Josephson Oscillation and Transition to Self-Trapping for Bose-Einstein-Condensates in a Triple-Well Trap

We investigate the tunnelling dynamics of Bose-Einstein-Condensates(BECs) in a symmetric as well as in a tilted triple-well trap within the framework of mean-field treatment. The eigenenergies as the functions of the zero-point energy difference between the tilted wells show a striking entangled star structure when the atomic interaction is large. We then achieve insight into the oscillation solutions around the corresponding eigenstates and observe several new types of Josephson oscillations. With increasing the atomic interaction, the Josephson-type oscillation is blocked and the self-trapping solution emerges. The condensates are self-trapped either in one well or in two wells but no scaling-law is observed near transition points. In particular, we find that the transition from the Josephson-type oscillation to the self-trapping is accompanied with some irregular regime where tunnelling dynamics is dominated by chaos. The above analysis is facilitated with the help of the Poicar\'{e} section method that visualizes the motions of BECs in a reduced phase plane.Comment: 10 pages, 11 figure

Mast cells and metabolic syndrome

AbstractMast cells are critical effectors in the development of allergic diseases and in many immunoglobulin E-mediated immune responses. These cells exert their physiological and pathological activities by releasing granules containing histamine, cytokines, chemokines, and proteases, including mast cell-specific chymase and tryptase. Like macrophages and T lymphocytes, mast cells are inflammatory cells, and they participate in the pathogenesis of inflammatory diseases such as cardiovascular complications and metabolic disorders. Recent observations suggested that mast cells are involved in insulin resistance and type 2 diabetes. Data from animal models proved the direct participation of mast cells in diet-induced obesity and diabetes. Although the mechanisms by which mast cells participate in these metabolic diseases are not fully understood, established mast cell pathobiology in cardiovascular diseases and effective mast cell inhibitor medications used in pre-formed obesity and diabetes in experimental models offer hope to patients with these common chronic inflammatory diseases. This article is part of a Special Issue entitled: Mast cells in inflammation

Scaling in directed dynamical small-world networks with random responses

A dynamical model of small-world network, with directed links which describe various correlations in social and natural phenomena, is presented. Random responses of every site to the imput message are introduced to simulate real systems. The interplay of these ingredients results in collective dynamical evolution of a spin-like variable S(t) of the whole network. In the present model, global average spreading length \langel L >_s and average spreading time _s are found to scale as p^-\alpha ln N with different exponents. Meanwhile, S behaves in a duple scaling form for N>>N^*: S ~ f(p^-\beta q^\gamma t'_sc), where p and q are rewiring and external parameters, \alpha, \beta, \gamma and f(t'_sc) are scaling exponents and universal functions, respectively. Possible applications of the model are discussed.Comment: 4 pages, 6 Figure

Plasma Cathepsin S and Cystatin C Levels and Risk of Abdominal Aortic Aneurysm: A Randomized Population–Based Study

Background: Human abdominal aortic aneurysm (AAA) lesions contain high levels of cathepsin S (CatS), but are deficient in its inhibitor, cystatin C. Whether plasma CatS and cystatin C levels are also altered in AAA patients remains unknown. Methods and Results: Plasma samples were collected from 476 male AAA patients and 200 age–matched male controls to determine CatS and cystatin C levels by ELISA. Student's t test demonstrated higher plasma levels of total, active, and pro–CatS in AAA patients than in controls (P<0.001). ROC curve analysis confirmed higher plasma total, active, and pro–CatS levels in AAA patients than in controls (P<0.001). Logistic regression suggested that plasma total (odds ratio [OR] = 1.332), active (OR = 1.21), and pro–CatS (OR = 1.25) levels were independent AAA risk factors that associated positively with AAA (P<0.001). Plasma cystatin C levels associated significantly, but negatively, with AAA (OR = 0.356, P<0.001). Univariate correlation demonstrated that plasma total and active CatS levels correlated positively with body–mass index, diastolic blood pressure, and aortic diameter, but negatively with the lowest ankle–brachial index (ABI). Plasma cystatin C levels also correlated negatively with the lowest ABI. Multivariate linear regression showed that plasma total, active, and pro–CatS levels correlated positively with aortic diameter and negatively with the lowest ABI, whereas plasma cystatin C levels correlated negatively with aortic diameter and the lowest ABI, after adjusting for common AAA risk factors. Conclusions: Correlation of plasma CatS and cystatin C with aortic diameter and the lowest ABI suggest these serological parameters as biomarkers for human peripheral arterial diseases and AAA

The preliminary strategies about the innovation of curriculum system of forensic medicine

法医学是应用医学、生物学、化学和其他自然科学理论和技术解决与法律有关的医学问题的一门应用学科。课程体系是指同一专业不同课程门类按照门类顺序排列，是教学内容和进程的总和，一门学科需要不断的调整和完善课程体系，才能适应学科的发展。本文从国内法医学课程设置的现状分析、国外法医学课程体系简况介绍、我国法医学课程体系改革和创新的必要性等几方面对我国法医学专业课程设置的改革进行讨论，提出可行的法医学专业课程体系改革措施和策略，与同行探讨，为法医学专业课程体系的改革提供借鉴。Forensic medicine is an applied science which solved the legal issues concerning with the medical science and utilized the theories and the technologies of medicine, biology, chemistry and other natural sciences. Curriculum system is the summation of teaching contents and teaching proceeding, including all courses of a discipline and arranged with a specific order. The curriculum system of a discipline requires adjustment and innovation to suit the developing circumstance. The present paper will firstly analyze the current status of curriculum system of forensic medicine in China; briefly introduce the oversea curriculum system of forensic medicine; and necessity of innovation of forensic curriculum system in China. Then give some reformatory strategies of China’s curriculum system of forensic medicine

Interleukin-17 Inhibits Adult Hippocampal Neurogenesis

Interleukin 17(A) (IL-17) is a potent pro-inflammatory cytokine that acts as a central regulator of inflammatory response within the brain, but its physiological roles under non-inflammatory conditions remain elusive. Here we report that endogenous IL-17 ablates neurogenesis in the adult dentate gyrus (DG) of hippocampus. Genetic deletion of IL-17 increased the number of adult-born neurons in the DG. Further, we found that IL-17 deletion altered cytokine network, facilitated basal excitatory synaptic transmission, enhanced intrinsic neuronal excitability, and increased expression of proneuronal genes in neuronal progenitor cells (NPCs). Our findings suggest a profound role of IL-17 in the negative regulation of adult hippocampal neurogenesis under physiology conditions

Effects of Ginkgo biloba Extract on Inflammatory Mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6) in TNBS-Induced Colitis in Rats

Inflammatory mediators play a criticial role in ulcerative colitis immune and inflammatory processes. The aim of the study was to investigate the effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-α, NF-κBp65, IL-6) in TNBS-induced colitis in rats. Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid (TNBS, 150 mg/kg). EGB in doses of (50, 100, 200 mg/kg) was administered for 4 weeks to protect colitis. The results showed that EGB could significantly ameliorate macroscopic and histological damage, evidently elevate the activities of SOD and reduce the contents of MDA, inhibit the protein and mRNA expressions of TNF-α, NF-κBp65, and IL-6 in the colon tissues of experimental colitis in a dose-dependent manner compared with the model group. We concluded that the probable mechanisms of EGB ameliorated inflammatory injury in TNBS-induced colitis in rats by its modulation of inflammatory mediators and antioxidatio

Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells

<p>Abstract</p> <p>Background</p> <p>Microglial activation plays an important role in neurodegenerative diseases through production of nitric oxide (NO) and several pro-inflammatory cytokines. Lipoxins (LXs) and aspirin-triggered LXs (ATLs) are considered to act as 'braking signals' in inflammation. In the present study, we investigated the effect of aspirin-triggered LXA₄(ATL) on infiammatory responses induced by lipopolysaccharide (LPS) in murine microglial BV-2 cells.</p> <p>Methods</p> <p>BV-2 cells were treated with ATL prior to LPS exposure, and the effects of such treatment production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were analysed by Griess reaction, ELISA, western blotting and quantitative RT-PCR. Moreover, we investigated the effects of ATL on LPS-induced nuclear factor-κB (NF-κB) activation, phosphorylation of mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) activation.</p> <p>Results</p> <p>ATL inhibited LPS-induced production of NO, IL-1β and TNF-α in a concentration-dependent manner. mRNA expressions for iNOS, IL-1β and TNF-α in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 (a LXA₄receptor antagonist). ATL significantly reduced nuclear translocation of NF-κB p65, degradation of the inhibitor IκB-α, and phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in BV-2 cells activated with LPS. Furthermore, the DNA binding activity of NF-κB and AP-1 was blocked by ATL.</p> <p>Conclusions</p> <p>This study indicates that ATL inhibits NO and pro-inflammatory cytokine production at least in part via NF-κB, ERK, p38 MAPK and AP-1 signaling pathways in LPS-activated microglia. Therefore, ATL may have therapeutic potential for various neurodegenerative diseases.</p