MALREKC00BB318C00F中文资料
MEMORY存储芯片MT29F64G08CBABA中文规格书
Output Driver ImpedanceThe output driver impedance is selected by MR1[5,1] during initialization. The selected value is able to maintain the tight tolerances specified if proper ZQ calibration is per-formed. Output specifications refer to the default output driver unless specifically sta-ted otherwise. A functional representation of the output buffer is shown below. The out-put driver impedance R ON is defined by the value of the external reference resistor RZQ as follows:•R ON,x = RZQ /y (with RZQ = 240ȍ ±1%; x = 34ȍ or 40ȍ with y = 7 or 6, respectively)The individual pull-up and pull-down resistors R ON(PU) and R ON(PD) are defined as fol-lows:•R ON(PU) = (V DDQ - V OUT )/|I OUT |, when R ON(PD) is turned off•R ON(PD) = (V OUT )/|I OUT |, when R ON(PU) is turned offFigure 28: Output DriverOutput driverChip in drive modeV DDQV SSQV OUTDQ34 Ohm Output Driver ImpedanceThe 34ȍ driver (MR1[5, 1] = 01) is the default driver. Unless otherwise stated, all timings and specifications listed herein apply to the 34ȍ driver only. Its impedance R ON is de-fined by the value of the external reference resistor RZQ as follows: R ON34 = RZQ/7 (with nominal RZQ = 240ȍ ±1%) and is actually 34.3ȍ ±1%.Table 38: DDR3L 34 Ohm Driver Impedance CharacteristicsNotes: 1.Tolerance limits assume RZQ of 240˖ ±1% and are applicable after proper ZQ calibra-tion has been performed at a stable temperature and voltage: V DDQ = V DD ; V SSQ = V SS ).Refer to DDR3L 34 Ohm Output Driver Sensitivity (page 69) if either the temperature or the voltage changes after calibration.2.Measurement definition for mismatch between pull-up and pull-down (MM PUPD ). Meas-ure both R ON(PU) and R ON(PD) at 0.5 × V DDQ :MM PUPD = ×100R ON(PU) - R ON(PD)R ON,nom3.For IT and AT devices, the minimum values are derated by 6% when the device operates between –40°C and 0°C (T C ).A larger maximum limit will result in slightly lower minimum currents.DDR3L 34 Ohm DriverUsing Table 39, the 34ȍ driver’s current range has been calculated and summarized in Table 40 (page 68) V DD = 1.35V , Table 41 for V DD = 1.45V , and Table 42 (page 69) for V DD = 1.283V . The individual pull-up and pull-down resistors R ON34(PD) and R ON34(PU)are defined as follows:•R ON34(PD) = (V OUT )/|I OUT |; R ON34(PU) is turned off•R ON34(PU) = (V DDQ - V OUT )/|I OUT |; R ON34(PD) is turned offTable 39: DDR3L 34 Ohm Driver Pull-Up and Pull-Down Impedance CalculationsTable 40: DDR3L 34 Ohm Driver I OH /I OL Characteristics: V DD = V DDQ = DDR3L@1.35VTable 41: DDR3L 34 Ohm Driver I OH /I OL Characteristics: V DD = V DDQ = DDR3L@1.45V 4Gb: x4, x8, x16 DDR3L SDRAM Output Driver Impedance。
MEMORY存储芯片N25Q008A11EF640E中文规格书
CRC[6] =D[67]^D[66]^D[65]^D[64]^D[62]^D[61]^D[58]^D[54]^D[52]^D[51]^D[50]^D[48]^D[47]^D[46]^D[43]^D[41]^D[38]^D[37]^D[33]^D[32]^D[29]^D[28]^D[26]^D[21]^D[19]^D[17]^D[16]^D[14]^D[12]^D[10]^D[6]^D[5]^D[4];CRC[7] =D[68]^D[67]^D[66]^D[65]^D[63]^D[62]^D[59]^D[55]^D[53]^D[52]^D[51]^D[49]^D[48]^D[47]^D[44]^D[42]^D[39]^D[38]^D[34]^D[33]^D[30]^D[29]^D[27]^D[22]^D[20]^D[18]^D[17]^D[15]^D[13]^D[11]^D[7]^D[6]^D[5];nextCRC8_D72 = CRC;Burst Ordering for BL8DDR4 supports fixed WRITE burst ordering [A2:A1:A0 = 0:0:0] when write CRC is ena-bled in BL8 (fixed).CRC Data Bit MappingTable 53: CRC Data Mapping for x4 Devices, BL8Table 54: CRC Data Mapping for x8 Devices, BL8A x16 device is treated as two x8 devices; a x16 device will have two identical CRC treesimplemented. CRC[7:0] covers data bits D[71:0], and CRC[15:8] covers data bitsD[143:72].Data Bus InversionThe DATA BUS INVERSION (DBI) function is supported only for x8 and x16 configura-tions (it is not supported on x4 devices). DBI opportunistically inverts data bits, and inconjunction with the DBI_n I/O, less than half of the DQs will switch LOW for a givenDQS strobe edge. The DBI function shares a common pin with the DATA MASK (DM)and TDQS functions. The DBI function applies to either or both READ and WRITE oper-ations: Write DBI cannot be enabled at the same time the DM function is enabled, andDBI is not allowed during MPR READ operation. Valid configurations for TDQS, DM,and DBI functions are shown below.Table 59: DBI vs. DM vs. TDQS Function MatrixDBI During a WRITE OperationIf DBI_n is sampled LOW on a given byte lane during a WRITE operation, the DRAM in-verts write data received on the DQ inputs prior to writing the internal memory array. IfDBI_n is sampled HIGH on a given byte lane, the DRAM leaves the data received on theDQ inputs noninverted. The write DQ frame format is shown below for x8 and x16 con-figurations (the x4 configuration does not support the DBI function).Table 60: DBI Write, DQ Frame Format (x8)Table 61: DBI Write, DQ Frame Format (x16)Figure 115: READ Postamble2t CK Mode1t CK Mode4Gb: x8, x16 Automotive DDR4 SDRAM Programmable Preamble Modes and DQS Postambles。
MEMORY存储芯片PC28F00AG18FE中文规格书
Device MT29F32G08ABAAAWP MT29F64G08AFAAAWP MT29F128G08AJAAAWP MT29F128G08AKAAAC5 MT29F128G08AMAAAC5 MT29F256G08AUAAAC5 MT29F32G08ABCABH1 MT29F64G08AECABH1 MT29F128G08AKCABH2 MT29F128G08AMCABH2 MT29F256G08AUCABH3 MT29F64G08AECABJ1 MT29F128G08AMCABJ2 MT29F256G08AUCABJ3 MT29F32G08ABAAAWP MT29F64G08AFAAAWP MT29F128G08AJAAAWP MT29F128G08AKAAAC5 MT29F128G08AMAAAC5 MT29F256G08AUAAAC5 MT29F32G08ABCABH1 MT29F64G08AECABH1 MT29F128G08AKCABH2 MT29F128G08AMCABH2 MT29F256G08AUCABH3 MT29F64G08AECABJ1 MT29F128G08AMCABJ2 MT29F256G08AUCABJ3
Table 8: Parameter Page Data Structure (Continued)
MEMORY存储芯片MT29F128G08CFABAWP_B中文规格书
READ LOCK REGISTERThe device is first selected by driving chip select (S#) LOW. The command code for theREAD LOCK REGISTER command is followed by a 3-byte address (A23-A0) pointing toany location inside the concerned sector (or subsector). Each address bit is latched-induring the rising edge of serial clock (C). Then the value of the lock register is shiftedout on serial data output (DQ1), each bit being shifted out at a maximum frequency f C during the falling edge of C.The READ LOCK REGISTER command is terminated by driving S# HIGH at any timeduring data output.Figure 17: READ LOCK REGISTER Command SequenceDQ[0]CDQ1Don’t CareAny READ LOCK REGISTER command issued while an ERASE, PROGRAM, or WRITEcycle is in progress is rejected without any effect on the cycle that is in progress.Values of b1 and b0 after power-up are defined in the table below.Table 14: Lock Register OutPAGE ERASEThe PAGE ERASE command sets to 1 (FFh) all bits inside the chosen page. Before thePAGE ERASE command can be accepted, a WRITE ENABLE command must have beenexecuted previously. After the WRITE ENABLE command has been decoded, the devicesets the write enable latch (WEL) bit.The PAGE ERASE command is entered by driving chip select (S#) LOW, followed by thecommand code, and three address bytes on serial data input (DQ0). Any address insidethe sector is a valid address for the PAGE ERASE command. S# must be driven LOW forthe entire duration of the sequence.S# must be driven HIGH after the eighth bit of the last address byte has been latched in.Otherwise the PAGE ERASE command is not executed. As soon as S# is driven HIGH,the self-timed PAGE ERASE cycle is initiated; the cycle's duration is t PE. While the PAGEERASE cycle is in progress, the status register may be read to check the value of the writein progress (WIP) bit. The WIP bit is 1 during the self-timed PAGE ERASE cycle, and is 0when the cycle is completed. At some unspecified time before the cycle is completed,the WEL bit is reset.A PAGE ERASE command applied to a page that is hardware or software protected is notexecuted.A PAGE ERASE command while an ERASE, PROGRAM, or WRITE cycle is in progress isrejected without having any effects on the cycle that is in progress.If RESET# is driven LOW while a PAGE ERASE cycle is in progress, the PAGE ERASE cycleis interrupted and the programmed data may be corrupted. On RESET going LOW, thedevice enters the reset mode and a time of t RHSL is then required before the device canbe reselected by driving Chip Select (S#) LOW.Figure 21: PAGE ERASE Command SequenceCDQ0Notes: 1.Address bits A23-A18 are don't care in the M25PE20. Address bits A23-A17 are don'tcare in the M25PE10.2.Address bits A23-A19 are don't care.3.Address bits A23-A20 are don't care.SUBSECTOR ERASEThe SUBSECTOR ERASE command sets to 1 (FFh) all bits inside the chosen subsector.Before the SUBSECTOR ERASE command can be accepted, a WRITE ENABLE com-mand must have been executed previously. After the WRITE ENABLE command has been decoded, the device sets the write enable latch (WEL) bit.The SUBSECTOR ERASE command is entered by driving chip select (S#) LOW, followed by the command code, and three address bytes on serial data input (DQ0). Any address inside the subsector is a valid address for the SUBSECTOR ERASE command. S# must be driven LOW for the entire duration of the sequence.S# must be driven HIGH after the eighth bit of the last address byte has been latched in.Otherwise the SUBSECTOR ERASE command is not executed. As soon as S# is driven HIGH, the self-timed SUBSECTOR ERASE cycle is initiated; the cycle's duration is t SSE .While the SUBSECTOR ERASE cycle is in progress, the status register may be read to check the value of the write in progress (WIP) bit. The WIP bit is 1 during the self-timed SUBSECTOR ERASE cycle, and is 0 when the cycle is completed. At some unspecified time before the cycle is complete, the WEL bit is reset.A SUBSECTOR ERASE command issued to a sector that is hardware or software protec-ted is not executed.Any SUBSECTOR ERASE command issued while an ERASE, PROGRAM, or WRITE cycle is in progress is rejected without any effect on the cycle that is in progress.If RESET# is driven LOW while a SUBSECTOR ERASE cycle is in progress, the SUBSEC-TOR ERASE cycle is interrupted and data may not be erased correctly. On RESET# going LOW, the device enters the RESET mode and a time of t RHSL is then required before the device can be reselected by driving S# LOW.Figure 22: SUBSECTOR ERASE Command SequenceDQ0CS#2134567892930310Notes: 1.Address bits A23-A18 are don't care in the M25PE20. Address bits A23-A17 are don'tcare in the M25PE10.2.Address bits A23-A19 are don't care .3.Address bits A23-A20 are don't care .SECTOR ERASEThe SECTOR ERASE command sets to 1 (FFh) all bits inside the chosen sector. Before the SECTOR ERASE command can be accepted, a WRITE ENABLE command must have been executed previously. After the WRITE ENABLE command has been decoded, the device sets the write enable latch (WEL) bit.The SECTOR ERASE command is entered by driving chip select (S#) LOW, followed by the command code, and three address bytes on serial data input (DQ0). Any address in-side the sector is a valid address for the SECTOR ERASE command. S# must be driven LOW for the entire duration of the sequence.S# must be driven HIGH after the eighth bit of the last address byte has been latched in.Otherwise the SECTOR ERASE command is not executed. As soon as S# is driven HIGH,the self-timed SECTOR ERASE cycle is initiated; the cycle's duration is t SE . While the SECTOR ERASE cycle is in progress, the status register may be read to check the value of the write in progress (WIP) bit. The WIP bit is 1 during the self-timed SECTOR ERASE cycle, and is 0 when the cycle is completed. At some unspecified time before the cycle is completed, the WEL bit is reset.A SECTOR ERASE command applied to a sector that contains a page that is hardware protected is not executed.Any SECTOR ERASE command while an ERASE, PROGRAM, or WRITE cycle is in pro-gress is rejected without having any effects on the cycle that is in progress.If RESET# is driven LOW while a SECTOR ERASE cycle is in progress, the SECTORERASE cycle is interrupted and the programmed data may be corrupted. On RESET go-ing LOW, the device enters the reset mode and a time of t RHSL is then required before the device can be reselected by driving Chip Select (S#) LOW.Figure 23: SECTOR ERASE Command SequenceCDQ0S#2134567892930310Notes: 1.Address bits A23-A18 are don't care in the M25PE20. Address bits A23-A17 are don'tcare in the M25PE10.2.Address bits A23-A19 are don't care .3.Address bits A23-A20 are don't care .。
MEMORY存储芯片MPC866TVR133A中文规格书
LPC2131_32_34_36_38All information provided in this document is subject to legal disclaimers.© NXP B.V. 2011. All rights reserved.Product data sheet Rev. 5.1 — 29 July 2011 19 of 45NXP Semiconductors LPC2131/32/34/36/38Single-chip 16/32-bit microcontrollers6.12.1Features•Compliant with Serial Peripheral Interface (SPI) specification.•Synchronous, Serial, Full Duplex, Communication.•Combined SPI master and slave.•Maximum data bit rate of one eighth of the input clock rate.6.13SSP serial I/O controllerThe LPC2131/32/34/36/38 each contain one Serial Synchronous Port controller (SSP).The SSP controller is capable of operation on a SPI, 4-wire SSI, or Microwire bus. It caninteract with multiple masters and slaves on the bus. However, only a single master and asingle slave can communicate on the bus during a given data transfer. The SSP supportsfull duplex transfers, with frames of 4 bits to 16 bits of data flowing from the master to theslave and from the slave to the master. Often only one of these data flows carriesmeaningful data.6.13.1Features•Compatible with Motorola SPI, 4-wire TI SSI and National Semiconductor Microwirebuses.•Synchronous Serial Communication.•Master or slave operation.•8-frame FIFOs for both transmit and receive.•Four bits to 16 bits per frame.6.14General purpose timers/external event countersThe Timer/Counter is designed to count cycles of the peripheral clock (PCLK) or anexternally supplied clock, and optionally generate interrupts or perform other actions atspecified timer values, based on four match registers. It also includes four capture inputsto trap the timer value when an input signal transitions, optionally generating an interrupt.Multiple pins can be selected to perform a single capture or match function, providing anapplication with ‘or’ and ‘and’, as well as ‘broadcast’ functions among them.At any given time only one of peripheral’s capture inputs can be selected as an externalevent signal source, i.e., timer’s clock. The rate of external events that can besuccessfully counted is limited to PCLK/2. In this configuration, unused capture lines canbe selected as regular timer capture inputs.6.14.1Features• A 32-bit Timer/Counter with a programmable 32-bit Prescaler.•External Event Counter or timer operation.•Four 32-bit capture channels per timer/counter that can take a snapshot of the timervalue when an input signal transitions. A capture event may also optionally generatean interrupt.•Four 32-bit match registers that allow:–Continuous operation with optional interrupt generation on match.LPC2131_32_34_36_38All information provided in this document is subject to legal disclaimers.© NXP B.V. 2011. All rights reserved.Product data sheet Rev. 5.1 — 29 July 2011 20 of 45NXP Semiconductors LPC2131/32/34/36/38Single-chip 16/32-bit microcontrollers–Stop timer on match with optional interrupt generation.–Reset timer on match with optional interrupt generation.•Four external outputs per timer/counter corresponding to match registers, with thefollowing capabilities:–Set LOW on match.–Set HIGH on match.–Toggle on match.–Do nothing on match.6.15Watchdog timerThe purpose of the watchdog is to reset the microcontroller within a reasonable amount oftime if it enters an erroneous state. When enabled, the watchdog will generate a systemreset if the user program fails to ‘feed’ (or reload) the watchdog within a predeterminedamount of time.6.15.1Features•Internally resets chip if not periodically reloaded.•Debug mode.•Enabled by software but requires a hardware reset or a watchdog reset/interrupt to bedisabled.•Incorrect/Incomplete feed sequence causes reset/interrupt if enabled.•Flag to indicate watchdog reset.•Programmable 32-bit timer with internal pre-scaler.•Selectable time period from (T cy(PCLK)⨯ 256⨯ 4) to (T cy(PCLK)⨯ 232⨯ 4) in multiples ofT cy(PCLK)⨯4.6.16Real-time clockThe Real-Time Clock (RTC) is designed to provide a set of counters to measure timewhen normal or idle operating mode is selected. The RTC has been designed to use littlepower, making it suitable for battery powered systems where the CPU is not runningcontinuously (Idle mode).6.16.1Features•Measures the passage of time to maintain a calendar and clock.•Ultra-low power design to support battery powered systems.•Provides Seconds, Minutes, Hours, Day of Month, Month, Year, Day of Week, andDay of Year.•Can use either the RTC dedicated 32 kHz oscillator input or clock derived from theexternal crystal/oscillator input at XTAL1. Programmable Reference Clock Dividerallows fine adjustment of the RTC.•Dedicated power supply pin can be connected to a battery or the main 3.3V.。
品牌机国产手机密码指令大全
品牌机国产手机密码指令大全YUKI was compiled on the morning of December 16, 2020品牌机国产手机密码指令大全国产手机, 品牌机, 指令, 密码, 大全本帖最后由天空之上！于 2010-6-25 19:16 编辑一、各种品牌手机中英文对照acer:：宏基 aiwa：爱华 alcatel（alc）：阿尔卡特amoi：夏新 apbw：亚太 apple：苹果arcoa：全虹 asus：华硕 aux：奥克斯benq：明基 benten：巨腾 bird（brd）：波导bosch：博士（博世） boss：宝石capitel：首信 casio：卡西欧 cect（cec）：中电通讯chabridge：中桥 chase：采星 cosun：侨兴daewoo：大宇 datang：大唐 daxian：大显dbtel：迪比特 denso：电送 dnet：迪奈特doeasy：多易随 docomo ：多科莫 dopod：多普达dragon:东方龙 eastcom（etcm）：东信 emol：易美ericsson：爱立信 fuli：富利galaxy：银河 gionee：金立 giya：基雅gplus：积加 great：伟松 gsl：权智（快译通）gstar:：吉事达 gvc：致福 hagenuk：汉佳诺haier(har)：海尔 hisense：海信 hitachi：日立hutel：秀特尔 hyundai：现代 innostream：盈讯jpg：金鹏 jrc：日本无线kejian(kjn)：科健 kenwood：建伍 kgt：和信konka(kon)：康佳 kpt：先进电讯 kyocera(kyea)：京瓷lenovo：联想 lucent：朗讯 lucky star：吉星malata：万利达 maxon：美晨 mitac：神达mitsubishi(trium)：三菱 motorola：摩托罗拉nec：日本电气 nett：雷特 nintaus：金正nixxo：尼索 nokia（nki）：诺基亚 nopo：星辰okwap：英资达 omron：欧姆龙palmax：帕玛斯(仁宝) panasonnic：松下 panda：熊猫penesas：天马 philips：飞利浦 photal：丰达putan：普天 qualcomm：高通 rowa：乐华sagem萨基姆 sanyo：三洋 samsung：三星sed：桑达 sendo:仙都 sewon：星王sharp：夏普 siemens：西门子 skynet：斯加耐特soutec：南方高科 sony：索尼 sobao：搜豹sonyerssion：索爱 soyea：数源 suohong：索鸿tcl：王牌 telsda：天时达 telson:泰尔信teltron：中讯天创 tinme：天梅（天美） tlink：神州龙tony：天珑（天龙） top：托普 toplux：天诺toshiba：东芝 toyo：东洋 transasia：泛亚ulycom：扬迪 uts：斯达康 victor：胜利vk：威科 vodafone：沃达丰 vtech：伟易达windows：视窗 xoceco：厦华ztc：中天伟业 zte：中兴品牌机系列二、手机密码（一）摩托罗拉摩托罗拉所有机锁：按menu+5+1/2t190解锁密码：t191解锁密码：3x8/2x88/998/8088/l2000/7689/t189/c289等初始密码为1234 ；话机密码为000000 ；解锁方法：如无测试卡，则先输入1234，如密码已更改，先按menu键会出现“修改开锁密码”，按ok键，然后输入000000就会显示四位数的话机密码，如保密码已更改，则只能用测试卡或软件工具解。
2000年以后新款奔驰电子控制模块中英文对照
ME2-SFI 引擎控制模块
ABS，ASR，ETS，ESP 防抱死刹车，牵引力，车身稳定，动力转向控制模块ETC 变速箱控制模块
ESM 电子排挡控制模块
DTR 车距控制模块
AIR MATIC。
ABC 空气悬挂控制模块
TPS 胎压控制模块
SRS 气囊控制模块
EIS 电子点火开关控制模块
OCP 车顶控制模块
UCP 上控制台控制模块
SAM-FL 左前保险丝，继电器，车身控制模块
SAM-FR 右前保险丝，继电器车身控制模块
R-SAM 后保险丝，车身控制模块
AHE 拖车监控模块
KG 无钥匙进入控制模块
SVMCM 特殊车辆控制模块
PSE 中控真空泵控制模块
HRA 头灯调整控制模块
DCM-FL 左前门控制模块
DCM-FR 右前门控制模块
DCM-RL 右后门车身控制模块
DCM-RR 右后门控制模块
ESA-R 右前电动座椅
ESA 电动座椅
OSB-FL 左前座椅充气椅背控制模块
OSB-FR 右前座椅充气椅背控制模块
OSB-R 后座椅充气椅背控制模块
ICM 仪表控制模组
SCM 方向盘控制模组
D2B 光纤控制模组
CDC CD换片机控制模组
VCS 语言控制模组
CTEL1 行动电话控制模组1
CTEL2 行动电话控制模组2
SOUND 音响控制模组
PTS 倒车雷达控制模组
TELE AID 紧急求救控制模组
TV 电视调频控制模组
DN 卫星定位控制模组
AAC 冷气空调控制模组
REAR-AC 后冷气控制模组
STH 暖气加热控制模组。
Expression of MiR200a, miR93, Metastasis-related Gene RECK and MMP2_MMP9 in Human Cervical C
Asian Pacific Journal of Cancer Prevention, Vol 14, 20132113DOI:/10.7314/APJCP .2013.14.3.2113MiR200a, miR93, RECK and MMP2/MMP9 Expression in Human Cervical CarcinomaAsian Pacific J Cancer Prev, 14 (3), 2113-2118IntroductionIn the worldwide, cervical cancer remains the third most common cancer in women globally after breast and colorectal cancer. However, 86% of all deaths caused by cervical cancer occur in developing countries (Arbyn et al., 2011). Data from the IARC GLOBOCAN 2008 database (http://globocan.iarc.fr/fact sheets/cancers/cervix.asp) estimate that there are 529, 512 new cases of cervical cancer diagnosed per year globally, corresponding to an age standardized incidence rate (ASIR) of 15.2/100,000 and 274,967 deaths. There is a striking difference in incidence of and mortality from cervical cancer in different regions of the world (Denny, 2012) So well-characteristic biomarkers are necessary for early diagnosis, to predict metastatic progression.Metastatic disease, rather than the primary tumor itself, is responsible for the death in most solid tumors, including cervical carcinoma (Lee et al., 1997; Welch et al., 2000; Yang et al., 2004). Degradation of basal membranes and the extracellular matrix (ECM) is essential for angiogenesis, invasion metastasis, and matrixDepartment of Obstetrics and Gynecology, the Second Affiliated Hospital of Jilin University, Changchun, Jilin, China *For correspondence: zanghu@AbstractAim and Background: Cervical cancer remains the third most common cancer in women globally after breast and colorectal cancer. Well-characterized biomarkers are necessary for early diagnosis and to predict metastatic progression and effective therapy. MiRNAs can regulate gene expression, cell growth, differentiation and apoptosis by targeting mRNAs for translational repression or degradation in tumor cells. The present study was conducted to assess expression of miR93, miR200a, RECK, MMP2, MMP9 in invasive cervical carcinoma, and analyze their clinical significance. Method: A total of 116 patients with invasive cervical carcinoma and 100 patients undergoing hysterectomy for benign lesions were retrospectively examined. Quantitative real-time PCR was performed to determine expression of miR93 and miR200a while RECK, MMP2, MMP9 and MVD were assessed by immunohistochemical staining. Results: Cervical carcinoma patients demonstrated up-regulation of miR-93, miR-200a, MMP2 and MMP9, with down-regulation of RECK as compared to benign lesion tissues. RECK was significantly inversely related to invasion and lymphatic metastasis. The 5-year survival rate for patients with strong RECK expression was significantly higher than that with weakly expressing tumors. Conclusion: MiR-93 and miR-200a are associated with metastasis and invasion of cervical carcinoma. Thus together with RECK they are potential prognostic markers for cervical carcinoma. RECK cooperating with MMP2, MMP9 expression is a significant prognostic factor correlated with long-term survival for patients with invasive cervical carcinoma.Keywords: miR-93 - miR-200a - RECK - MMP2 - MMP9 - MVD RESEARCH ARTICLEExpression of MiR200a, miR93, Metastasis-related Gene RECK and MMP2/MMP9 in Human Cervical Carcinoma - Relationship with PrognosisLing Wang, Qiang Wang, He-Lian Li, Li-Ying Han*metalloproteinases (MMPs) are potent enzymes that play a key role in these processes (Sabrina et al., 2012).Matrix Metalloproteinase 2 (MMP-2) (gelatinase A, 72 kDa) and Matrix Metalloproteinase 9 (MMP-9) (gelatinase B, 92 kDa) cleave type IV collagen and gelatin, which are the main structural components of the basal membrane (Toi et al., 1998). Expression of MMP-9 and MMP-2 has been implicated in the development and progression of many tumors, such as prostate, colorectal, breast cancer and cervical cancer (Liabakk et al., 1996; Kodate et al., 1997; Eissa et al., 2007; Rita et al., 2009).Several miRNAs are reported be associated with cervical carcinoma, Up-regulation of miR-200a and miR-93 promotes metastasis and tumor invasion. According to computational methodology current predictions-MicroCosm MMP2 is target gene to miR93, and TIMP1 is target gene to miR200a, while TIMP3 is target gene to miR93.MicroRNAs (miRNAs) is a novel class of small non-coding RNA molecules, 20-25 nucleotides in length, were shown to have important posttranscriptional gene regulatory functions. While miRNAs seed regionLing Wang et alAsian Pacific Journal of Cancer Prevention, Vol 14, 20132114which comprised of 2-8 nucleotides at 5’ end, target to special mRNA at 3’ untranslated region (UTR) (Bartel et al., 2009; Kim et al., 2009). If the complementarity of the miRNA-mRNA complex is perfect, miRNAs can exert translational repression function. However, if the complementarity is not perfect, the translation of the target mRNA is suppressed. To date, more than 1900 human mature miRNAs have been identified (http://www.miRbase. org/index. shtml), which are supposed to regulate more than 10% of protein coding genes (Wu et al., 2008), approximately one-third of expressed human genes contain miRNA regulatory target sites. Thus, this suggests that different clusters of miRNAs can regulate the cassette of specific genes which involve in one specific kind of cellular function together (Yang et al., 2003). It has been reported that RECK over-expression decreases the amount of active MMP-2 and MMP-9 and inhibits metastatic activity in vitro (Oh et al., 2001) and in vivo (Chang et al., 2008). RECK is a membrane-anchored glycoprotein of approximately 110 kDa containing multiple epidermal growth factor-like repeats and serine protease inhibitor-like domains. Down-regulation of RECK in several tumor cell lines and oncogene-transformed fibroblasts identified RECK as a common negative target for oncogenic signals. RECK low-expression, a hallmark of cancer, has been demonstrated to create a hypoxic tumor microenvironment.The aim of our study was to test the expression of miR200a and miR93 in cervical carcinoma, we propose the induction of the correlation between the expression of miR200a, miR93 and MMP2/9,RECK genes and to investigate whether miR200a, miR93 and MMP-2, MMP2/9 and RECK are expressed in a related pattern respectively in cervical carcinoma. Furthermore, we evaluate important prognostic parameters, analyzed the expression of RECK with 5-year survival rate, to conclude whether RECK is an independent factor to evaluate prognosis.Materials and MethodsTissue specimensCervical carcinoma specimens were obtained from patients undergone primary hysterectomy at the Department of Gynecology from Jan 2005 to Sep 2007, while control group were obtained from patients undergone hysterectomy for benign lesion. The specimens were frozen in liquid nitrogen at -80 ℃ within 30 minutes after isolated, and all cases were obtained from archives of the Department of Pathology in the Second Affiliated Hospital of Jilin University. The H&E stained slides of the cases were reviewed by gynecological pathologist. Morphology and protein expression were evaluated in consecutive sections. All protocols were reviewed and approved by the Ethical Committee of Second Affiliated Hospital of Jilin University. Written consent was obtained from all participating patients.Follow-upPatients were followed regularly for 5 years at the Second Affiliated Hospital of Jilin University. All patientswere followed until death or the study closing date (September 30, 2012). Disease-free survival (DFS) rate, which measured the first recurrence at any site, and overall survival (OS), measuring death from any case, were the two assessments used for prognostic analyses. Patients were re-examined (history, ultrasound examination, cervical screening test) once every 3 months during the first year, once every 6 months from the second year to the third year, and once every year after that. During the follow-up period, 6 patients were loss of follow up. 26 patients had disease recurrence and 36 patients died. miRNA isolationMiRNA was extracted from the tissue using the mirVana miRNA Isolation Kit (AM1561, Ambion) for hysterectomy specimen according to the protocols. The quantity and quality of the miRNA was verified with the NanoDrop spectrophotometer (Thermo Fisher Scientific Incorporated, Wilmington DE, USA) according to the manufacturer’s instructions.Quantitative real-time PCR (QPCR)miRNAs was reverse transcribed in a 20 μl reaction using the one step primescript miRNA cDNA Synthesis Kit (Takara, D350A). Forward primer sequences miR93: CAAAGTGCTGTTCGTGCAGGTAG, miR200a: GTAA CACTGTCTGGTAACGATGQPCR was performed on a BioMad Real-Time PCR System (ABI) using Power- SYBR Green PCR Master Mix (Takara, DRR081) in a 20 μl reaction and U6 as an endogenous control, miRlet-7 as positive control, result was determined using the 2-ΔΔCT . The QPCR experiments were run triplely within each experiment run, relative expression values were normalized to standard deviations from the mean.Immunohistochemical stainTo determine the expression of RECK, MMP2, MMP9 and MVD, immunohistochemical staining was carried out using the two-step plus poly-HRP method as described previously. After blocking with 3% hydrogen peroxide, the slides were incubated with primary anti-RECK antibody, anti-MMP2 antibody, anti-MMP9 antibody and CD34 antibody (1:50 goat mAb respectively; Santa Cruz Biotechnology, Santa Cruz, CA, USA). Afterwards, the slides were stained with the two-step plus poly-HRP antigoat IgG detection system (ZSGB-Bio, Beijing, China). For negative controls, the primary antibody was substituted with PBS in order to confirm the specificity of the primary antibody.Evaluation of immunohistochemical stainingTwo experienced investigators, who provided a consensus opinion of stain patterns by light microscopy, evaluated sections. RECK, MMP2 and MMP9 expression was estimated from the staining intensity and graded as follows: Grade 0, no staining (-); Grade 1, faint staining (+); Grade 2, moderate staining (++); and Grade 3, strong staining (+++). The positively stained area (distribution) was expressed as the percentage of the whole area under evaluation and scored as follows: 0, no staining; 1, 1~25% positive cells; 2, 26~50% positive cells; 3, 51~75%Asian Pacific Journal of Cancer Prevention, Vol 14, 20132115P0.0002 0.0193 0.0062Table 2. Correlation Between RECK Expression andVarious Clinicopathological Features in Cervical Cancer PatientsN RECK positive χ2 Pnegative positive (%)Stage I 64 33 31 48.44 6.198 0.1024 II 33 21 12 36.36 III 17 12 5 29.41 IV 2 2 0 0 Grade I 23 13 10 43.48 3.6204 0.1636 II 63 42 21 33.33 III 30 15 15 50 Invasive depth T2 66 43 23 34.85 0.0184 T3-T4 50 36 24 48 Lymph node status N1-N3 15 14 1 6.67 0.0237 N0 101 58 53 52.48 Squamous carcinoma 99 60 39 39.4 1 adenocarcinoma 17 11 6 35.29in Cervical Carcinoma in Relation to Normal TissueA BFigure 2. Expression of RECK, MMP2, MMP9. (A)expression of RECK in control group; (B) expression of RECK in cervical carcinoma; (C) expression of MMP2 in cervical carcinoma; (D) expression of MMP9 in cervical carcinoma; (E) MVD expression in control group; (F) expression of MVD in cervical carcinomapositive cells; and 4, 76~100% positive cells. Overall expression was then graded as low expression (score 0~2), intermediate expression (score 3~5), and high expression (score 6~7).Statistical analysisAnalysis were carried out by BioMad CFX system and statistical software SPSS 14.0 (SPSS, Chicago, IL, USA). The correlation of RECK, MMP2/9 expression with patients’ clinicopathological factors was analyzed by the Fisher’s exact test. The Kaplan-Meier method was used to estimate OS. Survival differences according to RECK expression were analyzed by the log-rank test. The risk ratio and its 95% confidence interval were recorded for each marker. P -values< 0.05 were considered statistically significant in all of the analysis.ResultsMean age of the total 116 patients was 49.3±2.39 years (24~77 years). 36 patients (31.03%) died, and 74 patients (63.79%) were alive at the end of research. Results of qPCR showed that miR93 and miR200a expression was higher in cervical carcinoma tissues (Figure 1A, Figure 1B). RECK was detected in the cytoplasm of normal cells (Figure 2A, Figure 2B), and of cervical carcinoma specimen its expression was much lower than that in control group, MMP9, MMP2 was detected in the cytoplasm of cells (Figure 2C, Figure 2D). MMP2 and MMP9 expression was significantly higher in cervical carcinoma than that in control group (Table 1). Accordingto Cox regression analysis result, the expression of MMP2 was positively related to expression of miR93 (P =0.0027) and miR200a (P =0.0016). However, higher expression of RECK related to lower expression of MMP2, MMP9. We also examined positive RECK staining in different clinopathological factors such as stage, grade, invasion depth and lymph node metastasis (Table 2). These data indicated that the frequency of RECK expression in high-grade was much higher than in low-grade cervical carcinoma. RECK expression, however, was significantly associated with lymph node metastasis (P =0.0237)Ling Wang et alAsian Pacific Journal of Cancer Prevention, Vol 14, 20132116and invasive depth (P =0.0184). Lymph node negative patients had higher RECK expression (53/101, 52.48%) than lymph node positive patients (1/15, 6.67%). Deeper invasive patients had lower RECK expression (24/50, 48%) than lower invasive patients (23/66, 34.85%). We found that histopathological grade, pathological TNM stage have no significance as prognostic predicators (Table 2). Multivariate analysis was carried out on the same set of patients for RECK expression and pathological predictors using the Cox regression model. The results indicated that RECK status (risk ratio, 3.312; P <0.05) was independent prognostic factor.Microscopic observation of MVD staining showed that in cervical carcinoma group, micro-vascular arranged disorderly, size and shape were irregular, thickness of vascular wall was nonuniform (Figure 2F), while in control group, clearer expression of micro-vascular endothelial cells were round or oval and in regular shape (Figure 2E). According to the Cox regression analysis, RECK expression in cervical carcinoma was negatively associated with MVD value (r=-0397, p =0.0495) (Table 3).To determine the relation between RECK expression and prognosis, Patients were divided into two groups on the basis of their prognosis. Our results indicated that patients with a poor prognosis(recurrence or metastasis) had low levels of RECK expression (P <0.05). Kaplan-Meier survival analysis showed that RECK positive patients also had significantly higher OS rates (P <0.05, log-rank test; Figure 3A).RECK positive patients had higher DFS rates compared with RECK negative patients (P =0.0387, log-rank test; Figure 3B).DiscussionAccumulating reports demonstrated that miRNAs have been observed in a variety of human cancers, and miRNA signatures accurately reflect the developmental lineagesand differential expression states of tumors by microarray profiling studies (Lu et al., 2005; Rosenfeld et al., 2008) Furthermore, they certified miRNAs involved in tumor cells invasion, apoptosis, angiogenesis and metastasis through regulation to target genes of corresponding signal pathways (MA et al., 2012). In previous research on human cervical cancer, expression of miR-15a, miR-20b, miR-21 and miR-224 is obviously increased in tissue and let-7c, miR-143, miR-199a-5p, miR-203 and miR-145 is reduced (Pereira et al., 2010; Wang et al., 2008). In our study, miRNAs expressions were quantified by using quantitative real-time PCR in which miR-93, miR-200a were up-regulated in cervical carcinoma tissue. Their expressions were accompanied by over-expression in MMP-2, MMP-9 and suppression in RECK gene.The miR-93 gene is located on chromosome 7q22.1, it can suppress proliferation and differentiation of cancer stem cells, while promoting tumor growth and malignant cells survival (Fang et al., 2011; Yu et al., 2011; Suling et al., 2012). In the present study, mir-93 expression was 5.29 fold higher compared to normal tissue. Our data are consistent with other reports indicating that mir-93 expression increased with cervical carcinoma (Lui et al., 2007). By microcosm predictor system, MMP2 has the target gene in 3’ UTR to miR-93, also TIMP3 is the proposal target gene of miR-93 ,whose sequence GAUGGACGUGCUUGUCGUGAAA was relatively complemented with CTTTCTATGTGCAAGGCACTTT in TIMP3 (/enright-srv /microcosm/htdocs/targets/v5). Endogenous angiogenesis inhibitors TIMPs are necessary to block the mitogenic stimuli in the vascular endothelium (Curran et al., 2000). TIMP3 is inhibitor of MMP2 and associated with actin and serve to stabilize microfilaments, so it act as tumor suppressor gene (Perry, 2001). miR93 was indentified up-regulated expression of MMP2 in cervical carcinoma, for the up-regulated mir-93, the inhibiting function of tumor suppressor genes TIMP3 maybe suppressed. But this hypothesis has not been certified. The miR-200a gene is located on chromosome 1P36.33, and can enhance invasion and growth of malignant cells. In this study, miR-200a was over-expressed by 3.65 folds in cervical carcinoma compared to normal tissues respectively. Similar studies indicated the miR-200a was up regulated which may supporting the concept that miR-200a functions as oncogene (Cong et al., 2013; Rasheed et al., 2013; Yu et al., 2013). In our study, the over-expression of miR-200a was associated with the over-expression of MMP2, MMP9. According to Microcosm target gene predictor system, TIMP1 is the corresponding target gene of miR-200a. miR-200a has been supposed to involve in down-regulating of TIMP1, whose inhibitor function to MMP2 and MMP9 is weakened and led to over-expression of MMP2 and MMP9. Similar research instructed that miR-200b is overexpressed in endometrial adenocarcinomas and enhances MMP2 activity by down regulating TIMP2 in human endometrial cancer cell Line HEC-1A cells (Dai et al., 2013). But the accurate mechanism in cervical carcinoma still need to certified in vitro until now.In this research, RECK expression is suppressedTable 3. Expression of MVD in Cervical Carcinoma and Control Tissue (n)P n MVD P RECK r (n/*400) (positive) [n(%)] Cervical carcinoma 116 19.4615±3.0718 0.000 48(40.31) -0.397Control group 100 12.0000±2.6629 0.0495 86(86.0)Figure 3. Kaplan–eier Analysis for Disease-free Survival (DFS) and Overall Survival (OS) Based on RECK Expression in Cervical Carcinoma Patients.(A) Kaplan–Meier analysis for OS based on RECK expression in patients with cervical carcinoma (P =0.0399, log–rank test); (B) Kaplan–Meier analysis for DFS based on RECK expression in patients with cervical carcinoma (P = 0.0387, log–rank test). RECK(+): RECK-positive patients (n =48 ); RECK(-): RECK-negative patients (n = 68)Asian Pacific Journal of Cancer Prevention, Vol 14, 20132117DOI:/10.7314/APJCP .2013.14.3.2113MiR200a, miR93, RECK and MMP2/MMP9 Expression in Human Cervical Carcinomain cervical carcinoma tissue when compared to benign lesion tissue. There are almost certainly pathways by which RECK is down-regulated in cancer. Hypoxia induces RECK down-regulation through the recruitment of HDAC1 and HIF-1α to the rHRE2 site in the promoter and the inhibition of hypoxic RECK silencing would be a therapeutic and preventive target for early tumorigenesis (Zhang et al., 2012). However, the CpG island promoter hypermethylation is associated silencing of tumor suppressor genes, which is the most recognized epigenetic disruption in human tumors (Rodriguez et al., 2011). Low RECK expression is closely correlated with high MMP2, MMP9 expression. In addition, increased expression of MMP2, MMP9 with decreased expression of RECK in invasive cervical carcinoma irrespective of histological grading supports the fact that RECK has a negative effect on the invasiveness of cervical cancer. Mori had found (Mori T et al., 2007) that MMP-2 activity, but not its mRNA expression, was significantly down-regulated in HT1080 cells after they were transferred into the RECK plasmid (Bin Zhang et al., 2009). Similarly, our results showed a negative correlation between RECK and MMP-2 protein expression. In HUVECs, specific inhibition of MMP-2 significantly antagonized the effect of RECK depletion on β1-integrin signaling, cell proliferation, and tube elongation (Namwat et al., 2011). Moreover, RECK-mediated suppression of MMP-9 promoter activity requires 12-O- tetradecanoylphorbol-13-acetate-responsive element (TRE) and KB sites. Moreover, the binding ability of Fra-1 and c-Jun to TRE within the MMP-9 promoter region was suppressed by RECK (Satoshi et al., 2007). In this research, MVD CD34 for tumors with lower-expression RECK is obviously increased, which indicates that RECK can inhibit angiogenesis. Targeting RECK specifically in tumor-associated vascular endothelial cells resulted in tumor regression (Takao et al., 2010).RECK positive patients showed higher 5-year survival rates and DFS rates. Furthermore, we found that RECK expression was significantly associated with lymph node metastasis and deeper invasion. HER-2/neu oncogene inhibits the expression of RECK to promote cell invasion (Tsung-Te et al., 2012). Hypermethylation of RECK promoter is also a common event in human ESCC, which occurs concurrently in tumor-adjacent normal mucosa and is correlated with poor prognosis in ESCC patients (Long NK et al., 2008). RECK displays as a metastasis suppressor and up-regulation of RECK expression could provide a potential therapy to improve the prognosis (Namwat et al., 2011).In conclusion, MiR-93, miR-200a is associated with metastasis and invasion of cervical carcinoma, thus MiR-93, miR-200a, RECK expression is a potentially prognostic marker for cervical carcinoma. RECK cooperating with MMP2, MMP9 expression is a significant prognostic factor correlated with long-term survival for patients with invasive cervical carcinoma.ReferencesArbyn M, Andersson K, Bergeron C, et al (2011). Cervicalcytology biobanks as a resource for molecular epidemiology. Methods Mol Biol , 675, 279-98.Bartel DP (2009). MicroRNAs, target recognition and regulatoryfunctions. Cell , 136, 215-33.Chang CK, Hung WC, Chang HC (2008). The Kazal motifs ofRECK protein inhibit MMP-9 secretion and activity and reduce metastasis of lung cancer cells in vitro and in vivo. J Cell Mol Med , 12, 12-6.Cong N, Du P , Zhang A, et al (2013). Downregulated microRNA-200a promotes EMT and tumor growth through the wnt/β-catenin pathway by targeting the E-cadherin repressors ZEB1/ZEB2 in gastric adenocarcinoma. Oncol Rep , 10, 3892-7.Curran S, Murray GI (2000). Matrix metalloproteinases,molecular aspects of their roles in tumour invasion and metastasis. Eur J Cancer , 36, 1621-30Dai Y, Xia W, Song T, et al (2013). MicroRNA-200b isoverexpressed in endometrial adenocarcinomas and enhances MMP2 activity by downregulating TIMP2 in human endometrial cancer cell line HEC-1A cells. Nucleic Acid Ther , 23, 29-34.Denny Lynette (2012). Cervical cancer, prevention andtreatment. Discov Med , 14, 125-11.Eissa S, Ali-Labib R, Swellam M, et al (2007). Noninvasivediagnosis of bladder cancer by detection of matrix metalloproteinases (MMP-2 and MMP-9) and their inhibitor (TIMP-2) in urine. Eur Urol , 52, 1388-96.Fang L, Deng Z, Shatseva T, et al (2011). MicroRNA miR-93promotes tumor growth and angiogenesis by targeting integrin-β8. Oncogene , 30, 806-21.Figueira RC, Gomes LR, Neto JS, et al (2009). Correlationbetween MMPs and their inhibitors in breast cancer tumor tissue specimens and in cell lines with different metastatic potential. BMC Cancer , 9, 20-5.Liu S, Patel SH, Ginestier C, et al (2012). MicroRNA93 regulatesproliferation and differentiation of normal and malignant breast stem cells. PLoS Genet , 8, e1002751.Kim VN, Han J, Siomi MC (2009). Biogenesis of small RNAsin animals. Nat Rev Mol Cell Biol , 10, 126-39.Kodate M, Kasai T, Hashimoto H, et al (1997). Expression ofmatrix metalloproteinase (gelatinase) in T1 adenocarcinoma of the lung. Pathol Int , 47, 461-9.Lee JH, Welch DR (1997). Suppression of metastasis in humanbreast carcinoma MDA-MB-435 cells after transfection with the metastasis suppressor gene, KiSS-1. Cancer Res , 57, 2384-7.Liabakk NB, Talbot I, Smith RA, et al (1996). Matrix metallo-proteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) type IV collagenase in colorectal cancer. Cancer Res , 56, 190-6.Lim LP, Lau NC, Garrett-Engele P, et al (2005). Microarrayanalysis shows that some microRNAs downregulate large numbers of target mRNAs. Nature , 433, 769-73.Long NK, Kato K, Yamashita T, et al (2008). Hypermethylationof the RECK gene predicts poor prognosis in oral squamous cell carcinomas. Oral Oncol , 44, 1052-8.Lu J, Getz G, Miska EA, et al (2005). MicroRNA expressionprofiles classify human cancers. Nature , 435, 834-8.Lui WO, Pourmand N, Patterson BK, Fire A (2007). Patternsof known and novel small RNAs in human cervical cancer. Cancer Res, 67, 6031-43.Ma D, Zhang YY , Guo YL, Li ZJ, Geng L (2012). Profiling ofmicroRNA-mRNA reveals roles of microRNAs in cervical cancer. Chin Med J , 125, 4270-76.Mori T, Moriuchi R, Okazaki E, et al (2007). Tgat oncoproteinfunctions as a inhibitor of RECK by association of the unique C-terminal region. Biochem Biophys Res Commun ,Ling Wang et alAsian Pacific Journal of Cancer Prevention, Vol 14, 20132118355, 937-43.Namwat N, Puetkasichonpasutha J, Loilome W, et al (2011).Downregulation of reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) is associated with enhanced expression of matrix metalloproteinases and cholangiocarcinoma metastases. J Gastroenterol, 46, 664-75.Oh J, Takahashi R, Kondo S, et al (2001). The membraneanchored MMP inhibitor RECK is a key regulator of extracellular matrix integrity and angiogenesis. Cell , 107, 789-800.Pereira PM, Marques JP, Soares AR, Carreto L, Santos MA(2010). MicroRNA expression variability in human cervical tissues. PLoS One , 5, e11780.Perry SV (2001). V ertebrate tropomyosin, distribution, propertiesand function. J Muscle Res Cell Motil , 22, 5-49.Rasheed SA, Teo CR, Beillard EJ, V oorhoeve M, Casey PJ(2013). MicroRNA-182 and microRNA-200a control G-protein subunit alpha-13 (GNA13) expression and cell invasion synergistically in prostate cancer. Cells J Biol Chem , 10, 1074-7.Rodriguez-Paredes M, Esteller M (2011). Cancer epigeneticsreaches mainstream oncology. Nat Med , 17, 330-9.Rosenfeld N, Aharonov R, Meiri E, Rosenwald S, et al (2008).MicroRNAs accurately identify cancer tissue origin. Nat Biotechnol, 26, 462-9.Reis ST, Leite KR, Piovesan LF, et al (2012). Increasedexpression of MMP-9 and IL-8 are correlated with poor prognosis of Bladder Cancer. BMC Urol , 12, 18-23.Takagi S, Simizu S, Osada H (2009). RECK negatively regulatesmatrix metalloproteinase-9 transcription. Cancer Res , 69, 1502-8.Miki T, Shamma A, Kitajima S, et al (2010). TThe ß1-integrin-dependent function of RECK in physiologic and tumor angiogenesis. Mol Cancer Res , 8, 665-76.TChung TT, Yeh CB, Li YC, et al (2012). Effect of RECK genepolymorphisms on hepatocellular carcinoma susceptibility and clinicopathologic features. Plos one , 7, e33517.Toi M, Ishigaki S, Tominaga T(1998). Metalloproteinases andtissue inhibitors of metallo-proteinases. Breast Cancer Res Treat , 52, 113-24.Wang X, Tang S, Le SY , et al(2008). Aberrant expression ofoncogenic and tumor-suppressive microRNAs in cervical cancer is required for cancer cell growth. PLoS One, 3, e2557.Welch DR, Steeg PS, Rinker-Schaeffer CW (2000). Molecularbiology of breast cancer metastasis. Genetic regulation of human breast carcinoma metastasis. Breast Cancer Res , 2, 408-16.Wu L, Belasco JG (2008). Let me count the ways, mechanisms ofgene regulation by miRNAs and siRNAs. Mol Cell, 29, 1-7.Yang J, Mani SA, Donaher JL, et al (2004). Twist, a masterregulator of morphogenesis, plays an essential role in tumor metastasis. Cell , 117, 927-39.Yang L, Parkin DM, Li L, Chen Y (2003). Time trends in cancermortality in China, 1987-1999. Int J Cancer , 106, 771-83.Yu SJ, Hu JY, Kuang XY, et al (2013). MicroRNA-200aPromotes Anoikis Resistance and Metastasis by Targeting YAP1 in Human Breast Cancer. Clin Cancer Res , 10, 1158-63.Yu XF, Zou J, Bao ZJ, Dong J (2011). miR-93 suppressesproliferation and colony formation of human colon cancer stem cells. World J Gastroenterol , 17, 4711-7.Zhang B, Zhang J, Xu ZY , Xie HL (2009). Expression of RECKand matrix metalloproteinase-2 in ameloblastoma. BMC Cancer , 9, 427-35.Zhang C, Ling Y , Zhang C, et al (2012). The silencing of RECKgene is associated with promoter hypermethylation and poorsurvival in hepatocellular carcinoma. Int J Biol Sci , 8, 451-8.。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
Document Number: 25009For technical questions, contact: aluminumcaps1@Aluminum CapacitorsRadial StyleEKCVishay RoedersteinFEATURES•Polarized Aluminum electrolytic capacitor •Small dimensions, high CU product •Extremely low impedance and R ESR values •Very high AC rating •Extremely long lifetime •High temperature rangeAPPLICATIONS•Industrial electronics, telecommunication systems,audio/video systems•Highly professional switching power supply units •Smoothing, filtering •Portable and mobile unitsComponent outlinesQUICK REFERENCE DATADESCRIPTIONUNIT VALUENominal case size (Ø D x L)mm 5 x 11.5 to 16 x 40Rated capacitance range C R µF 10 to 8200Capacitance tolerance %± 20Rated voltage rangeV 10 to 63Category temperature range°C - 55 to + 105Endurance test at upper category temperature hup to 8000Based on sectional specification IEC 60384/EN 130300Climatic category IEC 6006855/105/56SELECTION CHART FOR C R , U R AND RELEVANT NOMINAL CASE SIZES (Ø D x L in mm)C R (µF)RATED VOLTAGE (V)10162535506310→→→→→5 x 11.5 18→→→→ 5 x 11.5 6.3 x 11.527→→→ 5 x 11.5 --33→→→→→6.3 x 1539→→ 5 x 11.5 → 6.3 x 11.5-47→→→→→8 x 1256→ 5 x 11.5 → 6.3 x 11.5 6.3 x 1510 x 12.568→→→→8 x 128 x 1582 5 x 11.5 → 6.3 x 11.5 6.3 x 158 x 158 x 20100→→→8 x 1210 x 1610 x 20120→ 6.3 x 11.5 6.3 x 158 x 1210 x 1610 x 20150→→8 x 12→→10 x 25180 6.3 x 11.5 6.3 x 1510 x 12.58 x 1510 x 2010 x 30220 6.3 x 15→8 x 1510 x 1610 x 2512.5 x 20270→8 x 12→→→12.5 x 253308 x 128 x 158 x 2010 x 2012.5 x 2016 x 2039010 x 12.5→→10 x 25→12.5 x 304708 x 1510 x 1610 x 2012.5 x 2012.5 x 2512.5 x 35EKCVishay RoedersteinAluminum CapacitorsRadial Style For technical questions, contact: aluminumcaps1@Document Number: 25009GENERAL NOTE•For Standard Packaging Quantity (SPQ) and Minimum Order Quantity (MOQ) please refer to our price list or contact customer service•For other packaging forms please refer to Vishay Roederstein General Information560→→10 x 2512.5 x 2012.5 x 3012.5 x 406808 x 2010 x 20→12.5 x 2512.5 x 3516 x 30820→10 x 2510 x 30→12.5 x 4016 x 35100010 x 20→12.5 x 2516 x 2016 x 3016 x 40120010 x 2510 x 30→12.5 x 3516 x 35-150010 x 3012.5 x 2512.5 x 3012.5 x 4016 x 40-180012.5 x 20→12.5 x 3516 x 30--220012.5 x 2516 x 2012.5 x 4016 x 35--270012.5 x 3012.5 x 3516 x 3016 x 40--330012.5 x 3512.5 x 4016 x 35---390012.5 x 4016 x 3016 x 40---4700→16 x 35----560016 x 3016 x 40----680016 x 35-----820016 x 40-----SELECTION CHART FOR C R , U R AND RELEVANT NOMINAL CASE SIZES (Ø D x L in mm)C R(µF)RATED VOLTAGE (V)101625355063Document Number: 25009For technical questions, contact: aluminumcaps1@EKCAluminum CapacitorsRadial StyleVishay RoedersteinNoteUnless otherwise specified, all electrical values at T a =20 °C, P =80to 120kPa, RH =45to 75 %.ORDERING EXAMPLEEKC 3300 µF/25 V, ± 20 %, size: 16 x 35 mm Leads: LongOrdering code: MALREKC00JU433E00F Leads: ShortOrdering code: MALREKC05...ELECTRICAL DATASYMBOL DESCRIPTIONU R rated voltageC R rated capacitance at 120Hz tan δmax. dissipation factor at 120 Hz Z max. impedance at 100kHzI Rrated alternating current (rms) at 100 kHz and upper category temperatureELECTRICAL DATA AND ORDERING INFORMATIONU R (V)C R 120Hz (µF)NOMINAL CASE SIZE Ø D x L (mm)tan δ120 Hz Z100kHz/20 °C (Ω)I R 100 kHz/105 °C(mA)WEIGHT(g)CATALOG NUMBER (LONG LEADS)1082 5 x 11.5 0.190.751630.50MALREKC00AB282C00F 180 6.3 x 11.50.190.352730.80MALREKC00BB318C00F 220 6.3 x 150.190.25390 1.20MALREKC00BF322C00F 3308 x 120.190.17445 1.00MALREKC00PT333C00F 39010 x 12.50.190.12625 1.90MALREKC00DC339C00F 4708 x 150.190.13555 1.50MALREKC00PF347C00F 6808 x 200.190.095740 2.00MALREKC00PE368C00F 100010 x 200.190.0621040 3.00MALREKC00DE410C00F 120010 x 250.210.0521260 4.00MALREKC00DG412C00F 150010 x 300.210.0441440 4.80MALREKC00DJ415C00F 180012.5 x 200.210.0461340 4.00MALREKC00FE418C00F 220012.5 x 250.230.0341690 4.70MALREKC00FG422C00F 270012.5 x 300.230.0301950 5.40MALREKC00FJ427C00F 330012.5 x 350.250.0242220 5.90MALREKC00FU433C00F 390012.5 x 400.250.0222390 6.40MALREKC00FK439C00F 560016 x 300.290.02523508.80MALREKC00JJ456C00F 680016 x 350.310.022255010.0MALREKC00JU468C00F 820016 x 400.350.018290011.0MALREKC00JK482C00F 1656 5 x 11.5 0.160.751630.50MALREKC00AB256D00F 120 6.3 x 11.50.160.352730.80MALREKC00BB312D00F 180 6.3 x 150.160.253900.80MALREKC00BF318D00F 2708 x 120.160.17445 1.00MALREKC00PT327D00F 3308 x 150.160.13555 1.50MALREKC00PF333D00F 47010 x 160.160.084825 2.40MALREKC00DD347D00F 68010 x 200.160.0621040 3.00MALREKC00DE368D00F 82010 x 250.160.0521260 4.00MALREKC00DG382D00F 120010 x 300.180.0441440 4.80MALREKC00DJ412D00F 150012.5 x 250.180.0341690 4.70MALREKC00FG415D00F 220016 x 200.200.0381630 5.80MALREKC00JE422D00F 270012.5 x 350.200.0242220 5.90MALREKC00FU427D00F 330012.5 x 400.220.0222390 6.40MALREKC00FK433D00F 390016 x 300.220.02523508.80MALREKC00JJ439D00F 470016 x 350.240.022255010.0MALREKC00JU447D00F 560016 x 400.260.018290011.0MALREKC00JK456D00FEKCVishay RoedersteinAluminum CapacitorsRadial Style For technical questions, contact: aluminumcaps1@Document Number: 250092539 5 x 11.5 0.140.751630.50MALREKC00AB239E00F 82 6.3 x 11.50.140.352730.80MALREKC00BB282E00F 120 6.3 x 150.140.25390 1.20MALREKC00BF312E00F 1508 x 120.140.17445 1.00MALREKC00PT315E00F 18010 x 12.50.140.12625 1.90MALREKC00DC318E00F 2208 x 150.140.13555 1.50MALREKC00PF322E00F 3308 x 200.140.095740 2.00MALREKC00PE333E00F 47010 x 200.140.0621040 3.00MALREKC00DE347E00F 56010 x 250.140.0521260 4.00MALREKC00DG356E00F 82010 x 300.140.0441440 4.80MALREKC00DJ382E00F 100012.5 x 250.140.0341690 4.70MALREKC00FG410E00F 150012.5 x 300.160.0301950 5.40MALREKC00FJ415E00F 180012.5 x 350.160.0242220 5.90MALREKC00FU418E00F 220012.5 x 400.180.0222390 6.40MALREKC00FK422E00F 270016 x 300.180.02523508.80MALREKC00JJ427E00F 330016 x 350.200.022255010.0MALREKC00JU433E00F 390016 x 400.200.018290011.0MALREKC00JK439E00F 3527 5 x 11.5 0.120.751630.50MALREKC00AB227F00F 56 6.3 x 11.50.120.352730.80MALREKC00BB256F00F 82 6.3 x 150.120.25390 1.20MALREKC00BF282F00F 1008 x 120.120.17445 1.00MALREKC00PT310F00F 1208 x 120.120.17445 1.00MALREKC00PT312F00F 1808 x 150.120.13555 1.50MALREKC00PF318F00F 22010 x 160.120.084825 2.40MALREKC00DD322F00F 33010 x 200.120.0621040 3.00MALREKC00DE333F00F 39010 x 250.120.0521260 4.00MALREKC00DG339F00F 47012.5 x 200.120.0461340 4.00MALREKC00FE347F00F 56012.5 x 200.120.0461340 4.00MALREKC00FE356F00F 68012.5 x 250.120.0341690 4.70MALREKC00FG368F00F 100016 x 200.120.0381630 5.80MALREKC00JE410F00F 120012.5 x 350.140.0242220 5.90MALREKC00FU412F00F 150012.5 x 400.140.0222390 6.40MALREKC00FK415F00F 180016 x 300.140.02523508.80MALREKC00JJ418F00F 220016 x 350.160.022255010.0MALREKC00JU422F00F 270016 x 400.160.018290011.0MALREKC00JK427F00F 5018 5 x 11.5 0.10 1.201290.50MALREKC00AB218H00F 396.3 x 11.50.100.542190.80MALREKC00BB239H00F 56 6.3 x 150.100.34310 1.20MALREKC00BF256H00F 688 x 120.100.30340 1.00MALREKC00PT268H00F 828 x 150.100.20470 1.50MALREKC00PF282H00F 10010 x 160.100.137552.40MALREKC00DD310H00FELECTRICAL DATA AND ORDERING INFORMATIONU R (V)C R 120Hz (µF)NOMINAL CASE SIZE Ø D x L (mm)tan δ120 Hz Z100kHz/20 °C (Ω)I R 100 kHz/105 °C(mA)WEIGHT(g)CATALOG NUMBER (LONG LEADS)Document Number: 25009For technical questions, contact: aluminumcaps1@EKCAluminum CapacitorsRadial StyleVishay Roederstein12010 x 160.100.13755 2.40MALREKC00DD312H00F 18010 x 200.100.088945 3.00MALREKC00DE318H00F 22010 x 250.100.0731150 4.00MALREKC00DG322H00F 33012.5 x 200.100.0541260 4.00MALREKC00FE333H00F 47012.5 x 250.100.0441490 4.70MALREKC00FG347H00F 5056012.5 x 300.100.0391720 5.40MALREKC00FJ356H00F 68012.5 x 350.100.0331890 5.90MALREKC00FU368H00F 82012.5 x 400.100.0292030 6.40MALREKC00FK382H00F 100016 x 300.100.03021508.80MALREKC00JJ410H00F 120016 x 350.120.027232010.0MALREKC00JU412H00F 150016 x 400.120.024254011.0MALREKC00JK415H00F 6310 5 x 11.5 0.10 1.901030.50MALREKC00AB210J00F 18 6.3 x 11.50.10 1.001610.80MALREKC00BB218J00F 33 6.3 x 150.100.61233 1.20MALREKC00BF233J00F 478 x 120.100.47274 1.00MALREKC00PT247J00F 5610 x 12.50.100.27418 1.90MALREKC00DC256J00F 688 x 150.100.34360 1.50MALREKC00PF268J00F 828 x 200.100.21525 2.00MALREKC00PE282J00F 10010 x 200.100.16650 3.00MALREKC00DE310J00F 12010 x 200.100.16650 3.00MALREKC00DE312J00F 15010 x 250.100.13783 4.00MALREKC00DG315J00F 18010 x 300.100.10960 4.80MALREKC00DJ318J00F 22012.5 x 200.100.11870 4.00MALREKC00FE322J00F 27012.5 x 250.100.0741150 4.70MALREKC00FG327J00F 33016 x 200.100.0851100 5.80MALREKC00JE333J00F 39012.5 x 300.100.0681280 5.40MALREKC00FJ339J00F 47012.5 x 350.100.0631390 5.90MALREKC00FU347J00F 56012.5 x 400.100.0511530 6.40MALREKC00FK356J00F 68016 x 300.100.04617208.80MALREKC00JJ368J00F 82016 x 350.100.040191010.0MALREKC00JU382J00F 100016 x 400.100.036207011.0MALREKC00JK410J00FELECTRICAL DATA AND ORDERING INFORMATIONU R (V)C R 120Hz (µF)NOMINAL CASE SIZE ØD x L (mm)tan δ120 Hz Z100kHz/20 °C (Ω)I R 100 kHz/105 °C(mA)WEIGHT(g)CATALOG NUMBER (LONG LEADS)LOW TEMPERATURE BEHAVIOR (at 120Hz)IMPEDANCE RATIOZ (T2)/Z (T1)RATED VOLTAGE(V)T2/T110 ~ 5063- 55 °C/+ 20 °C36EKCVishay RoedersteinAluminum CapacitorsRadial Style For technical questions, contact: aluminumcaps1@Document Number: 25009ADDITIONAL ELECTRICAL DATAPARAMETER CONDITIONSVALUECurrent Leakage current(T est conditions: U R , 20 °C)After 2 minutes at U RI L2 ≤ 0.01 x C R x U Ror 3 µA(whichever is greater)ResistanceEquivalent series resistance (ESR)Calculated from tan δmax. ESR = tan δ/2 πf C R MULTIPLIER OF RIPPLE CURRENT (I R ) AS A FUNCTION OF FREQUENCYFREQUENCY(Hz)I R MULTIPLIER10 ~ 180 µF220 ~ 560 µF680 ~ 1800 µF2200 ~ 3900 µF4700 ~ 8200 µF1200.400.500.600.750.8510000.750.850.870.900.9510 0000.900.940.950.950.98100 0001.001.001.001.001.00TEST PROCEDURES AND REQUIREMENTSTESTPROCEDURE (QUICK REFERENCE)REQUIREMENTSLoad lifeT amb = 105 °C U R and I R appliedAfter 2000 hours Ø 5, Ø 6.3After 3000 hours Ø 8After 5000 hours Ø 10After 7000 hours Ø 12.5After 8000 hours Ø 16, Ø 18Δ C/C: ± 20 % of initial value I L ≤ spec. limittan δ ≤ 2 x spec. limitShelf lifeNo voltage applied After 1000 hAfter test: U R to be applied for 30 minutes 24 to 48 hours before measurementΔ C/C: ± 20 % of initial value I L ≤ spec.limittan δ ≤ 2 x spec. limitDisclaimer Legal Disclaimer NoticeVishayAll product specifications and data are subject to change without notice.Vishay Intertechnology, Inc., its affiliates, agents, and employees, and all persons acting on its or their behalf (collectively, “Vishay”), disclaim any and all liability for any errors, inaccuracies or incompleteness contained herein or in any other disclosure relating to any product.Vishay disclaims any and all liability arising out of the use or application of any product described herein or of any information provided herein to the maximum extent permitted by law. The product specifications do not expand or otherwise modify Vishay’s terms and conditions of purchase, including but not limited to the warranty expressed therein, which apply to these products.No license, express or implied, by estoppel or otherwise, to any intellectual property rights is granted by this document or by any conduct of Vishay.The products shown herein are not designed for use in medical, life-saving, or life-sustaining applications unless otherwise expressly indicated. Customers using or selling Vishay products not expressly indicated for use in such applications do so entirely at their own risk and agree to fully indemnify Vishay for any damages arising or resulting from such use or sale. Please contact authorized Vishay personnel to obtain written terms and conditions regarding products designed for such applications.Product names and markings noted herein may be trademarks of their respective owners.元器件交易网Document Number: 。