Search for a Solution of the Pioneer Anomaly

In 1972 and 1973 the Pioneer 10 and 11 missions were launched. They were the first to explore the outer solar system and achieved stunning breakthroughs in deep-space exploration. But beginning in about 1980 an unmodeled force of \sim 8 \times 10^{-8} cm/s^2, directed approximately towards the Sun, appeared in the tracking data. It later was unambiguously verified as being in the data and not an artifact. The cause remains unknown (although radiant heat remains a likely origin). With time more and more effort has gone into understanding this anomaly (and also possibly related effects). We review the situation and describe ongoing programs to resolve the issue.Comment: 24 pages 8 figure

Density distribution profile for internodes and nodes of Phyllostachys edulis (Moso bamboo) by computer tomography scanning

This study aims to quantify the density distribution, and specify the density distribution difference between internodes and nodes parts of Phyllostachys edulis (Moso Bamboo) in the radial, tangential and longitudinal directions. Due to the anatomical complexity of Moso bamboo, the measurement methods of bulk density are insufficient. In this work, Computed Tomography (CT) scanning has been selected to quantify the density distribution of Moso bamboo. Major findings from both anatomical analysis and CT scanning quantifications are that the Moso bamboo density of the internodes parts and the nodes parts reduce from the external surface to the internal surface of the culm wall in the radial direction. In the longitudinal direction, the internode parts of the Moso bamboo have relatively uniform density. Significant density fluctuation variations occur at the nodes parts of the Moso bamboo. The different proportions of the vascular bundles tissues and the parenchyma ground tissues dominate the density variation of the Moso bamboo in the radial direction. In the longitudinal direction, relatively uniform density of the internodes parts of the Moso bamboo is attributed to the straight vascular bundles. The significant density variation in the node parts is caused by the irregular intertwined vascular bundles

Commensal microbiota stimulate systemic neutrophil migration through induction of Serum amyloid A: Microbiota regulate systemic neutrophil function

Neutrophils serve critical roles in inflammatory responses to infection and injury, and mechanisms governing their activity represent attractive targets for controlling inflammation. The commensal microbiota is known to regulate the activity of neutrophils and other leucocytes in the intestine, but the systemic impact of the microbiota on neutrophils remains unknown. Here we utilized in vivo imaging in gnotobiotic zebrafish to reveal diverse effects of microbiota colonization on systemic neutrophil development and function. The presence of a microbiota resulted in increased neutrophil number and myeloperoxidase expression, and altered neutrophil localization and migratory behaviours. These effects of the microbiota on neutrophil homeostasis were accompanied by an increased recruitment of neutrophils to injury. Genetic analysis identified the microbiota-induced acute phase protein serum amyloid A (Saa) as a host factor mediating microbial stimulation of tissue-specific neutrophil migratory behaviours. In vitro studies revealed that zebrafish cells respond to Saa exposure by activating NF-κB, and that Saa-dependent neutrophil migration requires NF-κB-dependent gene expression. These results implicate the commensal microbiota as an important environmental factor regulating diverse aspects of systemic neutrophil development and function, and reveal a critical role for a Saa-NF-κB signalling axis in mediating neutrophil migratory responses

Elevated Ratio of Urinary Metabolites of Thromboxane and Prostacyclin Is Associated with Adverse Cardiovascular Events in ADAPT

Results from prevention trials, including the Alzheimer's Disease Anti-inflammatory Prevention Trial (ADAPT), have fueled discussion about the cardiovascular (CV) risks associated with non-steroidal anti-inflammatory drugs (NSAIDs). We tested the hypotheses that (i) adverse CV events reported among ADAPT participants (aged 70 years and older) are associated with increased ratio of urine 11-dehydrothromboxane B2 (Tx-M) to 2′3-donor–6-keto-PGF1 (PGI-M) attributable to NSAID treatments; (ii) coincident use of aspirin (ASA) would attenuate NSAID-induced changes in Tx-M/PGI-M ratio; and (iii) use of NSAIDs and/or ASA would not alter urine or plasma concentrations of F2-isoprostanes (IsoPs), in vivo biomarkers of free radical damage. We quantified urine Tx-M and PGI-M, and urine and plasma F2-IsoPs from 315 ADAPT participants using stable isotope dilution assays with gas chromatography/mass spectrometry, and analyzed these data by randomized drug assignment and self-report compliance as well as ASA use. Adverse CV events were significantly associated with higher urine Tx-M/PGI-M ratio, which seemed to derive mainly from lowered PGI-M. Participants taking ASA alone had reduced urine Tx-M/PGI-M compared to no ASA or NSAID; however, participants taking NSAIDs plus ASA did not have reduced urine Tx-M/PGI-M ratio compared to NSAIDs alone. Neither NSAID nor ASA use altered plasma or urine F2-IsoPs. These data suggest a possible mechanism for the increased risk of CV events reported in ADAPT participants assigned to NSAIDs, and suggest that the changes in the Tx-M/PGI-M ratio was not substantively mitigated by coincident use of ASA in individuals 70 years or older

NSAID Use Selectively Increases the Risk of Non-Fatal Myocardial Infarction: A Systematic Review of Randomised Trials and Observational Studies

Recent clinical trials and observational studies have reported increased coronary events associated with non steroidal anti-inflammatory drugs (NSAIDs). There appeared to be a disproportionate increase in non-fatal versus fatal events, however, numbers of fatal events in individual studies were too small, and event rates too low, to be meaningful.We undertook a pooled analysis to investigate the effect of NSAIDs on myocardial infarction (MI) risk with the specific aim to differentiate non-fatal from fatal events.We searched Pubmed (January, 1990 to March, 2010) for observational studies and randomised controlled trials that assessed the effect of NSAIDs (traditional or selective COX-2 inhibitors [coxibs]) on MI incidence separately for fatal and non-fatal events. Summary estimates of relative risk (RR) for non-fatal and fatal MIs were calculated with a random effects model.NSAID therapy carried a RR of 1.30 (95% CI, 1.20-1.41) for non-fatal MI with no effect on fatal MI (RR 1.02, 95% CI, 0.89-1.17) in six observational studies. Overall, the risk increase for non-fatal MI was 25% higher (95% CI, 11%-42%) than for fatal MI. The two studies that included only individuals with prior cardiovascular disease presented risk estimates for non-fatal MI on average 58% greater (95% CI, 26%-98%) than those for fatal MI. In nine randomised controlled trials, all investigating coxibs, the pooled RR estimate for non-fatal MI was 1.61 (95% CI, 1.04-2.50) and 0.86 (95% CI 0.51-1.47) for fatal MIs.NSAID use increases the risk of non-fatal MI with no substantial effect on fatal events. Such differential effects, with potentially distinct underlying pathology may provide insights into NSAID-induced coronary pathology. We studied the association between the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the risk of myocardial infarction (MI), separating non-fatal from fatal events, summarizing the evidence from both observational studies and randomised controlled trials. An increased risk of non-fatal MI was clearly found in both types of studies while use of NSAID did not confer an increased risk of fatal MI. Our findings provide support for the concept that thrombi generated under NSAID treatment could be different from spontaneous thrombi

Automatically Harnessing Sparse Acceleration

Sparse linear algebra is central to many scientific programs, yet compilers fail to optimize it well. High-performance libraries are available, but adoption costs are significant. Moreover, libraries tie programs into vendor-specific software and hardware ecosystems, creating non-portable code. In this paper, we develop a new approach based on our specification Language for implementers of Linear Algebra Computations (LiLAC). Rather than requiring the application developer to (re)write every program for a given library, the burden is shifted to a one-off description by the library implementer. The LiLAC-enabled compiler uses this to insert appropriate library routines without source code changes. LiLAC provides automatic data marshaling, maintaining state between calls and minimizing data transfers. Appropriate places for library insertion are detected in compiler intermediate representation, independent of source languages. We evaluated on large-scale scientific applications written in FORTRAN; standard C/C++ and FORTRAN benchmarks; and C++ graph analytics kernels. Across heterogeneous platforms, applications and data sets we show speedups of 1.1$\times$ to over 10$\times$ without user intervention.Comment: Accepted to CC 202

Description of the novel perchlorate-reducing bacteria Dechlorobacter hydrogenophilus gen. nov., sp. nov. and Propionivibrio militaris, sp. nov.

Novel dissimilatory perchlorate-reducing bacteria (DPRB) were isolated from enrichments conducted under conditions different from those of all previously described DPRB. Strain LT-1T was enriched using medium buffered at pH 6.6 with 2-(N-morpholino)ethanesulfonic acid (MES) and had only 95% 16S rRNA gene identity with its closest relative, Azonexus caeni. Strain MPT was enriched in the cathodic chamber of a perchlorate-reducing bioelectrical reactor (BER) and together with an additional strain, CR (99% 16S rRNA gene identity), had 97% 16S rRNA gene identity with Propionivibrio limicola. The use of perchlorate and other electron acceptors distinguished strains MPT and CR from P. limicola physiologically. Strain LT-1T had differences in electron donor utilization and optimum growth temperatures from A. caeni. Strains LT-1T and MPT are the first DPRB to be described in the Betaproteobacteria outside of the Dechloromonas and Azospira genera. On the basis of phylogenetic and physiological features, strain LT-1T represents a novel genus in the Rhodocyclaceae; strain MPT represents a novel species within the genus Propionivibrio. The names Dechlorobacter hydrogenophilus gen. nov., sp. nov and Propionivibrio militaris sp. nov. are proposed

A genetic assessment of the human-facilitated colonization history of black swans in Australia and New Zealand

Movement of species beyond their indigenous distribution can fundamentally alter the conservation status of the populations involved. If introductions are human-facilitated, introduced species could be considered pests. Characterizing the colonization history of introduced species can therefore be critical to formulating the objectives and nature of wildlife management strategies. The black swan (Cygnus atratus) is native to Australia but is considered a reintroduced species in New Zealand, where the endemic population was reported extinct during the 19th century. After the reintroduction of a small number of individuals from Australia, the New Zealand population expanded unexpectedly rapidly, which was attributed to simultaneous waves of migration from Australia. An alternative, but hitherto unformalized, hypothesis is that local extant populations remained and admixed with introduced individuals. To contribute to our understanding of the reintroduction history of the species, we investigated dispersal patterns and demographic histories of seven populations from Australia and New Zealand, using population genetic inferences from a microsatellite dataset. Our results on genetic structure, dispersal rates, and demographic histories provide mixed evidence on the origin of New Zealand black swans. The hypothesis that reintroduced individuals mixed with remaining local individuals and that the subsequent dramatic population expansion may have been due to genetic rescue of the inbred indigenous population cannot be discarded and needs further investigation.Publisher PDFPeer reviewe

Testing the “read-across hypothesis” by investigating the effects of ibuprofen on fish

Supplementary data related to this article can be found at http:// dx.doi.org/10.1016/j.chemosphere.2016.08.041Human pharmaceuticals present in the environment have the potential to cause adverse effects on non-target organisms. The “read-across hypothesis” stipulates that pharmaceuticals will exhibit similar biological effects across species (e.g. human and fish) if the molecular target has been conserved and the effective drug concentrations are reached (Cmax). We tested this hypothesis by evaluating if ibuprofen, a non-selective inhibitor of prostaglandins and the cyclooxygenase (COX) enzyme, can mimic its primary effect in humans, on fish, at comparable plasma concentrations. The endpoints, “prostaglandin E metabolite” (PGEM) levels and the mRNA expression of COX (ptgs gene), were measured in the gills of control and exposed fathead minnows (Pimephales promelas), using enzyme-immunoassay and quantitative real-time PCR (qPCR). Fish were exposed, for 24-72 h, to measured water concentrations of 9 (n= 12), 370 (n= 40) and 470 μg ibuprofen/L (n= 12). Water and blood plasma concentrations were determined using LC-MS/MS. Results showed that PGEM levels in fish exposed to 370 and 470 μg ibuprofen/L were significantly decreased compared to control fish, when mean plasma ibuprofen concentrations were 1.8 to 5.6-fold below the Cmax. The plasma ibuprofen concentrations and PGEM levels varied greatly between individuals. In fish exposed to 9 μg ibuprofen/L, when the mean plasma ibuprofen concentration was 224-fold below Cmax, no change in PGEM levels was observed. These data provide evidence for the read-across hypothesis, but suggest establishing a direct dose-response between internal plasma and PGEM is difficult, and would require significantly larger numbers of fish to overcome the inter-individual variation.This work was supported by Biotechnology and Biological Sci- ences Research Council (BBSRC) Industrial CASE Partnership Stu- dentship BB/I53257X/1 with AstraZeneca Safety Health and Environment Research Programme