Enhanced hydrogen storage in Ni/Ce composite oxides

The properties of dried (but not calcined) coprecipitated nickel ceria systems have been investigated in terms of their hydrogen emission characteristics following activation in hydrogen. XRD and BET data obtained on the powders show similarities to calcined ceria but it is likely that the majority of the material produced by the coprecipitation process is largely of an amorphous nature. XPS data indicate very little nickel is present on the outermost surface of the particles. Nevertheless, the thermal analytical techniques (TGA, DSC and TPD-MS) indicate that the hydrogen has access to the catalyst present and the nickel is able to generate hydrogen species capable of interacting with the support. Both unactivated and activated materials show two hydrogen emission features, viz. low temperature and high temperature emissions (LTE and HTE, respectively) over the temperature range 50 and 500 °C. A clear effect of hydrogen interaction with the material is that the activated sample not only emits much more hydrogen than the corresponding unactivated one but also at lower temperatures. H2 dissociation occurs on the reduced catalyst surface and the spillover mechanism transfers this active hydrogen into the ceria, possibly via the formation and migration of OH− species. The amount of hydrogen obtained (0.24 wt%) is 10× higher than those observed for calcined materials and would suggest that the amorphous phase plays a critical role in this process. The affiliated emissions of CO and CO2 with that of the HTE hydrogen (and consumption of water) strongly suggests a proportion of the hydrogen emission at this point arises from the water gas shift type reaction. It has not been possible from the present data to delineate between the various hydrogen storage mechanisms reported for ceria

TrkB Isoforms Differentially Affect AICD Production through Their Intracellular Functional Domains

We report that NTRK2, the gene encoding for the TrkB receptor, can regulate APP metabolism, specifically AICD levels. Using the human neuroblastoma cell line SH-SY5Y, we characterized the effect of three TrkB isoforms (FL, SHC, T) on APP metabolism by knockdown and overexpression. We found that TrkB FL increases AICD-mediated transcription and APP levels while it decreases sAPP levels. These effects were mainly mediated by the tyrosine kinase activity of the receptor and partially by the PLC-γ- and SHC-binding sites. The TrkB T truncated isoform did not have significant effects on APP metabolism when transfected by itself, while the TrkB SHC decreased AICD-mediated transcription. TrkB T abolished TrkB FL effects on APP metabolism when cotransfected with it while TrkB SHC cotransfected with TrkB FL still showed increased APP levels. In conclusion, we demonstrated that TrkB isoforms have differential effects on APP metabolism

Left ventricular function after valve repair for chronic mitral regurgitation: Predictive value of preoperative assessment of contractile reserve by exercise echocardiography

Objectives.We evaluated the value of preoperative assessment of left ventricular contractile reserve in predicting ventricular function after valve repair for minimally symptomatic mitral regurgitation.Background.The optimal timing for operation in minimally symptomatic patients with significant mitral regurgitation is controversial. Accurate preoperative assessment of left ventricular function is difficult, and the ability to predict postoperative function is limited. Previous studies in patients undergoing mitral valve replacement may not be applicable in the present era of valve repair.Methods.We performed exercise echocardiography in 139 patients with isolated mitral regurgitation and no coronary disease, 74 of whom subsequently underwent uncomplicated valve repair. We measured rest left ventricular end-systolic dimension, end-systolic wall stress and positive first derivative of left ventricular pressure (dP/dt). End-diastolic and end-systolic volumes and ejection fraction were measured preoperatively at rest, immediately after exercise and postoperatively.Results.Ejection fraction decreased postoperatively to 55 ± 10% from a rest preoperative value of 64 ± 9% (p < 0.001). Compared with patients with a postoperative ejection fraction ≥50% (n = 56), patients with postoperative ejection fraction <50% (n = 18) had a significantly lower preoperative exercise ejection fraction (57 ± 11% vs. 73 ± 9%, p < 0.0005), a larger exercise end-systolic volume index (32 ± 8 vs. 18 ± 7 cm3/m2, p < 0.0005) and a lower change in ejection fraction with exercise (−4 ± 8% vs. 9 ± 10%, p < 0.005). Preoperative rest indexes, including dP/dt, end-systolic wall stress and end-systolic volume index were less predictive, whereas exercise capacity, rest ejection fraction and end-systolic dimension were not predictive of postrepair ejection fraction. An exercise end-systolic volume index >25 cm3/m2 was the best predictor of postoperative dysfunction, with a sensitivity and specificity of 83%.Conclusions.In minimally symptomatic patients with mitral regurgitation, latent ventricular dysfunction may be indicated by a limited contractile reserve, manifest at exercise as an inadequate increase in ejection fraction and a larger end-systolic volume. These variables may also be used to predict left ventricular function after repair

Il10 Deficiency Rebalances Innate Immunity to Mitigate Alzheimer-Like Pathology

SummaryThe impact of inflammation suppressor pathways on Alzheimer’s disease (AD) evolution remains poorly understood. Human genetic evidence suggests involvement of the cardinal anti-inflammatory cytokine, interleukin-10 (IL10). We crossed the APP/PS1 mouse model of cerebral amyloidosis with a mouse deficient in Il10 (APP/PS1+Il10−/−). Quantitative in silico 3D modeling revealed activated Aβ phagocytic microglia in APP/PS1+Il10−/− mice that restricted cerebral amyloidosis. Genome-wide RNA sequencing of APP/PS1+Il10−/− brains showed selective modulation of innate immune genes that drive neuroinflammation. Il10 deficiency preserved synaptic integrity and mitigated cognitive disturbance in APP/PS1 mice. In vitro knockdown of microglial Il10-Stat3 signaling endorsed Aβ phagocytosis, while exogenous IL-10 had the converse effect. Il10 deficiency also partially overcame inhibition of microglial Aβ uptake by human Apolipoprotein E. Finally, the IL-10 signaling pathway was abnormally elevated in AD patient brains. Our results suggest that “rebalancing” innate immunity by blocking the IL-10 anti-inflammatory response may be therapeutically relevant for AD

DASHR: Database of Small Human Noncoding RNAs

Small non-coding RNAs (sncRNAs) are highly abundant RNAs, typically long, that act as key regulators of diverse cellular processes. Although thousands of sncRNA genes are known to exist in the human genome, no single database provides searchable, unified annotation, and expression information for full sncRNA transcripts and mature RNA products derived from these larger RNAs. Here, we present the Database of small human noncoding RNAs (DASHR) . DASHR contains the most comprehensive information to date on human sncRNA genes and mature sncRNA products. DASHR provides a simple user interface for researchers to view sequence and secondary structure, compare expression levels, and evidence of specific processing across all sncRNA genes and mature sncRNA products in various human tissues. DASHR annotation and expression data covers all major classes of sncRNAs including microRNAs (miRNAs), Piwi-interacting (piRNAs), small nuclear, nucleolar, cytoplasmic (sn-, sno-, scRNAs, respectively), transfer (tRNAs), and ribosomal RNAs (rRNAs). Currently, DASHR (v1.0) integrates 187 smRNA high-throughput sequencing (smRNA-seq) datasets with over 2.5 billion reads and annotation data from multiple public sources. DASHR contains annotations for ~48,000 human sncRNA genes and mature sncRNA products, 82% of which are expressed in one of more of the curated tissues. DASHR is available at http://lisanwanglab.org/DASHR

Elevation of methylated DNA in KILLIN/PTEN in the plasma of patients with thyroid and/or breast cancer

© 2014 Ng et al. Around 80% of mutations in the PTEN gene have been reported to be associated with diseases such as Cowden syndrome, which is an autosomal dominant disorder associated with an increased risk of developing breast, thyroid, and endometrial neoplasms. Recent studies have also demonstrated that KILLIN, which is located proximally to PTEN, shares the same transcription start site, and is assumed to be regulated by the same promoter, but is transcribed in the opposite direction. In this regard, we postulate that there may be a connection between KILLIN/PTEN genes and breast and thyroid cancers. Using real-time quantitative polymerase chain reaction (qPCR), we found that expression of KILLIN, but not PTEN, was significantly decreased in 23 Chinese women with a personal history of breast and thyroid cancer or a personal history of breast cancer and a family history of thyroid cancer, or vice versa, and at least two persons in the family with thyroid cancer or at a young age ,40 years, when compared with healthy controls (P<0.0001). No PTEN mutations were found in these 23 patients. We then developed a simple methylation-sensitive restriction enzyme digestion followed by real-time quantitative assay to quantify plasma methylated KILLIN/PTEN DNA in these patients. Plasma levels of methylated KILLIN/PTEN DNA were significantly increased in these patients when compared with healthy controls (P<0.05). This study shows that plasma methylated KILLIN/PTEN DNA was significantly elevated, suggesting hypermethylation of the KILLIN/PTEN promoter in breast and thyroid cancer patients.published_or_final_versio

Swine ANP32A supports avian influenza virus polymerase

Avian influenza viruses occasionally infect and adapt to mammals, including humans. Swine are often described as 'mixing vessels', being susceptible to both avian and human origin viruses, which allows the emergence of novel reassortants, such as the precursor to the 2009 H1N1 pandemic. ANP32 proteins are host factors that act as influenza virus polymerase cofactors. In this study we describe how swine ANP32A, uniquely among the mammalian ANP32 proteins tested, supports activity of avian origin influenza virus polymerases, and avian influenza virus replication. We further show that after the swine-origin influenza virus emerged in humans and caused the 2009 pandemic it evolved polymerase gene mutations that enabled it to more efficiently use human ANP32 proteins. We map the enhanced pro-viral activity of swine ANP32A to a pair of amino acids, 106 and 156, in the leucine-rich repeat and central domains and show these mutations enhance binding to influenza virus trimeric polymerase. These findings help elucidate the molecular basis for the 'mixing vessel' trait of swine and further our understanding of the evolution and ecology of viruses in this host.Importance Avian influenza viruses can jump from wild birds and poultry into mammalian species such as humans or swine, but only continue to transmit if they accumulate mammalian adapting mutations. Pigs appear uniquely susceptible to both avian and human strains of influenza and are often described as virus 'mixing vessels'. In this study, we describe how a host factor responsible for regulating virus replication, ANP32A, is different between swine and humans. Swine ANP32A allows a greater range of influenza viruses, specifically those from birds, to replicate. It does this through binding the virus polymerase more tightly than the human version of the protein. This work helps to explain the unique properties of swine as 'mixing vessels'

High-Dimensional Single-Cell Mapping of Central Nervous System Immune Cells Reveals Distinct Myeloid Subsets in Health, Aging, and Disease

Individual reports suggest that the central nervous system (CNS) contains multiple immune cell types with diverse roles in tissue homeostasis, immune defense, and neurological diseases. It has been challenging to map leukocytes across the entire brain, and in particular in pathology, where phenotypic changes and influx of blood-derived cells prevent a clear distinction between reactive leukocyte populations. Here, we applied high-dimensional single-cell mass and fluorescence cytometry, in parallel with genetic fate mapping systems, to identify, locate, and characterize multiple distinct immune populations within the mammalian CNS. Using this approach, we revealed that microglia, several subsets of border-associated macrophages and dendritic cells coexist in the CNS at steady state and exhibit disease-specific transformations in the immune microenvironment during aging and in models of Alzheimer's disease and multiple sclerosis. Together, these data and the described framework provide a resource for the study of disease mechanisms, potential biomarkers, and therapeutic targets in CNS disease

Impact of Allergic Reactions on Food-Specific IgE Concentrations and Skin Test Results

Although there is concern that food allergic reactions may negatively affect the natural history of food allergy, the impact of reactions on food-specific IgE (sIgE) or skin prick tests is unknown

Economic Impacts of Non-Native Forest Insects in the Continental United States

Reliable estimates of the impacts and costs of biological invasions are critical to developing credible management, trade and regulatory policies. Worldwide, forests and urban trees provide important ecosystem services as well as economic and social benefits, but are threatened by non-native insects. More than 450 non-native forest insects are established in the United States but estimates of broad-scale economic impacts associated with these species are largely unavailable. We developed a novel modeling approach that maximizes the use of available data, accounts for multiple sources of uncertainty, and provides cost estimates for three major feeding guilds of non-native forest insects. For each guild, we calculated the economic damages for five cost categories and we estimated the probability of future introductions of damaging pests. We found that costs are largely borne by homeowners and municipal governments. Wood- and phloem-boring insects are anticipated to cause the largest economic impacts by annually inducing nearly $1.7 billion in local government expenditures and approximately$830 million in lost residential property values. Given observations of new species, there is a 32% chance that another highly destructive borer species will invade the U.S. in the next 10 years. Our damage estimates provide a crucial but previously missing component of cost-benefit analyses to evaluate policies and management options intended to reduce species introductions. The modeling approach we developed is highly flexible and could be similarly employed to estimate damages in other countries or natural resource sectors