Holographic n-partite Information in Hyperscaling Violating Geometry

The $n$-partite information (nI) is formulated as a measure of multi-partite entanglement. Field theory computation revealed that the sign of nI is indefinite for $n\geq 3$, while holographic studies conjectured a sign property that holographic nI is non-negative/non-positive for even/odd $n$, with tripartite information (TI, $n=3$) proved. We investigate the aspects of nI with holographic duality. With a generically static bulk geometry, we give an alternate geometric proof that holographic TI for parallel disjoint boundary strips is non-positive, and illustrate that remarkably for larger $n$, the sign is indefinite. In hyperscaling violating geometry, we confirm the conjectured sign property for strips of equal length with equal separation distance, and self-consistently disprove this conjecture for $n>3$ with general configurations. Therefore, nI in field theories and holography exhibits compatibility except for $n=3$. We also discuss other properties of holographic nI with analytic computation: the monotonicity, linearity, relation to hyperscaling violating parameters, temperature and UV cutoff effects, and the physical implications. It is doubtful that nI is an effective measure of entanglement considering the indefinite sign, non-monotonicity, and quasi-linearity of its holographic dual. In this respect, we propose constraints on the multi-partite entanglement measures.Comment: 30 pages, 19 figure

Generalized Rindler Wedge and Holographic Observer Concordance

We study the most general horizons of accelerating observers and find that in a general spacetime, only spacelike surfaces satisfying a global condition could become horizons of well-defined accelerating observers, which we name the Rindler-convexity condition. The entanglement entropy associated with a Rindler-convex region is proportional to the area of the enclosing surface. This observer physics provides a novel perspective to define a well-defined subregion in spacetime, named the generalized Rindler wedge, whose degrees of freedom should be fully encoded within the subregion. We propose the holographic interpretation of generalized Rindler wedges and provide evidence from the observer correspondence, the subregion subalgebra duality, and the equality of the entanglement entropy, respectively. We introduce time/space cutoffs in the bulk to substantiate this proposition, generalize it, and establish a holographic observer concordance framework, which asserts that the partitioning of degrees of freedom through observation is holographically concordant.Comment: v2: 41 pages, 9 figures; major expansion for the GRW spacetime subregion duality and observer concordanc

Density alteration in non-physiological cells

In the present study an important phenomenon of cells was discovered: the change of intracellular density in cell's response to drug and environmental factors. For convenience, this phenomenon is named as "density alteration in non-physiological cells" ( DANCE). DANCE was determined by discontinuous sucrose gradient centrifugation (DSGC), in which cells were separated into several bands. The number and position of the bands in DSGC varied with the change of cell culture conditions, drugs, and physical process, indicating that cell's response to these factors was associated with alteration of intracellular density. Our results showed that the bands of cells were molecularly different from each other, such as the expression of some mRNAs. For most cells tested, intracellular density usually decreased when the cells were in bad conditions, in presence of drugs, or undergoing pathological changes. However, unlike other tissue cells, brain cells showed increased intracellular density in 24 hrs after the animal death. In addition, DANCE was found to be related to drug resistance, with higher drug-resistance in cells of lower intracellular density. Further study found that DANCE also occurred in microorganisms including bacteria and fungus, suggesting that DANCE might be a sensitive and general response of cells to drugs and environmental change. The mechanisms for DANCE are not clear. Based on our study the following causes were hypothesized: change of metabolism mode, change of cell membrane function, and pathological change. DANCE could be important in medical and biological sciences. Study of DANCE might be helpful to the understanding of drug resistance, development of new drugs, separation of new subtypes from a cell population, forensic analysis, and importantly, discovery of new physiological or pathological properties of cells

ERK3 Is Required for Metaphase-Anaphase Transition in Mouse Oocyte Meiosis

ERK3 (extracellular signal-regulated kinase 3) is an atypical member of the mitogen-activated protein (MAP) kinase family of serine/threonine kinases. Little is known about its function in mitosis, and even less about its roles in mammalian oocyte meiosis. In the present study, we examined the localization, expression and functions of ERK3 during mouse oocyte meiotic maturation. Immunofluorescent analysis showed that ERK3 localized to the spindles from the pre-MI stage to the MII stage. ERK3 co-localized with α-tubulin on the spindle fibers and asters in oocytes after taxol treatment. Deletion of ERK3 by microinjection of ERK3 morpholino (ERK3 MO) resulted in oocyte arrest at the MI stage with severely impaired spindles and misaligned chromosomes. Most importantly, the spindle assembly checkpoint protein BubR1 could be detected on kinetochores even in oocytes cultured for 10 h. Low temperature treatment experiments indicated that ERK3 deletion disrupted kinetochore-microtubule (K-MT) attachments. Chromosome spreading experiments showed that knock-down of ERK3 prevented the segregation of homologous chromosomes. Our data suggest that ERK3 is crucial for spindle stability and required for the metaphase-anaphase transition in mouse oocyte maturation

The Stellar "Snake" -- II: The Mass Function

We present a comprehensive investigation on the mass function (MF) of a snake-like stellar structure in the solar neighbourhood, building on our previous discovery. To ensure the reliability of the data, we reselect the member stars of the Stellar ``Snake'' in the latest {\it Gaia} Data Release 3 using the same approach as the initial series of articles. We also precisely measure the physical parameters of the clusters within the Stellar Snake. In light of the high completeness of the member stars in the cluster regions, we develop a simulated model color-magnitude diagram-based inference method to derive the mass function, binary fraction, and mass-ratio distribution of the clusters in the Stellar Snake. Notably, despite their similar ages and metallicity, we discover systematic variations in the MFs along the elongation direction of the Snake in the mass range of 0.5 to 2.0 M$_\odot$. The ``head'' of the Snake conforms to a canonical initial mass function with a power-law slope of $\alpha\sim-2.3$. Extending towards the ``tail,'' the MF becomes more top-light, indicating a deficiency of massive stars within these clusters. This result provides evidence for the delayed formation of massive stars in the clusters. Such clues give support to the hypothesis that the Stellar Snake constitutes as a hierarchically primordial structure.Comment: 19 pages, 15 figures, Accepted for publication on MNRA

miR-17/20 sensitization of breast cancer cells to chemotherapy-induced apoptosis requires Akt1.

The serine threonine kinase Akt1 has been implicated in the control of cellular metabolism, survival and growth. Herein, disruption of the ubiquitously expressed member of the Akt family of genes, Akt1, in the mouse, demonstrates a requirement for Akt1 in miRNA-mediated cellular apoptosis. The miR-17/20 cluster is known to inhibit breast cancer cellular proliferation through G1/S cell cycle arrest via binding to the cyclin D1 3\u27UTR. Here we show that miR-17/20 overexpression sensitizes cells to apoptosis induced by either Doxorubicin or UV irradiation in MCF-7 cells via Akt1. miR-17/20 mediates apoptosis via increased p53 expression which promotes Akt degradation. Akt1-/- mammary epithelial cells which express Akt2 and Akt3 demonstrated increased apoptosis to DNA damaging agents. Akt1 deficiency abolished the miR-17/20-mediated apoptosis. These results demonstrated a novel pathway through which miR17/20 regulate p53 and Akt controlling breast cancer cell apoptosis