Ephrin signalling controls brain size by regulating

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自适应谱线增强器在生物雷达中的应用

自适应谱线增强器在生物雷达中的应用
自适 应 谱 线 增 强器 在 生物 雷达 中 的应 用 陈 铁 军 , 等
白适 应 谱 线 增 强器 在 生 物 雷 达 中的应 用
Ap l a i ft e Ad p ie S e ta n a c n Bi a a pi t c on o h a t p c r lE h n eri or d r v
能力 , 其原理如 图 1 所示 。
因此 , 对采集信号处 理 的效果 直接决 定 了生命 探测仪
性能的优劣。

为解决这一 问题 , 基于变步长 自适应算法的各种信 号处理的方法不断 涌现 。传统 的变步长 自适应 算 一 法均需要预先给定参考信 号。但在救援环境 复杂以及 废墟下存活人体的个体差异 , 在生物雷达信号处理 中很
难找到一个 理想 的信号作 为参考信号。为解决 这一 问
图 1 自 适 应 谙 线 增 强 器 原 理 图
F g 1 T e p i cp eo d p ie s e t l n a c r i . h r i l fa a t p cr h n e n v ae
Ke wod :Boa a E rrc agn ae y r s ird r r h n igrt Ad pieset leh n e n L at a qae L ) Ma a R b s es o a t pcr na c met e s mensu r ( MS v a t b o ut s l n
自适应谱线增强器最早 是 由 Wir do w等 人于 17 95 年提 出的。 目前 , 基于 自适 应线性 组合器 的 自适 应谱
线增强器 已广泛应用 于频谱估算 、 谱线估 计 以及 窄带 检测等领域 。在窄带信 号加上 宽带信号 的情况 下 , 白 适应谱线增强方法无 需独立 的参考 信号就 能将信号分

STM32固件库使用手册的中文翻译版

STM32固件库使用手册的中文翻译版
该固态函数库通过校验所有库函数的输入值来实现实时错误检测。该动态校验提高了软件的鲁棒性。实时 检测适合于用户应用程序的开发和调试。但这会增加了成本,可以在最终应用程序代码中移去,以。
因为该固件库是通用的,并且包括了所有外设的功能,所以应用程序代码的大小和执行速度可能不是最优 的。对大多数应用程序来说,用户可以直接使用之,对于那些在代码大小和执行速度方面有严格要求的应 用程序,该固件库驱动程序可以作为如何设置外设的一份参考资料,根据实际需求对其进行调整。
1.3.1 变量 ................................................................................................................................................ 28 1.3.2 布尔型 ............................................................................................................................................ 28 1.3.3 标志位状态类型 ........................................................................................................................... 29 1.3.4 功能状态类型 .............................................................................................................

脑电信号处理算法优化方法

脑电信号处理算法优化方法

脑电信号处理算法优化方法脑电信号(Electroencephalogram, EEG)是一种记录大脑神经元电活动的非侵入性技术。

通过分析脑电信号,我们可以了解大脑的功能活动、认知过程和情绪等信息。

然而,由于脑电信号的特点复杂且噪声干扰大,因此需要经过一系列的信号处理算法来提取有用的信息。

本文将介绍一些脑电信号处理算法的优化方法。

1. 信号预处理脑电信号预处理是脑电信号处理的第一步,其目的是去除噪声干扰和对信号进行滤波处理。

通常的预处理方法包括滤波、去噪和伪迹消除。

滤波技术是预处理的关键步骤之一。

通常使用数字滤波器对原始脑电信号进行滤波处理,以去除高斯噪声和其他频率干扰。

常用的滤波算法包括低通滤波、高通滤波和带通滤波等。

为了更好地滤波脑电信号,我们可以采用优化滤波器设计方法,如基于优化算法的滤波器设计、自适应滤波器设计等。

在信号预处理中,去噪也是重要的一步。

脑电信号常常受到肌电噪声和眨眼等运动伪迹的干扰,而这些噪声干扰会降低信号质量。

为了去除这些噪声,我们可以采用经验模态分解(Empirical Mode Decomposition, EMD)方法或小波去噪方法。

经验模态分解可以将信号分解为多个固有模态函数和一个残差函数,通过将噪声与信号分离,实现去噪的目的。

而小波去噪方法则是通过使用小波分析技术,将噪声与信号分离。

2. 特征提取脑电信号中包含了丰富的信息,为了更好地理解脑电信号的意义,我们需要从中提取有效的特征。

常用的特征提取方法包括时域特征、频域特征和时频域特征。

时域特征是指对信号在时间上的统计特征进行分析,如均值、方差、标准差等。

频域特征则是对信号在频率上的统计特征进行分析,如功率谱密度、频率带能量等。

时频域特征则是综合考虑信号在时间和频率上的变化情况,如短时傅里叶变换、小波变换等。

为了更好地提取脑电信号的特征,我们可以采用机器学习算法进行特征选择和降维。

机器学习算法可以帮助我们从大量的特征中选择出对分类或识别任务最相关的特征,并将维度降低到更易处理的范围内。

Eph基因的表达及其与肿瘤的关系

Eph基因的表达及其与肿瘤的关系

Eph基因的表达及其与肿瘤的关系汤亲青,周晓军*南京大学医学院,南京军区总医院,南京(210002)E-mail:zhouxj1@摘要:Eph(促红细胞生成素产生肝细胞受体)基因是受体酪氨酸激酶家族中最大的一个亚群。

根据Eph受体家族的序列同源性,结构,及与配体的亲和力的不同而将其分为EphA受体和EphB受体亚家族. Eph的结构分成三个部分,即细胞外的配体结合区,细胞内部具有酪氨酸激酶活性的功能区和连接这两个区域的由疏水氨基酸组成的跨膜区。

Eph基因在神经系统的发育,血管和淋巴管的形成,肿瘤的发生发展中发挥重要作用。

探明Eph基因在神经系统疾病,脉管系统疾病以及肿瘤的发生、发展均有重要意义,并可能成为未来肿瘤及相关疾病治疗的靶点。

关键词:Eph,受体酪氨酸激酶,神经系统,血管,肿瘤0引言促红细胞生成素产生肝细胞受体(erythropoie-tin-producing hepatocyte receptor, Eph受体)激酶是受体酪氨酸激酶家族(receptor tyrosine kinases)中最大的一个亚群,其配体被命名为Ephrin。

Eph约由16个基因组成[1]。

根据Eph受体家族的序列同源性,结构,表达,分布及与配体的亲和力的不同而将其分为EphA受体和EphB受体亚家族。

EphA亚组包含10个成员EphA1-EphA10, EphB亚组包含6个成员EphB1-EphB6。

其中EphA9和EphA10是近年发现的[2,3]。

1 Eph家族蛋白结构特点Eph基因是一种膜结合的Ⅰ型糖蛋白,其结构分成三个部分,即细胞外的配体结合区,细胞内部具有酪氨酸激酶活性的功能区和连接这两个区域的由疏水氨基酸组成的跨膜区。

Eph受体亚族的胞外区包括一个N端球状结构域,一个半胱氨酸富含区,两个纤粘连蛋白Ⅲ型重复区,其胞外球状结构决定了受体与配体的结合特性及亚族特异性[4]。

Eph受体的胞内区包括具酪氨酸激酶活性的结构域(TK), SAM结构域和C端的PDZ -结构域结合基序,在Eph 受体的胞内C端发现有高度保守的SAM结构域,其保守Tyr932在疏水核埋藏形成SAM四聚物,为启动下游反应及为结合小分子质量磷酸酶提供适宜的接触部位[5]。

一种基于压缩感知的无冗余通道时间交织ADC随机化方法

一种基于压缩感知的无冗余通道时间交织ADC随机化方法

一种基于压缩感知的无冗余通道时间交织ADC随机化方法胡毅;王于波;李振国;姜亦刚;李靖;张帆
【期刊名称】《微电子学与计算机》
【年(卷),期】2022(39)2
【摘要】在时间交织ADC结构中,本文基于压缩感知理论提出一种无冗余通道随机化方法.利用随机数决定当前通道ADC是否采样,当有多个通道ADC空闲时随机选择某个通道进行采样,实现时间交织ADC的欠奈奎斯特随机化采样.在此基础上,基于观测矩阵和正交匹配追踪算法对时间交织ADC的数据进行重建,获得完整的ADC量化结果.通过MATLAB对本文提出的基于压缩感知的时间交织ADC通道随机化方法进行建模,在给定采样时间失配条件下,本方法将时间交织ADC的SFDR 从53.1 dB提高到65.5 dB,提升12.4 dB,有效提高了ADC的动态性能.
【总页数】6页(P101-106)
【作者】胡毅;王于波;李振国;姜亦刚;李靖;张帆
【作者单位】北京智芯微电子科技有限公司;电子科技大学;国网浙江省电力有限公司
【正文语种】中文
【中图分类】TN432
【相关文献】
1.双通道时间交织ADC采样系统的频域纠正补偿
2.基于PC软件的时间交织ADC 误差校准
3.一种速度可扩展的时间交织复位运放流水线ADC的设计
4.一种用于时
间交织型SAR ADC的电容校正技术5.超高速时间交织ADC通道失配后台校准算法
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协作频谱感知中快速自适应门限策略

协作频谱感知中快速自适应门限策略
第3 第6 2卷 期
21

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J u n l f e t o is& I f r a in Te h oo y o r a c r n c o El n o m to c n lg
J n 2 1 u .00
协作 频谱 感 知 中快 速 自适 应 门限策 略
Wu a 3 0 4 C ia h n4 0 7 , hn )
Ab t a t S e t u s n i g i e u c i n lp r o o n tv a i e wo k . n h t r g n o s n t r s t e s r c : p c r m e sn a k y f n t o a a tf rc g ii e r d o n t r s I e e o e e u e wo k , h s
险最 小 。
关键词 :认知无线电;协作频谱感知 ; 自适应门限;最 陡下 降法
中图分类号: N 2 T 9
文献标识码 : A
文章编 号: 09 8621)6 460 10— 9 ( 00. 0—6 5 0 1
D I 1. 2/PJ 16 09 09 O : 0 74S .14. 0. 8 1 3 . 2 0
夏文 芳 王 殊 龚世 民 刘 威
( 华中科技 大学 电子与信 息工程 系 武汉 摘 407) 3 0 4
要:频谱感知是认知无线电的一个重要组成部分 。 在异构 网络 中,认知节点的移动会 导致接 收信号强度和噪声
问题,该文提 出一种 自适应 门限参数 的协作频谱感知策略。该策略无需主用户信号、信道 以及环境噪声的任何 先
SepsD s n l rh (D )s sd o duthe o s f l op rt e o e adte pi ad t s n tee e et g i m S A iue js trs l l o e i ds n t laa ui t c A ot ta h d oa c av n ho m f o

3GPP TS 36.331 V13.2.0 (2016-06)

3GPP TS 36.331 V13.2.0 (2016-06)

3GPP TS 36.331 V13.2.0 (2016-06)Technical Specification3rd Generation Partnership Project;Technical Specification Group Radio Access Network;Evolved Universal Terrestrial Radio Access (E-UTRA);Radio Resource Control (RRC);Protocol specification(Release 13)The present document has been developed within the 3rd Generation Partnership Project (3GPP TM) and may be further elaborated for the purposes of 3GPP. The present document has not been subject to any approval process by the 3GPP Organizational Partners and shall not be implemented.This Specification is provided for future development work within 3GPP only. The Organizational Partners accept no liability for any use of this Specification. Specifications and reports for implementation of the 3GPP TM system should be obtained via the 3GPP Organizational Partners' Publications Offices.KeywordsUMTS, radio3GPPPostal address3GPP support office address650 Route des Lucioles - Sophia AntipolisValbonne - FRANCETel.: +33 4 92 94 42 00 Fax: +33 4 93 65 47 16InternetCopyright NotificationNo part may be reproduced except as authorized by written permission.The copyright and the foregoing restriction extend to reproduction in all media.© 2016, 3GPP Organizational Partners (ARIB, ATIS, CCSA, ETSI, TSDSI, TTA, TTC).All rights reserved.UMTS™ is a Trade Mark of ETSI registered for the benefit of its members3GPP™ is a Trade Mark of ETSI registered for the benefit of its Members and of the 3GPP Organizational PartnersLTE™ is a Trade Mark of ETSI currently being registered for the benefit of its Members and of the 3GPP Organizational Partners GSM® and the GSM logo are registered and owned by the GSM AssociationBluetooth® is a Trade Mark of the Bluetooth SIG registered for the benefit of its membersContentsForeword (18)1Scope (19)2References (19)3Definitions, symbols and abbreviations (22)3.1Definitions (22)3.2Abbreviations (24)4General (27)4.1Introduction (27)4.2Architecture (28)4.2.1UE states and state transitions including inter RAT (28)4.2.2Signalling radio bearers (29)4.3Services (30)4.3.1Services provided to upper layers (30)4.3.2Services expected from lower layers (30)4.4Functions (30)5Procedures (32)5.1General (32)5.1.1Introduction (32)5.1.2General requirements (32)5.2System information (33)5.2.1Introduction (33)5.2.1.1General (33)5.2.1.2Scheduling (34)5.2.1.2a Scheduling for NB-IoT (34)5.2.1.3System information validity and notification of changes (35)5.2.1.4Indication of ETWS notification (36)5.2.1.5Indication of CMAS notification (37)5.2.1.6Notification of EAB parameters change (37)5.2.1.7Access Barring parameters change in NB-IoT (37)5.2.2System information acquisition (38)5.2.2.1General (38)5.2.2.2Initiation (38)5.2.2.3System information required by the UE (38)5.2.2.4System information acquisition by the UE (39)5.2.2.5Essential system information missing (42)5.2.2.6Actions upon reception of the MasterInformationBlock message (42)5.2.2.7Actions upon reception of the SystemInformationBlockType1 message (42)5.2.2.8Actions upon reception of SystemInformation messages (44)5.2.2.9Actions upon reception of SystemInformationBlockType2 (44)5.2.2.10Actions upon reception of SystemInformationBlockType3 (45)5.2.2.11Actions upon reception of SystemInformationBlockType4 (45)5.2.2.12Actions upon reception of SystemInformationBlockType5 (45)5.2.2.13Actions upon reception of SystemInformationBlockType6 (45)5.2.2.14Actions upon reception of SystemInformationBlockType7 (45)5.2.2.15Actions upon reception of SystemInformationBlockType8 (45)5.2.2.16Actions upon reception of SystemInformationBlockType9 (46)5.2.2.17Actions upon reception of SystemInformationBlockType10 (46)5.2.2.18Actions upon reception of SystemInformationBlockType11 (46)5.2.2.19Actions upon reception of SystemInformationBlockType12 (47)5.2.2.20Actions upon reception of SystemInformationBlockType13 (48)5.2.2.21Actions upon reception of SystemInformationBlockType14 (48)5.2.2.22Actions upon reception of SystemInformationBlockType15 (48)5.2.2.23Actions upon reception of SystemInformationBlockType16 (48)5.2.2.24Actions upon reception of SystemInformationBlockType17 (48)5.2.2.25Actions upon reception of SystemInformationBlockType18 (48)5.2.2.26Actions upon reception of SystemInformationBlockType19 (49)5.2.3Acquisition of an SI message (49)5.2.3a Acquisition of an SI message by BL UE or UE in CE or a NB-IoT UE (50)5.3Connection control (50)5.3.1Introduction (50)5.3.1.1RRC connection control (50)5.3.1.2Security (52)5.3.1.2a RN security (53)5.3.1.3Connected mode mobility (53)5.3.1.4Connection control in NB-IoT (54)5.3.2Paging (55)5.3.2.1General (55)5.3.2.2Initiation (55)5.3.2.3Reception of the Paging message by the UE (55)5.3.3RRC connection establishment (56)5.3.3.1General (56)5.3.3.1a Conditions for establishing RRC Connection for sidelink communication/ discovery (58)5.3.3.2Initiation (59)5.3.3.3Actions related to transmission of RRCConnectionRequest message (63)5.3.3.3a Actions related to transmission of RRCConnectionResumeRequest message (64)5.3.3.4Reception of the RRCConnectionSetup by the UE (64)5.3.3.4a Reception of the RRCConnectionResume by the UE (66)5.3.3.5Cell re-selection while T300, T302, T303, T305, T306, or T308 is running (68)5.3.3.6T300 expiry (68)5.3.3.7T302, T303, T305, T306, or T308 expiry or stop (69)5.3.3.8Reception of the RRCConnectionReject by the UE (70)5.3.3.9Abortion of RRC connection establishment (71)5.3.3.10Handling of SSAC related parameters (71)5.3.3.11Access barring check (72)5.3.3.12EAB check (73)5.3.3.13Access barring check for ACDC (73)5.3.3.14Access Barring check for NB-IoT (74)5.3.4Initial security activation (75)5.3.4.1General (75)5.3.4.2Initiation (76)5.3.4.3Reception of the SecurityModeCommand by the UE (76)5.3.5RRC connection reconfiguration (77)5.3.5.1General (77)5.3.5.2Initiation (77)5.3.5.3Reception of an RRCConnectionReconfiguration not including the mobilityControlInfo by theUE (77)5.3.5.4Reception of an RRCConnectionReconfiguration including the mobilityControlInfo by the UE(handover) (79)5.3.5.5Reconfiguration failure (83)5.3.5.6T304 expiry (handover failure) (83)5.3.5.7Void (84)5.3.5.7a T307 expiry (SCG change failure) (84)5.3.5.8Radio Configuration involving full configuration option (84)5.3.6Counter check (86)5.3.6.1General (86)5.3.6.2Initiation (86)5.3.6.3Reception of the CounterCheck message by the UE (86)5.3.7RRC connection re-establishment (87)5.3.7.1General (87)5.3.7.2Initiation (87)5.3.7.3Actions following cell selection while T311 is running (88)5.3.7.4Actions related to transmission of RRCConnectionReestablishmentRequest message (89)5.3.7.5Reception of the RRCConnectionReestablishment by the UE (89)5.3.7.6T311 expiry (91)5.3.7.7T301 expiry or selected cell no longer suitable (91)5.3.7.8Reception of RRCConnectionReestablishmentReject by the UE (91)5.3.8RRC connection release (92)5.3.8.1General (92)5.3.8.2Initiation (92)5.3.8.3Reception of the RRCConnectionRelease by the UE (92)5.3.8.4T320 expiry (93)5.3.9RRC connection release requested by upper layers (93)5.3.9.1General (93)5.3.9.2Initiation (93)5.3.10Radio resource configuration (93)5.3.10.0General (93)5.3.10.1SRB addition/ modification (94)5.3.10.2DRB release (95)5.3.10.3DRB addition/ modification (95)5.3.10.3a1DC specific DRB addition or reconfiguration (96)5.3.10.3a2LWA specific DRB addition or reconfiguration (98)5.3.10.3a3LWIP specific DRB addition or reconfiguration (98)5.3.10.3a SCell release (99)5.3.10.3b SCell addition/ modification (99)5.3.10.3c PSCell addition or modification (99)5.3.10.4MAC main reconfiguration (99)5.3.10.5Semi-persistent scheduling reconfiguration (100)5.3.10.6Physical channel reconfiguration (100)5.3.10.7Radio Link Failure Timers and Constants reconfiguration (101)5.3.10.8Time domain measurement resource restriction for serving cell (101)5.3.10.9Other configuration (102)5.3.10.10SCG reconfiguration (103)5.3.10.11SCG dedicated resource configuration (104)5.3.10.12Reconfiguration SCG or split DRB by drb-ToAddModList (105)5.3.10.13Neighbour cell information reconfiguration (105)5.3.10.14Void (105)5.3.10.15Sidelink dedicated configuration (105)5.3.10.16T370 expiry (106)5.3.11Radio link failure related actions (107)5.3.11.1Detection of physical layer problems in RRC_CONNECTED (107)5.3.11.2Recovery of physical layer problems (107)5.3.11.3Detection of radio link failure (107)5.3.12UE actions upon leaving RRC_CONNECTED (109)5.3.13UE actions upon PUCCH/ SRS release request (110)5.3.14Proximity indication (110)5.3.14.1General (110)5.3.14.2Initiation (111)5.3.14.3Actions related to transmission of ProximityIndication message (111)5.3.15Void (111)5.4Inter-RAT mobility (111)5.4.1Introduction (111)5.4.2Handover to E-UTRA (112)5.4.2.1General (112)5.4.2.2Initiation (112)5.4.2.3Reception of the RRCConnectionReconfiguration by the UE (112)5.4.2.4Reconfiguration failure (114)5.4.2.5T304 expiry (handover to E-UTRA failure) (114)5.4.3Mobility from E-UTRA (114)5.4.3.1General (114)5.4.3.2Initiation (115)5.4.3.3Reception of the MobilityFromEUTRACommand by the UE (115)5.4.3.4Successful completion of the mobility from E-UTRA (116)5.4.3.5Mobility from E-UTRA failure (117)5.4.4Handover from E-UTRA preparation request (CDMA2000) (117)5.4.4.1General (117)5.4.4.2Initiation (118)5.4.4.3Reception of the HandoverFromEUTRAPreparationRequest by the UE (118)5.4.5UL handover preparation transfer (CDMA2000) (118)5.4.5.1General (118)5.4.5.2Initiation (118)5.4.5.3Actions related to transmission of the ULHandoverPreparationTransfer message (119)5.4.5.4Failure to deliver the ULHandoverPreparationTransfer message (119)5.4.6Inter-RAT cell change order to E-UTRAN (119)5.4.6.1General (119)5.4.6.2Initiation (119)5.4.6.3UE fails to complete an inter-RAT cell change order (119)5.5Measurements (120)5.5.1Introduction (120)5.5.2Measurement configuration (121)5.5.2.1General (121)5.5.2.2Measurement identity removal (122)5.5.2.2a Measurement identity autonomous removal (122)5.5.2.3Measurement identity addition/ modification (123)5.5.2.4Measurement object removal (124)5.5.2.5Measurement object addition/ modification (124)5.5.2.6Reporting configuration removal (126)5.5.2.7Reporting configuration addition/ modification (127)5.5.2.8Quantity configuration (127)5.5.2.9Measurement gap configuration (127)5.5.2.10Discovery signals measurement timing configuration (128)5.5.2.11RSSI measurement timing configuration (128)5.5.3Performing measurements (128)5.5.3.1General (128)5.5.3.2Layer 3 filtering (131)5.5.4Measurement report triggering (131)5.5.4.1General (131)5.5.4.2Event A1 (Serving becomes better than threshold) (135)5.5.4.3Event A2 (Serving becomes worse than threshold) (136)5.5.4.4Event A3 (Neighbour becomes offset better than PCell/ PSCell) (136)5.5.4.5Event A4 (Neighbour becomes better than threshold) (137)5.5.4.6Event A5 (PCell/ PSCell becomes worse than threshold1 and neighbour becomes better thanthreshold2) (138)5.5.4.6a Event A6 (Neighbour becomes offset better than SCell) (139)5.5.4.7Event B1 (Inter RAT neighbour becomes better than threshold) (139)5.5.4.8Event B2 (PCell becomes worse than threshold1 and inter RAT neighbour becomes better thanthreshold2) (140)5.5.4.9Event C1 (CSI-RS resource becomes better than threshold) (141)5.5.4.10Event C2 (CSI-RS resource becomes offset better than reference CSI-RS resource) (141)5.5.4.11Event W1 (WLAN becomes better than a threshold) (142)5.5.4.12Event W2 (All WLAN inside WLAN mobility set becomes worse than threshold1 and a WLANoutside WLAN mobility set becomes better than threshold2) (142)5.5.4.13Event W3 (All WLAN inside WLAN mobility set becomes worse than a threshold) (143)5.5.5Measurement reporting (144)5.5.6Measurement related actions (148)5.5.6.1Actions upon handover and re-establishment (148)5.5.6.2Speed dependant scaling of measurement related parameters (149)5.5.7Inter-frequency RSTD measurement indication (149)5.5.7.1General (149)5.5.7.2Initiation (150)5.5.7.3Actions related to transmission of InterFreqRSTDMeasurementIndication message (150)5.6Other (150)5.6.0General (150)5.6.1DL information transfer (151)5.6.1.1General (151)5.6.1.2Initiation (151)5.6.1.3Reception of the DLInformationTransfer by the UE (151)5.6.2UL information transfer (151)5.6.2.1General (151)5.6.2.2Initiation (151)5.6.2.3Actions related to transmission of ULInformationTransfer message (152)5.6.2.4Failure to deliver ULInformationTransfer message (152)5.6.3UE capability transfer (152)5.6.3.1General (152)5.6.3.2Initiation (153)5.6.3.3Reception of the UECapabilityEnquiry by the UE (153)5.6.4CSFB to 1x Parameter transfer (157)5.6.4.1General (157)5.6.4.2Initiation (157)5.6.4.3Actions related to transmission of CSFBParametersRequestCDMA2000 message (157)5.6.4.4Reception of the CSFBParametersResponseCDMA2000 message (157)5.6.5UE Information (158)5.6.5.1General (158)5.6.5.2Initiation (158)5.6.5.3Reception of the UEInformationRequest message (158)5.6.6 Logged Measurement Configuration (159)5.6.6.1General (159)5.6.6.2Initiation (160)5.6.6.3Reception of the LoggedMeasurementConfiguration by the UE (160)5.6.6.4T330 expiry (160)5.6.7 Release of Logged Measurement Configuration (160)5.6.7.1General (160)5.6.7.2Initiation (160)5.6.8 Measurements logging (161)5.6.8.1General (161)5.6.8.2Initiation (161)5.6.9In-device coexistence indication (163)5.6.9.1General (163)5.6.9.2Initiation (164)5.6.9.3Actions related to transmission of InDeviceCoexIndication message (164)5.6.10UE Assistance Information (165)5.6.10.1General (165)5.6.10.2Initiation (166)5.6.10.3Actions related to transmission of UEAssistanceInformation message (166)5.6.11 Mobility history information (166)5.6.11.1General (166)5.6.11.2Initiation (166)5.6.12RAN-assisted WLAN interworking (167)5.6.12.1General (167)5.6.12.2Dedicated WLAN offload configuration (167)5.6.12.3WLAN offload RAN evaluation (167)5.6.12.4T350 expiry or stop (167)5.6.12.5Cell selection/ re-selection while T350 is running (168)5.6.13SCG failure information (168)5.6.13.1General (168)5.6.13.2Initiation (168)5.6.13.3Actions related to transmission of SCGFailureInformation message (168)5.6.14LTE-WLAN Aggregation (169)5.6.14.1Introduction (169)5.6.14.2Reception of LWA configuration (169)5.6.14.3Release of LWA configuration (170)5.6.15WLAN connection management (170)5.6.15.1Introduction (170)5.6.15.2WLAN connection status reporting (170)5.6.15.2.1General (170)5.6.15.2.2Initiation (171)5.6.15.2.3Actions related to transmission of WLANConnectionStatusReport message (171)5.6.15.3T351 Expiry (WLAN connection attempt timeout) (171)5.6.15.4WLAN status monitoring (171)5.6.16RAN controlled LTE-WLAN interworking (172)5.6.16.1General (172)5.6.16.2WLAN traffic steering command (172)5.6.17LTE-WLAN aggregation with IPsec tunnel (173)5.6.17.1General (173)5.7Generic error handling (174)5.7.1General (174)5.7.2ASN.1 violation or encoding error (174)5.7.3Field set to a not comprehended value (174)5.7.4Mandatory field missing (174)5.7.5Not comprehended field (176)5.8MBMS (176)5.8.1Introduction (176)5.8.1.1General (176)5.8.1.2Scheduling (176)5.8.1.3MCCH information validity and notification of changes (176)5.8.2MCCH information acquisition (178)5.8.2.1General (178)5.8.2.2Initiation (178)5.8.2.3MCCH information acquisition by the UE (178)5.8.2.4Actions upon reception of the MBSFNAreaConfiguration message (178)5.8.2.5Actions upon reception of the MBMSCountingRequest message (179)5.8.3MBMS PTM radio bearer configuration (179)5.8.3.1General (179)5.8.3.2Initiation (179)5.8.3.3MRB establishment (179)5.8.3.4MRB release (179)5.8.4MBMS Counting Procedure (179)5.8.4.1General (179)5.8.4.2Initiation (180)5.8.4.3Reception of the MBMSCountingRequest message by the UE (180)5.8.5MBMS interest indication (181)5.8.5.1General (181)5.8.5.2Initiation (181)5.8.5.3Determine MBMS frequencies of interest (182)5.8.5.4Actions related to transmission of MBMSInterestIndication message (183)5.8a SC-PTM (183)5.8a.1Introduction (183)5.8a.1.1General (183)5.8a.1.2SC-MCCH scheduling (183)5.8a.1.3SC-MCCH information validity and notification of changes (183)5.8a.1.4Procedures (184)5.8a.2SC-MCCH information acquisition (184)5.8a.2.1General (184)5.8a.2.2Initiation (184)5.8a.2.3SC-MCCH information acquisition by the UE (184)5.8a.2.4Actions upon reception of the SCPTMConfiguration message (185)5.8a.3SC-PTM radio bearer configuration (185)5.8a.3.1General (185)5.8a.3.2Initiation (185)5.8a.3.3SC-MRB establishment (185)5.8a.3.4SC-MRB release (185)5.9RN procedures (186)5.9.1RN reconfiguration (186)5.9.1.1General (186)5.9.1.2Initiation (186)5.9.1.3Reception of the RNReconfiguration by the RN (186)5.10Sidelink (186)5.10.1Introduction (186)5.10.1a Conditions for sidelink communication operation (187)5.10.2Sidelink UE information (188)5.10.2.1General (188)5.10.2.2Initiation (189)5.10.2.3Actions related to transmission of SidelinkUEInformation message (193)5.10.3Sidelink communication monitoring (195)5.10.6Sidelink discovery announcement (198)5.10.6a Sidelink discovery announcement pool selection (201)5.10.6b Sidelink discovery announcement reference carrier selection (201)5.10.7Sidelink synchronisation information transmission (202)5.10.7.1General (202)5.10.7.2Initiation (203)5.10.7.3Transmission of SLSS (204)5.10.7.4Transmission of MasterInformationBlock-SL message (205)5.10.7.5Void (206)5.10.8Sidelink synchronisation reference (206)5.10.8.1General (206)5.10.8.2Selection and reselection of synchronisation reference UE (SyncRef UE) (206)5.10.9Sidelink common control information (207)5.10.9.1General (207)5.10.9.2Actions related to reception of MasterInformationBlock-SL message (207)5.10.10Sidelink relay UE operation (207)5.10.10.1General (207)5.10.10.2AS-conditions for relay related sidelink communication transmission by sidelink relay UE (207)5.10.10.3AS-conditions for relay PS related sidelink discovery transmission by sidelink relay UE (208)5.10.10.4Sidelink relay UE threshold conditions (208)5.10.11Sidelink remote UE operation (208)5.10.11.1General (208)5.10.11.2AS-conditions for relay related sidelink communication transmission by sidelink remote UE (208)5.10.11.3AS-conditions for relay PS related sidelink discovery transmission by sidelink remote UE (209)5.10.11.4Selection and reselection of sidelink relay UE (209)5.10.11.5Sidelink remote UE threshold conditions (210)6Protocol data units, formats and parameters (tabular & ASN.1) (210)6.1General (210)6.2RRC messages (212)6.2.1General message structure (212)–EUTRA-RRC-Definitions (212)–BCCH-BCH-Message (212)–BCCH-DL-SCH-Message (212)–BCCH-DL-SCH-Message-BR (213)–MCCH-Message (213)–PCCH-Message (213)–DL-CCCH-Message (214)–DL-DCCH-Message (214)–UL-CCCH-Message (214)–UL-DCCH-Message (215)–SC-MCCH-Message (215)6.2.2Message definitions (216)–CounterCheck (216)–CounterCheckResponse (217)–CSFBParametersRequestCDMA2000 (217)–CSFBParametersResponseCDMA2000 (218)–DLInformationTransfer (218)–HandoverFromEUTRAPreparationRequest (CDMA2000) (219)–InDeviceCoexIndication (220)–InterFreqRSTDMeasurementIndication (222)–LoggedMeasurementConfiguration (223)–MasterInformationBlock (225)–MBMSCountingRequest (226)–MBMSCountingResponse (226)–MBMSInterestIndication (227)–MBSFNAreaConfiguration (228)–MeasurementReport (228)–MobilityFromEUTRACommand (229)–Paging (232)–ProximityIndication (233)–RNReconfiguration (234)–RNReconfigurationComplete (234)–RRCConnectionReconfiguration (235)–RRCConnectionReconfigurationComplete (240)–RRCConnectionReestablishment (241)–RRCConnectionReestablishmentComplete (241)–RRCConnectionReestablishmentReject (242)–RRCConnectionReestablishmentRequest (243)–RRCConnectionReject (243)–RRCConnectionRelease (244)–RRCConnectionResume (248)–RRCConnectionResumeComplete (249)–RRCConnectionResumeRequest (250)–RRCConnectionRequest (250)–RRCConnectionSetup (251)–RRCConnectionSetupComplete (252)–SCGFailureInformation (253)–SCPTMConfiguration (254)–SecurityModeCommand (255)–SecurityModeComplete (255)–SecurityModeFailure (256)–SidelinkUEInformation (256)–SystemInformation (258)–SystemInformationBlockType1 (259)–UEAssistanceInformation (264)–UECapabilityEnquiry (265)–UECapabilityInformation (266)–UEInformationRequest (267)–UEInformationResponse (267)–ULHandoverPreparationTransfer (CDMA2000) (273)–ULInformationTransfer (274)–WLANConnectionStatusReport (274)6.3RRC information elements (275)6.3.1System information blocks (275)–SystemInformationBlockType2 (275)–SystemInformationBlockType3 (279)–SystemInformationBlockType4 (282)–SystemInformationBlockType5 (283)–SystemInformationBlockType6 (287)–SystemInformationBlockType7 (289)–SystemInformationBlockType8 (290)–SystemInformationBlockType9 (295)–SystemInformationBlockType10 (295)–SystemInformationBlockType11 (296)–SystemInformationBlockType12 (297)–SystemInformationBlockType13 (297)–SystemInformationBlockType14 (298)–SystemInformationBlockType15 (298)–SystemInformationBlockType16 (299)–SystemInformationBlockType17 (300)–SystemInformationBlockType18 (301)–SystemInformationBlockType19 (301)–SystemInformationBlockType20 (304)6.3.2Radio resource control information elements (304)–AntennaInfo (304)–AntennaInfoUL (306)–CQI-ReportConfig (307)–CQI-ReportPeriodicProcExtId (314)–CrossCarrierSchedulingConfig (314)–CSI-IM-Config (315)–CSI-IM-ConfigId (315)–CSI-RS-Config (317)–CSI-RS-ConfigEMIMO (318)–CSI-RS-ConfigNZP (319)–CSI-RS-ConfigNZPId (320)–CSI-RS-ConfigZP (321)–CSI-RS-ConfigZPId (321)–DMRS-Config (321)–DRB-Identity (322)–EPDCCH-Config (322)–EIMTA-MainConfig (324)–LogicalChannelConfig (325)–LWA-Configuration (326)–LWIP-Configuration (326)–RCLWI-Configuration (327)–MAC-MainConfig (327)–P-C-AndCBSR (332)–PDCCH-ConfigSCell (333)–PDCP-Config (334)–PDSCH-Config (337)–PDSCH-RE-MappingQCL-ConfigId (339)–PHICH-Config (339)–PhysicalConfigDedicated (339)–P-Max (344)–PRACH-Config (344)–PresenceAntennaPort1 (346)–PUCCH-Config (347)–PUSCH-Config (351)–RACH-ConfigCommon (355)–RACH-ConfigDedicated (357)–RadioResourceConfigCommon (358)–RadioResourceConfigDedicated (362)–RLC-Config (367)–RLF-TimersAndConstants (369)–RN-SubframeConfig (370)–SchedulingRequestConfig (371)–SoundingRS-UL-Config (372)–SPS-Config (375)–TDD-Config (376)–TimeAlignmentTimer (377)–TPC-PDCCH-Config (377)–TunnelConfigLWIP (378)–UplinkPowerControl (379)–WLAN-Id-List (382)–WLAN-MobilityConfig (382)6.3.3Security control information elements (382)–NextHopChainingCount (382)–SecurityAlgorithmConfig (383)–ShortMAC-I (383)6.3.4Mobility control information elements (383)–AdditionalSpectrumEmission (383)–ARFCN-ValueCDMA2000 (383)–ARFCN-ValueEUTRA (384)–ARFCN-ValueGERAN (384)–ARFCN-ValueUTRA (384)–BandclassCDMA2000 (384)–BandIndicatorGERAN (385)–CarrierFreqCDMA2000 (385)–CarrierFreqGERAN (385)–CellIndexList (387)–CellReselectionPriority (387)–CellSelectionInfoCE (387)–CellReselectionSubPriority (388)–CSFB-RegistrationParam1XRTT (388)–CellGlobalIdEUTRA (389)–CellGlobalIdUTRA (389)–CellGlobalIdGERAN (390)–CellGlobalIdCDMA2000 (390)–CellSelectionInfoNFreq (391)–CSG-Identity (391)–FreqBandIndicator (391)–MobilityControlInfo (391)–MobilityParametersCDMA2000 (1xRTT) (393)–MobilityStateParameters (394)–MultiBandInfoList (394)–NS-PmaxList (394)–PhysCellId (395)–PhysCellIdRange (395)–PhysCellIdRangeUTRA-FDDList (395)–PhysCellIdCDMA2000 (396)–PhysCellIdGERAN (396)–PhysCellIdUTRA-FDD (396)–PhysCellIdUTRA-TDD (396)–PLMN-Identity (397)–PLMN-IdentityList3 (397)–PreRegistrationInfoHRPD (397)–Q-QualMin (398)–Q-RxLevMin (398)–Q-OffsetRange (398)–Q-OffsetRangeInterRAT (399)–ReselectionThreshold (399)–ReselectionThresholdQ (399)–SCellIndex (399)–ServCellIndex (400)–SpeedStateScaleFactors (400)–SystemInfoListGERAN (400)–SystemTimeInfoCDMA2000 (401)–TrackingAreaCode (401)–T-Reselection (402)–T-ReselectionEUTRA-CE (402)6.3.5Measurement information elements (402)–AllowedMeasBandwidth (402)–CSI-RSRP-Range (402)–Hysteresis (402)–LocationInfo (403)–MBSFN-RSRQ-Range (403)–MeasConfig (404)–MeasDS-Config (405)–MeasGapConfig (406)–MeasId (407)–MeasIdToAddModList (407)–MeasObjectCDMA2000 (408)–MeasObjectEUTRA (408)–MeasObjectGERAN (412)–MeasObjectId (412)–MeasObjectToAddModList (412)–MeasObjectUTRA (413)–ReportConfigEUTRA (422)–ReportConfigId (425)–ReportConfigInterRAT (425)–ReportConfigToAddModList (428)–ReportInterval (429)–RSRP-Range (429)–RSRQ-Range (430)–RSRQ-Type (430)–RS-SINR-Range (430)–RSSI-Range-r13 (431)–TimeToTrigger (431)–UL-DelayConfig (431)–WLAN-CarrierInfo (431)–WLAN-RSSI-Range (432)–WLAN-Status (432)6.3.6Other information elements (433)–AbsoluteTimeInfo (433)–AreaConfiguration (433)–C-RNTI (433)–DedicatedInfoCDMA2000 (434)–DedicatedInfoNAS (434)–FilterCoefficient (434)–LoggingDuration (434)–LoggingInterval (435)–MeasSubframePattern (435)–MMEC (435)–NeighCellConfig (435)–OtherConfig (436)–RAND-CDMA2000 (1xRTT) (437)–RAT-Type (437)–ResumeIdentity (437)–RRC-TransactionIdentifier (438)–S-TMSI (438)–TraceReference (438)–UE-CapabilityRAT-ContainerList (438)–UE-EUTRA-Capability (439)–UE-RadioPagingInfo (469)–UE-TimersAndConstants (469)–VisitedCellInfoList (470)–WLAN-OffloadConfig (470)6.3.7MBMS information elements (472)–MBMS-NotificationConfig (472)–MBMS-ServiceList (473)–MBSFN-AreaId (473)–MBSFN-AreaInfoList (473)–MBSFN-SubframeConfig (474)–PMCH-InfoList (475)6.3.7a SC-PTM information elements (476)–SC-MTCH-InfoList (476)–SCPTM-NeighbourCellList (478)6.3.8Sidelink information elements (478)–SL-CommConfig (478)–SL-CommResourcePool (479)–SL-CP-Len (480)–SL-DiscConfig (481)–SL-DiscResourcePool (483)–SL-DiscTxPowerInfo (485)–SL-GapConfig (485)。

如何提高脑机接口技术中的信号稳定性

如何提高脑机接口技术中的信号稳定性

如何提高脑机接口技术中的信号稳定性在脑机接口技术(Brain-Computer Interface,BCI)领域中,信号稳定性是一个重要的挑战。

信号稳定性的提高可以有效增强脑机接口系统的性能,使其在各种实际应用中更加可靠和准确。

下面将介绍几种方法来提高脑机接口技术中的信号稳定性。

首先,信号预处理是提高信号稳定性的关键一步。

由于脑电图(Electroencephalogram,EEG)信号受到众多噪声源的干扰,例如肌肉活动、眼电活动和环境电磁干扰等,因此必须对信号进行有效的预处理。

常用的信号预处理方法包括滤波、伪迹去除和运动估计等。

滤波可以去除高频或低频噪声,以突出特定频带的信号成分;伪迹去除可以利用重采样和空间滤波等方法,消除源于肌肉活动和眼动的伪迹信号;运动估计可以通过检测和修正头部位置的变化,降低源于头部移动的伪迹信号。

其次,信号特征提取是提高信号稳定性的另一个关键环节。

在脑机接口系统中,通常需要从原始信号中提取出与特定脑活动相关的特征。

常见的信号特征包括时域特征、频域特征和时频域特征等。

时域特征包括振幅、幅值、斜率和相关系数等;频域特征包括功率谱密度、相干性和相位等;时频域特征则同时考虑了信号的时间和频率特性。

合理选择和优化特征提取方法可以有效降低信号的噪声干扰,提高信号稳定性。

此外,多模态融合是提高信号稳定性的一种有效手段。

融合不同模态的信息可以提供更完整和可靠的信号特征,从而提高脑机接口系统的性能。

例如,融合脑电图信号(EEG)和功能磁共振成像(fMRI)信号可以结合EEG高时分辨率和fMRI高空间分辨率的特点,提供更准确的脑区定位和脑活动监测;融合EEG和眼动信号可以明确用户的注意力和意图,提高脑机接口系统的控制精度和稳定性。

因此,多模态融合是提高信号稳定性的一种重要方法,可以综合利用不同模态之间的互补性和相关性。

此外,机器学习算法的应用也对提高信号稳定性具有重要意义。

在脑机接口技术中,基于机器学习的分类算法可以将提取的信号特征与预定义的类别进行关联,从而实现对脑活动的准确识别和分类。

堆叠自动编码器的训练方法详解(九)

堆叠自动编码器的训练方法详解(九)

堆叠自动编码器的训练方法详解自动编码器是一种无监督学习算法,它可以学习数据的有效表示,同时也可以用于特征提取和降维。

堆叠自动编码器(Stacked Autoencoder)是由多个自动编码器组成的深度神经网络模型,其训练方法相对于单个自动编码器更加复杂。

本文将对堆叠自动编码器的训练方法进行详细解析。

第一部分:单个自动编码器的训练在训练堆叠自动编码器之前,首先需要训练单个自动编码器。

自动编码器由编码器和解码器两部分组成,编码器将输入数据映射到隐藏层,解码器将隐藏层的表示映射回输入空间。

训练自动编码器的目标是最小化重构误差,即输入数据与解码器输出的差异。

常用的训练方法包括梯度下降和反向传播算法。

通过反向传播算法,可以计算出相对于重构误差的梯度,然后使用梯度下降算法更新自动编码器的参数。

在训练过程中,可以使用批量梯度下降或随机梯度下降来加速收敛。

第二部分:堆叠自动编码器的训练堆叠自动编码器由多个自动编码器组成,它的训练方法可以分为逐层训练和端到端训练两种方式。

逐层训练是指先训练每个单独的自动编码器,然后将它们堆叠在一起形成深度神经网络。

在逐层训练中,每个自动编码器的输入是上一层自动编码器的隐藏层表示。

通过逐层训练,可以逐步提高整个模型的性能,并且可以避免深度神经网络训练中的梯度消失和梯度爆炸问题。

端到端训练是指直接对堆叠自动编码器进行整体训练,而不是分阶段训练每个单独的自动编码器。

端到端训练可以更好地利用数据的信息,但是训练复杂度更高,需要更多的计算资源和更长的训练时间。

第三部分:正则化和优化在训练堆叠自动编码器时,为了提高模型的泛化能力和避免过拟合,可以采用正则化技术和优化算法。

正则化技术包括L1正则化和L2正则化,它们可以通过惩罚模型复杂度来减少过拟合。

此外,还可以使用dropout技术来随机丢弃隐藏层的部分神经元,以降低模型的复杂度。

优化算法是指在训练过程中寻找最优参数的方法。

除了传统的梯度下降算法,还可以使用动量法、自适应学习率算法等更高级的优化算法来加速训练过程。

大脑神经元信号处理流程

大脑神经元信号处理流程

大脑神经元信号处理流程下载温馨提示:该文档是我店铺精心编制而成,希望大家下载以后,能够帮助大家解决实际的问题。

文档下载后可定制随意修改,请根据实际需要进行相应的调整和使用,谢谢!并且,本店铺为大家提供各种各样类型的实用资料,如教育随笔、日记赏析、句子摘抄、古诗大全、经典美文、话题作文、工作总结、词语解析、文案摘录、其他资料等等,如想了解不同资料格式和写法,敬请关注!Download tips: This document is carefully compiled by theeditor. I hope that after you download them,they can help yousolve practical problems. The document can be customized andmodified after downloading,please adjust and use it according toactual needs, thank you!In addition, our shop provides you with various types ofpractical materials,such as educational essays, diaryappreciation,sentence excerpts,ancient poems,classic articles,topic composition,work summary,word parsing,copy excerpts,other materials and so on,want to know different data formats andwriting methods,please pay attention!大脑神经元信号处理是一个复杂的过程,涉及多个步骤和机制。

以下是一般情况下大脑神经元信号处理的流程:1. 信号接收:神经元通过其树突接收来自其他神经元或感觉器官的信号。

基于神经元振荡器的极限环目标围捕算法

基于神经元振荡器的极限环目标围捕算法

目录一、概述二、神经元振荡器的基本原理三、极限环目标围捕算法的原理四、实验与结果讨论五、结论六、参考文献一、概述神经元振荡器是一种具有自我激励和抑制作用的生物振荡器,其数学模型在人工智能和控制系统中具有广泛的应用。

极限环目标围捕算法是一种基于神经元振荡器的控制策略,可以实现对目标的快速、精准的围捕。

本文将介绍神经元振荡器的基本原理,并详细阐述极限环目标围捕算法的原理及其在实验中的应用。

二、神经元振荡器的基本原理1. 神经元振荡器的生物学基础神经元振荡器是一种生物神经元内在的振荡系统,它可以通过自身内部的相互激励和抑制相互作用产生周期性的电活动。

这种振荡活动在生物神经系统中起着重要的调控作用,类似于人工控制系统中的时钟信号。

神经元振荡器的数学模型通常由一组耦合的微分方程来描述其动态特性,这些方程描述了神经元内部离子通道的开闭过程以及细胞膜电位的变化。

2. 神经元振荡器的数学模型神经元振荡器的数学模型通常采用Hodgkin-Huxley模型或FitzHugh-Nagumo模型来描述。

这些模型可以有效地捕捉到神经元振荡器的自激励和抑制特性,对振荡器的频率和幅度变化进行了准确的描述。

通过对这些数学模型的分析,可以得出神经元振荡器的稳定性条件和工作方式,为控制系统设计提供了重要的理论基础。

三、极限环目标围捕算法的原理1. 极限环控制的基本原理极限环控制是一种基于系统内部振荡器的控制策略,它利用系统的自身振荡特性来实现对目标的精准控制。

极限环控制通过调节系统的相位和幅度,使系统输出与目标信号之间保持固定的相对位置关系,从而实现目标的追踪和围捕。

在传统的控制方法中,通常需要对系统进行建模和参数调节,而极限环控制则更加注重对系统的动态特性进行分析和利用。

2. 极限环目标围捕算法的设计极限环目标围捕算法是一种基于神经元振荡器的极限环控制策略,它利用神经元振荡器的自激励和抑制特性来实现对目标的围捕。

在这种算法中,系统的控制输入由神经元振荡器的输出信号决定,通过调节振荡器的频率和幅度,可以实现对目标的快速、精准的围捕。

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Ephrin signalling controls brain size by regulating apoptosis of neural progenitorsVanessa Depaepe 1,Nathalie Suarez-Gonzalez 1,Audrey Dufour 1,Lara Passante 1,Jessica A Gorski 2,Kevin R.Jones 2,Catherine Ledent 1&Pierre Vanderhaeghen 1Mechanisms controlling brain size include the regulation of neural progenitor cell proliferation,differentiation,survival and migration 1,2.Here we show that ephrin-A/EphA receptor signal-ling plays a key role in controlling the size of the mouse cerebral cortex by regulating cortical progenitor cell apoptosis.In vivo gain of EphA receptor function,achieved through ectopic expression of ephrin-A5in early cortical progenitors expressing EphA7,caused a transient wave of neural progenitor cell apoptosis,resulting in premature depletion of progenitors and a subsequent dramatic decrease in cortical size.In vitro treatment with soluble ephrin-A ligands similarly induced the rapid death of cultured dissociated cortical progenitors in a caspase-3-dependent manner,thereby confirming a direct effect of ephrin/Eph signalling on apoptotic cascades.Conversely,in vivo loss of EphA function,achieved through EphA7gene disruption,caused a reduction in apoptosis occurring normally in forebrain neural progenitors,resulting in an increase in cortical size and,in extreme cases,exencephalic forebrain overgrowth.Together,these results identify ephrin/Eph signalling as a physiological trigger for apoptosis that can alter brain size and shape by regulating the number of neural progenitors.Ephrin and Eph receptor genes have been implicated in the control of cell and axon guidance in many neural systems 3–5.To identify additional roles for ephrin/Eph genes in the developing forebrain,we generated a mouse transgenic line that allows ectopic expression of ephrin-A5under the control of the EphA7receptor promoter,taking advantage of their complementary patterns of expression.Ephrin-A5and EphA7are expressed as early as embryonic day (E)10.5in the forebrain.EphA7is preferentially expressed in cortical progenitors,and ephrin-A5is expressed in progenitors of the ventral telencepha-lon and the medial dorsal telencephalon (Fig.1a).Perinatally,they are expressed in complementary gradients in the cerebral cortex (Fig.1a and ref.6).To faithfully reproduce the EphA7expression pattern of the ephrin-A5transgene without interfering with EphA7function,we used a transgenic bacterial artificial chromosome (BAC)approach,in which a conditional,Cre-recombinase-dependent,lox/enhanced green fluorescent protein (eGFP)/lox/ephrin-A5expression cassette was placed under the control of EphA7regulatory elements using BAC recombineering 7,8(Fig.1b).The resulting transgenic mice (TGA7A5)expressed the conditional cassette in a pattern very similar to the endogenous pattern of EphA7,both at early and later stages of cortical development,as assessed by expression of the eGFP transgene (Fig.1c,d).No expression of the Flag-ephrin-A5transgene was detected in the absence of Cre-recombinase.To drive expression of the ephrin-A5transgene specifically in the developing cortex,we crossed this line with an Emx1IREScre line (Emx1-Cre)that promotes efficient and specificCre-recombination in the dorsal telencephalon from E10.5(ref.9).Although TGA7A5mice and Emx1-Cre mice did not show any overt phenotype (ref.9and data not shown),mice doubly transgenic for TGA7A5and Emx1-Cre (TG/Emx1-Cre)died at birth and showed a severe reduction in cerebral hemisphere size (up to threefold by E16.5;Fig.2a),with the rest of the brain appearing normal (Fig.2a,b).This reduction in cortical size was clearly visible as early as E12.5(Fig.2a,b),and was accompanied by a decrease in the tangential extent and radial thickness of the post-mitotic cortical plate at later stages (Fig.2b),suggesting that the phenotype resulted from an impairment in early neurogenesis in the dorsal forebrain.Such a phenotype could result from dysregulation of cell prolifer-ation,migration,differentiation or death.Staining for nestin revealed no decrease in the density of cortical progenitor cells (Fig.2c).To detect abnormal patterns of proliferation or cell cycle progression among cortical progenitors,we used 5-bromodeoxyur-idine (BrdU)pulse-labellings combined with Ki67staining (to mark proliferating cells).Both long and short time courses of BrdU/Ki67labelling showed a normal labelling index (the proportion of BrdU-labelled cells among Ki67þprogenitors)for cortical progenitors,suggesting that their proliferative pattern and cell cycle were unim-paired in the mutant,even though their total number was reduced (Fig.2c,e).Next,we measured the fraction of cells leaving the mitotic cycle (the quitting fraction,or the proportion of Ki672post-mitotic cells among BrdU-labelled cells)10.No difference was observed between the controls and mutants,suggesting that cortical neuro-genesis per se was occurring normally in the mutants (Fig.2e).In addition,analysis of pan-neural (MAP-2and Tuj1)and specific (reelin,calretinin,Tbr1,and Brn1)markers showed a normal proportion and position of neurons and progenitors at all stages examined (see Fig.2c,d and Supplementary Fig.1),confirming that neural differentiation and migration appeared to take place normally in TG/Emx1-Cre mutants.We next looked for dysregulation of cell death in the mutants (Fig.3).A large increase in the number of dying early cortical progenitors was observed at E11.5and E12.5,as labelled by terminal deoxynucleotidyltransferase-mediated dUTP nick end labelling (TUNEL)(Fig.3a,b).A similar increase was observed for cells immunoreactive for activated caspase-3,one of the main effectors of developmental apoptotic death 11,12(Fig.3a,b).Co-labelling for these apoptosis markers and nestin showed that the bulk (more than 90%)of dying cells were cortical progenitors (Fig.3c).This apoptosis was restricted both spatially and temporally in a pattern similar to that observed for EphA7and the ephrin-A5transgene 6(Figs 1a,c,d and 3b).Specifically,apoptosis was restricted to the developing cerebral cortex (Fig.3a,b)and was transient,peaking at E11.5–E12.5,reduced by E14.5and essentially absent by E17.5(Fig.3d,e),except for theLETTERS1Institut de Recherches Interdisciplinaires en Biologie Humaine et Mole´culaire (IRIBHM),University of Brussels,Campus Erasme,808Route de Lennik,B-1070Brussels,Belgium.2Department of Molecular,Cellular,and Developmental Biology,University of Colorado,Boulder,Colorado 80309,USA.activation of caspase-3in a few post-mitotic neurons in the cortical plate(Fig.3d).The rapid and transient nature of the induction of apoptosis of cortical progenitors upon ectopic expression of ephrin-A5,together with the lack of evidence for significant disruption of cell migration or differentiation,strongly indicated a direct pro-apoptotic effect of ephrin/Eph signalling in these cells.To test this hypothesis,we turned to an in vitro assay in which cultured cortical progenitors (at E12–E13,a stage at which most cortical progenitors express EphA7(data not shown))were challenged with EphA agonists (consisting of clustered ephrin-A5–Fc fragment fusion proteins). Ephrin stimulation of early cortical progenitors resulted in a rapid induction of cell death,as measured by TUNEL staning(Fig.3f).This cell death was inhibited by the pan-caspase inhibitor z-VAD-fmk (Fig.3f),and was concurrent with an increase in caspase-3activity (Fig.3g),indicating that ephrins can directly trigger cortical progenitor cell death through a caspase-dependent pathway. These gain-of-function data suggested a potentially important function for ephrin/Eph signalling in the regulation of progenitor cell death in the developing forebrain.To test for a physiological role of Eph signalling in this context,we next turned to a loss-of-function analysis,using EphA7knockout(EphA72/2)mice13.We found an approximately twofold decrease in cortical progenitor cell death at mid-neurogenesis(E13.5,which corresponds to a peak of apoptosis during cortical neurogenesis14,15),as assessed by quantification of TUNEL-positive and activated caspase-3-positive cortical progeni-tors,double-stained for nestin(Fig.4a–c).Notably,analysis of the labelling index,quitting fraction,and the expression of specific neural markers at the same stage of corticogenesis indicated that neural proliferation and differentiation proceeded normally in EphA72/2mutants(see Fig.4g and Supplementary Fig.2).In addition,EphA72/2mutants showed a significant increase inFigure1|Generation of EphA7/ephrin-A5transgenic mice.a,In situ hybridization(ISH)on forebrain sections shows complementary expression patterns of ephrin-A5and EphA7at E10.5and P0.DT,dorsal telencephalon; VT,ventral telencephalon.Arrowheads show the approximate boundaries of the neocortex.b,A BAC centred on EphA7exon-1was targeted with a conditional expression cassette to generate a transgenic mouse line (TGA7A5)allowing expression of eGFP under the control of EphA7regulatory sequences.After crossing this line with Emx1-Cre mice(TG/ Emx1-Cre)the eGFP cassette is removed by Cre recombinase,allowing expression of ephrin-A5in the DT.c,d,ISH on E12.5(c)and P0(d)brain sections illustrates the distribution of ephrin-A5,EphA7and the eGFP transgene.Arrowheads indicate boundaries of expression for ephrin-A5 versus EphA7/eGFP.Medial(M)is to the left(a,c),caudal is to the left(d), dorsal(D)is at the top in(a,c,d).Scale bar,200m m.NATURE|Vol435|30June2005LETTERSFigure2|Reduction in cortical size in TG/Emx1-Cre mutants.a,FromE14.5to P0the size of the cortex(Cx,arrows)of TG/Emx1-Cre mice is severely reduced,but the rest of the brain(MB,midbrain;HB,hindbrain)is normal in size.Quantification of cortical size at E16.5reveals a threefold reduction in TG/Emx1-Cre mice(results represent mean corticalarea^s.e.m.;P¼0.0022,n¼3per genotype).b,Coronal brain sections stained with cresyl violet,illustrating the reduction of the cortical plate in TG/Emx1-Cre mice(arrows and arrowheads).Scale bar,500m m.c,d,Coronal brain sections of mice at E12.5(c),E14.5and E16.5(d)stained with nestin,BrdU,Tuj1and MAP2.Despite the size reduction(red arrowheads),the overall cellular organization in the cortical plate(CP), intermediate zone(IZ)and ventricular zone(VZ)is normal in TG/Emx1-Cre mutants.Arrows in c indicate nestin-and BrdU-stained cortical cells. Scale bar in c and d,250m m.e,BrdU labelling(green)and Ki67staining (red)reveal normal labelling index and quitting fraction in the cortex of TG/Emx1-Cre mutants.PP,cortical preplate.Results represent the mean number^s.e.m.of counted cells(detected by BrdU or Ki67)from three animals per genotype.P¼0.2and0.9for labelling index after24h and1h, respectively;P¼0.4for quitting fraction.LETTERS NATURE|Vol435|30June2005Figure3|Ephrin-A/EphA stimulation triggers cortical progenitor cell apoptosis in vivo and in vitro.a,b,At E11.5(a)and E12.5(b),the DT of TG/Emx1-Cre animals shows an increase in the number of apoptotic cells,as labelled by TUNEL(red)or immunostained for activated caspase-3(red; Hoechst stain in green).Levels of apoptotic cells correlate with the expression of the ephrin-A5transgene(Flag-ephrin-A5,detected by ISH). Arrowheads indicate the limits of DT versus VT.c,Dual labelling ofTG/Emx1-Cre cortex with nestin(green)and caspase-3(red)shows that most apoptotic cells are nestinþ(white arrows).d,At later stages(E17.5),no increase in apoptosis is detected in the VZ,but a few apoptotic cells are found in the CP.Scale bar in b and d,125m m.e,Quantification of TUNELþcells in the cortex.Results represent mean number^s.e.m.of TUNELþcells normalized to the number of brain sections used(n¼3animals per genotype).Single asterisk,P¼0.02;two asterisks,P¼0.005;three asterisks,P,0.0001.f,Treatment of dissociated cortical progenitors with clustered ephrin-A5–Fc(100nM)induces a rapid increase in cell death, which is inhibited by the pan-caspase inhibitor z-V AD-fmk.Results represent the mean value^s.e.m.from six independent experiments performed in duplicate.Single asterisk,P¼0.0112(n¼6);two asterisks, P¼0.0065(n¼6).g,Clustered ephrin-A5–Fc(100nM)also induces a rapid increase in caspase-3activity.Single asterisk,P¼0.0411(n¼11);two asterisks,P¼0.0021(n¼11).Results represent the mean value^s.e.m. from11independent experiments performed in duplicate.All values are normalized to apoptosis under control conditions(100nM clustered Fc fragments).NATURE|Vol435|30June2005LETTERSFigure4|Decrease in cortical progenitor cell apoptosis and increase in forebrain size in EphA72/2mutants.a,Coronal brain sections immunostained for activated caspase-3(red,Hoechst in green)illustrate the decrease in apoptotic cell numbers in mutant cortex.Scale bar,125m m. b,Co-staining with nestin(green)and TUNEL(red)shows that most apoptotic cells correspond to nestinþcortical progenitors(white arrows). c,Quantification of cell death in E13.5EphA72/2and EphA7þ/2littermates. Results show mean values^s.e.m.of counted cells normalized to the number of brain sections counted(n¼5–7animals of each genotype). Single asterisk,P¼0.030(n¼5per genotype);two asterisks,P¼0.031 (n¼7per genotype).d,Results represent the mean value^s.e.m.of the cortical area at E13.5in EphA72/2and EphA7þ/2littermates,measured at two rostro-caudal levels(posterior and anterior).Single asterisk,P¼0.030; two asterisks,P¼0.004;three asterisks,P¼0.006(n¼7per genotype). e,f,Forebrain overgrowth in some EphA72/2mice,with ectopic proliferation(arrows in f)and cortical foldings(arrowhead in f).Scale bar, 250m m.g,BrdU labelling(green,performed after1h at E11.5or24h at E13.5)and Ki67staining(red).Labelling index and quitting fraction were normal in the cortex of EphA72/2mutants.Results represent the mean value^s.e.m.of counted cells(n¼5animals per genotype).P¼0.3and 0.47for the labelling index after24h and1h,respectively;P¼0.4for the quitting fraction.LETTERS NATURE|Vol435|30June2005cortical size(,20%,at different rostro-caudal levels at E13.5) (Fig.4d).Moreover,in a small proportion of cases(10%), EphA72/2embryos showed exencephalic overgrowth of forebrain tissue(Fig.4e)both in the ventral forebrain and cerebral cortex, characterized by heterotopic foci of proliferation and aberrant cortical foldings(Fig.4f).Together,the data indicate that ephrin/Eph signalling triggers pro-apoptotic pathways in early cortical progenitors,thereby controlling their number,and hence thefinal size of the forebrain.Although the prominent role of programmed cell death of post-mitotic neurons in brain development has been well established,the physiological meaning of apoptosis in neural progenitors has remained less clear11.Its influence on brain size was revealed by the analysis of mice in which apoptosis effectors and regulators have been knocked out:caspase-3–9and Apaf1mutants all display a severe exencephalic overgrowth of brain structures and reduction in neural progenitor apoptosis11,12,strikingly reminiscent of our observations in some EphA72/2mutants(Fig.4e,f).Although the low penetrance of this extreme phenotype did not allow us to establish a strict correlation with abnormal apoptosis rates,it probably results from a more severe dysregulation of cell death at earlier stages of forebrain development, as previously described for caspase mutants.A recent study identified caspases-3–9among genes that underwent positive selection during primate evolution16,suggesting that regulation of cell death might be one of the mechanisms underlying the expansion of the human cerebral cortex.Region-specific apoptosis of neural progenitors has also recently been proposed as a mechanism to restrict in time and space the size of distinct neural stem cell lineages in the Drosophila central nervous system17.In this context,future work will be needed to determine which ephrin ligand(s)interact physiologically with EphA7during early cortical neurogenesis.Ephrin-A5is present in the ventral telencephalon(see Fig.1and Supplementary Fig.3), suggesting that tangentially migrating ventral neurons could display ephrin-A5in the developing cortex.Ephrin-A3,expressed early in the cortical plate,and ephrin-A2,expressed in the ventricular zone (Supplementary Fig.3),could also act synergistically as cortical EphA7-ligands to provide spatial control of neural progenitor apoptosis.Ephrins have previously been proposed to control cell survival in vitro18,19,but with no physiological implication of ephrins in programmed cell death.Recent data have implicated apoptosis effectors and regulators in the control of axon or cell guidance20,21. Conversely,other cell and axon guidance factors have been shown to be involved in the control of cell death during development and in oncogenesis22–26.In most cases,apoptosis was shown to result from lack of activation of the receptors by their ligand,leading to the concept of dependence receptors.However,in the case of ephrins,apoptosis seems to result from direct stimulation by the ligand,similarly to Fas-ligand or neurotrophin-induced cell death27,28.Ephrin/Eph signalling was recently reported to mediate an anti-proliferative effect on adult neural progenitors,and thereby to influence neurogenesis in the adult olfactory bulb29.However,our study demonstrates a direct pro-apoptotic effect of ephrins on embryonic cortical progenitors,with no influence on their prolifer-ation.This further illustrates that ephrins,like neurotrophins,have evolved as pleiotropic factors that can control very different func-tions depending on the cellular context.Although the mechanisms allowing ephrin signalling to control guidance,apoptosis or prolifer-ation in a cell-specific manner remain unknown,the identification of ephrin/Eph receptor genes as positive regulators of apoptosis during forebrain neurogenesis uncovers a novel signalling pathway that could potentially be involved in other aspects of developmental or stem cell biology,and in oncogenesis.METHODSTransgenic mice.Generation and genotyping of Emx1IREScre(Emx1-Cre)knock-in and EphA7knockout mice were described previously9,13.For the generation of TGA7A5mice,a BAC homologous recombination method was used7,8(see Supplementary Information for details).A BAC clone of200 kilobases(kb),centred on the Epha7gene,was targeted with a conditional cassette containing an eGFP expression cassetteflanked by loxP sites,followed by Flag-tagged human ephrin-A5complementary DNA and a kanamycin-resistance cassette(Fig.1b).Homologous recombinant BACs,in which the first exon was replaced by the conditional cassette,were obtained using established methods7.TGA7A5mice were generated using microinjection of the recombinant BAC in C57BL/6£CBA F1zygotes and were screened using Southern blotting and polymerase chain reaction(PCR).In situ RNA hybridization and immunohistochemistry.In situ RNA hybrid-ization using digoxigenin-labelled RNA probes onfixed brain cryosections was performed as described30.Immunodetection was performed using standard methods(antibodies used are described in the Supplementary Methods).All stainings were performed on at least three embryos from each genotype tested.Quantitative studies of cell proliferation,cell cycle exit and cortical size.For BrdU labelling,timed-pregnant female mice were injected intraperitoneally with a single pulse(50mg kg21body weight)of BrdU,killed after1h or24h,and embryosfixed by perfusion with4%paraformaldehyde.Simultaneous staining of Ki67and BrdU,and quantification of labelling index and quitting fraction were performed according to the methods in ref.10.For each brain analysed,at least400cells,distributed across four sections,were counted.To quantify cortical size,cortical area was measured on two sets of six sections for each animal, corresponding to definedfiduciary marks(rostral pole of the thalamus,caudal pole of the internal caspule).Statistical analyses were performed using Student’s t test.Culture of dissociated cortical progenitors.Cortex was dissected from E12.5 embryos and dissociated mechanically in L15medium(Gibco)containing 30mM glucose.The suspension was centrifuged at2,000g for4min at208C and the pellet resuspended in culture medium(70%basal Eagle medium,25% Hanks’balanced salt solution,25mM glucose,1mM glutamine,50U ml21 penicillin,50m g ml21streptomycin,5%horse serum).Dissociated cortical cells were plated at a density of6–8£105cells per well in6-well plates pre-coated with poly-D-lysine(33m g ml21)and laminin(3m g ml21).Cultures were main-tained for24h in a humidified atmosphere at5%CO2,378C,then stimulated with100nM preclustered ephrin-A5–Fc or control Fc fragment,with or without 40m M z-V AD-fmk(R&D Systems).After treatment,cells were eitherfixed in4% paraformaldehyde in PBS for15min at room temperature(for TUNEL assays) or trypsinized(for caspase-3activity assays).TUNEL detection and caspase activity assays.TUNEL assays were performed using a commercially available kit and following to manufacturer’s instructions (TMR red,Roche Diagnostics).The number of apoptotic cells(detected by TUNEL assay and activated caspase-3immunoreactivity)was counted through-out the cerebral cortex in EphA72/2and EphA7þ/2littermates,and normalized to the number of brain sections analysed.For in vitro assays,the percentage of apoptotic cells was determined by counting the number of TUNEL-positive cells in1,000cells(visualized by Hoechst staining)for each duplicate from each independent experiment.Enzymatic assays for caspase-3activity were per-formed using a commercially available kit according to manufacturer’s 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Supplementary Information is linked to the online version of the paper at /nature.Acknowledgements We thank G.Vassart for continuous support and interest, and members of IRIBHM for help and advice,in particular muni,N.Gaspard,mbot,S.Pietri,J.Seibt and F.Pauwels.We also thank the Development Studies Hybridoma Bank;T.Ciossek for sharing the EphA7mutant mice;C.d’Enfert and J.-M.Ghigo for the gift of the pKOBEGA plasmid;A.de Kerchove for discussions about BAC recombineering;A.Deplano for help with pulse-field electrophoresis;S.Tajbakhsh for the gift of thefloxed eGFP cassette;F.Stewart for the gift of the frt-Neo cassette and the294-Flp bacteria;A.Goffinet for the gift of mouse reelin plasmid;R.Hevner for the gift of Tbr1 antibody;and F.Polleux for critically reading the manuscript.This work was funded by grants from the Belgian Funds for Scientific Research(FNRS and FRSM),the Belgian Queen Elizabeth Medical Foundation,the Belgian Interuniversity Attraction Poles Programme(to P.V.),and grants from the American Cancer Society and National Institutes of Health(to K.R.J).P.V.and C.L.are Research Associates,and L.P.is a Research Fellow,of the FNRS.A.D. and V.D.were supported by the Fonds pour la Recherche en Industrie et Agriculture(FRIA).Author Information Reprints and permissions information is available at/reprintsandpermissions.The authors declare no competingfinancial interests.Correspondence and requests for materials should be addressed to P.V.(pvdhaegh@ulb.ac.be).LETTERS NATURE|Vol435|30June2005。

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