Is there a trend in cirrus cloud cover due to aircraft traffic?

Trends in cirrus cloud cover have been estimated based on 16 years of data from ISCCP (International Satellite Cloud Climatology Project). The results have been spatially correlated with aircraft density data to determine the changes in cirrus cloud cover due to aircraft traffic. The correlations are only moderate, as many other factors have also contributed to changes in cirrus. Still we regard the results to be indicative of an impact of aircraft on cirrus amount. The main emphasis of our study is on the area covered by the METEOSAT satellite to avoid trends in the ISCCP data resulting from changing satellite viewing geometry. In Europe, which is within the METEOSAT region, we find indications of a trend of about 1-2% cloud cover per decade due to aircraft, in reasonable agreement with previous studies. The positive trend in cirrus in areas of high aircraft traffic contrasts with a general negative trend in cirrus. Extrapolation in time to cover the entire period of aircraft operations and in space to cover the global scale yields a mean estimate of 0.03 Wm^-2 (lower limit 0.01, upper limit 0.08 Wm^-2) for the radiative forcing due to aircraft induced cirrus. The mean is close to the value given by IPCC (1999) as an upper limit

Is there a trend in cirrus cloud cover due to aircraft traffic?

International audienceTrends in cirrus cloud cover have been estimated based on 16 years of data from ISCCP (International Satellite Cloud Climatology Project). The results have been spatially correlated with aircraft density data to determine the changes in cirrus could cover due to aircraft traffic. Main emphasis has been on the area covered by the METEOSAT satellite, to avoid trends in the ISCCP data resulting from changing satellite positions. An alternative retrieval of high clouds in this region has been used to complement the analysis based on ISCCP data. In Europe, which is within the METEOSAT region, we find indications of a trend of about 2%/decade due to aircraft, in reasonable agreement with previous studies. The positive trend in cirrus in areas of high aircraft traffic seems to have contrasted a general negative trend in cirrus. Extrapolation in time to cover the entire period of aircraft operations and in space to cover the global scale yields a best estimate of 0.05 Wm?2 for the radiative forcing due to aircraft. This is close to the value given by IPCC (1999) as an upper limit

Large-scale distributions of tropospheric nitric, formic, and acetic acids over the western Pacific basin during wintertime

We report here measurements of the acidic gases nitric (HNO3), formic (HCOOH), and acetic (CH3COOH) over the western Pacific basin during the February-March 1994 Pacific Exploratory Mission-West (PEM-West B). These data were obtained aboard the NASA DC-8 research aircraft as it flew missions in the altitude range of 0.3–12.5 km over equatorial regions near Guam and then further westward encompassing the entire Pacific Rim arc. Aged marine air over the equatorial Pacific generally exhibited mixing ratios of acidic gases \u3c100 parts per trillion by volume (pptv). Near the Asian continent, discrete plumes encountered below 6 km altitude contained up to 8 parts per billion by volume (ppbv) HNO3 and 10 ppbv HCOOH and CH3COOH. Overall there was a general correlation between mixing ratios of acidic gases with those of CO, C2H2, and C2Cl4, indicative of emissions from combustion and industrial sources. The latitudinal distributions of HNO3 and CO showed that the largest mixing ratios were centered around 15°N, while HCOOH, CH3COOH, and C2Cl4 peaked at 25°N. The mixing ratios of HCOOH and CH3COOH were highly correlated (r2 = 0.87) below 6 km altitude, with a slope (0.89) characteristic of the nongrowing season at midlatitudes in the northern hemisphere. Above 6 km altitude, HCOOH and CH3COOH were marginally correlated (r2 = 0.50), and plumes well defined by CO, C2H2, and C2Cl4 were depleted in acidic gases, most likely due to scavenging during vertical transport of air masses through convective cloud systems over the Asian continent. In stratospheric air masses, HNO3 mixing ratios were several parts per billion by volume (ppbv), yielding relationships with O3 and N2O consistent with those previously reported for NOy

Hsp90–Sgt1 and Skp1 target human Mis12 complexes to ensure efficient formation of kinetochore–microtubule binding sites

The Hsp90–Sgt1 chaperone and the ubiquitin ligase subunit Skp1 regulate the assembly and turnover of the kinetochore complex Mis12

Combined Characterisation of GOME and TOMS Total Ozone Using Ground-Based Observations from the NDSC

Several years of total ozone measured from space by the ERS-2 GOME, the Earth Probe Total Ozone Mapping Spectrometer (TOMS), and the ADEOS TOMS, are compared with high-quality ground-based observations associated with the Network for the Detection of Stratospheric Change (NDSC), over an extended latitude range and a variety of geophysical conditions. The comparisons with each spaceborne sensor are combined altogether for investigating their respective solar zenith angle (SZA) dependence, dispersion, and difference of sensitivity. The space- and ground-based data are found to agree within a few percent on average. However, the analysis highlights for both Global Ozone Monitoring Experiment (GOME) and TOMS several sources of discrepancies, including a dependence on the SZA at high latitudes and internal inconsistencies

Origin of Ozone NO(x) in the Tropical Troposphere: A Photochemical Analysis of Aircraft Observations Over the South Atlantic Basin

The photochemistry of the troposphere over the South Atlantic basin is examined by modeling of aircraft observations up to 12-km altitude taken during the TRACE A expedition in September-October 1992. A close balance is found in the 0 to 12-km column between photochemical production and loss Of O3, with net production at high altitudes compensating for weak net loss at low altitudes. This balance implies that O3 concentrations in the 0-12 km column can be explained solely by in situ photochemistry; influx from the stratosphere is negligible. Simulation of H2O2, CH3OOH, and CH2O concentrations measured aboard the aircraft lends confidence in the computations of O3 production and loss rates, although there appears to be a major gap in current understanding of CH2O chemistry in the marine boundary layer. The primary sources of NO(x) over the South Atlantic Basin appear to be continental (biomass burning, lightning, soils). There is evidence that NO(x) throughout the 0 to 12-km column is recycled from its oxidation products rather than directly transported from its primary sources. There is also evidence for rapid conversion of HNO3 to NO(x) in the upper troposphere by a mechanism not included in current models. A general representation of the O3 budget in the tropical troposphere is proposed that couples the large scale Walker circulation and in situ photochemistry. Deep convection in the rising branches of the Walker circulation injects NO(x) from combustion, soils, and lightning to the upper troposphere, leading to O3 production; eventually, the air subsides and net O3 loss takes place in the lower troposphere, closing the O3 cycle. This scheme implies a great sensitivity of the oxidizing power of the atmosphere to NO(x) emissions in the tropics

G2 checkpoint abrogation and checkpoint kinase-1 targeting in the treatment of cancer

Rigorous quality control steps, termed checkpoints, tightly regulate progression through the cell cycle. DNA-damaging chemotherapy and radiation activate functional cellular checkpoints. These checkpoints can facilitate DNA repair and promote cell death in unrepaired cells. There are at least three DNA damage checkpoints – at G1/S, S, and G2/M – as well as a mitotic spindle checkpoint. Most cancer cells harbour mutations in tumour suppressors and/or oncogenes, which impair certain cell checkpoints. Inhibiting the remaining cell checkpoints – particularly after exposure of cancer cells to chemotherapy and/or radiation – allows cell death, a strategy now being employed in cancer therapeutics. With our increasing knowledge of cell cycle regulation, many compounds have been developed to inhibit specific checkpoint components, particularly at the G2/M transition. One such target is checkpoint kinase-1 (Chk1). We review here the molecular framework of the cell cycle, the rationale for targeting Chk1, the preclinical concepts related to the development of Chk1 inhibitors, and the efficacy and safety results from Chk1 inhibitors now in phase I/II trials

High-Content, High-Throughput Analysis of Cell Cycle Perturbations Induced by the HSP90 Inhibitor XL888

BACKGROUND: Many proteins that are dysregulated or mutated in cancer cells rely on the molecular chaperone HSP90 for their proper folding and activity, which has led to considerable interest in HSP90 as a cancer drug target. The diverse array of HSP90 client proteins encompasses oncogenic drivers, cell cycle components, and a variety of regulatory factors, so inhibition of HSP90 perturbs multiple cellular processes, including mitogenic signaling and cell cycle control. Although many reports have investigated HSP90 inhibition in the context of the cell cycle, no large-scale studies have examined potential correlations between cell genotype and the cell cycle phenotypes of HSP90 inhibition. METHODOLOGY/PRINCIPAL FINDINGS: To address this question, we developed a novel high-content, high-throughput cell cycle assay and profiled the effects of two distinct small molecule HSP90 inhibitors (XL888 and 17-AAG [17-allylamino-17-demethoxygeldanamycin]) in a large, genetically diverse panel of cancer cell lines. The cell cycle phenotypes of both inhibitors were strikingly similar and fell into three classes: accumulation in M-phase, G2-phase, or G1-phase. Accumulation in M-phase was the most prominent phenotype and notably, was also correlated with TP53 mutant status. We additionally observed unexpected complexity in the response of the cell cycle-associated client PLK1 to HSP90 inhibition, and we suggest that inhibitor-induced PLK1 depletion may contribute to the striking metaphase arrest phenotype seen in many of the M-arrested cell lines. CONCLUSIONS/SIGNIFICANCE: Our analysis of the cell cycle phenotypes induced by HSP90 inhibition in 25 cancer cell lines revealed that the phenotypic response was highly dependent on cellular genotype as well as on the concentration of HSP90 inhibitor and the time of treatment. M-phase arrest correlated with the presence of TP53 mutations, while G2 or G1 arrest was more commonly seen in cells bearing wt TP53. We draw upon previous literature to suggest an integrated model that accounts for these varying observations