Analysis of a discrete-layout bimorph disk elements piezoelectric deformable mirror

We introduce a discrete-layout bimorph disk elements piezoelectric deformable mirror (DBDEPDM), driven by the circular flexural-mode piezoelectric actuators. We formulated an electromechanical model for analyzing the performance of the new deformable mirror. As a numerical example, a 21-actuators DBDEPDM with an aperture of 165 mm was modeled. The presented results demonstrate that the DBDEPDM has a stroke larger than 10  μm and the resonance frequency is 4.456 kHz. Compared with the conventional piezoelectric deformable mirrors, the DBDEPDM has a larger stroke, higher resonance frequency, and provides higher spatial resolution due to the circular shape of its actuators. Moreover, numerical simulations of influence functions on the model are provided

Role of disordered bipolar complexions on the sulfur embrittlement of nickel general grain boundaries

Minor impurities can cause catastrophic fracture of normally ductile metals. Here, a classic example is represented by the sulfur embrittlement of nickel, whose atomic-level mechanism has puzzled researchers for nearly a century. In this study, coupled aberration-corrected electron microscopy and semi-grand-canonical-ensemble atomistic simulation reveal, unexpectedly, the universal formation of amorphous-like and bilayer-like facets at the same general grain boundaries. Challenging the traditional view, the orientation of the lower-Miller-index grain surface, instead of the misorientation, dictates the interfacial structure. We also find partial bipolar structural orders in both amorphous-like and bilayer-like complexions (a.k.a. thermodynamically two-dimensional interfacial phases), which cause brittle intergranular fracture. Such bipolar, yet largely disordered, complexions can exist in and affect the properties of various other materials. Beyond the embrittlement mechanism, this study provides deeper insight to better understand abnormal grain growth in sulfur-doped Ni, and generally enriches our fundamental understanding of performance-limiting and more disordered interfaces

SINet: A Scale-insensitive Convolutional Neural Network for Fast Vehicle Detection

Vision-based vehicle detection approaches achieve incredible success in recent years with the development of deep convolutional neural network (CNN). However, existing CNN based algorithms suffer from the problem that the convolutional features are scale-sensitive in object detection task but it is common that traffic images and videos contain vehicles with a large variance of scales. In this paper, we delve into the source of scale sensitivity, and reveal two key issues: 1) existing RoI pooling destroys the structure of small scale objects, 2) the large intra-class distance for a large variance of scales exceeds the representation capability of a single network. Based on these findings, we present a scale-insensitive convolutional neural network (SINet) for fast detecting vehicles with a large variance of scales. First, we present a context-aware RoI pooling to maintain the contextual information and original structure of small scale objects. Second, we present a multi-branch decision network to minimize the intra-class distance of features. These lightweight techniques bring zero extra time complexity but prominent detection accuracy improvement. The proposed techniques can be equipped with any deep network architectures and keep them trained end-to-end. Our SINet achieves state-of-the-art performance in terms of accuracy and speed (up to 37 FPS) on the KITTI benchmark and a new highway dataset, which contains a large variance of scales and extremely small objects.Comment: Accepted by IEEE Transactions on Intelligent Transportation Systems (T-ITS

Vitamin B1 Helps to Limit Mycobacterium tuberculosis Growth via Regulating Innate Immunity in a Peroxisome Proliferator-Activated Receptor-γ-Dependent Manner

It is known that vitamin B1 (VB1) has a protective effect against oxidative retinal damage induced by anti-tuberculosis drugs. However, it remains unclear whether VB1 regulates immune responses during Mycobacterium tuberculosis (MTB) infection. We report here that VB1 promotes the protective immune response to limit the survival of MTB within macrophages and in vivo through regulation of peroxisome proliferator-activated receptor γ (PPAR-γ). VB1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced tumor necrosis factor-α and interleukin-6 expression at least in part by promoting nuclear factor-κB signaling. In addition, VB1 increases mitochondrial respiration and lipid metabolism and PPAR-γ integrates the metabolic and inflammatory signals regulated by VB1. Using both PPAR-γ agonists and deficient mice, we demonstrate that VB1 enhances anti-MTB activities in macrophages and in vivo by down-regulating PPAR-γ activity. Our data demonstrate important functions of VB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which VB1 exerts its function in macrophages

Immediately loaded fixed full-arch implant-retained prosthesis: a solution to the extreme defect in zone 2—a case report

Implants immediately loaded full-arch prosthesis in maxilla is always a challenge, especially when the zone 2 is extremely defected. To achieve a satisfying result, different therapeutic alternatives have been proposed, such as zygomatic implant, pterygoid implant; however, precise surgical skills limited its application

IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection

To our knowledge, no studies have examined the role of IL-17 production by neutrophils in immune defense against Mycobacterium tuberculosis (MTB) infection and the pathogenesis of rheumatoid arthritis (RA) caused by MTB infection. Here, we determined that neutrophils express IL-17 in an autocrine IL-6- and IL-23-dependent manner during MTB infection. MTB H37Rv-induced IL-6 production was dependent on the NF-κB, p38, and JNK signaling pathways; however, IL-23 production was dependent on NF-κB and EKR in neutrophils. Furthermore, we found that Toll-like receptor 2 (TLR2) and TLR4 mediated the activation of the kinases NF-κB, p38, ERK, and JNK and the production of IL-6, IL-23, and IL-17 in neutrophils infected with MTB H37Rv. Autocrine IL-17 produced by neutrophils played a vital role in inhibiting MTB H37Rv growth by mediating reactive oxygen species production and the migration of neutrophils in the early stages of infection. However, IL-17 production by neutrophils contributed to collagen-induced arthritis development during MTB infection. Our findings identify a protective mechanism against mycobacteria and the pathogenic role of MTB in arthritis development