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面向高吞吐量的NB‒IoT低轨卫星物联网资源调度

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太赫兹科学与电子信息学报 2024年第9期22卷 933-943,951页

作者：吉用华张晨张更新南京邮电大学通信与信息工程学院江苏南京210003 南京邮电大学通信与网络技术国家工程研究中心江苏南京210003

窄带物联网(NB-IoT)作为一种低功耗广域网技术,专门设计用于连接大量低功耗设备。基于该技术的低轨卫星物联网有着较低的传输损耗和时延,并且可以通过星座方式对地球实现无缝覆盖。然而,低轨卫星具有高度动态性,并且面临来自不同用户的... 详细信息

窄带物联网(NB-IoT)作为一种低功耗广域网技术,专门设计用于连接大量低功耗设备。基于该技术的低轨卫星物联网有着较低的传输损耗和时延,并且可以通过星座方式对地球实现无缝覆盖。然而,低轨卫星具有高度动态性,并且面临来自不同用户的QoS需求,这些因素使得现有资源调度算法的吞吐量性能受到了极大的影响。针对这些挑战,本文在海量物联网用户请求无线资源且时频资源有限的场景下,综合考虑卫星信道特性、不同用户间的可靠性与时延要求以及卫星高动态性引起的差分多普勒等因素,提出了一种面向高吞吐量的NB-IoT低轨卫星物联网资源调度算法。仿真结果表明,相比现有方法,提出的资源调度算法在系统吞吐量方面表现出显著的性能提升。

关键词：窄带物联网低轨卫星物联网资源调度

Voltage-dependent blockade by bupivacaine of cardiac sodium channels expressed in Xenopus oocytes

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Neuroscience Bulletin 2014年第4期30卷 697-710页

作者： Heng Zhang Hui ji Zhirui Liu yonghua ji Xinmin You Gang Ding Zhijun Cheng Lab of Neuropharmacology and Neurotoxicology Shanghai University Xinhua Hospital (Chongming) Shanghai Jiaotong University School of Medicine Xinhua Translational Institute for Cancer Pain

Bupivacaine ranks as the most potent and efficient drug among class I local anesthetics, but its high potential for toxic reactions severely limits its clinical use. Although bupivacaine-induced toxicity is mainly caused by substantial blockade of voltage-gated sodium channels （VGSCs）, how these hydrophobic molecules interact with the receptor sites to which they bind remains unclear. Navl.5 is the dominant isoform of VGSCs expressed in cardiac myocytes, and its dysfunction may be the cause of bupivacaine- triggered arrhythmia. Here, we investigated the effect of bupivacaine on Navl.5 within the clinical concentration range. The electrophysiological measurements on Navl.5 expressed in Xenopus oocytes showed that bupivacaine induced a voltage- and concentration-dependent blockade on the peak of/Na and the half-maximal inhibitory dose was 4.51 pmol/L. Consistent with other local anesthetics, bupivacaine also induced a use-dependent blockade on Navl.5 currents. The underlying mechanisms of this blockade may contribute to the fact that bupivacaine not only dose-dependently affected the gating kinetics of Nay1.5 but also accelerated the development of its open-state slow inactivation. These results extend our knowledge of the action of bupivacaine on cardiac sodium channels, and therefore contribute to the safer and more efficient clinical use of bupivacaine.

关键词： bupivacaine Nav1.5 voltage-dependentblockade inactivated state

Distribution and Functional Characteristics of Voltage-Gated Sodium Channels in Immature Cochlear Hair Cells

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Neuroscience Bulletin 2020年第1期36卷 49-65页

作者： You Zhou Chenchen Xia Manli Yi Xueling Wang Hao Wu yonghua ji Department of Otolaryngology-Head and Neck Surgery Ninth People’s HospitalShanghai Jiaotong University School of MedicineShanghai 200125China Ear Institute Shanghai Jiaotong University School of MedicineShanghai 200125China Shanghai Key Laboratory of Translational Medicine on Ear and Nose Diseases Shanghai 200125China Laboratory of Neuropharmacology and Neurotoxicology Shanghai UniversityShanghai 200444China Translational Institute for Cancer Pain Xinhua Hospital Chongming BranchShanghai 202150China

Voltage-gated sodium channels(VGSCs)are transiently expressed in cochlear hair cells before hearing onset and play an indispensable role in shaping spontaneous *** this study,we showed that Na^+currents shaped the spontaneous action potentials in developing mouse inner hair cells(IHCs)by decreasing the time required for the membrane potential to reach the action-potential *** immature IHCs,we identified 9 known VGSC subtypes(***-l.9ot),among which Navl.7a was the most highly expressed subtype and the main contributor to Na+currents in developing hair *** recordings of two cochlea-specific Navi.7 variants(CbmNavl.7a and CbmNavl.7b)revealed a novel loss-of-function mutation(C934R)at the extracellular linker between segments 5 and 6 of domain *** addition,post-transcriptional modification events,such as alternative splicing and RNA editing,amended the gating properties and kinetic features of CbmNavl.7a(C934).These results provide molecular and functional characteristics of VGSCs in mammalian IHCs and their contributions to spontaneous physiological activity during cochlear maturation.

关键词： Cochlear hair cell Spontaneous action potential Voltage-gated sodium channel Post-transcriptional modification Gating property Introduction

SCN9A Epileptic Encephalopathy Mutations Display a Gain-offunction Phenotype and Distinct Sensitivity to Oxcarbazepine

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Neuroscience Bulletin 2020年第1期36卷 11-24页

作者： Shuzhang Zhang Zhiping Zhang Yuan Shen Yudan Zhu Kun Du jingkang Guo yonghua ji jie Tao Institute of Biomembrane and Biopharmaceutics Shanghai UniversityShanghai 200444China Central Laboratory and Department of Neurology Putuo HospitalShanghai University of Traditional Chinese MedicineShanghai 200062China Department of Clinical Laboratory Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 202150China Xinhua Translational Institute for Cancer Pain Xinhua Hospital Chongming BranchShanghai 202150China Putuo Clinical Medical School Anhui Medical UniversityShanghai 200062China

Genetic mutants of voltage-gated sodium channels(VGSCs)are considered to be responsible for the increasing number of epilepsy *** research has indicated that mutations of one of the VGSC genes,SCN9A(Navl.7),result in febrile seizures and Dravet syndrome in *** these recent efforts,the electrophysiological basis of SCN9A mutations remains ***,we performed a genetic screen of patients with febrile seizures and identified a novel missense mutation of SCN9A(W1150R).Electrophysiological characterization of different SCN9A mutants in HEK293T cells,the previously-reported N641Y and K655R variants,as well as the newly-found W1150R variant,revealed that the current density of the W1150R and N641Y variants was significantly larger than that of the wild-type(WT)*** time constants of recovery from fast inactivation of the N641Y and K655R variants were markedly lower than in the WT *** W1150R variant caused a negative shift of the G-V curve in the voltage dependence of steady-state *** mutants displayed persistent currents larger than the WT *** addition,we found that oxcarbazepine(OXC),one of the antiepileptic drugs targeting VGSCs,caused a significant shift to more negative potential for the activation and inactivation in WT and mutant ***-induced inhibition of currents was weaker in the W1150R variant than in the ***,with administering OXC the time constant of the N641Y variant was longer than those of the other two SCN9A *** all,our results indicated that the point mutation W1150R resulted in a novel gain-of-function *** findings indicated that SCN9A mutants contribute to an increase in seizure,and show distinct sensitivity to OXC.

关键词： Voltage-gated sodium channel SCN9A Epilepsy Electrophysiological function Oxcarbazepine Sensitivity Introduction

Scorpion toxin BmKI directly activates Nav1.8 in primary sensory neurons to induce neuronal hyperexcitability in rats

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Protein & Cell 2015年第6期6卷 443-452页

作者： Pin Ye Yunlu jiao Zhenwei Li Liming Hua jin Fu Feng jiang Tong Liu yonghua ji Laboratory of Neuropharmacology and Neurotoxicology Shanghai University Shanghai 200436 China jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and the Second Affiliated Hospital of Soochow University Institute of Neuroscience Soochow University Suzhou 215021 China

Voltage-gated sodium channels （VGSCs） in primary sensory neurons play a key role in transmitting pain signals to the central nervous system. BmK I, a site-3 sodium channel-specific toxin from scorpion Buthus martensi Karsch, induces pain behaviors in rats. How- ever, the subtypes of VGSCs targeted by BmK I were not entirely clear. We therefore investigated the effects of BmK I on the current amplitude, gating and kinetic properties of Nav1.8, which is associated with neuronal hyperexcitability in DRG neurons. It was found that BmK I dose-dependently increased Nav1.8 current in small- sized （〈25 μm） acutely dissociated DRG neurons, which correlated with its inhibition on both fast and slow in- activation. Moreover, voltage-dependent activation and steady-state inactivation curves of Nay1.8 were shifted in a hyperpolarized direction. Thus, BmK I reduced the threshold of neuronal excitability and increased action potential firing in DRG neurons. In conclusion, our data clearly demonstrated that BmK I modulated Nav1.8 re- markably, suggesting BmK I as a valuable probe for studying Nay1.8. And Navl.8 is an important target re- lated to BmK I-evoked pain.

关键词： voltage-gated sodium channel Nay1.8,primary sensory neurons BmK I

PKA phosphorylation reshapes the pharmacological kinetics of site-4 sodium channel modulator

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PKA phosphorylation reshapes the pharmacological kinetics of...

第一届国际暨第十三次中国生物物理学术大会

作者： Zhirui Liu yonghua ji Lab of Neuropharmacology and Neurotoxicology Shanghai University

＜正＞The activity of the voltage-gated sodium channels（VGSCs）have been investigated to be subjected to PKA-mediated *** stimulation of a coexpressed β2-adrenergic receptor in Xenopus oocytes that increased the intracellular c AMP level,PKA was readily activated and suppressed the peak currents of sodium channel subtype r Nav1.2 without any

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Deciphering the Venomic Transcriptome of Killer-Wasp Vespa velutina

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Deciphering the Venomic Transcriptome of Killer-Wasp Vespa v...

第12届生物毒素研究及医药应用学术大会

作者： Zhirui Liu yonghua ji Laboratory of Neuropharmacology and Neurotoxicology Shanghai University

Since 2006,with the extensive occurrence of thousands injured and dozens of deaths caused by wasp stings,it has become a severe public health concern in *** wasp attacks cases intensively occurred in the summer of 2013,which resulted in 42 death and 1,675 injured in three cities in Shanxi *** the aim of understanding the toxic components of wasp venom,we took advantage of high-throughput sequencing platforms（Roche454 and Illminia HiSeq 2000） to uncover the global transcriptome of WASP *** distributing in China:（1） 293 putative toxin-encoding sequences were identified,and grouped into eight classes according to their possible working targets;（2） Among all the toxins grouped,hemostasis-impairing toxins and neurotoxins represented the two largest families of venomicproteins in ***;（3） 10 genes were found to be associating with toxic reactions and metabolisms;（4） However,hyaluronidase and antigen 5,the two well-known allergen families were not significantly verified in transcription *** study is the first comprehensive analysis of wasps toxin in the *** results clearly uncovered that the reason of death among wasp-attack victims may contribute to multiple organ failure induced by blood cycle toxin,neurotoxin and allergic factors,which expand the previous clinical interface to the attention of the allergic ***,the identification of 10 genes associating with toxic reactions and metabolisms is worthful of clarifying the assembly of "specific weapon" and enriching knowledges about toxin synthesis mechanism and injury mechanism of poisonous species.

关键词： Wasp V.velutina Transcriptome Venom Specific weapon

Dynamic expression of VGSCs subtypes Nav1.1,Nav1.2,Nav1.3 and Nav1.6 triggered by BmK I in rat hippocampus

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Dynamic expression of VGSCs subtypes Nav1.1,Nav1.2,Nav1.3 an...

第12届生物毒素研究及医药应用学术大会

作者： Hao Wu Hongyan Zhu yonghua ji Laboratory of Neuropharmacology and Neurotoxicology Shanghai University

BmK I（an-like toxin purified from the venom of Eastern Asian scorpion Buthus martensi Karsch） has been identified to a site-3 specific modulator of VGSCs with capacity ofinducing convulsive motor activities by intrahippocampal ***,BmK I was unilaterally injected to the hippocampus in rats to evoke convulsive motor activities,then the expression of VGSCs subtypes Nav1.1,Nav1.2,Nav1.3 and Nav1.6 were detected at 1 day,7 days,21 days and 63 days after BmK I *** revealed that the expression of Nav1.1,Nav1.2,Nav1.3and Nav1.6 was robustly up-regulated in the ipsilateral hippocampal CA1 and CA3 subregions at 7days,21 days after Bmk I injection compared with that of the contralateral side and control hippocampus,reaching the peak at 21 days after Bmk I ***,Nav1.1,Nav1.2,Nav1.3 and Nav1.6 immunoreactivities cannot be detected in the ipsilateral hippocampus at 63 days after BmK I ***,a large number of Nav1.1,Nav1.2,Nav1.3 and Nav1.6immunoreactivities were found to be localized in reactive astrocytes（GFAP-positive） at 7 days,21 days after BmK I *** real-time PCR also address the dramatic up-regulation of Nav1.1,Nav1.2,Nav1.3 and Nav1.6 expression at 21 days after BmK I injection with that of the contralateral side and control *** suggest that BmK I,a specific VGSCs modulator,not only can induce the seizure-like activities but also affect the expression of brain subtype VGSCs with time-dependent pattern.

关键词： BmK I Hippocampus Voltage-gated sodium channels Epilepsy

Spinal 5-HT3AR contributes to BmK I-induced inflammatory pain in rats

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Spinal 5-HT3AR contributes to BmK I-induced inflammatory pai...

第12届生物毒素研究及医药应用学术大会

作者： jin Fu Yu-Lu jiao yonghua ji Laboratory of Neuropharmacology and Neurotoxicology Shanghai University

Subcutaneous injection of BmK I could be adopted to well establish a novel pain ***,5-hydroxytryptamine（serotonin,5-HT） receptor is involved in regulating animal pain-related ***,the underlying mechanism of 5-HT3 R on BmK I-induced pain remains *** behavioral testing,RT-PCR and Western blotting were used to yield the following results:first,intraplantar（i.p1.） injection of BmK I（10 μg） induced elevated mRNA and protein levels of 5-HT3 AR in bilateral L4-L5 spinal cord;Second,intrathecal（i.t.） injection of ondansetron（a specific antagonist of 5-HT3AR） reduced spontaneous pain responses,attenuated unilateral thermal and bilateral mechanical hypersensitivity elicited by BmK I;Microglia could be activated by BmK I（***.） in both sides of L4-L5 spinal cord,and this effect was reversed by intrathecal pre-treatment with 5-HT3 AR ***,the 5-HT3 AR in L4-L5 spinal cord was almost co-localized with NeuN（a marker of nerve cell）,but not co-expressed with Iba-1（a marker of microglia）.Finally,the expression level of CX3CL1 and CX3CR1 was reduced by intrathecal pre-treatment with *** results indicate that both 5-HT3 AR signaling pathway and microglia are activated in the process of induction and maintenance of BmK I-induced pain ***,the results suggest that the neuronal 5-HT3 AR may communicate with microglia indirectly via CX3CL1 which is involved in regulating the BmK I-induced hyperalgesia and sensitization.~1

关键词： BmKI 5-HT Pain 5-HT3AR CX3CL1