scholarly journals Desipramine Ameliorates Cr(VI)-Induced Hepatocellular Apoptosis via the Inhibition of Ceramide Channel Formation and Mitochondrial PTP Opening

2014 ◽  
Vol 34 (6) ◽  
pp. 2128-2136 ◽  
Author(s):  
Lei Luo ◽  
Ying Xie ◽  
An Wang ◽  
Xinmin Liu ◽  
Fang Xiao ◽  
...  
Keyword(s):  
Channel Formation ◽  
Hepatocellular Apoptosis ◽  
Ptp Opening

Formation of Dislocation Channels in Neutron Irradiated Molybdenum

1972 ◽  
Vol 30 ◽  
pp. 672-673
Author(s):  
S. Mahajan
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Ambient Temperature ◽  
Room Temperature ◽  
Channel Formation ◽  
Early Stages ◽  
Transmission Electron ◽  
Three Stages ◽  
Two Stages ◽  
Polycrystalline Molybdenum

The evolution of dislocation channels in irradiated metals during deformation can be envisaged to occur in three stages: (i) formation of embryonic cluster free regions, (ii) growth of these regions into microscopically observable channels and (iii) termination of their growth due to the accumulation of dislocation damage. The first two stages are particularly intriguing, and we have attempted to follow the early stages of channel formation in polycrystalline molybdenum, irradiated to 5×1019 n. cm−2 (E > 1 Mev) at the reactor ambient temperature (∼ 60°C), using transmission electron microscopy. The irradiated samples were strained, at room temperature, up to the macroscopic yield point.Figure 1 illustrates the early stages of channel formation. The observations suggest that the cluster free regions, such as A, B and C, form in isolated packets, which could subsequently link-up to evolve a channel.

CYLD: A Key Regulator of Hepatocellular Apoptosis, Proliferation and Carcinogenesis

2010 ◽  
Vol 48 (01) ◽  
Author(s):  
T Urbanik ◽  
S Heine ◽  
M Wörns ◽  
N Hövelmeyer ◽  
RJ Boger ◽  
...  
Keyword(s):  
Hepatocellular Apoptosis

n-channel formation on semi-insulating InP surface by m.i.s.f.e.t.

1979 ◽  
Vol 15 (23) ◽  
pp. 743 ◽  
Author(s):  
Tsuyoshi Kawakami ◽  
Masamichi Okamura
Keyword(s):  
Channel Formation ◽  
Inp Surface

scholarly journals Jagged1-mediated myeloid Notch1 signaling activates HSF1/Snail and controls NLRP3 inflammasome activation in liver inflammatory injury

2019 ◽  
Vol 17 (12) ◽  
pp. 1245-1256 ◽  
Author(s):  
Yuting Jin ◽  
Changyong Li ◽  
Dongwei Xu ◽  
Jianjun Zhu ◽  
Song Wei ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Immune Cell ◽  
Ischemia Reperfusion ◽  
Inflammasome Activation ◽  
Inflammatory Injury ◽  
Notch1 Signaling ◽  
Caspase 1 ◽  
Hepatocellular Damage ◽  
Hepatocellular Apoptosis

AbstractNotch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response. Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue. However, it remains unknown whether Jagged1 (JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury. Here, we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion (IR)-induced liver injury. In a mouse model of liver IR injury, Notch1-proficient (Notch1FL/FL) mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain (NICD) and heat shock transcription factor 1 (HSF1) expression, whereas myeloid-specific Notch1 knockout (Notch1M-KO) aggravated hepatocellular damage even with concomitant JAG1 treatment. Compared to JAG1-treated Notch1FL/FL controls, Notch1M-KO mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver. The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation, while the adoptive transfer of HSF1-expressing macrophages to Notch1M-KO mice augmented Snail activation and mitigated IR-triggered liver inflammation. Moreover, the knockdown of Snail in JAG1-treated Notch1FL/FL livers worsened hepatocellular functioning, reduced TRX1 expression and increased TXNIP/NLRP3 expression. Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis, whereas the activation of Snail increased TRX1 expression and reduced TXNIP, NLRP3/caspase-1, and ROS production. Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation, which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury. Hence, the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury.

Convection and channel formation in solidifying Pb-Sn alloys

1997 ◽  
Vol 28 (3) ◽  
pp. 859-866 ◽  
Author(s):  
Michael I. Bergman ◽  
David R. Fearn ◽  
Jeremy Bloxham ◽  
Margarita C. Shannon
Keyword(s):  
Channel Formation
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