Does the Sun Shrink with Increasing Magnetic Activity?

We have analyzed the full set of SOHO/MDI f- and p-mode oscillation frequencies from 1996 to date in a search for evidence of solar radius evolution during the rising phase of the current activity cycle. Like Antia et al. (2000), we find that a significant fraction of the f-mode frequency changes scale with frequency; and that if these are interpreted in terms of a radius change, it implies a shrinking sun. Our inferred rate of shrinkage is about 1.5 km/y, which is somewhat smaller than found by Antia et al. We argue that this rate does not refer to the surface, but rather to a layer extending roughly from 4 to 8 Mm beneath the visible surface. The rate of shrinking may be accounted for by an increasing radial component of the rms random magnetic field at a rate that depends on its radial distribution. If it were uniform, the required field would be ~7 kG. However, if it were inwardly increasing, then a 1 kG field at 8 Mm would suffice. To assess contribution to the solar radius change arising above 4Mm, we analyzed the p-mode data. The evolution of the p-mode frequencies may be explained by a magnetic^M field growing with activity. The implications of the near-surface magnetic field changes depend on the anisotropy of the random magnetic field. If the field change is predominantly radial, then we infer an additional shrinking at a rate between 1.1-1.3 km/y at the photosphere. If on the other hand the increase is isotropic, we find a competing expansion at a rate of 2.3 km/y. In any case, variations in the sun's radius in the activity cycle are at the level of 10^{-5} or less, hence have a negligible contribution to the irradiance variations.Comment: 10 pages (ApJ preprint style), 4 figures; accepted for publication in Ap

The origin of pine pollen grains captured from air at Calypsobyen, Svalbard

Spitsbergen is the largest island in the Svalbard Archipelago (Norway) that has been permanently populated. The harsh Arctic climate prevents development of large vascular plants such as trees. A two-year aerobiological survey was conducted within the framework of two consecutive polar expeditions (2014 and 2015) in Spitsbergen (Calypsobyen, Bellsund). The air quality was measured continuously from June/July to August using a 7-day volumetric air sampler, Tauber trap and moss specimens. Collected air samples and gravimetric pollen deposits were processed following transfer to sterile laboratory conditions and analyzed with the aid of light microscopy. Days when pine pollen grains were detected in the air were selected for further analysis. Clusters of back-trajectories, computed using the Hybrid Single Particle Lagrangian Integrated Trajectory model in combination with ArcGIS software as well as the Flextra trajectory model, showed the movement of air masses to the sampling location at Hornsund, and thus indicated the likely origin of pollen grains. The GlobCover 2009 and CORINE Land Cover 2012 datasets were employed to establish the distribution of coniferous forests in the areas of interest. Conclusions were drawn based on the analyses of the circulation of air masses, using visualization of global weather conditions forecast to supercomputers. For the first time, we have demonstrated that pine pollen grains occurring in pine-free Spitsbergen, could originate from numerous locations, including Scandinavia, Iceland, Siberia and northern Canada. Pollen grains were transported via air masses for distances exceeding ~2000 km. Both air samples and gravimetric pollen deposits revealed the same pattern of Pinus pollen distributio

Properties of Flares-Generated Seismic Waves on the Sun

The solar seismic waves excited by solar flares (``sunquakes'') are observed as circular expanding waves on the Sun's surface. The first sunquake was observed for a flare of July 9, 1996, from the Solar and Heliospheric Observatory (SOHO) space mission. However, when the new solar cycle started in 1997, the observations of solar flares from SOHO did not show the seismic waves, similar to the 1996 event, even for large X-class flares during the solar maximum in 2000-2002. The first evidence of the seismic flare signal in this solar cycle was obtained for the 2003 ``Halloween'' events, through acoustic ``egression power'' by Donea and Lindsey. After these several other strong sunquakes have been observed. Here, I present a detailed analysis of the basic properties of the helioseismic waves generated by three solar flares in 2003-2005. For two of these flares, X17 flare of October 28, 2003, and X1.2 flare of January 15, 2005, the helioseismology observations are compared with simultaneous observations of flare X-ray fluxes measured from the RHESSI satellite. These observations show a close association between the flare seismic waves and the hard X-ray source, indicating that high-energy electrons accelerated during the flare impulsive phase produced strong compression waves in the photosphere, causing the sunquake. The results also reveal new physical properties such as strong anisotropy of the seismic waves, the amplitude of which varies significantly with the direction of propagation. The waves travel through surrounding sunspot regions to large distances, up to 120 Mm, without significant decay. These observations open new perspectives for helioseismic diagnostics of flaring active regions on the Sun and for understanding the mechanisms of the energy release and transport in solar flares.Comment: 12 pages, 4 figures, submitted to Ap

β-Catenin Signaling Increases during Melanoma Progression and Promotes Tumor Cell Survival and Chemoresistance

Beta-catenin plays an important role in embryogenesis and carcinogenesis by controlling either cadherin-mediated cell adhesion or transcriptional activation of target gene expression. In many types of cancers nuclear translocation of beta-catenin has been observed. Our data indicate that during melanoma progression an increased dependency on the transcriptional function of beta-catenin takes place. Blockade of beta-catenin in metastatic melanoma cell lines efficiently induces apoptosis, inhibits proliferation, migration and invasion in monolayer and 3-dimensional skin reconstructs and decreases chemoresistance. In addition, subcutaneous melanoma growth in SCID mice was almost completely inhibited by an inducible beta-catenin knockdown. In contrast, the survival of benign melanocytes and primary melanoma cell lines was less affected by beta-catenin depletion. However, enhanced expression of beta-catenin in primary melanoma cell lines increased invasive capacity in vitro and tumor growth in the SCID mouse model. These data suggest that beta-catenin is an essential survival factor for metastatic melanoma cells, whereas it is dispensable for the survival of benign melanocytes and primary, non-invasive melanoma cells. Furthermore, beta-catenin increases tumorigenicity of primary melanoma cell lines. The differential requirements for beta-catenin signaling in aggressive melanoma versus benign melanocytic cells make beta-catenin a possible new target in melanoma therapy

Breast cancer-specific mutations in CK1ε inhibit Wnt/β-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration

Introduction Breast cancer is one of the most common types of cancer in women. One of the genes that were found mutated in breast cancer is casein kinase 1 epsilon (CK1ε). Because CK1ε is a crucial regulator of the Wnt signaling cascades, we determined how these CK1ε mutations interfere with the Wnt pathway and affect the behavior of epithelial breast cancer cell lines. Methods We performed in silico modeling of various mutations and analyzed the kinase activity of the CK1ε mutants both in vitro and in vivo. Furthermore, we used reporter and small GTPase assays to identify how mutation of CK1ε affects different branches of the Wnt signaling pathway. Based on these results, we employed cell adhesion and cell migration assays in MCF7 cells to demonstrate a crucial role for CK1ε in these processes. Results In silico modeling and in vivo data showed that autophosphorylation at Thr 44, a site adjacent to the breast cancer point mutations in the N-terminal lobe of human CK1ε, is involved in positive regulation of the CK1ε activity. Our data further demonstrate that, in mammalian cells, mutated forms of CK1ε failed to affect the intracellular localization and phosphorylation of Dvl2; we were able to demonstrate that CK1ε mutants were unable to enhance Dvl-induced TCF/LEF-mediated transcription, that CK1ε mutants acted as loss-of-function in the Wnt/β-catenin pathway, and that CK1ε mutants activated the noncanonical Wnt/Rac-1 and NFAT pathways, similar to pharmacological inhibitors of CK1. In line with these findings, inhibition of CK1 promoted cell migration as well as decreased cell adhesion and E-cadherin expression in the breast cancer-derived cell line MCF7. Conclusions In summary, these data suggest that the mutations of CK1ε found in breast cancer can suppress Wnt/β-catenin as well as promote the Wnt/Rac-1/JNK and Wnt/NFAT pathways, thus contributing to breast cancer development via effects on cell adhesion and migration. In terms of molecular mechanism, our data indicate that the breast cancer point mutations in the N-terminal lobe of CK1ε, which are correlated with decreased phosphorylation activities of mutated forms of CK1ε both in vitro and in vivo, interfere with positive autophosphorylation at Thr 4

Digital ulcers predict a worse disease course in patients with systemic sclerosis

Objective: Systemic sclerosis (SSc) is a systemic autoimmune disease with high morbidity and significant mortality. There is a great need of predictors that would allow risk stratification of patients with SSc and ultimately initiation of treatment early enough to ensure optimal clinical results. In this study, we evaluated whether a history of digital ulcers (HDU) at presentation may be a predictor of vascular outcomes and of overall clinical worsening and death in patients with SSc. Methods: Patients from the EULAR Scleroderma Trials and Research (EUSTAR) database, satisfying at inclusion the 1980 American College of Rheumatology classification criteria for SSc, who had a follow-up of at least 3 years since baseline or who have died, were included in the analysis. HDU at presentation as a predictor of disease worsening or death was evaluated by Cox proportional hazards regression analysis. Results :3196 patients matched the inclusion criteria (male sex 13.2%, 33.4% diffuse subset). At presentation, 1092/3196 patients had an HDU (34.1%). In multivariable analysis adjusting for age, gender and all parameters considered potentially significant, HDU was predictive for the presence of active digital ulcers (DUs) at prospective visits (HR (95% CI)): 2.41(1.91 to 3.03), p<0.001, for an elevated systolic pulmonary arterial pressure on heart ultrasound (US-PAPs):1.36 (1.03 to 1.80), p=0.032, for any cardiovascular event (new DUs, elevated US-PAPs or LV failure):3.56 (2.26 to 5.62), p<0.001, and for death (1.53 (1.16 to 2.02), p=0.003). Conclusions :In patients with SSc, HDU at presentation predicts the occurrence of DUs at follow-up and is associated with cardiovascular worsening and decreased survival

Racial differences in systemic sclerosis disease presentation: a European Scleroderma Trials and Research group study

Objectives. Racial factors play a significant role in SSc. We evaluated differences in SSc presentations between white patients (WP), Asian patients (AP) and black patients (BP) and analysed the effects of geographical locations.Methods. SSc characteristics of patients from the EUSTAR cohort were cross-sectionally compared across racial groups using survival and multiple logistic regression analyses.Results. The study included 9162 WP, 341 AP and 181 BP. AP developed the first non-RP feature faster than WP but slower than BP. AP were less frequently anti-centromere (ACA; odds ratio (OR) = 0.4, P < 0.001) and more frequently anti-topoisomerase-I autoantibodies (ATA) positive (OR = 1.2, P = 0.068), while BP were less likely to be ACA and ATA positive than were WP [OR(ACA) = 0.3, P < 0.001; OR(ATA) = 0.5, P = 0.020]. AP had less often (OR = 0.7, P = 0.06) and BP more often (OR = 2.7, P < 0.001) diffuse skin involvement than had WP.AP and BP were more likely to have pulmonary hypertension [OR(AP) = 2.6, P < 0.001; OR(BP) = 2.7, P = 0.03 vs WP] and a reduced forced vital capacity [OR(AP) = 2.5, P < 0.001; OR(BP) = 2.4, P < 0.004] than were WP. AP more often had an impaired diffusing capacity of the lung than had BP and WP [OR(AP vs BP) = 1.9, P = 0.038; OR(AP vs WP) = 2.4, P < 0.001]. After RP onset, AP and BP had a higher hazard to die than had WP [hazard ratio (HR) (AP) = 1.6, P = 0.011; HR(BP) = 2.1, P < 0.001].Conclusion. Compared with WP, and mostly independent of geographical location, AP have a faster and earlier disease onset with high prevalences of ATA, pulmonary hypertension and forced vital capacity impairment and higher mortality. BP had the fastest disease onset, a high prevalence of diffuse skin involvement and nominally the highest mortality