An Interval Algebra-based Modeling and Routing Method in Bus Delay Tolerant Network

( Haiquan Wang ),( Weijian Ma ),( Hengkun Shi ),( Chunhe Xia ) 한국인터넷정보학회 2015 KSII Transactions on Internet and Information Syst Vol.9 No.4

In bus delay-tolerant networks, the route of bus is determinate but its arrival time is indeterminate. However, most conventional approaches predict future contact without considering its uncertainty, which makes a limitation on routing performance. A novel approach is proposed by employing interval algebra to characterize the contact`s uncertainty and time-varying nature. The contact is predicted by using the Bayesian estimation to achieve a better routing performance. Simulation results show that this approach achieves a good balance between delivery latency and delivery ratio.

HSP70 attenuates compression-induced apoptosis of nucleus pulposus cells by suppressing mitochondrial fission via upregulating the expression of SIRT3

Hu Binwu,Wang Peng,Zhang Shuo,Liu Weijian,Lv Xiao,Shi Deyao,Zhao Lei,Liu Hongjian,Wang Baichuan,Chen Songfeng,Shao Zengwu 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Compression-induced apoptosis of nucleus pulposus (NP) cells plays a pivotal role in the pathogenesis of intervertebral disc degeneration (IVDD). Recent studies have shown that the dysregulation of mitochondrial fission and fusion is implicated in the pathogenesis of a variety of diseases. However, its role in and regulatory effects on compression-induced apoptosis of NP cells have not yet been fully elucidated. Heat shock protein 70 (HSP70) is a major cytoprotective heat shock protein, but its physiological role in IVDD, especially its effect on mitochondrial fission and fusion, is still unknown. Herein, we found that compression could induce mitochondrial fission, which ultimately trigger apoptosis of NP cells via the mitochondrial apoptotic pathway. In addition, we identified the cytoprotective effects of HSP70 on NP cells, and we found that promoting the expression of HSP70 could protect NP cells from abnormal mechanical loading in vitro and in vivo. Finally, we showed that HSP70 inhibited compression-induced mitochondrial fission by promoting SIRT3 expression, thereby attenuating mitochondrial dysfunction and the production of reactive oxygen species and ultimately inhibiting the mitochondrial apoptotic pathway in NP cells. In conclusion, our results demonstrated that HSP70 could attenuate compression-induced apoptosis of NP cells by suppressing mitochondrial fission via upregulating SIRT3 expression. Promoting the expression of HSP70 might be a novel strategy for the treatment of IVDD.

Dexmedetomidine alleviates blood-brain barrier disruption in rats after cerebral ischemia-reperfusion by suppressing JNK and p38 MAPK signaling

Zhu Canmin,Wang Dili,Chang Chang,Liu Aofei,Zhou Ji,Yang Ting,Jiang Yuanfeng,Li Xia,Jiang Weijian 대한약리학회 2024 The Korean Journal of Physiology & Pharmacology Vol.28 No.3

Dexmedetomidine displays multiple mechanisms of neuroprotection in ameliorating ischemic brain injury. In this study, we explored the beneficial effects of dexmedetomidine on blood-brain barrier (BBB) integrity and neuroinflammation in cerebral ischemia/reperfusion injury. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h and reperfusion for 24 h to establish a rat model of cerebral ischemia/reperfusion injury. Dexmedetomidine (9 g/kg) was administered to rats 30 min after MCAO through intravenous injection, and SB203580 (a p38 MAPK inhibitor, 200 g/kg) was injected intraperitoneally 30 min before MCAO. Brain damages were evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, Nissl staining, and brain water content assessment. BBB permeability was examined by Evans blue staining. Expression levels of claudin-5, zonula occludens-1, occludin, and matrix metalloproteinase-9 (MMP-9) as well as M1/M2 phenotypes-associated markers were assessed using immunofluorescence, RT-qPCR, Western blotting, and gelatin zymography. Enzyme-linked immunosorbent assay was used to examine inflammatory cytokine levels. We found that dexmedetomidine or SB203580 attenuated infarct volume, brain edema, BBB permeability, and neuroinflammation, and promoted M2 microglial polarization after cerebral ischemia/reperfusion injury. Increased MMP-9 activity by ischemia/reperfusion injury was inhibited by dexmedetomidine or SB203580. Dexmedetomidine inhibited the activation of the ERK, JNK, and p38 MAPK pathways. Moreover, activation of JNK or p38 MAPK reversed the protective effects of dexmedetomidine against ischemic brain injury. Overall, dexmedetomidine ameliorated brain injury by alleviating BBB permeability and promoting M2 polarization in experimental cerebral ischemia/reperfusion injury model by inhibiting the activation of JNK and p38 MAPK pathways.

Antisense oligodeoxynucleotides against dynamin-related protein 1 reduce remifentanilinduced hyperalgesia by modulating spinal N-methyl-D-aspartate receptor expression in rats

Songyi Zhou,Yizhao Pan,Yan Zhang,Lijun Gu,Leikai Ma,Qingqing Xu,Weijian Wang,Jiehao Sun 대한통증학회 2023 The Korean Journal of Pain Vol.36 No.3

Background: Spinal N-methyl-D-aspartate (NMDA) receptor activation is attributed to remifentanil-induced hyperalgesia (RIH). However, the specific mechanism and subsequent treatment is still unknown. Previous studies have shown that the dynamin-related protein 1 (DRP1)-mitochondria-reactive oxygen species (ROS) pathway plays an important role in neuropathic pain. This study examined whether antisense oligodeoxynucleotides against DRP1 (AS-DRP1) could reverse RIH. Methods: The authors first measured changes in paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) at 24 hours before remifentanil infusion and 4, 8, 24, and 48 hours after infusion. The expression levels of DRP1 and NR2B were measured after behavioral testing using Western blotting. In addition, DRP1 expression was knocked down by intrathecal administration of AS-DRP1 to investigate the effects of DRP1 on RIH. The behavioral testing, the expression levels of spinal DRP1 and NR2B, and dorsal mitochondrial superoxide were measured. Changes in mitochondrial morphology were assessed using electron microscopy. Results: After remifentanil exposure, upregulation of spinal DRP1 and NR2B was observed along with a reduction in PWMT and PWTL. In addition, AS-DRP1 improved RIH-induced PWTL and PWMT (P < 0.001 and P < 0.001) and reduced remifentanil-mediated enhancement of spinal DRP1 and NR2B expression (P = 0.020 and P = 0.022). More importantly, AS-DRP1 reversed RIH-induced mitochondrial fission (P = 0.020) and mitochondrial superoxide upregulation (P = 0.031). Conclusions: These results indicate that AS-DRP1 could modulate NMDA receptor expression to prevent RIH through the DRP1-mitochondria-ROS pathway.

Member capacity-based progressive collapse analysis of transmission towers under wind load

Yong-Quan Li,Yong Chen,Guohui Shen,Wenjuan Lou,Weijian Zhao,Hao Wang 한국풍공학회 2021 Wind and Structures, An International Journal (WAS Vol.33 No.4

The wind-induced collapse of transmission towers has raised many concerns. Progressive collapse analysis is recognized as a promising method for the assessment of the collapse-resistant capacity of the transmission tower. The finite element model of an actual transmission tower is firstly built for the analysis, in which the dynamic behavior of the member in failure is taken into account to be in accord with the actual tower collapse. The analysis considering the main design load cases is conducted in advance to determine the case under which the tower has the potential to collapse. The incremental dynamic analysis in association with the explicit time integration algorithm is employed to perform a progressive collapse analysis, where the wind loads are simulated by using the linear filtering method, and the developed failure criterion with axial force and bending moment involved is based on the stability bearing capacity of the members. It is found the tower collapse begins with the horizontal bracing member near the waist. Then, the adjacent members, including the leg members, fail sequentially, and the tower collapses eventually with a shear-type failure. The demand to capacity ratio (DCR) in terms of bearing capacity of the member is defined to quantify the structural behavior, the location of the member that has the potential to fail, and when the initial failure occurs are thereby identified. It is concluded that compared to the member capacity-based analysis, the ultimate strain-based analysis, which is most likely to be an inelastic dynamic analysis permitting a large deformation, may overestimate the bearing capacity of the structure in wind-induced collapse.