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Random sampling and reconstruction of signals with finite rate of innovation
Yingchun Jiang,Junjian Zhao 대한수학회 2022 대한수학회보 Vol.59 No.2
In this paper, we mainly study the random sampling and reconstruction of signals living in the subspace $V^p(\Phi,\Lambda)$ of $L^p(\mathbb{R}^d)$, which is generated by a family of molecules $\Phi$ located on a relatively separated subset $\Lambda\subset \mathbb{R}^d$. The space $V^p(\Phi,\Lambda)$ is used to model signals with finite rate of innovation, such as stream of pulses in GPS applications, cellular radio and ultra wide-band communication. The sampling set is independently and randomly drawn from a general probability distribution over $\mathbb{R}^d$. Under some proper conditions for the generators $\Phi=\{\phi_\lambda:\lambda\in \Lambda\}$ and the probability density function $\rho$, we first approximate $V^{p}(\Phi,\Lambda)$ by a finite dimensional subspace $V^{p}_N(\Phi,\Lambda)$ on any bounded domains. Then, we prove that the random sampling stability holds with high probability for all signals in $V^{p}(\Phi,\Lambda)$ whose energy concentrate on a cube when the sampling size is large enough. Finally, a reconstruction algorithm based on random samples is given for signals in $V^{p}_N(\Phi,\Lambda)$.
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Guangwei Liu,Hanqiao Jiang,Junjian Li,Min Wang,Fuzhen Chen,Shuaiwei Ding,Xiangan Lu 한국공업화학회 2015 Journal of Industrial and Engineering Chemistry Vol.26 No.-
This paper presents gels with asphalt particle (GAP) as a novel composite profile control system, which has better sealing effect for plugging channeling in fractured reservoir. This composite agent was prepared by modified asphalt particle and polymer gels served as suspension. Laboratory core–flood tests showed good injectiviy of GAP solution in high permeability zone with a high plugging rate. Also, the enhance oil recovery mechanism of GAP and polymer gels in fractured reservoir were compared by parallel core–flood test. Simulation results indicate longer response time and better enhance oil recovery for GAP than polymer gels in fractured system.
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EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1
Xiang, Yaoxian,Zhu, Lei,He, Zijian,Xu, Lei,Mao, Yuhang,Jiang, Junjian,Xu, Jianguang The Korean Neurosurgical Society 2022 Journal of Korean neurosurgical society Vol.65 No.6
Objective : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.
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Xiang Yaoxian,Dai Junxi,Li Yao,You Zongqi,Zhang Junpeng,Huang Xinying,Nie Shuqi,Chen Yujie,Xu Lei,Liu Fengming,Jiang Junjian,Xu Jianguang 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Neutrophils are the earliest master inflammatory regulator cells recruited to target tissues after direct infection or injury. Although inflammatory factors are present in muscle that has been indirectly disturbed by peripheral nerve injury, whether neutrophils are present and play a role in the associated inflammatory process remains unclear. Here, intravital imaging analysis using spinning-disk confocal intravital microscopy was employed to dynamically identify neutrophils in denervated muscle. Slice digital scanning and 3D-view reconstruction analyses demonstrated that neutrophils escape from vessels and migrate into denervated muscle tissue. Analyses using reactive oxygen species (ROS) inhibitors and flow cytometry demonstrated that enhanced ROS activate neutrophils after denervation. Transcriptome analysis revealed that the vast majority of neutrophils in denervated muscle were of the CXCR2 subtype and were recruited by CXCL1. Most of these cells gradually disappeared within 1 week via P53-mediated apoptosis. Experiments using specific blockers confirmed that neutrophils slow the process of denervated muscle atrophy. Collectively, these results indicate that activated neutrophils are recruited via chemotaxis to muscle tissue that has been indirectly damaged by denervation, where they function in delaying atrophy.
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