Study of KIC 8561221 observed by Kepler: an early red giant showing depressed dipolar modes

The continuous high-precision photometric observations provided by the CoRoT and Kepler space missions have allowed us to better understand the structure and dynamics of red giants using asteroseismic techniques. A small fraction of these stars shows dipole modes with unexpectedly low amplitudes. The reduction in amplitude is more pronounced for stars with higher frequency of maximum power. In this work we want to characterize KIC 8561221 in order to confirm that it is currently the least evolved star among this peculiar subset and to discuss several hypotheses that could help explain the reduction of the dipole mode amplitudes. We used Kepler short- and long-cadence data combined with spectroscopic observations to infer the stellar structure and dynamics of KIC 8561221. We then discussed different scenarios that could contribute to the reduction of the dipole amplitudes such as a fast rotating interior or the effect of a magnetic field on the properties of the modes. We also performed a detailed study of the inertia and damping of the modes. We have been able to characterize 37 oscillations modes, in particular, a few dipole modes above nu_max that exhibit nearly normal amplitudes. We have inferred a surface rotation period of around 91 days and uncovered the existence of a variation in the surface magnetic activity during the last 4 years. As expected, the internal regions of the star probed by the l = 2 and 3 modes spin 4 to 8 times faster than the surface. With our grid of standard models we are able to properly fit the observed frequencies. Our model calculation of mode inertia and damping give no explanation for the depressed dipole modes. A fast rotating core is also ruled out as a possible explanation. Finally, we do not have any observational evidence of the presence of a strong deep magnetic field inside the star.Comment: Accepted in A&A. 17 pages, 16 figure

Comparative actions of progesterone, medroxyprogesterone acetate, drospirenone and nestorone on breast cancer cell migration and invasion

<p>Abstract</p> <p>Background</p> <p>Limited information is available on the effects of progestins on breast cancer progression and metastasis. Cell migration and invasion are central for these processes, and require dynamic cytoskeletal and cell membrane rearrangements for cell motility to be enacted.</p> <p>Methods</p> <p>We investigated the effects of progesterone (P), medroxyprogesterone acetate (MPA), drospirenone (DRSP) and nestorone (NES) alone or with 17β-estradiol (E2) on T47-D breast cancer cell migration and invasion and we linked some of these actions to the regulation of the actin-regulatory protein, moesin and to cytoskeletal remodeling.</p> <p>Results</p> <p>Breast cancer cell horizontal migration and invasion of three-dimensional matrices are enhanced by all the progestins, but differences are found in terms of potency, with MPA being the most effective and DRSP being the least. This is related to the differential ability of the progestins to activate the actin-binding protein moesin, leading to distinct effects on actin cytoskeleton remodeling and on the formation of cell membrane structures that mediate cell movement. E2 also induces actin remodeling through moesin activation. However, the addition of some progestins partially offsets the action of estradiol on cell migration and invasion of breast cancer cells.</p> <p>Conclusion</p> <p>These results imply that P, MPA, DRSP and NES alone or in combination with E2 enhance the ability of breast cancer cells to move in the surrounding environment. However, these progestins show different potencies and to some extent use distinct intracellular intermediates to drive moesin activation and actin remodeling. These findings support the concept that each progestin acts differently on breast cancer cells, which may have relevant clinical implications.</p

New evidence regarding hormone replacement therapies is urgently required. Transdermal postmenopausal hormone therapy differs from oral hormone therapy in risks and benefits

Controversies about the safety of different postmenopausal hormone therapies (HTs) started 30 years ago and reached a peak in 2003 after the publication of the results from the Women Health Initiative (WHI) trial and the Million Women Study (MWS) [Writing group for the women's health initiative investigations. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA 2002;288:321–33; Million women study collaborators. Breast cancer and hormone-replacement therapy in the million women study. Lancet 2003;362:419–27]. The single HT formulation used in the WHI trial for non hysterectomized women—an association of oral conjugated equine estrogens (CEE–0.625 mg/day) and a synthetic progestin, medroxyprogesterone acetate (MPA–2.5 mg/day)—increases the risks of venous thromboembolism, cardiovascular disease, stroke and breast cancer. The MWS, an observational study, showed an increased breast cancer risk in users of estrogens combined with either medroxyprogesterone acetate (MPA), norethisterone, or norgestrel. It is unclear and questionable to what extent these results might be extrapolated to other HRT regimens, that differ in their doses, compositions and administration routes, and that were not assessed in the WHI trial and the MWS. Significant results were achieved with the publication of the WHI estrogen-only arm study [Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA 2004;291:1701–1712] in which hormone therapy was reserved to women who had carried out hysterectomy. What emerged from this study will allow us to have some important argument to develop