Constraints and tests of the OPERA superluminal neutrinos

The superluminal neutrinos detected by OPERA indicates Lorentz invariance violation (LIV) of the neutrino sector at the order of $10^{-5}$. We study the implications of the result in this work. We find that such a large LIV implied by OPERA data will make the neutrino production process $\pi \to \mu + \nu_\mu$ kinematically forbidden for neutrino energy greater than about 5 GeV. The OPERA detection of neutrinos at 40 GeV can constrain the LIV parameter to be smaller than $3\times 10^{-7}$. Furthermore the neutrino decay in the LIV framework will modify the neutrino spectrum greatly. The atmospheric neutrino spectrum measured by IceCube can constrain the LIV parameter to the level of $10^{-12}$. The future detection of astrophysical neutrinos of Galactic sources is expected to be able to give even stronger constraint on the LIV parameter of neutrinos.Comment: 5 pages (2 column), 4 figures; published in Phys. Rev. Let

Insights into long noncoding RNAs of naked mole rat (Heterocephalus glaber) and their potential association with cancer resistance

Additional file 4: Table S3. Differential expressed lncRNAs identified in naked mole rat (Heterocephalus glaber) genome

Hypoxia-inducible factor-2a is associated with ABCG2 expression, histology-grade and Ki67 expression in breast invasive ductal carcinoma

<p>Abstract</p> <p>Background</p> <p>Breast cancer is the most common cancer and the leading cause of cancer mortality in women worldwide. Hypoxia is an important factor involved in the progression of solid tumors and has been associated with various indicators of tumor metabolism, angiogenesis and metastasis. But little is known about the contribution of Hypoxia-Inducible Factor-2a (HIF-2a) to the drug resistance and the clinicopathological characteristics in breast cancer.</p> <p>Methods</p> <p>Immunohistochemistry was employed on the tissue microarray paraffin sections of surgically removed samples from 196 invasive breast cancer patients with clinicopathological data. The correlations between the expression of HIF-2a and ABCG2 as well as other patients' clinicopathological data were investigated.</p> <p>Results</p> <p>The results showed that HIF-2a was expressed in different intensities and distributions in the tumor cells of the breast invasive ductal carcinoma. A positive staining for HIF-2a was defined as a brown staining observed mainly in the nucleus. A statistically significant correlation was demonstrated between HIF-2a expression and ABCG2 expression (p = 0.001), histology-grade (p = 0.029), and Ki67 (p = 0. 043) respectively.</p> <p>Conclusion</p> <p>HIF-2a was correlated with ABCG2 expression, histology-grade and Ki67 expression in breast invasive ductal carcinoma. HIF-2a could regulate ABCG2 in breast cancer cells, and could be a novel potential bio-marker to predict chemotherapy effectiveness. The hypoxia/HIF-2a/ABCG2 pathway could be a new mechanism of breast cancer multidrug-resistance.</p> <p>Virtual slides</p> <p>http://www.diagnosticpathology.diagnomx.eu/vs/2965948166714795</p

The chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) controls cellular quiescence by hyperpolarizing the cell membrane during diapause in the crustacean Artemia

Cellular quiescence, a reversible state in which growth, proliferation, and other cellular activities are arrested, is important for self-renewal, differentiation, development, regeneration, and stress resistance. However, the physiological mechanisms underlying cellular quiescence remain largely unknown. In the present study, we used embryos of the crustacean Artemia in the diapause stage, in which these embryos remain quiescent for prolonged periods, as a model to explore the relationship between cell-membrane potential (V-mem) and quiescence. We found that V-mem is hyperpolarized and that the intracellular chloride concentration is high in diapause embryos, whereas V-mem is depolarized and intracellular chloride concentration is reduced in postdiapause embryos and during further embryonic development. We identified and characterized the chloride ion channel protein cystic fibrosis transmembrane conductance regulator (CFTR) of Artemia (Ar-CFTR) and found that its expression is silenced in quiescent cells of Artemia diapause embryos but remains constant in all other embryonic stages. Ar-CFTR knockdown and GlyH-101-mediated chemical inhibition of Ar-CFTR produced diapause embryos having a high V-mem and intracellular chloride concentration, whereas control Artemia embryos released free-swimming nauplius larvae. Transcriptome analysis of embryos at different developmental stages revealed that proliferation, differentiation, and metabolism are suppressed in diapause embryos and restored in postdiapause embryos. Combined with RNA sequencing (RNA-Seq) of GlyH-101-treated MCF-7 breast cancer cells, these analyses revealed that CFTR inhibition down-regulates the Wnt and Aurora Kinase A (AURKA) signaling pathways and up-regulates the p53 signaling pathway. Our findings provide insight into CFTR-mediated regulation of cellular quiescence and V-mem in the Artemia model