Measurement-induced nonlocality in arbitrary dimensions in terms of the inverse approximate joint diagonalization

Here we focus on the measurement induced nonlocality and present a redefinition in terms of the skew information subject to a broken observable. It is shown that the obtained quantity possesses an obvious operational meaning, can tackle the noncontractivity of the measurement induced nonlocality and has analytic expressions for many quantum states. Most importantly, an inverse approximate joint diagonalization algorithm, due to its simplicity, high efficiency, stability, and state independence, is presented to provide almost analytic expressions for any quantum state, which can also shed light on other aspects in physics

GPER-induced signaling is essential for the survival of breast cancer stem cells.

G protein-coupled estrogen receptor-1 (GPER), a member of the G protein-coupled receptor (GPCR) superfamily, mediates estrogen-induced proliferation of normal and malignant breast epithelial cells. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here we showed greater expression of GPER in BCSCs than non-BCSCs of three patient-derived xenografts of ER- /PR+ breast cancers. GPER silencing reduced stemness features of BCSCs as reflected by reduced mammosphere forming capacity in vitro, and tumor growth in vivo with decreased BCSC populations. Comparative phosphoproteomics revealed greater GPER-mediated PKA/BAD signaling in BCSCs. Activation of GPER by its ligands, including tamoxifen (TMX), induced phosphorylation of PKA and BAD-Ser118 to sustain BCSC characteristics. Transfection with a dominant-negative mutant BAD (Ser118Ala) led to reduced cell survival. Taken together, GPER and its downstream signaling play a key role in maintaining the stemness of BCSCs, suggesting that GPER is a potential therapeutic target for eradicating BCSCs

The Information Of The Milky Way From 2MASS Whole Sky Star Count: The Bimodal Color Distributions

The J-Ks color distribution (CD) with a bin size of 0.05 magnitude for the entire Milky Way has been carried out by using the Two Micron All Sky Survey Point Source Catalog (2MASS PSC). The CDs are bimodal, which has a red peak at 0.8 < J-Ks < 0.85 and a blue peak at 0.3 < J-Ks < 0.4. The colors of the red peak are more or less the same for the whole sky, but that of the blue peak depend on Galactic latitude, (J-Ks ~ 0.35 at low Galactic latitudes and 0.35 < J-Ks < 0.4 for other sky areas). The blue peak dominates the bimodal CDs at low Galactic latitudes and becomes comparable with the red peak in other sky regions. In order to explain the bimodal distribution and the global trend shown by the all sky 2MASS CDs, we assemble an empirical HR diagram, which is composed by observational-based near infrared HR diagrams and color magnitude diagrams, and incorporate a Milky Way model. In the empirical HR diagram, the main sequence stars turnoff the thin disk is relatively bluer, (J-Ks)0 = 0.31, when we compare with the thick disk which is (J-Ks)0 = 0.39. The age of the thin/thick disk is roughly estimated to be around 4-5/8-9 Gyr according to the color-age relation of the main sequence turnoff. In general, the 2MASS CDs can be treated as a tool to census the age of stellar population of the Milky Way in a statistical manner and to our knowledge this is a first attempt to measure the age.Comment: Accepted by ApJ on Sept. 11 201

Loss of vesicular dopamine release precedes tauopathy in degenerative dopaminergic neurons in a Drosophila model expressing human tau.

While a number of genome-wide association studies have identified microtubule-associated protein tau as a strong risk factor for Parkinson's disease (PD), little is known about the mechanism through which human tau can predispose an individual to this disease. Here, we demonstrate that expression of human wild-type tau is sufficient to disrupt the survival of dopaminergic neurons in a Drosophila model. Tau triggers a synaptic pathology visualized by vesicular monoamine transporter-pHGFP that precedes both the age-dependent formation of tau-containing neurofibrillary tangle-like pathology and the progressive loss of DA neurons, thereby recapitulating the pathological hallmarks of PD. Flies overexpressing tau also exhibit progressive impairments of both motor and learning behaviors. Surprisingly, contrary to common belief that hyperphosphorylated tau could aggravate toxicity, DA neuron degeneration is alleviated by expressing the modified, hyperphosphorylated tau(E14). Together, these results show that impairment of VMAT-containing synaptic vesicle, released to synapses before overt tauopathy may be the underlying mechanism of tau-associated PD and suggest that correction or prevention of this deficit may be appropriate targets for early therapeutic intervention