Explanation of the activity sensitivity of Mn I 5394.7 \AA

There is a long-standing controversy concerning the reason why the Mn I 5394.7 A line in the solar irradiance spectrum brightens more at larger activity than most other photospheric lines. The claim that this activity sensitivity is caused by spectral interlocking to chromospheric emission in Mg II h & k is disputed. Classical one-dimensional modeling is used for demonstration; modern three-dimensional MHD simulation for verification and analysis. The Mn I 5394.7 A line thanks its unusual sensitivity to solar activity to its hyperfine structure. This overrides the thermal and granular Doppler smearing through which the other, narrower, photospheric lines lose such sensitivity. We take the nearby Fe I 5395.2 A line as example of the latter and analyze the formation of both lines in detail to demonstrate and explain granular Doppler brightening. We show that this affects all narrow lines. Neither the chromosphere nor Mg II h & k play a role, nor is it correct to describe the activity sensitivity of Mn I 5394.7 A through plage models with outward increasing temperature contrast. The Mn I 5394.7 A line represents a proxy diagnostic of strong-field magnetic concentrations in the deep solar photosphere comparable to the G band and the blue wing of H-alpha, but not a better one than these. The Mn I lines are more promising as diagnostic of weak fields in high-resolution Stokes polarimetry.Comment: 12 pages, 8 figures, accepted by A&

Photospheric Dynamic Model of Magnetic Reconnection

We present a dynamic model of the atmospheric magnetic field in which magnetic loop footpoints are controlled by photospheric flows computed through a N-body algorithm. This simulation reproduces a system whose behaviour is characterized by small scale (e.g., granular) advection flows that interact to form large spatial organization scales (e.g., meso- and super-granulation). In this model the passive advection of magnetic footpoints through photospheric spatio-temporal correlated flows causes the magnetic field to reconfigure as a consequence of magnetic reconnection processes. This approach, based on the dynamic model of multiple magnetic loops tep{b8 Hu03} and on an advective-interaction model proposed by tet{b8 Ra03}, naturally accounts for the observed probability distribution functions and waiting time statistics of the emitted magnetic energy

Dissecting the role of microRNAs in prostate cancer metastasis: implications for the design of novel therapeutic approaches

Metastatic prostate cancer is a lethal disease that remains incurable despite the recent approval of new drugs, thus making the development of alternative treatment approaches urgently needed. A more precise understanding of the molecular mechanisms underlying prostate cancer dissemination could lead to the identification of novel therapeutic targets for the design of efficient anti-metastatic strategies. MicroRNA (miRNAs) are endogenous, small non-coding RNA molecules acting as key regulators of gene expression at post-transcriptional level. It has been clearly established that altered miRNA expression is a common hallmark of cancer. In addition, emerging evidence suggests their direct involvement in the metastatic cascade. In this review, we present a comprehensive overview of the data generated in experimental tumor models indicating that specific miRNAs may impinge on the different stages of prostate cancer metastasis, including (i) the regulation of epithelial-to-mesenchymal transition and cell migration/invasion, (ii) the interplay between cancer cells and the surrounding stroma, (iii) the control of angiogenesis, (iv) the regulation of anoikis, and (v) the colonization of distant organs. Moreover, we show preliminary evidence of the clinical relevance of some of these miRNAs, in terms of association with tumor aggressiveness/dissemination and clinical outcome, as emerged from translation studies carried out in prostate cancer patient cohorts. We also discuss the potential and the current limitations of manipulating metastasis-related miRNAs, by mimicking or inhibiting them, as a strategy for the development of novel therapeutic approaches for the advanced disease.</p