184 research outputs found

    The seasonal cycle of N_2O

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    We have carried out an empirical study of the seasonal cycle of nitrous oxide (N_2O) using the data archived by the National Oceanic and Atmospheric Administration – Climate Monitoring and Diagnostics Laboratory (NOAA-CMDL) Global Cooperative Air Sampling Network from 1977 to 2000. In order to isolate the seasonal cycle, we first detrended the data using least square polynomial fits. The remaining variability was averaged to extract the seasonal cycle, which has an amplitude of about 0.8 ppbv. The statistical significance of the seasonal signal was established using the multitaper method and Welch's method for power spectrum analysis

    Temporal and spatial patterns of the interannual variability of total ozone in the tropics

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    The recently constructed gridded Merged Ozone Data (MOD) set, combining the monthly mean column abundances collected by the Total Ozone Mapping Spectrometer (TOMS) and the Solar Backscatter Ultraviolet (SBUV and SBUV/2) instruments, provides a nearly continuous record from late 1978 to 2000 on a 5° × 10° latitude-longitude grid. The precision of these measurements and their calibration allow very small signals, ∼1% of total column ozone, to be clearly seen. Using MOD, we have carried out an empirical orthogonal function (EOF) study of the temporal and spatial patterns of the interannual variability of total column ozone in the tropics. The first four EOFs of our study capture over 93% of the variance of the deseasonalized data. The leading two EOFs of our study, respectively accounting for 42% and 33% of the variance, display structures attributable to the quasi-biennial oscillation(QBO), with influence from a decadal oscillation. The third EOF (15% of the variance) represents an interaction between the QBO and an annual cycle. The fourth EOF (3% of the variance) is related to the El Niño - Southern Oscillation. This EOF decomposition is robust; nearly identical patterns occur in the decomposition of various equatorial latitude bands of MOD and similar patterns occur in the analysis of the deseasonalized TOMS data set, a shorter record with a more finely resolved spatial grid. For comparison, similar decompositions were performed for dynamical fields from the reanalysis product from the National Centers for Environmental Prediction and the National Center for Atmospheric Research. Using these analyses, we found possible connections between the deduced patterns in ozone and the climate variables

    Quasi-biennial oscillation and quasi-biennial oscillation--annual beat in the tropical total column ozone: A two-dimensional model simulation

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    The National Centers for Environmental Prediction–Department of Energy Reanalysis 2 data are used to calculate the monthly mean meridional circulation and eddy diffusivity from 1979 to 2002 for use in the California Institute of Technology–Jet Propulsion Laboratory two-dimensional (2-D) chemistry and transport model (CTM). This allows for an investigation of the impact of dynamics on the interannual variability of the tropical total column ozone for all years for which the Total Ozone Mapping Spectrometer and the Solar Backscatter Ultraviolet merged total ozone data are available. The first two empirical orthogonal functions (EOFs) of the deseasonalized and detrended stratospheric stream function capture 88% of the total variance on interannual timescales. The first EOF, accounting for over 70% of the interannual variance, is related to the quasi-biennial oscillation (QBO) and its interaction with annual cycles, the QBO-annual beat (QBO-AB). The 2-D CTM provides realistic simulations of the seasonal and interannual variability of ozone in the tropics. The equatorial ozone anomaly from the model is close to that derived from the observations. The phase and amplitude of the QBO are well captured by the model. The magnitude of the QBO signal is somewhat larger in the model than it is in the data. The QBO-AB found in the simulated ozone agrees well with that in the observed data

    A Negative Feedback Loop That Limits the Ectopic Activation of a Cell Type–Specific Sporulation Sigma Factor of Bacillus subtilis

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    Two highly similar RNA polymerase sigma subunits, σF and σG, govern the early and late phases of forespore-specific gene expression during spore differentiation in Bacillus subtilis. σF drives synthesis of σG but the latter only becomes active once engulfment of the forespore by the mother cell is completed, its levels rising quickly due to a positive feedback loop. The mechanisms that prevent premature or ectopic activation of σG while discriminating between σF and σG in the forespore are not fully comprehended. Here, we report that the substitution of an asparagine by a glutamic acid at position 45 of σG (N45E) strongly reduced binding by a previously characterized anti-sigma factor, CsfB (also known as Gin), in vitro, and increased the activity of σG in vivo. The N45E mutation caused the appearance of a sub-population of pre-divisional cells with strong activity of σG. CsfB is normally produced in the forespore, under σF control, but sigGN45E mutant cells also expressed csfB and did so in a σG-dependent manner, autonomously from σF. Thus, a negative feedback loop involving CsfB counteracts the positive feedback loop resulting from ectopic σG activity. N45 is invariant in the homologous position of σG orthologues, whereas its functional equivalent in σF proteins, E39, is highly conserved. While CsfB does not bind to wild-type σF, a E39N substitution in σF resulted in efficient binding of CsfB to σF. Moreover, under certain conditions, the E39N alteration strongly restrains the activity of σF in vivo, in a csfB-dependent manner, and the efficiency of sporulation. Therefore, a single amino residue, N45/E39, is sufficient for the ability of CsfB to discriminate between the two forespore-specific sigma factors in B. subtilis

    Right-to-left shunt with hypoxemia in pulmonary hypertension

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    <p>Abstract</p> <p>Background</p> <p>Hypoxemia is common in pulmonary hypertension (PH) and may be partly related to ventilation/perfusion mismatch, low diffusion capacity, low cardiac output, and/or right-to-left (RL) shunting.</p> <p>Methods</p> <p>To determine whether true RL shunting causing hypoxemia is caused by intracardiac shunting, as classically considered, a retrospective single center study was conducted in consecutive patients with precapillary PH, with hypoxemia at rest (PaO<sub>2 </sub>< 10 kPa), shunt fraction (Qs/Qt) greater than 5%, elevated alveolar-arterial difference of PO<sub>2 </sub>(AaPO<sub>2</sub>), and with transthoracic contrast echocardiography performed within 3 months.</p> <p>Results</p> <p>Among 263 patients with precapillary PH, 34 patients were included: pulmonary arterial hypertension, 21%; PH associated with lung disease, 47% (chronic obstructive pulmonary disease, 23%; interstitial lung disease, 9%; other, 15%); chronic thromboembolic PH, 26%; miscellaneous causes, 6%. Mean pulmonary artery pressure, cardiac index, and pulmonary vascular resistance were 45.8 ± 10.8 mmHg, 2.2 ± 0.6 L/min/m<sup>2</sup>, and 469 ± 275 dyn.s.cm<sup>-5</sup>, respectively. PaO<sub>2 </sub>in room air was 6.8 ± 1.3 kPa. Qs/Qt was 10.2 ± 4.2%. AaPO<sub>2 </sub>under 100% oxygen was 32.5 ± 12.4 kPa. Positive contrast was present at transthoracic contrast echocardiography in 6/34 (18%) of patients, including only 4/34 (12%) with intracardiac RL shunting. Qs/Qt did not correlate with hemodynamic parameters. Patients' characteristics did not differ according to the result of contrast echocardiography.</p> <p>Conclusion</p> <p>When present in patients with precapillary PH, RL shunting is usually not related to reopening of patent <it>foramen ovale</it>, whatever the etiology of PH.</p

    Temporal Proteome and Lipidome Profiles Reveal Hepatitis C Virus-Associated Reprogramming of Hepatocellular Metabolism and Bioenergetics

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    Proteomic and lipidomic profiling was performed over a time course of acute hepatitis C virus (HCV) infection in cultured Huh-7.5 cells to gain new insights into the intracellular processes influenced by this virus. Our proteomic data suggest that HCV induces early perturbations in glycolysis, the pentose phosphate pathway, and the citric acid cycle, which favor host biosynthetic activities supporting viral replication and propagation. This is followed by a compensatory shift in metabolism aimed at maintaining energy homeostasis and cell viability during elevated viral replication and increasing cellular stress. Complementary lipidomic analyses identified numerous temporal perturbations in select lipid species (e.g. phospholipids and sphingomyelins) predicted to play important roles in viral replication and downstream assembly and secretion events. The elevation of lipotoxic ceramide species suggests a potential link between HCV-associated biochemical alterations and the direct cytopathic effect observed in this in vitro system. Using innovative computational modeling approaches, we further identified mitochondrial fatty acid oxidation enzymes, which are comparably regulated during in vitro infection and in patients with histological evidence of fibrosis, as possible targets through which HCV regulates temporal alterations in cellular metabolic homeostasis
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