Ammonium removal from landfill leachate by chemical precipitation

Accepted ManuscriptPublishe

Using Neural Networks for Relation Extraction from Biomedical Literature

Using different sources of information to support automated extracting of relations between biomedical concepts contributes to the development of our understanding of biological systems. The primary comprehensive source of these relations is biomedical literature. Several relation extraction approaches have been proposed to identify relations between concepts in biomedical literature, namely, using neural networks algorithms. The use of multichannel architectures composed of multiple data representations, as in deep neural networks, is leading to state-of-the-art results. The right combination of data representations can eventually lead us to even higher evaluation scores in relation extraction tasks. Thus, biomedical ontologies play a fundamental role by providing semantic and ancestry information about an entity. The incorporation of biomedical ontologies has already been proved to enhance previous state-of-the-art results.Comment: Artificial Neural Networks book (Springer) - Chapter 1

Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

Generation of integration-free neural progenitor cells from cells in human urine

Human neural stem cells hold great promise for research and therapy in neural disease. We describe the generation of integration-free and expandable human neural progenitor cells (NPCs). We combined an episomal system to deliver reprogramming factors with a chemically defined culture medium to reprogram epithelial-like cells from human urine into NPCs (hUiNPCs). These transgene-free hUiNPCs can self-renew and can differentiate into multiple functional neuronal subtypes and glial cells in vitro. Although functional in vivo analysis is still needed, we report that the cells survive and differentiate upon transplant into newborn rat brain.postprin

Determination of the number of J/ψ events with J/ψ → inclusive decays

postprin

Higher-order multipole amplitude measurement in ψ ′→γχ c2

Using 106×106 ψ ′ events collected with the BESIII detector at the BEPCII storage ring, the higher-order multipole amplitudes in the radiative transition ψ ′→γχ c2→γπ +π -/γK +K - are measured. A fit to the χ c2 production and decay angular distributions yields M2=0.046±0. 010±0.013 and E3=0.015±0.008±0.018, where the first errors are statistical and the second systematic. Here M2 denotes the normalized magnetic quadrupole amplitude and E3 the normalized electric octupole amplitude. This measurement shows evidence for the existence of the M2 signal with 4.4σ statistical significance and is consistent with the charm quark having no anomalous magnetic moment. © 2011 American Physical Society.published_or_final_versio

Self-sustained combustion of CO with transient changes and reaction mechanism over CuCe0.75Zr0.25O delta powder for honeycomb ceramic catalyst

A CuCe0.75Zr0.25O delta catalyst was prepared by the sol-gel method and successfully coated on honeycomb ceramic (HC) carrier. The activity of CuCe0.75Zr0.25O delta/HC was determined by the CO-TPO + FLIR, with the results performing that the critical condition for CO self-sustained combustion is 3 vol% CO + 3 vol% O-2/N-2 at 0.5 L/min. As the CO concentration increases from 1 vol% CO to 3 vol% CO, the induction process ( T-15) shifts to rapid ignition with a transient change for the CO oxidation reaction. The furnace temperature for CO self-sustained combustion decreases with increasing the CO and O-2 concentrations. Upon increasing the CO2 concentration, however, furnace temperature is needed to increase and realize CO complete conversion. The thermal stability test combined with SEM + EDX results indicate that the CuCe0.75Zr0.25O delta/HC retains an excellent thermal stability after a 200 h, and the high-temperature region remains at 225 +/- 1 degrees C during the CO self-combustion reaction. The activity of catalyst is reduced slightly after the 200 h test because of the carbon deposition on the catalyst surface, but such a slight deactivation can be eliminated by the air oxidation method. In situ IR results show a competitive adsorption of CO/O-2 and CO2 on the Cu-Ce active sites, indicating that the addition of gaseous CO2 performs an inhibition of CO oxidation. CO preferentially adsorbs linearly at Cu+ sites to form carbonyls that react with lattice oxygen to produce CO2 to release, which can be ascribed to M-K mechanism. The L-H mechanism is less important, which involves the relatively weak reaction of adsorbed CO and adsorbed oxygen on the Cu-Ce active sites to form carbonate species

Two-photon widths of the χ c0,2 states and helicity analysis for χ c2→γγ

Based on a data sample of 106×106 ψ ′ events collected with the BESIII detector, the decays ψ ′→γχ c0,2, χ c0,2→γγ are studied to determine the two-photon widths of the χ c0,2 states. The two-photon decay branching fractions are determined to be B(χ c0→γγ)=(2. 24±0.19±0.12±0.08)×10 -4 and B(χ c2→γγ)=(3.21±0.18±0. 17±0.13)×10 -4. From these, the two-photon widths are determined to be Γ γγ(χ c0)=(2. 33±0.20±0.13±0.17)keV, Γ γγ(χ c2)=(0.63±0.04±0. 04±0.04)keV, and R=Γ γγ(χ c2)/ Γ γγ(χ c0)=0.271±0. 029±0.013±0.027, where the uncertainties are statistical, systematic, and those from the PDG B(ψ ′→γχ c0,2) and Γ(χ c0,2) errors, respectively. The ratio of the two-photon widths for helicity λ=0 and helicity λ=2 components in the decay χ c2→γγ is measured for the first time to be f 0/2=Γγγλ= 0(χ c2)/Γγγλ=2(χ c2)=0. 00±0.02±0.02. © 2012 American Physical Society.published_or_final_versio

Contribution of human hematopoietic stem cells to liver repair

Immune-deficient mouse models of liver damage allow examination of human stem cell migration to sites of damage and subsequent contribution to repair and survival. In our studies, in the absence of a selective advantage, transplanted human stem cells from adult sources did not robustly become hepatocytes, although some level of fusion or hepatic differentiation was documented. However, injected stem cells did home to the injured liver tissue and release paracrine factors that hastened endogenous repair and enhanced survival. There were significantly higher levels of survival in mice with a toxic liver insult that had been transplanted with human stem cells but not in those transplanted with committed progenitors. Transplantation of autologous adult stem cells without conditioning is a relatively safe therapy. Adult stem cells are known to secrete bioactive factors that suppress the local immune system, inhibit fibrosis (scar formation) and apoptosis, enhance angiogenesis, and stimulate recruitment, retention, mitosis, and differentiation of tissue-residing stem cells. These paracrine effects are distinct from the direct differentiation of stem cells to repair tissue. In patients at high risk while waiting for a liver transplant, autologous stem cell therapy could be considered, as it could delay the decline in liver function

XIAP impairs Smac release from the mitochondria during apoptosis

X-linked inhibitor of apoptosis protein (XIAP) is a potent inhibitor of caspases 3, 7 and 9, and mitochondrial Smac (second mitochondria-derived activator of caspase) release during apoptosis inhibits the activity of XIAP. In this study we show that cytosolic XIAP also feeds back to mitochondria to impair Smac release. We constructed a fluorescent XIAP-fusion protein by labelling NH2- and COOH-termini with Cerulean fluorescent protein (C-XIAP-C). Immunoprecipitation confirmed that C-XIAP-C retained the ability to interact with Smac and impaired extrinsically and intrinsically activated apoptosis in response to tumour necrosis factor-related apoptosis-inducing ligand/cycloheximide and staurosporine. In C-XIAP-C-expressing cells, cytochrome c release from mitochondria proceeded normally, whereas Smac release was significantly prolonged and incomplete. In addition, physiological expression of native XIAP prolonged or limited Smac release in HCT-116 colon cancer cells and primary mouse cortical neurons. The Smac-binding capacity of XIAP, but not caspase inhibition, was central for mitochondrial Smac retention, as evidenced in experiments using XIAP mutants that cannot bind to Smac or effector caspases. Similarly, the release of a Smac mutant that cannot bind to XIAP was not impaired by C-XIAP-C expression. Full Smac release could however be provoked by rapid cytosolic C-XIAP-C depletion upon digitonin-induced plasma membrane permeabilization. Our findings suggest that although mitochondria may already contain pores sufficient for cytochrome c release, elevated amounts of XIAP can selectively impair and limit the release of Smac