Effects of relative humidity on aerosol light scattering in the Arctic

Aerosol particles experience hygroscopic growth in the ambient atmosphere. Their optical properties – especially the aerosol light scattering – are therefore strongly dependent on the ambient relative humidity (RH). In-situ light scattering measurements of long-term observations are usually performed under dry conditions (RH>30–40%). The knowledge of this RH effect is of eminent importance for climate forcing calculations or for the comparison of remote sensing with in-situ measurements. This study combines measurements and model calculations to describe the RH effect on aerosol light scattering for the first time for aerosol particles present in summer and fall in the high Arctic. For this purpose, a field campaign was carried out from July to October 2008 at the Zeppelin station in Ny-Ålesund, Svalbard. The aerosol light scattering coefficient σ<sub>sp</sub>(λ) was measured at three distinct wavelengths (λ=450, 550, and 700 nm) at dry and at various, predefined RH conditions between 20% and 95% with a recently developed humidified nephelometer (WetNeph) and with a second nephelometer measuring at dry conditions with an average RH<10% (DryNeph). In addition, the aerosol size distribution and the aerosol absorption coefficient were measured. The scattering enhancement factor <i>f</i>(RH, λ) is the key parameter to describe the RH effect on σ<sub>sp</sub>(λ) and is defined as the RH dependent σ<sub>sp</sub>(RH, λ) divided by the corresponding dry σ<sub>sp</sub>(RH<sub>dry</sub>, λ). During our campaign the average <i>f</i>(RH=85%, λ=550 nm) was 3.24±0.63 (mean ± standard deviation), and no clear wavelength dependence of <i>f</i>(RH, λ) was observed. This means that the ambient scattering coefficients at RH=85% were on average about three times higher than the dry measured in-situ scattering coefficients. The RH dependency of the recorded <i>f</i>(RH, λ) can be well described by an empirical one-parameter equation. We used a simplified method to retrieve an apparent hygroscopic growth factor <i>g</i>(RH), defined as the aerosol particle diameter at a certain RH divided by the dry diameter, using the WetNeph, the DryNeph, the aerosol size distribution measurements and Mie theory. With this approach we found, on average, <i>g</i>(RH=85%) values to be 1.61±0.12 (mean±standard deviation). No clear seasonal shift of <i>f</i>(RH, λ) was observed during the 3-month period, while aerosol properties (size and chemical composition) clearly changed with time. While the beginning of the campaign was mainly characterized by smaller and less hygroscopic particles, the end was dominated by larger and more hygroscopic particles. This suggests that compensating effects of hygroscopicity and size determined the temporal stability of <i>f</i>(RH, λ). During sea salt influenced periods, distinct deliquescence transitions were observed. At the end we present a method on how to transfer the dry in-situ measured aerosol scattering coefficients to ambient values for the aerosol measured during summer and fall at this location

Ground-based and airborne in-situ measurements of the Eyjafjallajökull volcanic aerosol plume in Switzerland in spring 2010

The volcanic aerosol plume resulting from the Eyjafjallajökull eruption in Iceland in April and May 2010 was detected in clear layers above Switzerland during two periods (17–19 April 2010 and 16–19 May 2010). In-situ measurements of the airborne volcanic plume were performed both within ground-based monitoring networks and with a research aircraft up to an altitude of 6000 m a.s.l. The wide range of aerosol and gas phase parameters studied at the high altitude research station Jungfraujoch (3580 m a.s.l.) allowed for an in-depth characterization of the detected volcanic aerosol. Both the data from the Jungfraujoch and the aircraft vertical profiles showed a consistent volcanic ash mode in the aerosol volume size distribution with a mean optical diameter around 3 ± 0.3 μm. These particles were found to have an average chemical composition very similar to the trachyandesite-like composition of rock samples collected near the volcano. Furthermore, chemical processing of volcanic sulfur dioxide into sulfate clearly contributed to the accumulation mode of the aerosol at the Jungfraujoch. The combination of these in-situ data and plume dispersion modeling results showed that a significant portion of the first volcanic aerosol plume reaching Switzerland on 17 April 2010 did not reach the Jungfraujoch directly, but was first dispersed and diluted in the planetary boundary layer. The maximum PM<sub>10</sub> mass concentrations at the Jungfraujoch reached 30 μgm<sup>−3</sup> and 70 μgm<sup>−3</sup> (for 10-min mean values) duri ng the April and May episode, respectively. Even low-altitude monitoring stations registered up to 45 μgm<sup>−3</sup> of volcanic ash related PM<sub>10</sub> (Basel, Northwestern Switzerland, 18/19 April 2010). The flights with the research aircraft on 17 April 2010 showed one order of magnitude higher number concentrations over the northern Swiss plateau compared to the Jungfraujoch, and a mass concentration of 320 (200–520) μgm<sup>−3</sup> on 18 May 2010 over the northwestern Swiss plateau. The presented data significantly contributed to the time-critical assessment of the local ash layer properties during the initial eruption phase. Furthermore, dispersion models benefited from the detailed information on the volcanic aerosol size distribution and its chemical composition

Surface Deposition and Imaging of Large Ag Clusters Formed in He Droplets

The utility of a continuous beam of He droplets for the assembly and surface deposition of Ag clusters, ~ 300 - 6 000, is studied with transmission electron microscopy. Images of the clusters on amorphous carbon substrates obtained at short deposition times have provided for a measure of the size distribution of the metal clusters. The average sizes of the deposited clusters are in good agreement with an energy balance based estimate of Ag cluster growth in He droplets. Measurements of the deposition rate indicate that upon impact with the surface the He-embedded cluster is attached with high probability. The stability of the deposited clusters on the substrate is discussed.Comment: 24 pages, 5 figure

Impaired CK1 Delta Activity Attenuates SV40-Induced Cellular Transformation In Vitro and Mouse Mammary Carcinogenesis In Vivo

Simian virus 40 (SV40) is a powerful tool to study cellular transformation in vitro, as well as tumor development and progression in vivo. Various cellular kinases, among them members of the CK1 family, play an important role in modulating the transforming activity of SV40, including the transforming activity of T-Ag, the major transforming protein of SV40, itself. Here we characterized the effects of mutant CK1δ variants with impaired kinase activity on SV40-induced cell transformation in vitro, and on SV40-induced mammary carcinogenesis in vivo in a transgenic/bi-transgenic mouse model. CK1δ mutants exhibited a reduced kinase activity compared to wtCK1δ in in vitro kinase assays. Molecular modeling studies suggested that mutation N172D, located within the substrate binding region, is mainly responsible for impaired mutCK1δ activity. When stably over-expressed in maximal transformed SV-52 cells, CK1δ mutants induced reversion to a minimal transformed phenotype by dominant-negative interference with endogenous wtCK1δ. To characterize the effects of CK1δ on SV40-induced mammary carcinogenesis, we generated transgenic mice expressing mutant CK1δ under the control of the whey acidic protein (WAP) gene promoter, and crossed them with SV40 transgenic WAP-T-antigen (WAP-T) mice. Both WAP-T mice as well as WAP-mutCK1δ/WAP-T bi-transgenic mice developed breast cancer. However, tumor incidence was lower and life span was significantly longer in WAP-mutCK1δ/WAP-T bi-transgenic animals. The reduced CK1δ activity did not affect early lesion formation during tumorigenesis, suggesting that impaired CK1δ activity reduces the probability for outgrowth of in situ carcinomas to invasive carcinomas. The different tumorigenic potential of SV40 in WAP-T and WAP-mutCK1δ/WAP-T tumors was also reflected by a significantly different expression of various genes known to be involved in tumor progression, specifically of those involved in wnt-signaling and DNA repair. Our data show that inactivating mutations in CK1δ impair SV40-induced cellular transformation in vitro and mouse mammary carcinogenesis in vivo

Cross-species comparison of aCGH data from mouse and human BRCA1- and BRCA2-mutated breast cancers

Background: Genomic gains and losses are a result of genomic instability in many types of cancers. BRCA1- and BRCA2-mutated breast cancers are associated with increased amounts of chromosomal aberrations, presumably due their functions in genome repair. Some of these genomic aberrations may harbor genes whose absence or overexpression may give rise to cellular growth advantage. So far, it has not been easy to identify the driver genes underlying gains and losses. A powerful approach to identify these driver genes could be a cross-species comparison of array comparative genomic hybridization (aCGH) data from cognate mouse and human tumors. Orthologous regions of mouse and human tumors that are commonly gained or lost might represent essential genomic regions selected for gain or loss during tumor development. Methods: To identify genomic regions that are associated with BRCA1- and BRCA2-mutated breast cancers we compared aCGH data from 130 mouse Brca1?/?;p53?/?, Brca2?/?;p53?/? and p53?/? mammary tumor groups with 103 human BRCA1-mutated, BRCA2-mutated and non-hereditary breast cancers. Results: Our genome-wide cross-species analysis yielded a complete collection of loci and genes that are commonly gained or lost in mouse and human breast cancer. Principal common CNAs were the well known MYCassociated gain and RB1/INTS6-associated loss that occurred in all mouse and human tumor groups, and the AURKA-associated gain occurred in BRCA2-related tumors from both species. However, there were also important differences between tumor profiles of both species, such as the prominent gain on chromosome 10 in mouse Brca2?/?;p53?/? tumors and the PIK3CA associated 3q gain in human BRCA1-mutated tumors, which occurred in tumors from one species but not in tumors from the other species. This disparity in recurrent aberrations in mouse and human tumors might be due to differences in tumor cell type or genomic organization between both species. Conclusions: The selection of the oncogenome during mouse and human breast tumor development is markedly different, apart from the MYC gain and RB1-associated loss. These differences should be kept in mind when using mouse models for preclinical studies.MediamaticsElectrical Engineering, Mathematics and Computer Scienc

New particle formation in the free troposphere : A question of chemistry and timing

New particle formation (NPF) is the source of over half of the atmosphere's cloud condensation nuclei, thus influencing cloud properties and Earth's energy balance. Unlike in the planetary boundary layer, few observations of NPF in the free troposphere exist. We provide observational evidence that at high altitudes, NPF occurs mainly through condensation of highly oxygenated molecules (HOMs), in addition to taking place through sulfuric acid-ammonia nucleation. Neutral nucleation is more than 10 times faster than ion-induced nucleation, and growth rates are size-dependent. NPF is restricted to a time window of 1 to 2 days after contact of the air masses with the planetary boundary layer; this is related to the time needed for oxidation of organic compounds to form HOMs. These findings require improved NPF parameterization in atmospheric models.Peer reviewe

Omeprazole Inhibits Proliferation and Modulates Autophagy in Pancreatic Cancer Cells

BACKGROUND: Omeprazole has recently been described as a modulator of tumour chemoresistance, although its underlying molecular mechanisms remain controversial. Since pancreatic tumours are highly chemoresistant, a logical step would be to investigate the pharmacodynamic, morphological and biochemical effects of omeprazole on pancreatic cancer cell lines. METHODOLOGY/PRINCIPAL FINDINGS: Dose-effect curves of omeprazole, pantoprazole, gemcitabine, 5-fluorouracil and the combinations of omeprazole and 5-fluorouracil or gemcitabine were generated for the pancreatic cancer cell lines MiaPaCa-2, ASPC-1, Colo357, PancTu-1, Panc1 and Panc89. They revealed that omeprazole inhibited proliferation at probably non-toxic concentrations and reversed the hormesis phenomena of 5-fluorouracil. Electron microscopy showed that omeprazole led to accumulation of phagophores and early autophagosomes in ASPC-1 and MiaPaCa-2 cells. Signal changes indicating inhibited proliferation and programmed cell death were found by proton NMR spectroscopy of both cell lines when treated with omeprazole which was identified intracellularly. Omeprazole modulates the lysosomal transport pathway as shown by Western blot analysis of the expression of LAMP-1, Cathepsin-D and β-COP in lysosome- and Golgi complex containing cell fractions. Acridine orange staining revealed that the pump function of the vATPase was not specifically inhibited by omeprazole. Gene expression of the autophagy-related LC3 gene as well as of Bad, Mdr-1, Atg12 and the vATPase was analysed after treatment of cells with 5-fluorouracil and omeprazole and confirmed the above mentioned results. CONCLUSIONS: We hypothesise that omeprazole interacts with the regulatory functions of the vATPase without inhibiting its pump function. A modulation of the lysosomal transport pathway and autophagy is caused in pancreatic cancer cells leading to programmed cell death. This may circumvent common resistance mechanisms of pancreatic cancer. Since omeprazole use has already been established in clinical practice these results could lead to new clinical applications