Organic aerosol formation downwind from the Deepwater Horizon oil spill.

A large fraction of atmospheric aerosols are derived from organic compounds with various volatilities. A National Oceanic and Atmospheric Administration (NOAA) WP-3D research aircraft made airborne measurements of the gaseous and aerosol composition of air over the Deepwater Horizon (DWH) oil spill in the Gulf of Mexico that occurred from April to August 2010. A narrow plume of hydrocarbons was observed downwind of DWH that is attributed to the evaporation of fresh oil on the sea surface. A much wider plume with high concentrations of organic aerosol (>25 micrograms per cubic meter) was attributed to the formation of secondary organic aerosol (SOA) from unmeasured, less volatile hydrocarbons that were emitted from a wider area around DWH. These observations provide direct and compelling evidence for the importance of formation of SOA from less volatile hydrocarbons

Atmospheric emissions from the deepwater Horizon spill constrain air-water partitioning, hydrocarbon fate, and leak rate

The fate of deepwater releases of gas and oil mixtures is initially determined by solubility and volatility of individual hydrocarbon species; these attributes determine partitioning between air and water. Quantifying this partitioning is necessary to constrain simulations of gas and oil transport, to predict marine bioavailability of different fractions of the gas-oil mixture, and to develop a comprehensive picture of the fate of leaked hydrocarbons in the marine environment. Analysis of airborne atmospheric data shows massive amounts (∼258,000 kg/day) of hydrocarbons evaporating promptly from the Deepwater Horizon spill; these data collected during two research flights constrain air-water partitioning, thus bioavailability and fate, of the leaked fluid. This analysis quantifies the fraction of surfacing hydrocarbons that dissolves in the water column (∼33% by mass), the fraction that does not dissolve, and the fraction that evaporates promptly after surfacing (∼14% by mass). We do not quantify the leaked fraction lacking a surface expression; therefore, calculation of atmospheric mass fluxes provides a lower limit to the total hydrocarbon leak rate of 32,600 to 47,700 barrels of fluid per day, depending on reservoir fluid composition information. This study demonstrates a new approach for rapid-response airborne assessment of future oil spills. Copyright 2011 by the American Geophysical Union

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

The Perfect Family: Decision Making in Biparental Care

Background Previous theoretical work on parental decisions in biparental care has emphasized the role of the conflict between evolutionary interests of parents in these decisions. A prominent prediction from this work is that parents should compensate for decreases in each other\u27s effort, but only partially so. However, experimental tests that manipulate parents and measure their responses fail to confirm this prediction. At the same time, the process of parental decision making has remained unexplored theoretically. We develop a model to address the discrepancy between experiments and the theoretical prediction, and explore how assuming different decision making processes changes the prediction from the theory. Model Description We assume that parents make decisions in behavioral time. They have a fixed time budget, and allocate it between two parental tasks: provisioning the offspring and defending the nest. The proximate determinant of the allocation decisions are parents\u27 behavioral objectives. We assume both parents aim to maximize the offspring production from the nest. Experimental manipulations change the shape of the nest production function. We consider two different scenarios for how parents make decisions: one where parents communicate with each other and act together (the perfect family), and one where they do not communicate, and act independently (the almost perfect family). Conclusions/Significance The perfect family model is able to generate all the types of responses seen in experimental studies. The kind of response predicted depends on the nest production function, i.e. how parents\u27 allocations affect offspring production, and the type of experimental manipulation. In particular, we find that complementarity of parents\u27 allocations promotes matching responses. In contrast, the relative responses do not depend on the type of manipulation in the almost perfect family model. These results highlight the importance of the interaction between nest production function and how parents make decisions, factors that have largely been overlooked in previous models

MicroRNAs in pulmonary arterial remodeling

Pulmonary arterial remodeling is a presently irreversible pathologic hallmark of pulmonary arterial hypertension (PAH). This complex disease involves pathogenic dysregulation of all cell types within the small pulmonary arteries contributing to vascular remodeling leading to intimal lesions, resulting in elevated pulmonary vascular resistance and right heart dysfunction. Mutations within the bone morphogenetic protein receptor 2 gene, leading to dysregulated proliferation of pulmonary artery smooth muscle cells, have been identified as being responsible for heritable PAH. Indeed, the disease is characterized by excessive cellular proliferation and resistance to apoptosis of smooth muscle and endothelial cells. Significant gene dysregulation at the transcriptional and signaling level has been identified. MicroRNAs are small non-coding RNA molecules that negatively regulate gene expression and have the ability to target numerous genes, therefore potentially controlling a host of gene regulatory and signaling pathways. The major role of miRNAs in pulmonary arterial remodeling is still relatively unknown although research data is emerging apace. Modulation of miRNAs represents a possible therapeutic target for altering the remodeling phenotype in the pulmonary vasculature. This review will focus on the role of miRNAs in regulating smooth muscle and endothelial cell phenotypes and their influence on pulmonary remodeling in the setting of PAH

Collision Mortality Has No Discernible Effect on Population Trends of North American Birds

Avian biodiversity is threatened by numerous anthropogenic factors and migratory species are especially at risk. Migrating birds frequently collide with manmade structures and such losses are believed to represent the majority of anthropogenic mortality for North American birds. However, estimates of total collision mortality range across several orders of magnitude and effects on population dynamics remain unknown. Herein, we develop a novel method to assess relative vulnerability to anthropogenic threats, which we demonstrate using 243,103 collision records from 188 species of eastern North American landbirds. After correcting mortality estimates for variation attributable to population size and geographic overlap with potential collision structures, we found that per capita vulnerability to collision with buildings and towers varied over more than four orders of magnitude among species. Species that migrate long distances or at night were much more likely to be killed by collisions than year-round residents or diurnal migrants. However, there was no correlation between relative collision mortality and long-term population trends for these same species. Thus, although millions of North American birds are killed annually by collisions with manmade structures, this source of mortality has no discernible effect on populations

Desulfotomaculum varum sp. nov., a moderately thermophilic sulfate-reducing bacterium isolated from a microbial mat colonizing a Great Artesian Basin bore well runoff channel

A strictly anaerobic moderately thermophilic bacterium, designated strain RH04-3T (T = type strain), was isolated from a red colored microbial mat that colonizes a Great Artesian Basin (GAB) bore well (Registered Number 17263) runoff channel at 66 °C. The cells of strain RH04-3T were straight to slightly curved, sporulating, Gram-positive rods (2.0–5.0 × 1.0 μm) that grew optimally at 50 °C (temperature growth range between 37 and 55 °C) and at pH 7 (pH growth range of 5.0 and 8.5). Growth was inhibited by NaCl concentrations ≥1.5% (w/v), and by chloramphenicol, streptomycin, tetracycline, penicillin and ampicillin. The strain utilized fructose, mannose, glycerol, lactate, pyruvate and H2 in the presence of sulfate, and fermented pyruvate in the absence of sulfate. Strain RH04-3T reduced sulfate, sulfite, thiosulfate and elemental sulfur, but not nitrate, nitrite, iron(III), arsenate(V), vanadium(V) or cobalt(III) as terminal electron acceptors. The G + C content of DNA was 52.4 ± 0.8 mol % as determined by the thermal denaturation (Tm) method. 16S rRNA sequence analysis indicated that strain RH04-3T was a member of the genus Desulfotomaculum and was most closely related to Desulfotomaculum putei (similarity value of 95.2%) and Desulfotomaculum hydrothermale (similarity value of 93.6%). On the basis of phylogenetic and phenotypic characteristics, strain RH04-3T is considered to represent a novel species of the genus Desulfotomaculum, for which the name Desulfotomaculum varum sp. nov. is proposed. The type strain RH04-3T = JCM 16158T = KCTC 5794T

Brain and Spinal Cord Interaction: Protective Effects of Exercise Prior to Spinal Cord Injury

We have investigated the effects of a spinal cord injury on the brain and spinal cord, and whether exercise provided before the injury could organize a protective reaction across the neuroaxis. Animals were exposed to 21 days of voluntary exercise, followed by a full spinal transection (T7–T9) and sacrificed two days later. Here we show that the effects of spinal cord injury go beyond the spinal cord itself and influence the molecular substrates of synaptic plasticity and learning in the brain. The injury reduced BDNF levels in the hippocampus in conjunction with the activated forms of p-synapsin I, p-CREB and p-CaMK II, while exercise prior to injury prevented these reductions. Similar effects of the injury were observed in the lumbar enlargement region of the spinal cord, where exercise prevented the reductions in BDNF, and p-CREB. Furthermore, the response of the hippocampus to the spinal lesion appeared to be coordinated to that of the spinal cord, as evidenced by corresponding injury-related changes in BDNF levels in the brain and spinal cord. These results provide an indication for the increased vulnerability of brain centers after spinal cord injury. These findings also imply that the level of chronic activity prior to a spinal cord injury could determine the level of sensory-motor and cognitive recovery following the injury. In particular, exercise prior to the injury onset appears to foster protective mechanisms in the brain and spinal cord

From rehabilitation to recovery: protocol for a randomised controlled trial evaluating a goal-based intervention to reduce depression and facilitate participation post-stroke

<p>Abstract</p> <p>Background</p> <p>There is much discourse in healthcare about the importance of client-centred rehabilitation, however in the realm of community-based therapy post-stroke there has been little investigation into the efficacy of goal-directed practice that reflects patients' valued activities. In addition, the effect of active involvement of carers in such a rehabilitation process and their subsequent contribution to functional and emotional recovery post-stroke is unclear. In community based rehabilitation, interventions based on patients' perceived needs may be more likely to alter such outcomes. In this paper, we describe the methodology of a randomised controlled trial of an integrated approach to facilitating patient goal achievement in the first year post-stroke. The effectiveness of this intervention in reducing the severity of post-stroke depression, improving participation status and health-related quality of life is examined. The impact on carers is also examined.</p> <p>Methods/Design</p> <p>Patients (and their primary carers, if available) are randomly allocated to an intervention or control arm of the study. The intervention is multimodal and aims to screen for adverse stroke sequelae and address ways to enhance participation in patient-valued activities. Intervention methods include: telephone contacts, written information provision, home visitation, and contact with treating health professionals, with further relevant health service referrals as required. The control involves treatment as usual, as determined by inpatient and community rehabilitation treating teams. Formal blinded assessments are conducted at discharge from inpatient rehabilitation, and at six and twelve months post-stroke. The primary outcome is depression. Secondary outcome measures include participation and activity status, health-related quality of life, and self-efficacy.</p> <p>Discussion</p> <p>The results of this trial will assist with the development of a model for community-based rehabilitation management for stroke patients and their carers, with emphasis on goal-directed practice to enhance home and community participation status. Facilitation of participation in valued activities may be effective in reducing the incidence or severity of post-stroke depression, as well as enhancing the individual's perception of their health-related quality of life. The engagement of carers in the rehabilitation process will enable review of the influence of the broader social context on recovery.</p> <p>Trial registration</p> <p>Australia and New Zealand Clinical Trials Register (ANZCTR): <a href="http://www.anzctr.org.au/ACTRN12608000042347.aspx">ACTRN12608000042347</a></p