PD-Flow: A Point Cloud Denoising Framework with Normalizing Flows

Point cloud denoising aims to restore clean point clouds from raw observations corrupted by noise and outliers while preserving the fine-grained details. We present a novel deep learning-based denoising model, that incorporates normalizing flows and noise disentanglement techniques to achieve high denoising accuracy. Unlike existing works that extract features of point clouds for point-wise correction, we formulate the denoising process from the perspective of distribution learning and feature disentanglement. By considering noisy point clouds as a joint distribution of clean points and noise, the denoised results can be derived from disentangling the noise counterpart from latent point representation, and the mapping between Euclidean and latent spaces is modeled by normalizing flows. We evaluate our method on synthesized 3D models and real-world datasets with various noise settings. Qualitative and quantitative results show that our method outperforms previous state-of-the-art deep learning-based approaches

Galactic Disk Bulk Motions as Revealed by the LSS-GAC DR2

We report a detailed investigation of the bulk motions of the nearby Galactic stellar disk, based on three samples selected from the LSS-GAC DR2: a global sample containing 0.57 million FGK dwarfs out to $\sim$ 2 kpc, a local subset of the global sample consisting $\sim$ 5,400 stars within 150 pc, and an anti-center sample containing $\sim$ 4,400 AFGK dwarfs and red clump stars within windows of a few degree wide centered on the Galactic anti-center. The global sample is used to construct a three-dimensional map of bulk motions of the Galactic disk from the solar vicinity out to $\sim$ 2 kpc with a spatial resolution of $\sim$ 250 pc. Typical values of the radial and vertical components of bulk motion range from $-$15 km s$^{-1}$ to 15 km s$^{-1}$, while the lag behind the circular speed dominates the azimuthal component by up to $\sim$ 15 km s$^{-1}$. The map reveals spatially coherent, kpc-scale stellar flows in the disk, with typical velocities of a few tens km s$^{-1}$. Bending- and breathing-mode perturbations are clearly visible, and vary smoothly across the disk plane. Our data also reveal higher-order perturbations, such as breaks and ripples, in the profiles of vertical motion versus height. From the local sample, we find that stars of different populations exhibit very different patterns of bulk motion. Finally, the anti-center sample reveals a number of peaks in stellar number density in the line-of-sight velocity versus distance distribution, with the nearer ones apparently related to the known moving groups. The "velocity bifurcation" reported by Liu et al. (2012) at Galactocentric radii 10--11 kpc is confirmed. However, just beyond this distance, our data also reveal a new triple-peaked structure.Comment: 27 pages, 17 figures, Accepted for publication in a special issue of Research in Astronomy and Astrophysics on LAMOST science

p38b Mitogen-Activated Protein Kinase Signaling Mediates Exenatide-Stimulated Microglial b-Endorphin Expression

ABSTRACT Recent discoveries established that activation of glucagon-like peptide-1 receptors (GLP-1Rs) mediates neuroprotection and antinociception through microglial b-endorphin expression. This study aimed to explore the underlying signaling mechanisms of microglial b-endorphin. GLP-1Rs and b-endorphin were coexpressed in primary cultures of microglia. Treatment with the GLP-1R agonist exenatide concentration-dependently stimulated microglial expression of the b-endorphin precursor gene proopiomelanocortin (POMC) and peptides, with EC 50 values of 4.1 and 7.5 nM, respectively. Exenatide also significantly increased intracellular cAMP levels and expression of pprotein kinase A (PKA), p-p38, and p-cAMP response element binding protein (CREB) in cultured primary microglia. Furthermore, exenatide-induced microglial expression of POMC was completely blocked by reagents that specifically inhibit adenylyl cyclase and activation of PKA, p38, and CREB. In addition, knockdown of p38b (but not p38a) using short interfering RNA (siRNA) eliminated exenatide-induced microglial p38 phosphorylation and POMC expression. In contrast, lipopolysaccharide increased microglial activation of p38, and knockdown of p38a (but not p38b) partially suppressed expression of proinflammatory factors (including tumor necrosis factor-a, interleukin-1b, and interleukin-6). Exenatideinduced phosphorylation of p38 and CREB was also totally blocked by the PKA inhibitor and siRNA/p38b, but not by siRNA/p38a. Seven-day intrathecal injections of siRNA/p38b (but not siRNA/p38a) completely blocked exenatide-induced spinal p38 activation, b-endorphin expression, and mechanical antiallodynia in rats with established neuropathy, although siRNA/p38b and siRNA/p38a were not antiallodynic. To our knowledge, our results are the first to show a causal relationship between the PKA-dependent p38b mitogen-activated protein kinase/CREB signal cascade and GLP-1R agonismmediated microglial b-endorphin expression. The differential role of p38a and p38b activation in inflammation and nociception was also highlighted

Plasma Lipoprotein-associated Phospholipase A2 in Patients with Metabolic Syndrome and Carotid Atherosclerosis

<p>Abstract</p> <p>Background</p> <p>Lipoprotein-associated phospholipase A₂(Lp-PLA₂) is a recently identified and potentially useful plasma biomarker for cardiovascular and atherosclerotic diseases. However, the correlation between the Lp-PLA₂activity and carotid atherosclerosis remains poorly investigated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the potential role of Lp-PLA₂as a comprehensive marker of metabolic syndrome in individuals with and without carotid atherosclerosis.</p> <p>Methods</p> <p>We documented 118 consecutive patients with MetS and 70 age- and sex-matched healthy subjects served as controls. The patients were further divided into two groups: 39 with carotid plaques and 79 without carotid plaques to elucidate the influence of Lp-PLA₂on carotid atherosclerosis. The plasma Lp-PLA₂activity was measured by using ELISA method and carotid intimal-media thickness (IMT) was performed by ultrasound in all participants.</p> <p>Results</p> <p>Lp-PLA₂activity was significantly increased in MetS subgroups when compared with controls, and was higher in patients with carotid plaques than those without plaques (<it>P </it>< 0.05). Furthermore, we found that significant difference in Lp-PLA₂was obtained between patients with three and four disorders of metabolic syndrome (<it>P </it>< 0.01). Age (β = 0.183, <it>P </it>= 0.029), LDL-cholesterol (β = 0.401, <it>P </it>= 0.000) and waist-hip ratio (β = 0.410, <it>P </it>= 0.000) emerged as significant and independent determinants of Lp-PLA₂activity. Multiple stepwise regression analysis revealed that LDL-cholesterol (β = 0.309, <it>P </it>= 0.000), systolic blood pressure (β = 0.322, <it>P </it>= 0.002) and age (β = 0.235, <it>P </it>= 0.007) significantly correlated with max IMT, and Lp-PLA₂was not an independent predictor for carotid IMT.</p> <p>Conclusions</p> <p>Lp-PLA₂may be a modulating factor for carotid IMT via age and LDL-cholesterol, not independent predictor in the pathophysiological process of carotid atherosclerosis in patients with MetS.</p

Immunologic Changes during Pandemic (H1N1) 2009, China

We analyzed changes in immunologic values over time for 28 hospitalized patients with pandemic (H1N1) 2009. Levels of interleukin-6, interferon-γ, and interleukin-10 increased 1 day after illness onset and then decreased to baseline levels. Levels of virus-specific antibody were undetectable 1 day after illness onset and peaked 36 days later

Bromido{dicyclo­hexyl[2′-(dimethyl­amino)biphenyl-2-yl]phosphine-κP}[2-(4,6-dimethyl­pyrimidin-2-yl)ferrocenyl-κ2 C 1,N]palladium(II) dichloro­methane solvate

In the title compound, [FePdBr(C5H5)(C11H10N2)(C26H36NP)]·CH2Cl2, the Pd atom displays a distorted square-planar coordination environment. The five-membered metallacycle adopts an envelope conformation with the coordinated cyclo­penta­dienyl C atom 0.4222 (4) Å out of plane. The dihedral angle between the pyrimidinyl ring and substituted cyclo­penta­dienyl ring is 21.47 (2)°. In the crystal structure, the dimeric unit is generated through the C—H⋯π contact via a crystallographic inversion centre, while the C—H⋯Cl contacts in the dimeric centre link the dichlormethane mol­ecules with the Pd complex mol­ecules

Bostrycin inhibits proliferation of human lung carcinoma A549 cells via downregulation of the PI3K/Akt pathway

<p>Abstract</p> <p>Background</p> <p>Bostrycin is a novel compound isolated from marine fungi that inhibits proliferation of many cancer cells. However, the inhibitory effect of bostrycin on lung cancers has not been reported. This study is to investigate the inhibitory effects and mechanism of bostrycin on human lung cancer cells in vitro.</p> <p>Methods</p> <p>We used MTT assay, flow cytometry, microarray, real time PCR, and Western blotting to detect the effect of bostrycin on A549 human pulmonary adenocarcinoma cells.</p> <p>Results</p> <p>We showed a significant inhibition of cell proliferation and induction of apoptosis in bostrycin-treated lung adenocarcinoma cells. Bostrycin treatment caused cell cycle arrest in the G0/G1 phase. We also found the upregulation of microRNA-638 and microRNA-923 in bostrycin-treated cells. further, we found the downregulation of p110α and p-Akt/PKB proteins and increased activity of p27 protein after bostrycin treatment in A549 cells.</p> <p>Conclusions</p> <p>Our study indicated that bostrycin had a significant inhibitory effect on proliferation of A549 cells. It is possible that upregulation of microRNA-638 and microRNA-923 and downregulaton of the PI3K/AKT pathway proteins played a role in induction of cell cycle arrest and apoptosis in bostrycin-treated cells.</p