3,182 research outputs found

    Asymptotic normalization of mirror states and the effect of couplings

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    Assuming that the ratio between asymptotic normalization coefficients of mirror states is model independent, charge symmetry can be used to indirectly extract astrophysically relevant proton capture reactions on proton-rich nuclei based on information on stable isotopes. The assumption has been tested for light nuclei within the microscopic cluster model. In this work we explore the Hamiltonian independence of the ratio between asymptotic normalization coefficients of mirror states when deformation and core excitation is introduced in the system. For this purpose we consider a phenomenological rotor + N model where the valence nucleon is subject to a deformed mean field and the core is allowed to excite. We apply the model to 8Li/8B, 13C/13N, 17O/17F, 23Ne/23Al, and 27Mg/27P. Our results show that for most studied cases, the ratio between asymptotic normalization coefficients of mirror states is independent of the strength and multipolarity of the couplings induced. The exception is for cases in which there is an s-wave coupled to the ground state of the core, the proton system is loosely bound, and the states have large admixture with other configurations. We discuss the implications of our results for novae.Comment: 8 pages, 2 figures, submitted to PR

    miRNA-489 Induces Immunogenic Cell Death in Triple Negative Breast Cancer Cells

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    It has been well established that microRNAs (miRNAs) play an important role in the regulation of gene expression and consequently promoting or downregulating molecular pathways. When dysregulated, miRNAs have been found to serve as important biomarkers for cancer diagnosis and influence tumor initiation and progression. It has been previously established that miRNA-489 is a tumor suppressor microRNA, and it directly targets cell proliferative pathways like the HER2-SHP2-MAPK pathway. In this study, we focus on the role of miRNA-489, in the induction of immunogenic cell death (ICD) in triple-negative breast cancer cell lines. We first examined the effects of miRNA-489 on two main ICD hallmarks and showed that overexpression of miRNA-489 triggered the extracellular release of ATP and the relocalization of calreticulin (CRT) to the surface of the tumor cells. It was shown for the first time that miRNA- 489 induces ER stress through the upregulation of markers like PERK, IRE1 alpha, and eIF2 alpha, which triggers the release of damage-associated molecular patterns (DAMPs), leading to CRT exposure on the tumor cell surface and ATP release. Lastly, miRNA-489-induced ICD was further confirmed by the promotion of tumor cell phagocytosis by macrophages. Overall, our results suggested that miRNA-489 overexpression, without any corresponding ICD inducer, was able to elevate a phagocytotic and immunogenic response, through the trigger of DAMPS, relocalization of CRT on the cellular surface, and release of ATP
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