In order to research the hot deformation of Inconel 625 deposited metal, the Inconel 625 flux-cored wire was surfaced on carbon steel by GMAW. The true stress–strain curves of the deposited metal ...were obtained by high-temperature tensile test at temperatures of 600–900 °C and strain rate of 8.33 × 10
−5
s
−1
. The tensile fracture morphology and microstructure were observed by OM, SEM, XRD and TEM, and the thermal deformation behavior and strengthening mechanism of the Inconel 625 deposited metal were analyzed. The results show that the longitudinal section of the tensile fracture of specimen can be judged to be mainly composed of
γ
austenite, MC and Laves phase at different temperatures. And the flow stress decreases with the increase of temperature. The tensile stress–strain curves of the specimens show obvious work-hardening behavior after yielding at RT, 600 °C and 700 °C, while it decreases obviously, and the stress basically maintains a constant at 760 °C, 800 °C and 900 °C. When the temperature is 700 °C, the plasticity of the sample has a low valley, that is medium temperature brittleness. Inconel 625 deposited metal is divided into three stages by Arrhenius relation: the low-temperature zone (
T
≤ 600 °C), the medium-temperature zone (600 °C <
T
≤ 760 °C) and the high-temperature zone (
T
> 760 °C). In the low-temperature zone, it consists of
a
/2 < 110 > dislocation pairs cutting the precipitates or continuous cutting matrix channel and stacking faults of precipitates (continuous stacking fault). The strengthening mechanism is dominated by dislocations cutting
γ
-phase. With the increase of temperature, some dislocation bands and loops appear in the microstructure, and the dislocation bypass mechanism (Orowan mechanism) has been initiated; in the medium-temperature zone, the complex dislocation reactions occur and form dislocation locks and tangles at 700 °C; it is a mixed mechanism of dislocation cutting and bypassing; in the high-temperature zone, a large number of dislocation loops appear in the microstructure, and some irregular dislocation networks can be observed. With the increase of temperature, the dislocation networks become more regular. It shows that the bypass mechanism of dislocation is the main deformation mechanism.
In order to investigate the corrosion behavior of Inconel 625 deposited metal in molten KCl and MgCl2, the corrosion behavior of deposited metal immersed in molten salt for 60 h at 700 °C and 900 °C ...was studied by static corrosion immersion method. X-ray diffraction (XRD) and Geminisem300 were used to systematically study the phase composition, corrosion morphology and element distribution of the deposited metal. The results show that: the corrosion weight loss of the deposited metal showed an increasing trend at both temperatures, but the increasing range was different in different time intervals. The corrosion weight loss of the deposited metal increased slowly in the first 10 h, and increased sharply in the 10 h-60 h. It can be found that 10 h is the cut-off point of corrosion behavior. The corrosion rate is 0.03 mm/year at 700 °C and 0.50 mm/year at 900 °C for 10 h. The corrosion resistance of the deposited metal at 700 °C is better than that at 900 °C, which is due to the formation of dense MgO on the surface of the deposited metal at 700 °C, which hinders the corrosion reaction; at 900 °C, the content of CrCl3 on the surface of the deposited metal increases, resulting in a 'shell breaking effect', which destroys the MgO shell and forms NiCr2O4 with spinel structure. Its corrosion resistance is thus weakened.
Hepcidin is an antimicrobial peptide, which also negatively regulates iron in circulation by controlling iron absorption from dietary sources and iron release from macrophages. Hepcidin is ...synthesized mainly in the liver, where hepcidin is regulated by iron loading, inflammation and hypoxia. Recently, we have demonstrated that bone morphogenetic protein (BMP)-hemojuvelin (HJV)-SMAD signaling is central for hepcidin regulation in hepatocytes. Hepcidin is also expressed by macrophages. Studies have shown that hepcidin expression by macrophages increases following bacterial infection, and that hepcidin decreases iron release from macrophages in an autocrine and/or paracrine manner. Although previous studies have shown that lipopolysaccharide (LPS) can induce hepcidin expression in macrophages, whether hepcidin is also regulated by BMPs in macrophages is still unknown. Therefore, we examined the effects of BMP signaling on hepcidin expression in RAW 264.7 and J774 macrophage cell lines, and in primary peritoneal macrophages. We found that BMP4 or BMP6 alone did not have any effect on hepcidin expression in macrophages although they stimulated Smad1/5/8 phosphorylation and Id1 expression. In the presence of LPS, however, BMP4 and BMP6 were able to stimulate hepcidin expression in macrophages, and this stimulation was abolished by the NF-κB inhibitor Ro1069920. These results suggest that hepcidin expression is regulated differently in macrophages than in hepatocytes, and that BMPs regulate hepcidin expression in macrophages in a LPS-NF-κB dependent manner.
Considering the possibility to build an
e
+
e
−
collider at the energies around
Z
-boson resonance with a luminosity so high as
L
∝ 10
34
cm
−2
s
−1
(even higher) and the abilities of a modern ...synthesis detector, we systematically calculate the exclusive two body processes of the heavy quarkonium production:
e
+
e
−
annihilates into a heavy quarkonium and a photon, involving the initial state radiation (i.e. ISR) cases, at the energies around the
Z
-boson resonance. Since the couplings of
Z
-boson to quarks contain an axial vector term as well as a vector one, a charmonium such as
J
/ψ or η
c
or
h
c
or χ
cJ
…, or a bottomonium such as ϒ or η
b
or
h
b
or χ
bJ
…, associating with a photon, may be produced respectively via
Z
-boson annihilation. If we call such a collider with so high luminosity and running around the
Z
-boson resonance as a
Z
-factory, then our results obtained here indicate that experimental studies of the various heavy quarkona (their ground and excited states) via the two-body processes at a
Z
-factory have outstanding advantages, especially, the production of the possible states with quantum numbers
J
PC
= 1
−−
via ISR.
The inflammatory status of epicardial adipose tissue (EAT) is one of the factors leading to the development of related diseases such as coronary artery disease (CAD). The thickness of CAD EAT ...increases and is accompanied with increased macrophage infiltration and heightened inflammatory responses. However, microRNAs (miRNAs) regulating the inflammatory responses of macrophages in CAD EAT remain unclear.
miRNA expression profiles of CAD EATs and non-CAD EATs were determined by miRNA microarrays. Quantitative real-time reverse transcription-polymerase chain reaction, Western blotting, immunohistochemical assay, and fluorescence in-situ hybridization were adopted to detect miR-3614 expression and function in EATs and macrophages. The interaction between miR-3614 and tumor necrosis factor receptor-associated factor 6 (TRAF6) was identified using an online website combined with a dual-luciferase reporter assay. Enzyme-linked immunosorbent assay was performed to detect the expression of inflammatory cytokines.
The decreased expression of miR-3614 was identified in CAD EAT. The level of miR-3614 was down-regulated by lipopolysaccharide (LPS) in macrophages, whereas LPS-induced inflammatory injury can be reduced by miR-3614 overexpression. TRAF6 was predicted and verified to be a target of miR-3614. The phosphorylated levels of kinases in the mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB pathways were inhibited by miR-3614 overexpression. Importantly, the knockdown of TRAF6 inhibited the LPS-induced inflammatory cytokine expressions in cells.
A novel negative feedback loop by miR-3614 possibly contribute to the regulation of inflammatory processes via targeting the TRAF6/MAPK/NF-κB pathway in EATs and prevents an overwhelming inflammatory response.
•miR-3614 is down-expressed in epicardial adipose tissue (EAT) with coronary artery disease (CAD).•Studies with cultured macrophages suggest that miR-3614 can be stimulated by toll-like receptor activators.•miR-3614 targeted TRAF6 to repress the MAPKs/NF-κB pathway in macrophages.•miR-3614 suppress inflammatory response through MAPKs/NF-κB pathway in CAD EAT, which decreases expression of the TRAF6.
The regulation of the actin cytoskeleton and membrane trafficking is coordinated in mammalian cells. One of the regulators of membrane traffic, the small GTP-binding protein ARF1, also activates ...phosphatidylinositol kinases that in turn affect actin polymerization. ARFGAP1 is a GTPase activating protein (GAP) for ARF1 that is found on Golgi membranes. We present evidence that ARFGAP1 not only serves as a GAP for ARF1, but also can affect the actin cytoskeleton.
As cells attach to a culture dish foci of actin appear prior to the cells flattening and spreading. We have observed that overexpression of a truncated ARFGAP1 that lacks catalytic activity for ARF, called GAP273, caused these foci to persist for much longer periods than non-transfected cells. This phenomenon was dependent on the level of GAP273 expression. Furthermore, cell spreading after re-plating or cell migration into a previously scraped area was inhibited in cells transfected with GAP273. Live cell imaging of such cells revealed that actin-rich membrane blebs formed that seldom made protrusions of actin spikes or membrane ruffles, suggesting that GAP273 interfered with the regulation of actin dynamics during cell spreading. The over-expression of constitutively active alleles of ARF6 and Rac1 suppressed the effect of GAP273 on actin. In addition, the activation of Rac1 by serum, but not that of RhoA or ARF6, was inhibited in cells over-expressing GAP273, suggesting that Rac1 is a likely downstream effector of ARFGAP1. The carboxyl terminal 65 residues of ARFGAP1 were sufficient to produce the effects on actin and cell spreading in transfected cells and co-localized with cortical actin foci.
ARFGAP1 functions as an inhibitor upstream of Rac1 in regulating actin cytoskeleton. In addition to its GAP catalytic domain and Golgi binding domain, it also has an actin regulation domain in the carboxyl-terminal portion of the protein.
Electron-ion collider in China Anderle, Daniele P.; Bertone, Valerio; Cao, Xu ...
Frontiers of Physics,
12/2021, Letnik:
16, Številka:
6
Journal Article
Recenzirano
Odprti dostop
Lepton scattering is an established ideal tool for studying inner structure of small particles such as nucleons as well as nuclei. As a future high energy nuclear physics project, an Electron-ion ...collider in China (EicC) has been proposed. It will be constructed based on an upgraded heavy-ion accelerator, High Intensity heavy-ion Accelerator Facility (HIAF) which is currently under construction, together with a new electron ring. The proposed collider will provide highly polarized electrons (with a po- larization of 80%) and protons (with a polarization of 70%) with variable center of mass energies from 15 to 20 GeV and the luminosity of (2-3)×10 33 cm −2*s −1. Polarized deuterons and Helium-3, as well as unpolarized ion beams from Carbon to Uranium, will be also available at the EicC.
The main foci of the EicC will be precision measurements of the structure of the nucleon in the sea quark region, including 3D tomography of nucleon; the partonic structure of nuclei and the parton interaction with the nuclear environment; the exotic states, especially those with heavy flavor quark contents. In addition, issues fundamental to understanding the origin of mass could be addressed by measurements of heavy quarkonia near-threshold production at the EicC. In order to achieve the above-mentioned physics goals, a hermetical detector system will be constructed with cutting-edge technologies.
This document is the result of collective contributions and valuable inputs from experts across the globe. The EicC physics program complements the ongoing scientific programs at the Jefferson Laboratory and the future EIC project in the United States. The success of this project will also advance both nuclear and particle physics as well as accelerator and detector technology in China.
In order to reduce the lane departure accident caused by driver’s negligence, LDWS (lane departure warning system) has become increasingly popular and important. However, most researches proposed ...mainly focus on how to detect lane markings. In this paper, we propose an improved lane departure warning algorithm based on fusion of F-Kalman filter (kalman filter based on fuzzy logic) and F-TLC (time to lane crossing based on fuzzy logic). First of all, least square method is used to calculate the distance between vehicle and lane markings. Then the estimation of vehicle states in the future is generated by means of the traditional kalman filter. To better work for lateral offset estimation, a fuzzy model is adopted to change the size of covariance matrices, which is used to adjust the traditional kalman filter in time. Finally, we further put forward to utilize F-TLC to generate multi-grade alarm. Extensive experiments are conducted on different conditions. Experimental results indicate that our warning method works efficiently. The average time consumed for system in each frame is 20.0216 ms. The proposed method possesses good robustness, and can be widely us\ed in LDWS.
Kirsten rat sarcoma (KRAS) mutant cancers, which constitute the vast majority of pancreatic tumors, are characterized by their resistance to established therapies and high mortality rates. Here, we ...developed a novel and extremely effective combinational therapeutic approach to target KRAS mutant tumors through the generation of a cytotoxic oxidative stress. At high concentrations, vitamin C (VC) is known to provoke oxidative stress and selectively kill KRAS mutant cancer cells, although its effects are limited when it is given as monotherapy. We found that the combination of VC and the oxidizing drug arsenic trioxide (ATO) is an effective therapeutic treatment modality. Remarkably, its efficiency is dependent on chirality of VC as its enantiomer d‐optical isomer of VC (d‐VC) is significantly more potent than the natural l‐optical isomer of VC. Thus, our results demonstrate that the oxidizing combination of ATO and d‐VC is a promising approach for the treatment of KRAS mutant human cancers.
What's new?
A new combination therapy could effectively fight Kirsten rat sarcoma (KRAS)‐mutant cancers. Although KRAS mutations frequently crop up in human cancers, therapies targeting them have proved difficult to find. In our study, the authors tested a novel approach to kill the cancer cells by inducing oxidative stress with vitamin C and arsenic trioxide. The combo successfully killed cancer cells, with one surprising twist. When the researchers tested the therapy in a mouse xenograft model, they found that the tumor‐shrinking action depended on the chirality of the vitamin C molecule. The D isomer showed much greater efficacy than the naturally occurring L isomer.
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