Ozone and alkyl nitrate formation from the Deepwater Horizon oil spill atmospheric emissions

Ozone (O3), alkyl nitrates (RONO2), and other photochemical products were formed in the atmosphere downwind from the Deepwater Horizon (DWH) oil spill by photochemical reactions of evaporating hydrocarbons with NOx (=NO+NO2) emissions from spill response activities. Reactive nitrogen species and volatile organic compounds (VOCs) were measured from an instrumented aircraft during daytime flights in the marine boundary layer downwind from the area of surfacing oil. A unique VOC mixture, where alkanes dominated the hydroxyl radical (OH) loss rate, was emitted into a clean marine environment, enabling a focused examination of O3 and RONO 2 formation processes. In the atmospheric plume from DWH, the OH loss rate, an indicator of potential O3 formation, was large and dominated by alkanes with between 5 and 10 carbons per molecule (C 5-C10). Observations showed that NOx was oxidized very rapidly with a 0.8h lifetime, producing primarily C6-C10 RONO2 that accounted for 78% of the reactive nitrogen enhancements in the atmospheric plume 2.5h downwind from DWH. Both observations and calculations of RONO2 and O3 production rates show that alkane oxidation dominated O3 formation chemistry in the plume. Rapid and nearly complete oxidation of NOx to RONO2 effectively terminated O3 production, with O3 formation yields of 6.0±0.5 ppbv O3 per ppbv of NOx oxidized. VOC mixing ratios were in large excess of NOx, and additional NOx would have formed additional O3 in this plume. Analysis of measurements of VOCs, O3, and reactive nitrogen species and calculations of O3 and RONO2 production rates demonstrate that NOx-VOC chemistry in the DWH plume is explained by known mechanisms. Copyright 2012 by the American Geophysical Union

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

Biallelic JAK1 mutations in immunodeficient patient with mycobacterial infection

Mutations in genes encoding components of the immune system cause primary immunodeficiencies. Here, we study a patient with recurrent atypical mycobacterial infection and early-onset metastatic bladder carcinoma. Exome sequencing identified two homozygous missense germline mutations, P733L and P832S, in the JAK1 protein that mediates signalling from multiple cytokine receptors. Cells from this patient exhibit reduced JAK1 and STAT phosphorylation following cytokine stimulations, reduced induction of expression of interferon-regulated genes and dysregulated cytokine production; which are indicative of signalling defects in multiple immune response pathways including Interferon-γ production. Reconstitution experiments in the JAK1-deficient cells demonstrate that the impaired JAK1 function is mainly attributable to the effect of the P733L mutation. Further analyses of the mutant protein reveal a phosphorylation-independent role of JAK1 in signal transduction. These findings clarify JAK1 signalling mechanisms and demonstrate a critical function of JAK1 in protection against mycobacterial infection and possibly the immunological surveillance of cancer.Wellcome Trust (095198/Z/10/Z and 090233/Z/09/Z); Higher Education Funding Council for England; Great Ormond Street Hospital Children’s Charity; National Institute for Health Research (NIHR); Great Ormond Street Hospital Biomedical Research Centre; NIHR Cambridge Biomedical Research Centre; Alfonso Martin Escudero Foundatio

A valley-spin qubit in a carbon nanotube

Although electron spins in III-V semiconductor quantum dots have shown great promise as qubits, a major challenge is the unavoidable hyperfine decoherence in these materials. In group IV semiconductors, the dominant nuclear species are spinless, allowing for qubit coherence times that have been extended up to seconds in diamond and silicon. Carbon nanotubes are a particularly attractive host material, because the spin-orbit interaction with the valley degree of freedom allows for electrical manipulation of the qubit. In this work, we realise such a qubit in a nanotube double quantum dot. The qubit is encoded in two valley-spin states, with coherent manipulation via electrically driven spin resonance (EDSR) mediated by a bend in the nanotube. Readout is performed by measuring the current in Pauli blockade. Arbitrary qubit rotations are demonstrated, and the coherence time is measured via Hahn echo. Although the measured decoherence time is only 65 ns in our current device, this work offers the possibility of creating a qubit for which hyperfine interaction can be virtually eliminated

Autoinflammatory periodic fever, immunodeficiency, and thrombocytopenia (PFIT) caused by mutation in actinregulatory gene WDR1

The importance of actin dynamics in the activation of the inflammasome is becoming increasingly apparent. IL-1β, which is activated by the inflammasome, is known to be central to the pathogenesis of many monogenic autoinflammatory diseases. However, evidence from an autoinflammatory murine model indicates that IL-18, the other cytokine triggered by inflammasome activity, is important in its own right. In this model, autoinflammation was caused by mutation in the actin regulatory gene WDR1 We report a homozygous missense mutation in WDR1 in two siblings causing periodic fevers with immunodeficiency and thrombocytopenia. We found impaired actin dynamics in patient immune cells. Patients had high serum levels of IL-18, without a corresponding increase in IL-18-binding protein or IL-1β, and their cells also secreted more IL-18 but not IL-1β in culture. We found increased caspase-1 cleavage within patient monocytes indicative of increased inflammasome activity. We transfected HEK293T cells with pyrin and wild-type and mutated WDR1 Mutant protein formed aggregates that appeared to accumulate pyrin; this could potentially precipitate inflammasome assembly. We have extended the findings from the mouse model to highlight the importance of WDR1 and actin regulation in the activation of the inflammasome, and in human autoinflammation

Gossip as a Burdened Virtue

Gossip is often serious business, not idle chitchat. Gossip allows those oppressed to privately name their oppressors as a warning to others. Of course, gossip can be in error. The speaker may be lying or merely have lacked sufficient evidence. Bias can also make those who hear the gossip more or less likely to believe the gossip. By examining the social functions of gossip and considering the differences in power dynamics in which gossip can occur, we contend that gossip may be not only permissible but virtuous, both as the only reasonable recourse available and as a means of resistance against oppression

Immunobiological effects of gemcitabine and capecitabine combination chemotherapy in advanced pancreatic ductal adenocarcinoma

Background: Preclinical studies suggest that chemotherapy may enhance the immune response against pancreatic cancer. Methods: The levels of granulocyte macrophage-colony-stimulating factor (GM-CSF) and interleukin-6 (IL-6) and the associated inflammatory marker C-reactive protein (CRP) were assessed in 38 patients receiving gemcitabine and capecitabine combination chemotherapy for advanced pancreatic cancer within the TeloVac trial. Apoptosis (M30) and total immune response (delayed-type hypersensitivity and/or T-cell response) were also assessed and levels of apoptosis induction correlated with immune response. The telomerase GV1001 vaccine was given either sequentially (n=18) or concomitantly (n=24) with the combination chemotherapy. Results: There were no differences between baseline and post-treatment levels of CRP (P=0.19), IL-6 (P=0.19) and GM-CSF (P=0.71). There was a positive correlation between post-chemotherapy CRP and IL-6 levels (r=0.45, P=0.005) and between CRP with carbohydrate antigen-19-9 (CA19-9) levels at baseline (r=0.45, P=0.015) and post treatment (r=0.40, P=0.015). The change in CRP and IL-6 levels was positively correlated (r=0.40, P=0.012). Hazard ratios (95% CI) for baseline CA19-9 (1.30 (1.07–1.59), P=0.009) and CRP (1.55 (1.00–2.39), P=0.049) levels were each independently predictive of survival. The M30 mean matched differences between pre- and post-chemotherapy showed evidence of apoptosis in both the sequential (P=0.058) and concurrent (P=0.0018) chemoimmunotherapy arms. Respectively, 5 of 10 and 9 of 20 patients had a positive immune response but there was no association with apoptosis. Conclusions: Combination gemcitabine and capecitabine chemotherapy did not affect circulating levels of GM-CSF, IL-6 and CRP. Chemotherapy-induced apoptosis was not associated with the immunogenicity induced by the GV1001 vaccine in advanced pancreatic cancer

Differing myocardial response to a single session of hemodialysis in end-stage renal disease with and without type 2 diabetes mellitus and coronary artery disease

BACKGROUND: Though hemodialysis (HD) acutely improves cardiac function, the impact of background diseases like coronary artery disease (CAD) and Type 2 diabetes (DM) in the setting of end-stage renal disease (ESRD) is not known. Tissue velocity echocardiography (TVE) offers a fast choice to follow changes in myocardial function after HD in ESRD with concomitant DM and /or CAD. METHODS: 46 subjects (17 with ESRD, Group 1; 15 with DM, Group 2; 14 with DM+CAD, Group 3) underwent standard and TVE prior to and shortly after HD. Besides standard Doppler variables, regional myocardial systolic and diastolic velocities, as well as systolic strain rate were post processed. RESULTS: Compared with pre-HD, post-HD body weight (kg) significantly decreased in all the three groups (51 ± 9 vs. 48 ± 8, 62 ± 10 vs.59 ± 10, and 61 ± 9 vs. 58 ± 9 respectively; all p < 0.01). Left ventricular end diastolic dimensions (mm) also decreased post- HD (46 ± 5 vs. 42 ± 7, 53 ± 7 vs. 50 ± 7, 51 ± 7 vs. 47 ± 8 respectively; all p < 0.01). Regional longitudinal peak systolic velocity in septum (cm/s) significantly increased post-HD in Group 1(5.7 ± 1.6 vs. 7.2 ± 2.3; p < 0.001) while remained unchanged in the other two groups. Similar trends were noted in other left ventricular walls. When the myocardial velocities (cm/s) were computed globally, the improvement was seen only in Group 1 (6.3 ± 1.5 vs. 7.9 ± 2.0; p < 0.001). Global early regional diastolic velocity (cm/s) improved in Group 1, remained unchanged in Group 2, while significantly decreased in Group 3(-5.9 ± 1.3 vs. -4.1 ± 1.8; p < 0.01). Global systolic strain rate (1/sec) increased in the first 2 Groups but remained unchanged (-0.87 ± 0.4 vs. -0.94 ± 0.3; p = ns) in Group 3. CONCLUSION: A single HD session improves LV function only in ESRD without coexistent DM and/or CAD. The present data suggest that not only dialysis-dependent changes in loading conditions but also co-existent background diseases determine the myocardial response to HD

The dependence of dijet production on photon virtuality in ep collisions at HERA

The dependence of dijet production on the virtuality of the exchanged photon, Q^2, has been studied by measuring dijet cross sections in the range 0 < Q^2 < 2000 GeV^2 with the ZEUS detector at HERA using an integrated luminosity of 38.6 pb^-1. Dijet cross sections were measured for jets with transverse energy E_T^jet > 7.5 and 6.5 GeV and pseudorapidities in the photon-proton centre-of-mass frame in the range -3 < eta^jet <0. The variable xg^obs, a measure of the photon momentum entering the hard process, was used to enhance the sensitivity of the measurement to the photon structure. The Q^2 dependence of the ratio of low- to high-xg^obs events was measured. Next-to-leading-order QCD predictions were found to generally underestimate the low-xg^obs contribution relative to that at high xg^obs. Monte Carlo models based on leading-logarithmic parton-showers, using a partonic structure for the photon which falls smoothly with increasing Q^2, provide a qualitative description of the data.Comment: 35 pages, 6 eps figures, submitted to Eur.Phys.J.

Beauty photoproduction measured using decays into muons in dijet events in ep collisions at s\sqrt{s}=318 GeV

The photoproduction of beauty quarks in events with two jets and a muon has been measured with the ZEUS detector at HERA using an integrated luminosity of 110 pb$^{- 1}$. The fraction of jets containing b quarks was extracted from the transverse momentum distribution of the muon relative to the closest jet. Differential cross sections for beauty production as a function of the transverse momentum and pseudorapidity of the muon, of the associated jet and of $x_{\gamma}^{jets}$, the fraction of the photon's momentum participating in the hard process, are compared with MC models and QCD predictions made at next-to-leading order. The latter give a good description of the data.Comment: 32 pages, 6 tables, 7 figures Table 6 and Figure 7 revised September 200