Spectroscopy of 26^{26}F

The structure of the weakly-bound $^{26}_{\;\;9}$F$_{17}$ odd-odd nucleus, produced from $^{27,28}$Na nuclei, has been investigated at GANIL by means of the in-beam $\gamma$-ray spectroscopy technique. A single $\gamma$-line is observed at 657(7) keV in $^{26}_{9}$F which has been ascribed to the decay of the excited J=$2^+$ state to the J=1$^+$ ground state. The possible presence of intruder negative parity states in $^{26}$F is also discussed.Comment: 3 pages, 1 figure, accepted for publication in Physical Review

Spectroscopy around 36^{36}Ca

Expérience GANILInternational audienceAn experiment was performed to study excited states in neutron-deficient nuclei around Ca. A one-neutron knockout reaction was used to produce $^{36}$Ca ions from a $^{37}$Ca secondary beam, and in-beam $\gamma$-rays were measured. The $2^+$ energy in $^{36}$Ca is compared to the mirror nucleus $^{36}$S to deduce information on the isospin dependence of the nuclear force near the proton drip line. The energy of the first excited $2^+$ state in $^{36}$Ca and the cross section for the 1-neutron knock-out reaction from $^{37}$Ca at $\sim$ 45 · AMeV were obtained. Furthermore, for two other $T_z$ = −2 nuclei, $^{28}$S and $^{32}$Ar, the de-excitation of the first $2^+$ state has been observed

Regulation of microRNA biogenesis and turnover by animals and their viruses

Item does not contain fulltextMicroRNAs (miRNAs) are a ubiquitous component of gene regulatory networks that modulate the precise amounts of proteins expressed in a cell. Despite their small size, miRNA genes contain various recognition elements that enable specificity in when, where and to what extent they are expressed. The importance of precise control of miRNA expression is underscored by functional studies in model organisms and by the association between miRNA mis-expression and disease. In the last decade, identification of the pathways by which miRNAs are produced, matured and turned-over has revealed many aspects of their biogenesis that are subject to regulation. Studies in viral systems have revealed a range of mechanisms by which viruses target these pathways through viral proteins or non-coding RNAs in order to regulate cellular gene expression. In parallel, a field of study has evolved around the activation and suppression of antiviral RNA interference (RNAi) by viruses. Virus encoded suppressors of RNAi can impact miRNA biogenesis in cases where miRNA and small interfering RNA pathways converge. Here we review the literature on the mechanisms by which miRNA biogenesis and turnover are regulated in animals and the diverse strategies that viruses use to subvert or inhibit these processes

Search for Dark Matter and Supersymmetry with a Compressed Mass Spectrum in the Vector Boson Fusion Topology in Proton-Proton Collisions at root s=8 TeV

Peer reviewe

First in-beam γ -ray study of the level structure of neutron-rich S 39

International audienceThe neutron-rich S39 nucleus has been studied using binary grazing reactions produced by the interaction of a 215-MeV beam of S36 ions with a thin Pb208 target. The magnetic spectrometer, PRISMA, and the γ-ray array, CLARA, were used in the measurements. Gamma-ray transitions of the following energies were observed: 339, 398, 466, 705, 1517, 1656, and 1724 keV. Five of the observed transitions have been tentatively assigned to the decay of excited states with spins up to (11/2−). The results of a state-of-the-art shell-model calculation of the level scheme of S39 using the SDPF-U effective interaction are also presented. The systematic behavior of the excitation energy of the first 11/2− states in the odd-A isotopes of sulfur and argon is discussed in relation to the excitation energy of the first excited 2+ states of the adjacent even-A isotopes. The states of S39 that have the components in their wave functions corresponding to three neutrons in the 1f7/2 orbital outside the N=20 core have also been discussed within the context of the 0 ℏω shell-model calculations presented here

NCI60 Cancer Cell Line Panel Data and RNAi Analysis Help Identify EAF2 as a Modulator of Simvastatin and Lovastatin Response in HCT-116 Cells

Simvastatin and lovastatin are statins traditionally used for lowering serum cholesterol levels. However, there exists evidence indicating their potential chemotherapeutic characteristics in cancer. In this study, we used bioinformatic analysis of publicly available data in order to systematically identify the genes involved in resistance to cytotoxic effects of these two drugs in the NCI60 cell line panel. We used the pharmacological data available for all the NCI60 cell lines to classify simvastatin or lovastatin resistant and sensitive cell lines, respectively. Next, we performed whole-genome single marker case-control association tests for the lovastatin and simvastatin resistant and sensitive cells using their publicly available Affymetrix 125K SNP genomic data. The results were then evaluated using RNAi methodology. After correction of the p-values for multiple testing using False Discovery Rate, our results identified three genes (NRP1, COL13A1, MRPS31) and six genes (EAF2, ANK2, AKAP7, STEAP2, LPIN2, PARVB) associated with resistance to simvastatin and lovastatin, respectively. Functional validation using RNAi confirmed that silencing of EAF2 expression modulated the response of HCT-116 colon cancer cells to both statins. In summary, we have successfully utilized the publicly available data on the NCI60 cell lines to perform whole-genome association studies for simvastatin and lovastatin. Our results indicated genes involved in the cellular response to these statins and siRNA studies confirmed the role of the EAF2 in response to these drugs in HCT-116 colon cancer cells

Wnt signaling in triple-negative breast cancer

Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC. We review the complex molecular nature of TNBC and the emerging therapies that are currently under investigation for the treatment of this disease