The Homeostatic Regulation of Our Social Neural Architecture

2004 ◽  
pp. 33-36
Author(s):  
Gerald A. Cory
1992 ◽  
Author(s):  
William Ross ◽  
Ennio Mingolla

Author(s):  
Hanna Mazzawi ◽  
Xavi Gonzalvo ◽  
Aleks Kracun ◽  
Prashant Sridhar ◽  
Niranjan Subrahmanya ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kojiro Mukai ◽  
Emari Ogawa ◽  
Rei Uematsu ◽  
Yoshihiko Kuchitsu ◽  
Fumika Kiku ◽  
...  

AbstractCoat protein complex I (COP-I) mediates the retrograde transport from the Golgi apparatus to the endoplasmic reticulum (ER). Mutation of the COPA gene, encoding one of the COP-I subunits (α-COP), causes an immune dysregulatory disease known as COPA syndrome. The molecular mechanism by which the impaired retrograde transport results in autoinflammation remains poorly understood. Here we report that STING, an innate immunity protein, is a cargo of the retrograde membrane transport. In the presence of the disease-causative α-COP variants, STING cannot be retrieved back to the ER from the Golgi. The forced Golgi residency of STING results in the cGAS-independent and palmitoylation-dependent activation of the STING downstream signaling pathway. Surf4, a protein that circulates between the ER/ ER-Golgi intermediate compartment/ Golgi, binds STING and α-COP, and mediates the retrograde transport of STING to the ER. The STING/Surf4/α-COP complex is disrupted in the presence of the disease-causative α-COP variant. We also find that the STING ligand cGAMP impairs the formation of the STING/Surf4/α-COP complex. Our results suggest a homeostatic regulation of STING at the resting state by retrograde membrane traffic and provide insights into the pathogenesis of COPA syndrome.


Author(s):  
Wei Jia ◽  
Wei Xia ◽  
Yang Zhao ◽  
Hai Min ◽  
Yan-Xiang Chen

AbstractPalmprint recognition and palm vein recognition are two emerging biometrics technologies. In the past two decades, many traditional methods have been proposed for palmprint recognition and palm vein recognition and have achieved impressive results. In recent years, in the field of artificial intelligence, deep learning has gradually become the mainstream recognition technology because of its excellent recognition performance. Some researchers have tried to use convolutional neural networks (CNNs) for palmprint recognition and palm vein recognition. However, the architectures of these CNNs have mostly been developed manually by human experts, which is a time-consuming and error-prone process. In order to overcome some shortcomings of manually designed CNN, neural architecture search (NAS) technology has become an important research direction of deep learning. The significance of NAS is to solve the deep learning model’s parameter adjustment problem, which is a cross-study combining optimization and machine learning. NAS technology represents the future development direction of deep learning. However, up to now, NAS technology has not been well studied for palmprint recognition and palm vein recognition. In this paper, in order to investigate the problem of NAS-based 2D and 3D palmprint recognition and palm vein recognition in-depth, we conduct a performance evaluation of twenty representative NAS methods on five 2D palmprint databases, two palm vein databases, and one 3D palmprint database. Experimental results show that some NAS methods can achieve promising recognition results. Remarkably, among different evaluated NAS methods, ProxylessNAS achieves the best recognition performance.


2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Shanshan Liu ◽  
Xiuxin Jiang ◽  
Xiuru Cui ◽  
Jingjing Wang ◽  
Shangming Liu ◽  
...  

AbstractHuman antigen R (HuR) is a widespread RNA-binding protein involved in homeostatic regulation and pathological processes in many diseases. Atherosclerosis is the leading cause of cardiovascular disease and acute cardiovascular events. However, the role of HuR in atherosclerosis remains unknown. In this study, mice with smooth muscle-specific HuR knockout (HuRSMKO) were generated to investigate the role of HuR in atherosclerosis. HuR expression was reduced in atherosclerotic plaques. As compared with controls, HuRSMKO mice showed increased plaque burden in the atherosclerotic model. Mechanically, HuR could bind to the mRNAs of adenosine 5′-monophosphate-activated protein kinase (AMPK) α1 and AMPKα2, thus increasing their stability and translation. HuR deficiency reduced p-AMPK and LC3II levels and increased p62 level, thereby resulting in defective autophagy. Finally, pharmacological AMPK activation induced autophagy and suppressed atherosclerosis in HuRSMKO mice. Our findings suggest that smooth muscle HuR has a protective effect against atherosclerosis by increasing AMPK-mediated autophagy.


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