Many-body dynamics of a Bose system with attractive interactions on a ring

We investigate the many-body dynamics of an effectively attractive one-dimensional Bose system confined in a toroidal trap. The mean-field theory predicts that a bright-soliton state will be formed when increasing the interparticle interaction over a critical point. The study of quantum many-body dynamics in this paper reveals that there is a modulation instability in a finite Bose system correspondingly. We show that Shannon entropy becomes irregular near and above the critical point due to quantum correlations. We also study the dynamical behavior of the instability by exploring the momentum distribution and the fringe visibility, which can be verified experimentally by releasing the trapComment: 6 pages,5 figure

Reversible Transition Between Thermodynamically Stable Phases with Low Density of Oxygen Vacancies on SrTiO3_3(110) Surface

The surface reconstruction of SrTiO$_3$(110) is studied with scanning tunneling microscopy and density functional theory (DFT) calculations. The reversible phase transition between (4$\times$1) and (5$\times$1) is controlled by adjusting the surface metal concentration [Sr] or [Ti]. Resolving the atomic structures of the surface, DFT calculations verify that the phase stability changes upon the chemical potential of Sr or Ti. Particularly, the density of oxygen vacancies is low on the thermodynamically stabilized SrTiO$_3$(110) surface.Comment: Accepted by Physical Review Letter

Analysis on the evolution process of BFW-like model with explosive percolation of multiple giant components

Recently, the modified BFW model on random graph [Phys. Rev. Lett., 106, 115701 (2011)], which shows a strongly discontinuous percolation transition with multiple giant components, has attracted much attention from physicists, statisticians and materials scientists. In this paper, by establishing the theoretical expression of evolution equations on the modified BFW model, the steady-state and evolution process are analyzed and a close correspondence is built between the values of parameter \alpha and the number of giant components in steady-states, which fits very well with the numerical simulations. In fact, with the value of \alpha decreasing to 0.25, the error between theoretical and numerical results is smaller than 4% and trends to 0 rapidly. Furthermore, the sizes of giant components for different evolution strategies can also be obtained by solving some constraints derived from the evolution equations. The analysis of the steady-state and evolution process is of great help to explain why the percolation of modified BFW model is explosive and how explosive it is.Comment: 12 pages, 5 figure

Telmisartan prevents weight gain and obesity through activation of peroxisome proliferator-activated receptor-delta-dependent pathways

Abstract—Telmisartan shows antihypertensive and several pleiotropic effects that interact with metabolic pathways. In the present study we tested the hypothesis that telmisartan prevents adipogenesis in vitro and weight gain in vivo through activation of peroxisome proliferator-activated receptor (PPAR)-–dependent pathways in several tissues. In vitro, telmisartan significantly upregulated PPAR- expression in 3T3-L1 preadipocytes in a time- and dose-dependent manner. Other than enhancing PPAR- expression by 68.217.3 % and PPAR- activity by 102.09.0%, telmisartan also upregulated PPAR- expression, whereas neither candesartan nor losartan affected PPAR- expression. In vivo, long-term administration of telmisartan significantly reduced visceral fat and prevented high-fat diet-induced obesity in wild-type mice and hypertensive rats but not in PPAR- knockout mice. Administration of telmisartan did not influence food intake in mice. Telmisartan influenced several lipolytic and energy uncoupling related proteins (UCPs) and enhanced phosphorylated protein kinase A and hormone sensitive lipase but reduced perilipin expression and finally inhibited adipogenesis in 3T3-L1 preadipocytes. Telmisartan-associated reduction of adipogenesis in preadipocytes was significantly blocked after PPAR- gene knockout. Chronic telmisartan treatment upregulated the expressions of protein kinase A, hormone-sensitive lipase, and uncoupling protein 1 but reduced perilipin expression in adipose tissue and increased uncoupling protein 2 and 3 expression in skeletal muscle in wild-type mice but not in PPAR- knockout mice. We conclude that telmisartan prevents adipogenesis and weight gain through activation of PPAR-–dependent lipolyti

Characteristics of tumor infiltrating lymphocyte and circulating lymphocyte repertoires in pancreatic cancer by the sequencing of T cell receptors

Pancreatic cancer has a poor prognosis and few effective treatments. The failure of treatment is partially due to the high heterogeneity of cancer cells within the tumor. T cells target and kill cancer cells by the specific recognition of cancer-associated antigens. In this study, T cells from primary tumor and blood of sixteen patients with pancreatic cancer were characterized by deep sequencing. T cells from blood of another eight healthy volunteers were also studied as controls. By analyzing the complementary determining region 3 (CDR3) gene sequence, we found no significant differences in the T cell receptor (TCR) repertoires between patients and healthy controls. Types and length of CDR3 were similar among groups. However, two clusters of patients were identified according to the degree of CDR3 overlap within tumor sample group. In addition, clonotypes with low frequencies were found in significantly higher numbers in primary pancreatic tumors compared to blood samples from patients and healthy controls. This study is the first to characterize the TCR repertoires of pancreatic cancers in both primary tumors and matched blood samples. The results imply that specific types of pancreatic cancer share potentially important immunological characteristics