2.5 +/- 0.2 vs. 3.5 +/- 0.3 pA/pF; P < 0.05). Rapid delayed-rectifier K+ current (I(Kr)) density and activation voltage-dependence showed no sex differences. Female dogs had significantly larger slow delayed-rectifier K+ current (I(Ks)) in epicardium and endocardium (e.g., at +40 mV; tail densities, female vs. male; epicardium: 1.3 +/- 0.1 vs. 0.8 +/- 0.1 pA/pF; P < 0.001; endocardium: 1.2 +/- 0.1 vs. 0.7 +/- 0.1 pA/pF; P < 0.05), but there were no sex differences in midmyocardial I(Ks). Female dogs had larger L-type Ca2+ current (I(Ca,L)) densities in all layers than male dogs (e.g., at -20 mV, female vs. male, epicardium: -4.2 +/- 0.4 vs. -3.2 +/- 0.2 pA/pF; midmyocardium: -4.5 +/- 0.5 vs. -3.3 +/- 0.3 pA/pF; endocarium: -4.5 +/- 0.4 vs. -3.2 +/- 0.3 pA/pF; P < 0.05 for each). We conclude that there are sex-based transmural differences in ionic currents that may underlie sex differences in transmural cardiac repolarization.     

Theiler's Murine Encephalomyelitis Virus Leader Protein Is the Only Nonstructural Protein Tested That Induces Apoptosis When Transfected into Mammalian Cells

Theiler''s murine encephalomyelitis virus (TMEV) induces two distinct cell death programs, necrosis and apoptosis. The apoptotic pathway is of particular interest because TMEV persists in the central nervous system of mice, largely in infiltrating macrophages, which undergo apoptosis. Infection of murine macrophages in culture induces apoptosis that is Bax dependent through the intrinsic or mitochondrial pathway, restricting infectious-virus yields and raising the possibility that apoptosis represents a mechanism to attenuate TMEV yet promote macrophage-to-macrophage spread during persistent infection. To help define the cellular stressors and upstream signaling events leading to apoptosis during TMEV infection, we screened baby hamster kidney (BHK-21) cells transfected to express individual nonstructural genes (except 3B) of the low-neurovirulence BeAn virus strain for cell death. Only expression of the leader protein led to apoptosis, as assessed by fluorescence-activated cell sorting analysis of propidium iodide- and annexin V-stained transfected cells, immunoblot analysis of poly(ADP-ribose) polymerase and caspase cleavages, electron microscopy, and inhibition of apoptosis by the pancaspase inhibitor qVD-OPh. After transfection, Bak and not Bax expression increased, suggesting that the apical pathway leading to activation of these Bcl-2 multi-BH-domain proapoptotic proteins differs in BeAn virus infection versus L transfection. Mutation to remove the CHCC Zn finger motif from L, a motif required by L to mediate inhibition of nucleocytoplasmic trafficking, significantly reduced L-protein-induced apoptosis in both BHK-21 and M1-D macrophages.Theiler''s murine encephalomyelitis viruses (TMEV), members of the genus Cardiovirus in the family Picornaviridae, are highly cytolytic RNA viruses. Mice experimentally infected with a low-neurovirulence TMEV, such as BeAn virus, develop persistent infection in the central nervous system (CNS) and an inflammatory demyelinating disease, providing an experimental analogue for multiple sclerosis. BeAn virus persists primarily in macrophages in the CNS of infected mice. Schlitt et al. (34) found that 74% of TUNEL-positive cells in infected spinal cords (primarily in CNS lesions) were T and B lymphocytes and 8% were macrophages, although virus genomes were detected in <1% of apoptotic cells, consistent with infection of only a low percentage of macrophages and the fact that TMEV does not infect T or B lymphocytes in culture. Thus, some means other than direct infection was responsible for apoptosis of most CNS macrophages, including TMEV triggering apoptosis through tumor necrosis factor alpha or tumor necrosis factor alpha-related apoptosis-inducing ligand by binding death receptors on activated macrophages in vitro, as reported elsewhere (17).Infection of mouse macrophages induces apoptosis (16, 26) mediated by Bax through the intrinsic or mitochondrial pathway and severely restricts the yield of progeny virus (37). Thus, apoptosis may be a mechanism to attenuate the virus yet promote macrophage-to-macrophage spread through phagocytosis of infected apoptotic blebs during persistence (37). In contrast, TMEV infection in other rodent cells tested thus far, including baby hamster kidney (BHK-21) cells, produces necrotic cell death with high virus yields. The contrasting outcomes of TMEV infection point to the existence of two distinct virus-induced cell death programs.The genes of an increasing number of RNA viruses have been shown to encode proteins that trigger apoptosis. Among picornaviruses, coxsackievirus B3 1B (VP2) (12, 13), avian encephalomyocarditis virus 1C (VP3) (24) and 2C (25), enterovirus 71 2A (20), and poliovirus 2A (10) and 3C protease (3C^pro) (3) induce apoptosis, mostly through the intrinsic pathway. Coxsackievirus B3 VP2 has been shown to interact with the proapoptotic Siva protein in a yeast two-hybrid screen (12), but exactly how the VP2-Siva interaction or any of the other picornavirus proteins initiates the apoptotic cascade remains unknown.To gain insight into the upstream signaling events that lead to apoptosis, we tested the ability of individual BeAn virus nonstructural genes to induce apoptosis in uninfected BHK-21 cells. Only the leader (L) protein resulted in apoptosis and mutation of the CHCC Zn finger motif in L significantly reduced L protein-induced apoptosis.