scholarly journals Role of the geodesic acoustic mode shearing feedback loop in transport bifurcations and turbulence spreading

2010 ◽  
Vol 17 (3) ◽  
pp. 032309 ◽  
Author(s):  
K. Miki ◽  
P. H. Diamond
2018 ◽  
Vol 25 (1) ◽  
pp. 012317 ◽  
Author(s):  
K. N. Geng ◽  
D. F. Kong ◽  
A. D. Liu ◽  
T. Lan ◽  
C. X. Yu ◽  
...  

2019 ◽  
Vol 4 (5) ◽  
Author(s):  
Kevin Rosenberg ◽  
Sean Symon ◽  
Beverley J. McKeon
Keyword(s):  

2021 ◽  
Vol 22 (16) ◽  
pp. 8472
Author(s):  
Senem Aykul ◽  
Jordan Maust ◽  
Vijayalakshmi Thamilselvan ◽  
Monique Floer ◽  
Erik Martinez-Hackert

Adipose tissues (AT) expand in response to energy surplus through adipocyte hypertrophy and hyperplasia. The latter, also known as adipogenesis, is a process by which multipotent precursors differentiate to form mature adipocytes. This process is directed by developmental cues that include members of the TGF-β family. Our goal here was to elucidate, using the 3T3-L1 adipogenesis model, how TGF-β family growth factors and inhibitors regulate adipocyte development. We show that ligands of the Activin and TGF-β families, several ligand traps, and the SMAD1/5/8 signaling inhibitor LDN-193189 profoundly suppressed 3T3-L1 adipogenesis. Strikingly, anti-adipogenic traps and ligands engaged the same mechanism of action involving the simultaneous activation of SMAD2/3 and inhibition of SMAD1/5/8 signaling. This effect was rescued by the SMAD2/3 signaling inhibitor SB-431542. By contrast, although LDN-193189 also suppressed SMAD1/5/8 signaling and adipogenesis, its effect could not be rescued by SB-431542. Collectively, these findings reveal the fundamental role of SMAD1/5/8 for 3T3-L1 adipogenesis, and potentially identify a negative feedback loop that links SMAD2/3 activation with SMAD1/5/8 inhibition in adipogenic precursors.


2014 ◽  
Vol 21 (10) ◽  
pp. 102506 ◽  
Author(s):  
Haijun Ren ◽  
Chao Dong

2010 ◽  
Author(s):  
N. Chakrabarti ◽  
P. N. Guzdar ◽  
R. G. Kleva ◽  
R. Singh ◽  
P. K. Kaw ◽  
...  

Author(s):  
Yahui Wang ◽  
Tao Wang ◽  
Shizhao Wei ◽  
Zhiyong Qiu

Abstract The parametric decay process of a reversed shear Alfv\'{e}n eigenmeode (RSAE) into a geodesic acoustic mode (GAM) and a kinetic reversed shear Alfv\'{e}n eigenmode (KRSAE) is investigated using nonlinear gyrokinetic theory. The excitation conditions mainly require the pump RSAE amplitude to exceed a certain threshold, which could be readily satisfied in burning plasmas operated in steady-state advanced scenario. This decay process can contribute to thermal plasma heating and confinement improvement.


2017 ◽  
Vol 57 (12) ◽  
pp. 126048 ◽  
Author(s):  
J. Seidl ◽  
J. Krbec ◽  
M. Hron ◽  
J. Adamek ◽  
C. Hidalgo ◽  
...  

2018 ◽  
Vol 115 (47) ◽  
pp. E11168-E11177 ◽  
Author(s):  
Iksung Jin ◽  
Hiroshi Udo ◽  
Russell Nicholls ◽  
Huixiang Zhu ◽  
Eric R. Kandel ◽  
...  

Whereas short-term plasticity is often initiated on one side of the synapse, long-term plasticity involves coordinated changes on both sides, implying extracellular signaling. We have investigated the possible signaling role of an Aplysia neurotrophin (ApNT) in facilitation induced by serotonin (5HT) at sensory-to-motor neuron synapses in culture. ApNT is an ortholog of mammalian BDNF, which has been reported to act as either an anterograde, retrograde, or autocrine signal, so that its pre- and postsynaptic sources and targets remain unclear. We now report that ApNT acts as a presynaptic autocrine signal that forms part of a positive feedback loop with ApTrk and PKA. That loop stimulates spontaneous transmitter release, which recruits postsynaptic mechanisms, and presynaptic protein synthesis during the transition from short- to intermediate-term facilitation and may also initiate gene regulation to trigger the transition to long-term facilitation. These results suggest that a presynaptic ApNT feedback loop plays several key roles during consolidation of learning-related synaptic plasticity.


2015 ◽  
Vol 22 (6) ◽  
pp. 062508 ◽  
Author(s):  
A. Storelli ◽  
L. Vermare ◽  
P. Hennequin ◽  
Ö. D. Gürcan ◽  
G. Dif-Pradalier ◽  
...  

2015 ◽  
Vol 35 (6) ◽  
pp. 2192-2202 ◽  
Author(s):  
Guohua Lou ◽  
Yanning Liu ◽  
Shanshan Wu ◽  
Jihua Xue ◽  
Fan Yang ◽  
...  

Background: The anti-tumor effects of quercetin have been reported, but the underlying molecular mechanisms remain to be elucidated. The aim of present study was to explore the role of miRNA in the anticancer effects of quercetin. Methods: The differential miRNAs expression between the HepG2 and Huh7 cells treated by quercetin were detected by microarray. The xCELLigence, Flow cytometry, RT-PCR and Western blot were used to analyze the cell proliferation, cell apoptosis, cell cycle arrest, anti-tumor genes, and protein expression. Results: miR-34a was up-regulated in HepG2 cells treated by quercetin exhibiting wild-type p53. When inhibiting the miR-34a, the sensitivity of the cells to quercetin decreased and the expression of the SIRT1 was up-regulated, but the acetylation of p53 and the expression of some genes related to p53 down-regulated. Conclusion: miR-34a plays an important role in the anti-tumor effects of querctin in HCC, miR-34a may be a tiemolecule between the p53 and SIRT1 and is composed of a p53/miR-34a/SIRT1 signal feedback loop, which could enhance apoptosis signal and significantly promote cell apoptosis.


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