Pomeranchuk cooling of the SU(2N2N) ultra-cold fermions in optical lattices

We investigate the thermodynamic properties of a half-filled SU(2N) Fermi-Hubbard model in the two-dimensional square lattice using the determinantal quantum Monte Carlo simulation, which is free of the fermion "sign problem". The large number of hyperfine-spin components enhances spin fluctuations, which facilitates the Pomeranchuk cooling to temperatures comparable to the superexchange energy scale at the case of SU$(6)$. Various quantities including entropy, charge fluctuation, and spin correlations have been calculated.Comment: 7 page

The New Formulation of Higgs Effective Field Theory

We present the explicit construction of the effective field theory (EFT) of standard model mass eigenstates. The EFT, which is invariant under $U(1)_{\text{e.m.}}\times SU(3)_c$, is constructed based on the on-shell method and Young Tableau technique. This EFT serves as a new formulation of the Higgs EFT (HEFT), which can describe the infrared effects of new physics at the electroweak symmetry-breaking phase with greater conciseness. The current HEFT operator basis has a clear physical interpretation, making it more accessible for research in phenomenology. A complete list of HEFT operator bases for any-point vertices up to any dimension could be provided, and three- and four-point bases are provided as examples. Additionally, this framework realized as a Mathematica program can be used to construct the EFT of any type of dark matter or particles with any spin

Role of CD28/B7 costimulation and IL-12/IL-10 interaction in the radiation-induced immune changes

BACKGROUND: The present paper aims at studying the role of B7/CD28 interaction and related cytokine production in the immunological changes after exposure to different doses of ionizing radiation. RESULTS: The stimulatory effect of low dose radiation (LDR) on the proliferative response of lymphocytes to Con A was found to require the presence of APCs. The addition of APCs obtained from both low- and high-dose-irradiated mice to splenic lymphocytes separated from low-dose-irradiated mice caused stimulation of lymphocyte proliferation. B7-1/2 expression on APCs was up-regulated after both low and high doses of radiation. There was up-regulation of CD28 expression on splenic and thymic lymphocytes after LDR and its suppression after high dose radiation (HDR), and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) expression showed changes in the opposite direction. IL-12 secretion by macrophages was stimulated after both low and high doses of radiation, but IL-10 synthesis by splenocytes was suppressed by low dose radiation and up-regulated by high dose radiation. CONCLUSION: The status of CD28/CTLA-4 expression on T lymphocytes in the presence of up-regulated B7 expression on APCs determined the outcome of the immune changes in response to radiation, i.e., up-regulation of CD28 after LDR resulted in immunoenhancement, and up-regulation of CTLA-4 associated with down-regulation of CD28 after HDR led to immunosuppression. Both low and high doses of radiation up-regulated B7-1/2 expression on APCs. After LDR, the stimulated proliferative effect of increased IL-12 secretion by APCs, reinforced by the suppressed secretion of IL-10, further strengthened the intracellular signaling induced by B7-CD28 interaction

Planets Across Space and Time (PAST) IV: The Occurrence and Architecture of Kepler Planetary Systems as a Function of Kinematic Age Revealed by the LAMOST-Gaia-Kepler Sample

One of the fundamental questions in astronomy is how planetary systems form and evolve. Measuring the planetary occurrence and architecture as a function of time directly addresses this question. In the fourth paper of the Planets Across Space and Time (PAST) series, we investigate the occurrence and architecture of Kepler planetary systems as a function of kinematic age by using the LAMOST-Gaia-Kepler sample. To isolate the age effect, other stellar properties (e.g., metallicity) have been controlled. We find the following results. (1) The fraction of stars with Kepler-like planets ($F_{\text{Kep}}$) is about 50% for all stars; no significant trend is found between $F_{\text{Kep}}$ and age. (2) The average planet multiplicity ($\bar{N}_p$) exhibits a decreasing trend (~2$\sigma$ significance) with age. It decreases from $\bar{N}_p$~3 for stars younger than 1 Gyr to $\bar{N}_p$~1.8 for stars about 8 Gyr. (3) The number of planets per star ($\eta=F_{\text{Kep}}\times\bar{N}_p$) also shows a decreasing trend (~2-3$\sigma$ significance). It decreases from $\eta$~1.6-1.7 for young stars to $\eta$~1.0 for old stars. (4) The mutual orbital inclination of the planets ($\sigma_{i,k}$) increases from $1.2^{+1.4}_{-0.5}$ to $3.5^{+8.1}_{-2.3}$ as stars aging from 0.5 to 8 Gyr with a best fit of $\log{\sigma_{i,k}}=0.2+0.4\times\log{\frac{\text{Age}}{\text{1Gyr}}}$. Interestingly, the Solar System also fits such a trend. The nearly independence of $F_{\text{Kep}}$~50% on age implies that planet formation is robust and stable across the Galaxy history. The age dependence of $\bar{N}_p$ and $\sigma_{i,k}$ demonstrates planetary architecture is evolving, and planetary systems generally become dynamically hotter with fewer planets as they age.Comment: 27 pages, 20 figures, 4tables, accepted for publication in A

Planets Across Space and Time (PAST). III. Morphology of the Planetary Radius Valley as a Function of Stellar Age and Metallicity in the Galactic Context Revealed by the LAMOST-Gaia-Kepler Sample

The radius valley, a dip in the radius distribution of exoplanets at ~1.9 Earth radii separates compact rocky Super-Earths and Sub-Neptunes with lower density. Various hypotheses have been put forward to explain the radius valley. Characterizing the radius valley morphology and its correlation to stellar properties will provide crucial observation constraints on its origin mechanism and deepen the understanding of planet formation and evolution. In this paper, the third part of the Planets Across the Space and Time (PAST) series, using the LAMOST-Gaia-Kepler catalog, we perform a systematical investigation into how the radius valley morphology varies in the Galactic context, i.e., thin/thick galactic disks, stellar age and metallicity abundance ([Fe/H] and [alpha/Fe]). We find that (1) The valley becomes more prominent with the increase of both age and [Fe/H]. (2) The number ratio of super-Earths to sub-Neptunes monotonically increases with age but decreases with [Fe/H] and [alpha/Fe]. (3) The average radius of planets above the valley (2.1-6 Earth radii) decreases with age but increases with [Fe/H]. (4) In contrast, the average radius of planets below the valley (R < 1.7 Earth radii) is broadly independent on age and metallicity. Our results demonstrate that the valley morphology as well as the whole planetary radius distribution evolves on a long timescale of giga-years, and metallicities (not only Fe but also other metal elements, e.g., Mg, Si, Ca, Ti) play important roles in planet formation and in the long term planetary evolution.Comment: Accepted for pubilication in AJ, 20 Pages, 10 figures, 2 Tables (Appendix: 13 Figures

Drugging the “Undruggable” DNA-binding Domain of STAT3 for Inhibition of Cancer Cell Migration and Invasion

poster abstractSignal transducer and activator of transcription 3 (STAT3) is constitutively activated in malignant tumors, and its activation is associated with high histological grade and advanced cancer stage. STAT3 has been shown to play important roles in multiple aspects of cancer aggressiveness including migration, invasion, survival, self-renewal, angiogenesis, and tumor cell immune evasion by regulating the expression of multiple downstream target genes. Thus, inhibiting STAT3 promises an attracting strategy for treatment of advanced tumors with metastatic potential. Previously, we identified a STAT3 inhibitor, inS3-54, by targeting the “undruggable” DNA-binding site of STAT3 using an improved in-silico screening approach. To further develop this inhibitor, we identified 79 analogues of inS3-54 for the structure-activity relationship analysis. Further study of five effective analogues shows that four analogues (#1, 18, 26, and 69) inhibit STAT3-dependent colony formation of hematopoietic progenitor cells, indicating a higher selectivity for STAT3 than their parental compound, inS3-54 and another analogue #74. These compounds also (1) inhibit STAT3-specific DNA binding activity; (2) suppress proliferation of cancer cells that have constitutively activated STAT3; and (3) inhibit migration and invasion of cancer cells. In addition, analogue #26-conjugated Sepharose beads could also pull down STAT3, revealing a possible direct binding between STAT3 and the inhibitor. Taken together, we conclude that it is possible to inhibit STAT3 by targeting its DNA-binding domain for discovery of anticancer therapeutics and for treatment of metastatic cancers

The Modulatory Role of CYP3A4 in Dictamnine-Induced Hepatotoxicity

Dictamni Cortex (DC) has been reported to be associated with acute hepatitis in clinic and may lead to a selective sub-chronic hepatotoxicity in rats. Nevertheless, the potent toxic ingredient and the underlying mechanism remain unknown. Dictamnine (DTN), the main alkaloid from DC, possesses a furan ring which was suspected of being responsible for hepatotoxicity via metabolic activation primarily by CYP3A4. Herein, the present study aimed to evaluate the role of CYP3A4 in DTN-induced liver injury. The in vitro results showed that the EC50 values in primary human hepatocytes (PHH), L02, HepG2 and NIH3T3 cells were correlated with the CYP3A4 expression levels in corresponding cells. Furthermore, the toxicity was increased in CYP3A4-induced PHH by rifampicin, and CYP3A4 over-expressed (OE) HepG2 and L02 cells. Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). In addition, the hepatotoxicity of DTN in enzyme induction/inhibition mice was further investigated in the aspects of biochemistry, histopathology, and pharmacokinetics. Administration of DTN in combination with KTZ resulted in attenuated liver injury, including lower alanine transaminase and aspartate transaminase activities and greater AUC and Cmax of serum DTN, whereas, pretreatment with dexamethasone aggravated the injury. Collectively, our findings illustrated that DTN-induced hepatotoxicity correlated well with the expression of CYP3A4, namely inhibition of CYP3A4 alleviated the toxicity both in vitro and in vivo, and induction aggravated the toxicity effects

A simulation study on the measurement of D0-D0bar mixing parameter y at BES-III

We established a method on measuring the \dzdzb mixing parameter $y$ for BESIII experiment at the BEPCII $e^+e^-$ collider. In this method, the doubly tagged $\psi(3770) \to D^0 \overline{D^0}$ events, with one $D$ decays to CP-eigenstates and the other $D$ decays semileptonically, are used to reconstruct the signals. Since this analysis requires good $e/\pi$ separation, a likelihood approach, which combines the $dE/dx$, time of flight and the electromagnetic shower detectors information, is used for particle identification. We estimate the sensitivity of the measurement of $y$ to be 0.007 based on a $20fb^{-1}$ fully simulated MC sample.Comment: 6 pages, 7 figure

Aurora-A down-regulates IkappaBα via Akt activation and interacts with insulin-like growth factor-1 induced phosphatidylinositol 3-kinase pathway for cancer cell survival

<p>Abstract</p> <p>Background</p> <p>The mitotic Aurora-A kinase exerts crucial functions in maintaining mitotic fidelity. As a bona fide oncoprotein, Aurora-A aberrant overexpression leads to oncogenic transformation. Yet, the mechanisms by which Aurora-A enhances cancer cell survival remain to be elucidated.</p> <p>Results</p> <p>Here, we found that Aurora-A overexpression was closely correlated with clinic stage and lymph node metastasis in tongue carcinoma. Aurora-A inhibitory VX-680 suppressed proliferation, induced apoptosis and markedly reduced migration in cancer cells. We further showed that insulin-like growth factor-1, a PI3K physiological activator, reversed VX-680-decreased cell survival and motility. Conversely, wortmannin, a PI3K inhibitor, combined with VX-680 showed a synergistic effect on inducing apoptosis and suppressing migration. In addition, Aurora-A inhibition suppressed Akt activation, and VX-680-induced apoptosis was attenuated by Myr-Akt overexpression, revealing a cross-talk between Aurora-A and PI3K pathway interacting at Akt activation. Significantly, we showed that suppression of Aurora-A decreased phosphorylated Akt and was associated with increased IkappaBα expression. By contrast, Aurora-A overexpression upregulated Akt activity and downregulated IkappaBα, these changes were accompanied by nuclear translocation of nuclear factor-κB and increased expression of its target gene Bcl-xL. Lastly, Aurora-A overexpression induced IkappaBα reduction was abrogated by suppression of Akt either chemically or genetically.</p> <p>Conclusion</p> <p>Taken together, our data established that Aurora-A, via activating Akt, stimulated nuclear factor-κB signaling pathway to promote cancer cell survival, and promised a novel combined chemotherapy targeting both Aurora-A and PI3K in cancer treatment.</p