An Exponential Decay Model for the Deterministic Correlations in Axial Compressors

International audienceThe average-passage equation system (APES) provides a rigorous mathematical framework to account for the UBRI in steady state environment by introducing the deterministic correlations (DC). How to model the DC is the key in APES method. The primary purpose of this study is to develop a DC model for compressor routine design. A 3D viscous unsteady and time-averaging CFD flow solver is developed to investigate the APES technique. Steady, unsteady and time-averaging simulations are conducted on the investigation of the UBRI in the first stage of NASA 67 compressor. Based on DC characteristics and its effects on time-averaged flow, an exponential decay DC model is proposed and implemented into the time-averaging solver. Based on the unsteady simulation, the proposed model is validated by comparing DC distributions and mean flow fields. The comparison indicates that the proposed model can take into account the major part of UBRI and provide significant improvements for predicting spanwise distributions of flow properties in axial compressors, compared with the steady mixing plane method

Active Multiple Plasmon-Induced Transparency with Graphene Sheets Resonators in Mid-Infrared Frequencies

A multiple plasmon-induced transparency (PIT) device operated in the mid-infrared region has been proposed. The designed model is comprised of one graphene ribbon as main waveguide and two narrow graphene sheets resonators. The phase coupling between two graphene resonators has been investigated. The multimode PIT resonances have been found in both cases and can be dynamically tuned via varying the chemical potential of graphene resonators without optimizing its geometric parameters. In addition, this structure can get multiple PIT effect by equipping extra two sheets on the symmetric positions of graphene waveguide. The simulation results based on finite element method (FEM) are in good agreement with the resonance theory. This work may pave new way for graphene-based thermal plasmonic devices applications

Evidence for Dirac Fermions in a honeycomb lattice based on silicon

Silicene, a sheet of silicon atoms in a honeycomb lattice, was proposed to be a new Dirac-type electron system similar as graphene. We performed scanning tunneling microscopy and spectroscopy studies on the atomic and electronic properties of silicene on Ag(111). An unexpected $\sqrt{3}\times \sqrt{3}$ reconstruction was found, which is explained by an extra-buckling model. Pronounced quasi-particle interferences (QPI) patterns, originating from both the intervalley and intravalley scattering, were observed. From the QPI patterns we derived a linear energy-momentum dispersion and a large Fermi velocity, which prove the existence of Dirac Fermions in silicene.Comment: 6 pages, 4 figure

Association between COX-2 rs2745557 polymorphism and prostate cancer risk: a systematic review and meta-analysis

<p>Abstract</p> <p>Background</p> <p>Evidence is accumulating that chronic inflammation may have an important role in prostate cancer (PCa). The COX-2 polymorphism rs2745557 (+202 C/T) has been extensively investigated as a potential risk factor for PCa, but the results have thus far been inconclusive. This meta-analysis was performed to derive a more precise estimation of the association.</p> <p>Methods</p> <p>A comprehensive search was conducted to identify all case-control studies of COX-2 rs2745557 polymorphism and PCa risk. We used odds ratios (ORs) to assess the strength of the association, and 95% confidence intervals (CIs) give a sense of the precision of the estimate. Statistical analyses were performed by Review Manage, version 5.0 and Stata 10.0.</p> <p>Results</p> <p>A total of 8 available studies were considered in the present meta-analysis, with 11356 patients and 11641 controls for rs2745557. When all groups were pooled, there was no evidence that rs2745557 had significant association with PCa under co-dominant, recessive, over-dominant, and allelic models. However, our analysis suggested that rs2745557 was associated with a lower PCa risk under dominant model in overall population (OR = 0.85, 95%CI = 0.74-0.97, P = 0.02). When stratifying for race, there was a significant association between rs2745557 polymorphism and lower PCa risk in dominant model comparison in the subgroup of Caucasians (OR = 0.86, 95%CI = 0.75-0.99, P = 0.04), but not in co-dominant, recessive, over-dominant and allelic comparisons.</p> <p>Conclusion</p> <p>Based on our meta-analysis, COX-2 rs2745557 was associated with a lower PCa risk under dominant model in Caucasians.</p

The noncanonical BMP signaling pathway plays an important role in club cell regeneration

The bronchiole is a major site for the development of several life‐threatening disorders, including chronic obstructive pulmonary disease and lung adenocarcinomas. The bronchiolar epithelium is composed of club cells and ciliated epithelial cells, with club cells serving as progenitor cells. Presently, the identity of the cells involved in regeneration of bronchiolar epithelium and the underlying mechanisms remain incompletely understood. Here, we show that Prrx1, a homeobox transcription factor, can mark club cells in adult mice during homeostasis and regeneration. We further show that the noncanonical signaling pathway of BMPs, BMPR1A‐Tak1‐p38MAPK, plays a critical role in club cell regeneration. Ablation of Bmpr1a, Tak1, or Mapk14 (encoding p38α) in Prrx1+ club cells caused minimal effect on bronchiolar epithelium homeostasis, yet it resulted in severe defects in club cell regeneration and bronchiole repair in adult mice. We further show that this pathway supports proliferation and expansion of the regenerating club cells. Our findings thus identify a marker for club cells and reveal a critical role for the BMP noncanonical pathway in club cell regeneration.Schematic representation of our results showing the critical roles of the noncanonical signaling pathway of BMPs, (BMPR1A‐Tak1‐p38MAPK) in club cell regeneration. Naphthalene (NA) is metabolized by CYP‐2F2, which is expressed exclusively in club cells, generating cytotoxic epoxide that kills the club cells within 1.5 days after NA exposure. Under normal conditions, hyperplastic growth occurs at day 3 and the bronchiolar epithelium is restored at day 7. We show that ablation of Bmpr1a, Tak1, or Mapk14 (encoding p38α) in club cells resulted in severe defects in regeneration and bronchiole repair in adult mice.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154263/1/stem3125_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154263/2/stem3125.pd

p38α MAPK regulates proliferation and differentiation of osteoclast progenitors and bone remodeling in an aging-dependent manner.

Bone mass is determined by the balance between bone formation, carried out by mesenchymal stem cell-derived osteoblasts, and bone resorption, carried out by monocyte-derived osteoclasts. Here we investigated the potential roles of p38 MAPKs, which are activated by growth factors and cytokines including RANKL and BMPs, in osteoclastogenesis and bone resorption by ablating p38α MAPK in LysM+monocytes. p38α deficiency promoted monocyte proliferation but regulated monocyte osteoclastic differentiation in a cell-density dependent manner, with proliferating p38α-/- cultures showing increased differentiation. While young mutant mice showed minor increase in bone mass, 6-month-old mutant mice developed osteoporosis, associated with an increase in osteoclastogenesis and bone resorption and an increase in the pool of monocytes. Moreover, monocyte-specific p38α ablation resulted in a decrease in bone formation and the number of bone marrow mesenchymal stem/stromal cells, likely due to decreased expression of PDGF-AA and BMP2. The expression of PDGF-AA and BMP2 was positively regulated by the p38 MAPK-Creb axis in osteoclasts, with the promoters of PDGF-AA and BMP2 having Creb binding sites. These findings uncovered the molecular mechanisms by which p38α MAPK regulates osteoclastogenesis and coordinates osteoclastogenesis and osteoblastogenesis