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Controller Backup and Replication for Reliable Multi-domain SDN
( Junli Mao ),( Lishui Chen ),( Jiacong Li ),( Yi Ge ) 한국인터넷정보학회 2020 KSII Transactions on Internet and Information Syst Vol.14 No.12
Software defined networking (SDN) is considered to be one of the most promising paradigms in the future. To solve the scalability and performance problem that a single and centralized controller suffers from, the distributed multi-controller architecture is adopted, thus forms multi-domain SDN. In a multi-domain SDN network, it is of great importance to ensure a reliable control plane. In this paper, we focus on the reliability problem of multi-domain SDN against controller failure from perspectives of backup controller deployment and controller replication. We firstly propose a placement algorithm for backup controllers, which considers both the reliability and the cost factors. Then a controller replication mechanism based on shared data storage is proposed to solve the inconsistency between the active and standby controllers. We also propose a shared data storage layout method that considers both reliability and performance. Besides, a fault recovery and repair process is designed based on the controller backup and shared data storage mechanism. Simulations show that our approach can recover and repair controller failure. Evaluation results also show that the proposed backup controller placement approach is more effective than other methods.
Chung, Ge-Hoon,Kim, Tae-Hyung,Shin, Hye-Won,Chae, Eun-Hee,Yi, Han-Ju,Moon, Hong-Sik,Kim, Hyun-Jin,Kim, Joong-Soo,Jung, Sung-Jun,Oh, Seog-Bae The Korean Society of Pharmacology 2012 The Korean Journal of Physiology & Pharmacology Vol.16 No.4
In this study, we determined mode of action of a novel carbamoyloxy arylalkanoyl arylpiperazine compound (SKL-NP) on hyperpolarization-activated cyclic nucleotide-gated (HCN) channel currents ($I_h$) that plays important roles in neuropathic pain. In small or medium-sized dorsal root ganglion (DRG) neurons (< $40{\mu}m$ in diameter) exhibiting tonic firing and prominent $I_h$, SKL-NP inhibited $I_h$ and spike firings in a concentration dependent manner ($IC_{50}=7.85{\mu}M$). SKL-NP-induced inhibition of $I_h$ was blocked by pretreatment of pertussis toxin (PTX) and N-ethylmaleimide (NEM) as well as 8-Br-cAMP, a membrane permeable cAMP analogue. These results suggest that SKL-NP modulates $I_h$ in indirect manner by the activation of a Gi-protein coupled receptor that decreases intracellular cAMP concentration. Taken together, SKL-NP has the inhibitory effect on HCN channel currents ($I_h$) in DRG neurons of rats.
Ying-Wang,Yi-guo Chen,Wan-shuang Zhao,Di Li,Ya-han Xu,Meng-di Li,Jin Chen,Zhi-jun Kou,Qi-ge Wang,Nsoa dimitri Joseph 사단법인약침학회 2018 Journal of Acupuncture & Meridian Studies Vol.11 No.3
This study aims to investigate the possible mechanisms of electroacupuncture (EA) at PC6to improve myocardial ischemia (MI) by regulating the cardiac transient outward potassiumcurrent channel (Ito). According to the random number table, the mice were dividedinto six groups of six mice each: control group, MI group, PC6, LU7 (Lieque-point), ST36(Zusanli-point), and nonacupoint group. Mice in the control group were injected with saline(20 mg/kg, 24 hours interval), and the other ASIC3 / mice were injected subcutaneouslytwice with isoproterenol (ISO) (20 mg/kg, 24 hours interval). In thepreexperiment, 5 mg/kg, 10 mg/kg, 20 mg/kg, and 30 mg/kg of ISO were used, andthe results showed that 5 mg/kg and 10 mg/kg of ISO both could induce acute MI, butshorter duration of sustained MI. On the other hand, an injection of 30 mg/kg can makethe mice experience arrhythmia or die immediately, and EA was operated at PC6, LU7,ST36 acupoints, and nonacupoint in the mice of PC6, LU7, ST36, and nonacupoint groups,respectively, after injecting twice. Then Western blotting techniques (Western Blot) wereused to analyze the protein expressions of Kv1.4, Kv4.2, Kv4.3, and KchIP2. The results ofthis experiment showed that the protein expressions of Kv1.4, Kv4.2, Kv4.3, and KChIP2 inMI group were significantly lower than those in the control group (p < 0.01). Comparedwith MI group, the results of PC6, LU7, and ST36 groups obviously increased (p < 0.05). Furthermore, the expressions of PC6 group were higher than LU7 group and ST36 group(p < 0.05). And electrocardiogram’s T-waves showed obvious pathological changes inthe MI group compared to the control group (p < 0.01). After EA, the abnormal T-waves voltage of ECG in PC6, LU7, and ST36 groups was improved (p < 0.05). In addition, therate change of PC6 group was larger than that of both LU7 and ST36 groups (p < 0.05). But the T-waves voltage of the nonacupoint group was not significantly different than thatof the MI group (p > 0.05).
Choi, Yeong-Jin,Jun, Young-Joon,Kim, Dong Yeon,Yi, Hee-Gyeong,Chae, Su-Hun,Kang, Junsu,Lee, Juyong,Gao, Ge,Kong, Jeong-Sik,Jang, Jinah,Chung, Wan Kyun,Rhie, Jong-Won,Cho, Dong-Woo Elsevier 2019 Biomaterials Vol.206 No.-
<P><B>Abstract</B></P> <P>Volumetric muscle loss (VML) is an irrecoverable injury associated with muscle loss greater than 20%. Although hydrogel-based 3D engineered muscles and the decellularized extracellular matrix (dECM) have been considered for VML treatment, they have shown limited efficacy. We established a novel VML treatment with dECM bioink using 3D cell printing technology. Volumetric muscle constructs composed of cell-laden dECM bioinks were generated with a granule-based printing reservoir. The 3D cell printed muscle constructs exhibited high cell viability without generating hypoxia and enhanced <I>de novo</I> muscle formation in a VML rat model. To improve functional recovery, prevascularized muscle constructs that mimic the hierarchical architecture of vascularized muscles were fabricated through coaxial nozzle printing with muscle and vascular dECM bioinks. Spatially printing tissue-specific dECM bioinks offers organized microenvironmental cues for the differentiation of each cell and improves vascularization, innervation, and functional recovery. Our present results suggest that a 3D cell printing and tissue-derived bioink-based approach could effectively generate biomimetic engineered muscles to improve the treatment of VML injuries.</P>
Chu, Jia-Qi,Jing, Kai-Peng,Gao, Xiang,Li, Peng,Huang, Rui,Niu, Yan-Ru,Yan, Shou-Quan,Kong, Jun-Chao,Yu, Cai-Yuan,Shi, Ge,Fan, Yi-Ming,Lee, Young-Ha,Zhou, Yu,Quan, Juan-Hua Landes Bioscience 2017 Cell Cycle Vol.16 No.5
<P>Autophagy and apoptosis are critical for controlling Toxoplasma gondii (T. gondii) infection. T. gondii infection during pregnancy can damage the fetus and cause birth defects; however, the molecular mechanisms of this process are poorly understood. This study aims to determine the activities of autophagy and apoptosis as well as their regulatory mechanisms during T. gondii infection by using human umbilical cord mesenchymal stem cells (hUC-MSCs) as a model of congenital diseases. LC3B, a hallmark protein of autophagy was incrementally upregulated with the infection duration, whereas p62 was downregulated in T. gondii-infected hUC-MSCs. Concurrent to this result, the invasion of T. gondii into hUC-MSCs increased in a time-dependent manner. The expression levels of Bcl-2 family proteins including Bcl-2, Bcl-xL, Bim, Bax, Bid and Bak were not altered; however, Mcl-1 levels in hUC-MSCs were dramatically decreased upon T. gondii infection. In addition, at 24h post-infection, cleaved PARP and cleaved caspase-3 protein levels were elevated in hUC-MSCs. Importantly, Mcl-1 overexpression reduced the levels of autophagy- and apoptosis-related proteins in T. gondii-infected hUC-MSCs. Mcl-1 proteins were primarily expressed in the fraction containing mitochondria and strongly interacted with Beclin-1 under normal conditions; however, these interactions were remarkably attenuated by T. gondii infection. These results suggest that mitochondrial Mcl-1 is an essential signaling mediator regulating the activation of autophagy and apoptosis during T. gondii infection.</P>
K-doping effect of the superconductivity in K2xFeTe1-xSx (0.07 ≤ x ≤ 0.3)
Cheng Cheng,Zhenjie Feng,Qing Li,Tao Li,Qiang Hou,Fei Chen,Zhongmin Ou,Jun-Yi Ge,Shixun Cao,Jincang Zhang 한국물리학회 2019 Current Applied Physics Vol.19 No.4
Bulk samples of K doping K2xFeTe1-xSx with x=0.07, 0.1, 0.2, 0.3 are successfully prepared by using easy-to-use stable compound K2S as the reactant. The lattice constant calculated from X-ray diffraction patterns indicate that K ions enter the Fe-Te-S layers. K doping is beneficial enhance the superconductivity transition temperature from the R-T curves. The apparent diamagnetic signal is observed in M-T curves when the content of K is smaller than 0.1. However, differential curves (dM/dT) in K-rich samples appear sharp slope mutations, which means that the Meissner effect signal is covered by the increased excess ferromagnetic ions. The number of excess Fe magnetic ions is proportional to K content, which may play an important role in determining the superconductivity.
Anomalous magnetization jumps in granular Pb superconducting films
Zhang An-Lei,Jiang Wan-Yan,Chen Xing-Hong,Zhang Xiao-Ke,Lu Wen-Lai,Chen Fei,Feng Zhen-Jie,Cao Shi-Xun,Zhang Jin-Cang,Ge Jun-Yi 한국물리학회 2022 Current Applied Physics Vol.35 No.-
In granular superconductors, the grain boundaries are closely related to the vortex dynamics and the macroscopic superconducting properties. In our research, Pb films with different grain sizes were prepared by tuning the substrate temperature. With the grain size decreasing, Pb films are prone to feature the anomalous magnetization jumps in the M − T curves, while in the M − H curves flux avalanche happens. Both phenomena appear in the same region of the H − T phase diagram and thus are considered to have the same origin. The further theoretical analysis shows that with grain size decreasing the pinning mechanism evolves from a mixed δTc and δl pinning to the δl pinning mechanism. The results shed light on the study of pinning mechanism for granular superconductors and is beneficial to the potential application of manipulating vortex pinning by regulation of intrinsic defects.