Adversarial PoseNet: A Structure-aware Convolutional Network for Human Pose Estimation

For human pose estimation in monocular images, joint occlusions and overlapping upon human bodies often result in deviated pose predictions. Under these circumstances, biologically implausible pose predictions may be produced. In contrast, human vision is able to predict poses by exploiting geometric constraints of joint inter-connectivity. To address the problem by incorporating priors about the structure of human bodies, we propose a novel structure-aware convolutional network to implicitly take such priors into account during training of the deep network. Explicit learning of such constraints is typically challenging. Instead, we design discriminators to distinguish the real poses from the fake ones (such as biologically implausible ones). If the pose generator (G) generates results that the discriminator fails to distinguish from real ones, the network successfully learns the priors.Comment: Fixed typos. 14 pages. Demonstration videos are http://v.qq.com/x/page/c039862eira.html, http://v.qq.com/x/page/f0398zcvkl5.html, http://v.qq.com/x/page/w0398ei9m1r.htm

The Sparse-Grid-Based Adaptive Spectral Koopman Method

The adaptive spectral Koopman (ASK) method was introduced to numerically solve autonomous dynamical systems that lay the foundation of numerous applications across different fields in science and engineering. Although ASK achieves high accuracy, it is computationally more expensive for multi-dimensional systems compared with conventional time integration schemes like Runge-Kutta. In this work, we combine the sparse grid and ASK to accelerate the computation for multi-dimensional systems. This sparse-grid-based ASK (SASK) method uses the Smolyak structure to construct multi-dimensional collocation points as well as associated polynomials that are used to approximate eigenfunctions of the Koopman operator of the system. In this way, the number of collocation points is reduced compared with using the tensor product rule. We demonstrate that SASK can be used to solve partial differential equations based-on their semi-discrete forms. Numerical experiments illustrate that SASK balances the accuracy with the computational cost, and hence accelerates ASK.Comment: 21 pages, 5 figure

3-Amino-4,6-dimethyl­thieno[2,3-b]pyridine-2-carbonitrile

The mol­ecule of the title compound, C10H9N3S, is almost planar, with a dihedral angle of 1.38 (4)° between the thio­phene and pyridine rings. In the crystal packing, mol­ecules are linked into layers parallel to the ab plane by inter­molecular N—H⋯N hydrogen bonds and by π⋯π stacking inter­actions involving adjacent pyridine and thio­phene rings with a centroid–centroid distance of 3.537 (3) Å

"En Face" detection of nitric oxide and superoxide in endothelial layer of intact arteries

Endothelium-derived nitric oxide (NO) produced from endothelial NO-synthase (eNOS) is one of the most important vasoprotective molecules in cardiovascular physiology. Dysfunctional eNOS such as uncoupling of eNOS leads to decrease in NO bioavailability and increase in superoxide anion (O₂.−) production, and in turn promotes cardiovascular diseases. Therefore, appropriate measurement of NO and O₂.− levels in the endothelial cells are pivotal for research on cardiovascular diseases and complications. Because of the extremely labile nature of NO and O₂.−, it is difficult to measure NO and O₂.− directly in a blood vessel. Numerous methods have been developed to measure NO and O₂.− production. It is, however, either insensitive, or non-specific, or technically demanding and requires special equipment. Here we describe an adaption of the fluorescence dye method for en face simultaneous detection and visualization of intracellular NO and O₂.− using the cell permeable diaminofluorescein-2 diacetate (DAF-2DA) and dihydroethidium (DHE), respectively, in intact aortas of an obesity mouse model induced by high-fat-diet feeding. We could demonstrate decreased intracellular NO and enhanced O₂.− levels in the freshly isolated intact aortas of obesity mouse as compared to the control lean mouse. We demonstrate that this method is an easy technique for direct detection and visualization of NO and O₂.− in the intact blood vessels and can be widely applied for investigation of endothelial (dys)function under (physio)pathological conditions

An asymptotically compatible probabilistic collocation method for randomly heterogeneous nonlocal problems

In this paper we present an asymptotically compatible meshfree method for solving nonlocal equations with random coefficients, describing diffusion in heterogeneous media. In particular, the random diffusivity coefficient is described by a finite-dimensional random variable or a truncated combination of random variables with the Karhunen-Lo\`{e}ve decomposition, then a probabilistic collocation method (PCM) with sparse grids is employed to sample the stochastic process. On each sample, the deterministic nonlocal diffusion problem is discretized with an optimization-based meshfree quadrature rule. We present rigorous analysis for the proposed scheme and demonstrate convergence for a number of benchmark problems, showing that it sustains the asymptotic compatibility spatially and achieves an algebraic or sub-exponential convergence rate in the random coefficients space as the number of collocation points grows. Finally, to validate the applicability of this approach we consider a randomly heterogeneous nonlocal problem with a given spatial correlation structure, demonstrating that the proposed PCM approach achieves substantial speed-up compared to conventional Monte Carlo simulations

Arginase-II activates mTORC1 through myosin-1b in vascular cell senescence and apoptosis

Type-II L-arginine:ureahydrolase, arginase-II (Arg-II), is shown to activate mechanistic target of rapamycin complex 1 (mTORC1) pathway and contributes to cell senescence and apoptosis. In an attempt to elucidate the underlying mechanism, we identified myosin-1b (Myo1b) as a mediator. Overexpression of Arg-II induces re-distribution of lysosome and mTOR but not of tuberous sclerosis complex (TSC) from perinuclear area to cell periphery, dissociation of TSC from lysosome and activation of mTORC1- ribosomal protein S6 kinase 1 (S6K1) pathway. Silencing Myo1b prevents all these alterations induced by Arg-II. By overexpressing Myo1b or its mutant with point mutation in its pleckstrin homology (PH) domain we further demonstrate that this effect of Myo1b is dependent on its PH domain that is required for Myo1b-lysosome association. Notably, Arg-II promotes association of Myo1b with lysosomes. In addition, we show that in senescent vascular smooth muscle cells with elevated endogenous Arg-II, silencing Myo1b prevents Arg-II-mediated lysosomal positioning, dissociation of TSC from lysosome, mTORC1 activation and cell apoptosis. Taken together, our study demonstrates that Myo1b mediates the effect of Arg-II in activating mTORC1-S6K1 through promoting peripheral lysosomal positioning, that results in spatial separation and thus dissociation of TSC from lysosome, leading to hyperactive mTORC1-S6K1 signaling linking to cellular senescence/apoptosis

P38 mitogen-activated protein kinase is involved in arginase-II-mediated eNOS-Uncoupling in Obesity

Background Endothelial nitric oxide synthase (eNOS)-uncoupling links obesity-associated insulin resistance and type-II diabetes to the increased incidence of cardiovascular disease. Studies have indicated that increased arginase is involved in eNOS-uncoupling through competing with the substrate L-arginine. Given that arginase-II (Arg-II) exerts some of its biological functions through crosstalk with signal transduction pathways, and that p38 mitogen-activated protein kinase (p38mapk) is involved in eNOS-uncoupling, we investigated here whether p38mapk is involved in Arg-II-mediated eNOS-uncoupling in a high fat diet (HFD)-induced obesity mouse model. Methods Obesity was induced in wild type (WT) and Arg-II-deficient (Arg-II-/-) mice on C57BL/6 J background by high-fat diet (HFD, 55% fat) for 14 weeks starting from age of 7 weeks. The entire aortas were isolated and subjected to 1) immunoblotting analysis of the protein level of eNOS, Arg-II and p38mapk activation; 2) arginase activity assay; 3) endothelium-dependent and independent vasomotor responses; 4) en face staining of superoxide anion and NO production with Dihydroethidium and 4,5-Diaminofluorescein Diacetate, respectively, to assess eNOS-uncoupling. To evaluate the role of p38mapk, isolated aortas were treated with p38mapk inhibitor SB203580 (10 μmol/L, 1 h) prior to the analysis. In addition, the role of p38mapk in Arg-II-induced eNOS-uncoupling was investigated in cultured human endothelial cells overexpressing Arg-II in the absence or presence of shRNA against p38mapk. Results HFD enhanced Arg-II expression/activity and p38mapk activity, which was associated with eNOS-uncoupling as revealed by decreased NO and enhanced L-NAME-inhibitable superoxide in aortas of WT obese mice. In accordance, WT obese mice revealed decreased endothelium-dependent relaxations to acetylcholine despite of higher eNOS protein level, whereas Arg-II-/- obese mice were protected from HFD-induced eNOS-uncoupling and endothelial dysfunction, which was associated with reduced p38mapk activation in aortas of the Arg-II-/- obese mice. Moreover, overexpression of Arg-II in human endothelial cells caused eNOS-uncoupling and augmented p38mapk activation. The Arg-II-induced eNOS-uncoupling was prevented by silencing p38mapk. Furthermore, pharmacological inhibition of p38mapk recouples eNOS in isolated aortas from WT obese mice. Conclusions Taking together, we demonstrate here for the first time that Arg-II causes eNOS-uncoupling through activation of p38 mapk in HFD-induced obesity