Exact solution of gyration radius of individual's trajectory for a simplified human mobility model

Gyration radius of individual's trajectory plays a key role in quantifying human mobility patterns. Of particular interests, empirical analyses suggest that the growth of gyration radius is slow versus time except the very early stage and may eventually arrive to a steady value. However, up to now, the underlying mechanism leading to such a possibly steady value has not been well understood. In this Letter, we propose a simplified human mobility model to simulate individual's daily travel with three sequential activities: commuting to workplace, going to do leisure activities and returning home. With the assumption that individual has constant travel speed and inferior limit of time at home and work, we prove that the daily moving area of an individual is an ellipse, and finally get an exact solution of the gyration radius. The analytical solution well captures the empirical observation reported in [M. C. Gonz`alez et al., Nature, 453 (2008) 779]. We also find that, in spite of the heterogeneous displacement distribution in the population level, individuals in our model have characteristic displacements, indicating a completely different mechanism to the one proposed by Song et al. [Nat. Phys. 6 (2010) 818].Comment: 4 pages, 4 figure

Mice with cardiac-restricted angiotensin-converting enzyme (ACE) have atrial enlargement, cardiac arrhythmia, and sudden death

Journal ArticleTo investigate the local effects of angiotensin II on the heart, we created a mouse model with 100-fold normal cardiac angiotensin-converting enzyme (ACE), but no ACE expression in kidney or vascular endothelium. This was achieved by placing the endogenous ACE gene under the control of the α-myosin heavy chain promoter using targeted homologous recombination. These mice, called ACE 8/8, have cardiac angiotensin II levels that are 4.3-fold those of wild-type mice. Despite near normal blood pressure and a normal renal function, ACE 8/8 mice have a high incidence of sudden death. Both histological analysis and in vivo catheterization of the heart showed normal ventricular size and function. In contrast, both the left and right atria were three times normal size. ECG analysis showed atrial fibrillation and cardiac block. In conclusion, increased local production of angiotensin II in the heart is not sufficient to induce ventricular hypertrophy or fibrosis. Instead, it leads to atrial morphological changes, cardiac arrhythmia, and sudden death

Hes1 Potentiates T Cell Lymphomagenesis by Up-Regulating a Subset of Notch Target Genes

Background: Hairy/Enhancer of Split (Hes) proteins are targets of the Notch signaling pathway and make up a class of basic helix-loop-helix (bHLH) proteins that function to repress transcription. Data from Hes1 deficient mice suggested that Hes1, like Notch1, is necessary for the progression of early T cell progenitors. Constitutive activation of Notch is known to cause T cell leukemia or lymphoma but whether Hes1 has any oncogenic activity is not known. Methodology/Principal Findings: We generated mice carrying a Hes1 transgene under control of the proximal promote of the lck gene. Hes1 expression led to a reduction in numbers of total thymocytes, concomitant with the increased percentage and number of immature CD8 + (ISP) T cells and sustained CD25 expression in CD4 + CD8 + double positive (DP) thymocytes. Hes1 transgenic mice develop thymic lymphomas at about 20 weeks of age with a low penetrance. However, expression of Hes1 significantly shortens the latency of T cell lymphoma developed in Id1 transgenic mice, where the function of bHLH E proteins is inhibited. Interestingly, Hes1 increased expression of a subset of Notch target genes in premalignant ISP and DP thymocytes, which include Notch1, Notch3 and c-myc, thus suggesting a possible mechanism for lymphomagenesis. Conclusions/Significance: We have demonstrated for the first time that Hes1 potentiates T cell lymphomagenesis, by upregulating a subset of Notch target genes and by causing an accumulation of ISP thymocytes particularly vulnerable to oncogenic transformation

Suppression of ILC2 differentiation from committed T cell precursors by E protein transcription factors

Current models propose that group 2 innate lymphoid cells (ILC2s) are generated in the bone marrow. Here, we demonstrate that subsets of these cells can differentiate from multipotent progenitors and committed T cell precursors in the thymus, both in vivo and in vitro. These thymic ILC2s exit the thymus, circulate in the blood, and home to peripheral tissues. Ablation of E protein transcription factors greatly promotes the ILC fate while impairing B and T cell development. Consistently, a transcriptional network centered on the ZBTB16 transcription factor and IL-4 signaling pathway is highly up-regulated due to E protein deficiency. Our results show that ILC2 can still arise from what are normally considered to be committed T cell precursors, and that this alternative cell fate is restrained by high levels of E protein activity in these cells. Thymus-derived lung ILC2s of E protein-deficient mice show different transcriptomes, proliferative properties, and cytokine responses from wild-type counterparts, suggesting potentially distinct functions

Piceatannol, a Dietary Polyphenol, Alleviates Adipose Tissue Loss in Pre-Clinical Model of Cancer-Associated Cachexia via Lipolysis Inhibition

Cancer-associated cachexia (CAC) is the nutrition-independent loss of lean muscle and adipose tissues, and results in reduced chemotherapy effectiveness and increased mortality. Preventing adipose loss is considered a key target in the early stages of cachexia. Lipolysis is considered the central driver of adipose loss in CAC. We recently found that piceatannol, but not its analogue resveratrol, exhibits an inhibitory effect on lipolysis. The objective of this study was to investigate the role of piceatannol in cancer-associated lipolysis and cachexia-induced weight loss. Cancer cell-induced lipolysis in adipocytes was stimulated using cancer-conditioned media (CCM) or co-culture with human pancreatic cancer cells and the cachexia-associated cytokines TNF-α and interleukin-6 in 3T3-L1 adipocytes. C26 colon carcinoma-bearing mice were modeled using CAC in vivo. Piceatannol reduced cancer-associated lipolysis by at least 50% in both CCM and cytokine-induced lipolysis in vitro. Further gene and protein analysis confirmed that piceatannol modulated the stability of lipolytic proteins. Moreover, piceatannol protected tumor-bearing mice against weight-loss in early stages of CAC largely through preserving adipose tissue, with no effect on survival. This study demonstrates the use of a dietary compound to preserve adipose in models of early stage CAC and provides groundwork for further investigation of piceatannol or piceatannol-rich foods as alternative medicine in the preservation of body fat mass and future CAC therapy

Time-reversal symmetry breaking superconducting ground state in the doped Mott insulator on the honeycomb lattice

The emergence of superconductivity in doped Mott insulators has been debated for decades. In this paper, we report the theoretical discovery of a time-reversal symmetry breaking superconducting ground state in the doped Mott insulator (described by the well known t-J model) on honeycomb lattice, based on a recently developed variational method: the Grassmann tensor product state approach. As a benchmark, we use exact diagonalization and density-matrix renormalization methods to check our results on small clusters. We find systematic consistency for the ground-state energy as well as other physical quantities, such as the staggered magnetization. At low doping, the superconductivity coexists with antiferromagnetic ordering.Comment: 7 pages, 9 figures (published version

Cosmological Evolution of Interacting Dark Energy Models with Mass Varying Neutrinos

In this paper we consider the cosmological implications of dark energy models with a coupled system of a dynamical scalar field (the quintessence) and the neutrinos. By detailed numerical calculations we study the various possibilities on the evolution and the fates of the universe in this class of models. Our results show that due to the interaction with quintessence, neutrinos could be dominant over the quintessence in the future universe, however would eventually decay away.Comment: One typographical error corrected, references updated and presentation improve