![]() ![]() Material Ledger production startup • Why the material is not active for Material Ledger being the Plant active? Values and price differences are collected (material movements, purchasing, incoices, production order settlements, debits/credits). ![]() • The actual quantity structure is built with goods issues and activities to production, goods receipts from production, material transfers. At period -end closing (transaction CKMLCP): • • The steps in CKMLCP have to be executed in the correct sequence. • A periodic unit price (PUP) is determined and used to update V-Price in Acc1-view in Material Master. Dear SAP Community Member, In order to fully benefit from what the SAP. Activate Valuation Areas for Material Ledger. IS-Retail and Material Ledger. I created a new plant ZZVS which I copied from an already existing plant 1010 in standard SAP. Activate the Material ledger. Activatipon of material ledger. • The price (and exchange rate) differences are distributed to consumption and to ending inventory. • The inventory can be revaluated with the actual price determined. Use the transaction CKMSTART to ensure that you can start extending materials to a plant that has material ledger activated. This has been a problem for me at a recent client as we’re going through pre-implementation data load cycles. The strategy I use to create the material master follows this sequence: basic data, plant data, storage location data, and sales data. The plant data is where I extend the accounting & costing views and also where I hit some errors because the plant did not have the material ledger set as “productive”. So I added logic into my plant data LSMW to catch these situations. Let’s look at CKMSTART. Below you can see the selection screen for the transaction. You are able to “startup” several plants at once, if needed, but can only execute for one exchange rate type. In the example below, I’m going to start material ledger for plant 1400 and exchange rate type M. I do not claim to be a material ledger expert and probably never will be, so I cannot speak to the configuration of or consequences from using material ledger. I can say that in this situation, no master or transactional data existed for that plant (1400) prior to material ledger activation. Thus, some of the activities that CKMSTART executes when plant data does exist are not addressed here. As with many SAP transactions, there is a test mode and I highly recommend that you use it here. Recognizing that no data exists, the background processing option is not necessary. This is the picture of CKMSTART after execution in test mode. All green lights means that things are good to go. Below is the picture of CKMSTART after execution with “Test run” unchecked. Do not be worried that there is a red light at the end of this list. Not being an expert in material ledger, I got a little worried myself. My FICO colleague assured me that this is normal for this situation and is a response to the second to last step shown in the screenshot above (“Company codes in which ML and FI can be reconciled”). The result of this startup is that an entry is made in table CKLMV allowing you to extend materials to the plant. The indicator in the red box below (MLBWI) tells you that material ledger is “live’ in for that valuation area (BWKEY). For this client, the valuation area is equivalent to the plant. You can see another key indicator in the table T001K. Again, by valuation area you have an indicator identified in the red box (MLBWA) that tells you material ledger is activated. This is not the same as being “live”. This is one of the configuration settings when a plant is identified for material ledger. Thus, in my LSMW to extend plant data, I added some logic to prohibit extending materials where this entry does not exist. I checked both of the tables mentioned above and looked for values the fields identified. This check looks something like this: SELECT SINGLE a~bwkey INTO t_bwkey FROM ( t001k AS a INNER JOIN ckmlv AS b ON a~bwkey = b~bwkey ) WHERE a~bwkey = src_data-werks AND a~mlbwa = 'X' AND b~mlbwi = 'X'. If no value is found from this SELECT, then the transaction is skipped in the LSMW. I am using the SAP direct input program RMDATIND to load the material master data. Although this program has a test mode, this test mode does not capture when a valuation area is not “live” with material medger. I should say that the test mode for this program is definitely recommended to identify many other problems that might be present in your data – testing whether material ledger is “live” is, unfortunately, not one of those that it can pinpoint.
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At the menu screen,select menu and scroll down to contacts, hit select,then select names, find the number you want to add voice dial to, select details,select options,scroll down to 'add voice tag' Hit select and follow the instructions. One tip: when you program the voice call, you should be in the enviroment thet you usually use the voice dial. If you set it up in a quite place like your home and then try to use voice dial in a noisy place, it probably will not work. Also talking louder does not help. Hope that helps. ![]() If not, you probably have a problem with the phone itself. Posted on Oct 19, 2009. Hi, These are the secret hidden codes of 6230i Please use hard reset and soft reset only when it is necessary because it will formats your mobile phone.and also be carefull with gprs deleting code. Soft Reset *#7370# Shows phone software version *#0000# Production serial No *#7760# Warranty information *#92702689# Bluetooth information*#2820# Deletes GPRS and MMS settings *#335738# Hard reset *#7780# Reset phone timers *#73# 0 (hold for a second) Gprs connection. 1 (hold for a second) voice mail. Please do rate the solution if the issue is resolved or post a comment for further assistance. ![]() ![]() Thank you for using fixya have a nice day:-) Aug 02, 2010|. Hi Kazgear, Voice Dial: Important: Be sure your phone supports the voice dialing function and that it is activated. Record at least one voice tag. (Please refer to the instructions in your phone’s user manual.) Note: Voice dialing entries must be stored in the phone’s memory, not on the SIM card! Press the Accept Button (1) for 1 second. A voice dial beep will be heard on the kit to prompt the user to say the voice tag of the contact to call. Say the voice tag exactly as how you recorded it. Jun 22, 2010 Just a demo on how to configure MTN GPRS settings manually on a Nokia 6230. It should work like this for most Nokia phones http://www.multidox.net/blog/1. May 15, 2013 How to open a gprs on nokia 2220s? But don't forget to activate an internet plan on your number. How can i open my gprs, my phone is nokia 6230i? The voice will be played back to you, and then the phone will dial the number automatically. Her's a.pdf file of the user manual, which you can save to your computer: Hope this helps:) Season's Greetings! Chris (ziraffa) Nov 29, 2008|. Hi marrick, Voice Dial: Important: Be sure your phone supports the voice dialing function andthat it is activated. Record at least one voice tag. (Please refer tothe instructions in your phone’s user manual.) Note: Voice dialingentries must be stored in the phone’s memory, not on the SIM card! Press the Accept Button (1) for 1 second. A voice dial beep will be heard on the kit to prompt the user to say the voice tag of the contact to call. Say the voice tag exactly as how you recorded it. The voice will be played back to you, and then the phone will dial the number automatically. Her's a.pdf file of the user manual, which you can save to your computer: Hope this helps:) Season's Greetings! Chris (ziraffa) Nov 21, 2008|. ![]() Hiya psychomania - Here's a question on an even older phone - but a lovable piece of Nokia machinery; the 6820b. Its a close family friend, but has suddenly started accepting selected telephone numbers as 'Data Calls' only and has on the lower screen 'infrared'. There's also a capital 'D' in a sqare box next to the number (if the number is recognised). Some incoming calls still come in as normal calls, and are answered in the normal way, and there seems nothing common to each group of numbers (neither mobile/fixed line, or country specific/area, or whatever). The normal Carphonewarehouse types all start off looking supremely confident (perhaps a little disparaging at the phone until they see the swing-out keyboard) but all have failed to fix our problem. Any ideas of where I can find some pointers on these discussion boards? Is this a configuration problem (can't think what we've done; but possible) or is this a firmware problem or just time to put this fab phone in the box with all my other Nokia ex-companions?? All best Paul aka. Hi I own a 6230i which is currently on the UK Virgin Mobile network. I'm trying to setup dial-up WAP access (not GPRS which works fine on this phone) to the web but am having problems. I've found all the settings on the web and created a personal configuration, but cannot get it to work. When trying to connect to the web this way the number dials, but is quickly followed by the message 'No response. Can anybody please tell me if it is possible use dial-up WAP on the 6230i, and if so exactly what I need to do to get it working! Hi I own a 6230i which is currently on the UK Virgin Mobile network. I'm trying to setup dial-up WAP access (not GPRS which works fine on this phone) to the web but am having problems. I've found all the settings on the web and created a personal configuration, but cannot get it to work. When trying to connect to the web this way the number dials, but is quickly followed by the message 'No response. Can anybody please tell me if it is possible use dial-up WAP on the 6230i, and if so exactly what I need to do to get it working! I have just purchased a 6230i for use with a Tomtom Go 700 satellite navigation unit. I also want to use the 6230i to receive my emails. I have an O2 pay and go tariff. Whenever I try to access my emails, I get a display on my phone which says 'Subscribe to GPRS first'. This also happens when I try to access the Internet from the Tomtom when I want to use the 'Traffic UK' service on the Tomtom. Bluetooth and the phone connection between the 6230i and the Tomtom works OK. I have downloaded the standard and advanced settings from the Nokia website to my phone, so I think I am correctly subscribing to GPRS. Is there another separate GPRS subscription which I have to get from O2 which is not already included in my O2 pay and go tariff? Thanks in advance for anyone's help with this. Hello; I have a problem with my 9300i. I bought 9300i last week to replace my 6230. In the past, I used palm Tx with 6230i GPRS modem. To use this old cople, i have to set it in: setting=connectivity=GPRS. In this menu, I make new 'active access point' Alias for access point:TRE gprs acces point: TRE051 that all! With this setting, my Palm work to send data. But now,I have 9300i,and the menu 'connectivity' is not there! I can't create 'acces point'! I don't now how to use 9300i modem with Palm Tx NB: I'must use the Palm software for my job! PLEASE HELP ME!!! Thanks Nicolas. I have Nokia 6230i connected to PC using Bluetooth and I want to set up my internet connection using dial-up number from fixed line operator (yes the old internet connection using a phone line and modem - with dialing an ISP number - except that I don’t have phone line) not GPRS. I am guessing that I don’t have modem initialization command because I can call that dial up number from my phone manually, but when I try to dial it from dial-up network connection I get strange sound and no call is made, however number shows up on phones display. I have Nokia 6230i connected to PC using Bluetooth and I want to set up my internet connection using dial-up number from fixed line operator (yes the old internet connection using a phone line and modem - with dialing an ISP number - except that I don’t have phone line) not GPRS. I am guessing that I don’t have modem initialization command because I can call that dial up number from my phone manually, but when I try to dial it from dial-up network connection I get strange sound and no call is made, however number shows up on phones display. I've had my phone for about 6 months now and have never succeeded in getting any settings for mms, email and web browser. I have requested settings via SMS from both the Nokia and Virgin Mobile (my provider) websites, but after loads of attempts none of the SMS settings messages ever reached my phone. I've contacted Virgin but all they could suggest is that I input the settings manually which I have done but still with no success - the message 'Subscribe to GPRS first' keeps showing up - although my GPRS setting is switched on?!? If I don't have any luck soon I'm going to have to get a new phone - does anyone have any suggestions? 19-Apr-2006 04:03 PM vicky1706 wrote: Hi there, you need to go into CONFIGURATION then PERSONAL CONFIGURATION SETTINGS then OPTIONS then ADD NEW then choose MULTIMEDIA MSG. Put in all the settings your provider has given you. You will need to carry out the same thing for WEB. I had exactly this same problem with my Nokia 6230i, hope this helps, it took me a good few months as well to figure it out. Let me know if you have any further queries. Thanks for that vicky. I'm getting sore thumbs trying to get it to work too. The problem I'm having though is more to do with checking my email with the 6230i. Sorry that wasn't clear on my previous posting. Have you had any luck with that? I've written to virgin mobile several times but they seem unable to help. I'm after the GPRS settings from them, such as: Access Point Name: Data bearer (GSM or GPRS?): Dial up number (if GSM): Gateway IP (proxy) address: Proxy port: There are several postings on some websites (but I can't make these work either. When I use this data and try and retrieve email, all I get is a prolonged connecting message that eventually gives up. I used to have a graphite 6230 and it worked fine on that, but the phone broke so I can't check the settings I had on that. Anyway, just hoping someone has had some success and can pass on the solution to me. Can anyone advise if they have had any success using a HP iPAQ 914c Business Messenger to work on a Vodafone monthly contract and use the GPRS/3G services? I just got one of these handsets and it is fantastic but I am unable to get GPRS/3G (or MMS) to work and I am on my 2nd Sim card. I did contact Vodafone UK customer services before getting the 914c to confirm that it would work and was told that it would. I have since called Vodafone UK tech support and told that they wont help me as it not an approved handset and they don't sell it. I am awaiting assistance from HP Support but they think that it should work with a Vodafone Sim. Has anyone got any ideas? Anyone else got a 914c? Hi Jason I'm sorry to hear that you are having problems here. Have you tried all of the settings listed on this page? Has this ever worked at all? What happens if you put your SIM into another mobile phone with a working internet connection? Are you able to get online with this? (We need to know if this is a problem with the settings on the handset or the network and this will tell us the answer) Please let us know the answer to the above questions and we'll be more than happy to help you further Thanks Wayne eForum Team Hi Wayne, Sorry for the delay in my answer, I was waiting for the reply from my provider. This is what the reply i got: GPRS has been reprovisioned for you as a precaution. Please turn the phone off and remove the SIM and battery, and wait 2 minutes before putting it back together and turning it on. Please retest the settings. Should the service still not work, please contact the manufacturer of the phone and ask them to assist you in setting up the GPRS profile. If they ask, it will need to be configured for the Vodafone network. Should you continue to experence issues, please advise us and what error messages you get. I did try the settings I got from slimtel, using the sim in my 6288 too using the automatic sms settings received from AAPT and Vodafone with no success. I have a feeling the service is not active since it should be succcefull in the 6288 with AAPT and vodafone automatic settings. Thanks, Jason. Hi brianh110881, First things first, welcome to the Vodafone eForum! It's always great to see new faces As we don't range this particular device ourselves, I'm afraid I have no set instructions myself for the settings. That being said I can try and suggest as much information as possible. You mentioned you had the IP settings already; these are not required for data access on our network so can I ask what have you got here? Just to confirm the other settings are correct, do you have the following? Password = web. Username = web. APN = internet. If there are any other users who can give more specific instructions or have managed to configure such a device themselves, please let me know Cheers, Ben eForum Team. 1)With my IPAQ hw6945 I may share files with a normal PC via WIFI or only internet conn?2)With my IPAQ hw6945 I can browse(wifi b) but I can NOT send/receive email in windows mobile outlook.well?I think when send/receive go for a gprs connection unsuccessfully. Well how modify use wifi connection instead(for email if I had prior enabled it)? If needed create a connection[wifi] and make it default, what to choose for the wifi connection type. In drop down list of conections(I do not see wifi)? For wifi from AP is needed vpn or proxy server or.?please note I can browse success only email the problem at wifi (I do not use gprs)! AP/ROUTER: Thomson 585 v7. 1)With my IPAQ hw6945 I may share files with a normal PC via WIFI or only internet conn?2)With my IPAQ hw6945 I can browse(wifi b) but I can NOT send/receive email in windows mobile outlook.well?I think when send/receive go for a gprs connection unsuccessfully. Well how modify use wifi connection instead(for email if I had prior enabled it)? If needed create a connection[wifi] and make it default, what to choose for the wifi connection type. In drop down list of conections(I do not see wifi)? For wifi from AP is needed vpn or proxy server or.?please note I can browse success only email the problem at wifi (I do not use gprs)! AP/ROUTER: Thomson 585 v7. I have a 6230i (3.46) and have installed an application called smsbug which requires access to the web via GPRS! The problem is that although i have downloaded the GPRS settings (Vodafone UK Prepay) and i can browse the web normally,this particular application cannot access the web! I have seen a 6230i with Orange and the details of the default configuration settings include web,mms and applications! Tried this application in that phone and worked fine! I am wondering if there is a way I can do that in my phone also or perhaps you can send me the GPRS settings via sms which will enable web access to the applications. I am looking forward for your answer thank you in advance. P.s I have already contacted Vodafone for this matter and I was told that I should ask Nokia for these settings. I have a 6230i (3.46) and have installed an application called smsbug which requires access to the web via GPRS! The problem is that although i have downloaded the GPRS settings (Vodafone UK Prepay) and i can browse the web normally,this particular application cannot access the web! I have seen a 6230i with Orange and the details of the default configuration settings include web,mms and applications! Tried this application in that phone and worked fine! I am wondering if there is a way I can do that in my phone also or perhaps you can send me the GPRS settings via sms which will enable web access to the applications. I am looking forward for your answer thank you in advance. P.s I have already contacted Vodafone for this matter and I was told that I should ask Nokia for these settings. Hi I have a 6230i but I am unable to access e.mail messages using the message menu ( I can access via wap ). I have an 02.co.uk e.mail account which i would like to access quickly via the phone. I got some settings from the internet which I downloaded to the phone. However, if I try 'retrieve messages' I get the message 'subscribe to GPRS first'. I cannot understand this as I am subscribed to GPRS and use it to access the internet, with which I have no problems. I have been told different things from o2, depending on who you talk to within that organisation. Some say that this service is not available with pay as you go, others that my phone is faulty and some that just scratch their head. Does anyone have a definative answer? Sorry for long posting. I have recently purchased a 6230i to replace my 6310i. I previously used a CA-42 USB cable for the 6310i but that is reported by the 6230i as incompatible - grrh. And now I am trying to set up the Bluetooth connectivity. I have (eventually) managed to get the 6230i paired to my Laptop using a Belkin USB Bluetooth and the Belkin software running on WinXP (IBM T41 laptop). PC Suite runs but seems to be a little unreliable over Bluetooth - will address that by sourcing a DKU-2 cable. However, I have problems with pairing the 6230i with my Sony HBH-600 headset (works perfectly with 6310i) I can get the 6230i to discover the headset either by searching for audio enhancements or by setting up a new pair, however it always fails to set up the connection (never asks for passkey). Similarly I cannot get my Ipaq 5550 to pair with the 6230i. I can start the pairing from the Ipaq which finds the 6230i but the 6230i never acknowledges the pairing attempt which then fails. If I start the pairing process from the 6230i it finds the Ipaq and attempts to pair but never asks to setup a passkey - the Ipaq does not seems to receive the pairing attempt. I have set the auto connect option to yes and no with no difference. Any suggestions? Needless to say all this worked perfectly with the 6310i. Project Manager Reuters. Hi all, I've been using my Nokia 6230i (bought Dec 05) as a GPRS modem to synch my inbox on my HP Ipaq (via bluetooth) for a few weeks now and everythign had been dandy. However in the last week I've been having GPRS problems. I can connect and my mailbox will start synching with the Exchange server fine and pulling down attachments and then all of a sudden the GPRS connection will drop out without any warning and the synch will not complete. It says something like 'GPRS connection ended' on the phone screen. The same thing happens when I just browse the internet on my Ipaq, the GPRS connection drops out, sometimes after a few minutes, sometimes after 20 seconds or so. I've tried changing alot of settings on the phone and Ipaq and the only conclusion I can come to is that the phone maybe malfunctioning. The firmware on the phone is 03.50. What is the lastest firmware update for this phone and is their a problem with GPRS known with this firmware version? Can anyone give me any advice. Thanks for reading, and thanks in advance. Hi I'm reactivating this topic in order to know if somebody has found a solution. I've exactly the same problem with a GPRS connection which is cut after about 1 min, the setting by itself working correctly. For specialists the connection log is saying 'ipcp down' when the connection is lost. I confirm it is a Nokia problem, and something linked between data GPRS and bluetooth. In my case, it happens always the same way on my nokia 6230 (firmware V 03.15 - model RH12) when the GPRS modem is used by various devices: a Palm Tungsten E2, a brand new MacBook Pro with factory bluetooth, a PowerBook with D-Link DBT120 USB bluetooth dongle. I've no problem when using the wap directly on the phone. I've tested on the powerBook the IR connection: it works fine. It's also fine with a USB to Nokia cable on the MacBook. So it's not a problem due to my provider (Orange), nor the GPRS part of the phone. When the problem occurs, the Nokia phone considers that it is still connected to the computer, and I need to switch off the phone to take control on bluetooth again (the disconnect choice in the bluetooth part of the menu is not working). As I've no bluetooth replacement solution for my Palm, I would be very happy if someone knows how to fix it (reset something in the phone, apply a patch, etc.) Thanks by advance for your answers Jean - from France. Hi All, I have a 6230i which is locked to Vodafone (v3.62 RM-72). I use it occasionally as a modem for collecting email and surfing from Windows XP on my Sony Vaio laptop. Connection is via Bluetooth. The problem is that the GPRS connection fails after about 30 seconds or 1 minute and sometimes the phone restarts itself. I'm convinced the problem is with Bluetooth because when I use an old laptop with infrared it works perfectly well. Previously I had a 6230 (not the i) which had a similar problem and apparently the solution was to replace the D400/TIKU processor. Can anyone suggest a solution for this one? It's making me tear my hair out!! Hi All, I have a 6230i which is locked to Vodafone (v3.62 RM-72). I use it occasionally as a modem for collecting email and surfing from Windows XP on my Sony Vaio laptop. Connection is via Bluetooth. The problem is that the GPRS connection fails after about 30 seconds or 1 minute and sometimes the phone restarts itself. I'm convinced the problem is with Bluetooth because when I use an old laptop with infrared it works perfectly well. Previously I had a 6230 (not the i) which had a similar problem and apparently the solution was to replace the D400/TIKU processor. Can anyone suggest a solution for this one? It's making me tear my hair out!! Hi Pip, Welcome to the Nokia Support Discussions Boards. When requesting help with this sort of iissue it can help if you let everyone know a bit more about your setup. Do you know what bluetooth drivers you're using, what version of windows you have, or which version of PC suite you have? You can find this by selecting Help/About Nokia PC Suite from the menus at the top of pc suite. The current version for the 6230I is 6.6.18 which you can download from www.nokia.com/pcs If you have pc suite 6.6.18 already I would recommend clicking on get connected and following the wizard through. Regards, Andrewc. Just purchased a Linksys WCF11 wireless card for an inherited Ipaq 2200. Set up goes fine UNTIL the blue bar reaches 100%. Then a message pops up in a frame titled 'Invalid Windows CE Setup Files' that says, 'Application manager cannot install this application on your mobile device due to an invalid setup file. Reinstall and try again.' I have tried a soft reset, hard reset, and changing options in the setup.nothing seems to help. I even tried dragging the files to the Ipaq through ActiveSync, which did not work. Thanks in advance for your consideration. Hi, Appreciate that Activesync is not the most stable of products but version 3.8 was working fine between my Tosh Tablet and iPAQ 6515. Installed Intellisync Mobile Suite Version 6.5 yesterday and is working fine on the iPAQ through GPRS but Activesync no longer works between the Tosh/iPAQ and this is my route for updating software on the iPAQ. I have read about a similar problem and that uninstalling Intellsync on the laptop fixed it and given that my iPAQ works through GPRS I don 't see the need for any Intellisync client on the Tosh? I suppose its understandable that two 'sync ' products may have problems coexisting on the same device but before uninstalling is there anything to try? I have tried EVERY suggestion in relation to ActiveSync!!! Anyone any thoughts on this? BTW: Intellisync Mobile Suite really does seem to be an excellent product. We get it through our SEA agreement so is an excellent deal. Have used it on a Treo 650 and now the iPAQ very successfully! I have a issue where I can get a user to work with GPRS on Dell x51 device with GPRS. When I get the same user to try and work with a Hp iPaq 210/214 device, I get subscribe to packet data. I have gone in the registry with of the iPaq. HKEY-Local_Machine - Unimodem - Init and then inserted the dial up string of: AT+CGDCONT=1,IP, name of providercr Name of the provider is our own companies APN. I have spoken with our mobile phone carrier who is BT and they have the correct APN at their end. I cant understand how I can get it to work on a Dell x 51 (WM5) and not on Hp 214 (WM6) I need to try and get this user to work on a Hp iPaq 210/214.Any ideas would be great? Hi Everyone, I'm excited about getting Ovi setup and working. I currently use the PC Suite via bluetooth to sync my Outlook to my Nokia 6230i which works perfectly. I created an Ovi Account, added my device, received an sms from Ovi and saved the settings. All good so far. However when I select Synchronise from the Menu - Organiser - Sync - Server Sync menu I get the following message 'Synchronise selected data? Unnamed Ovi.com' I select Yes Then i get this error 'Synchronisation failed' 'Contacts:Failed Calendar:Failed Notes:Failed' I have tried changing the settings to just Contacts and I get the same issue. It's odd as it doesn't even seem to try and connect. I get no GPRS icon, no delay just an error straight away. I assume that this is going to start a GPRS connection? I have tried changing my GPRS settings to 'always on' which didn't help. I have also checked and I can brose the web ok and pickup my email on the gmail app. Can anyone give me some tips or general info on anything else I can check or try? Hello, I have an Ipaq HW6910 with WM5and have recently installed ActiveSync 4.5 on my PC, I have a hand bit of software that allows me to use my Ipaq as if it's another monitor so I can control just by moving my mouse off the screen. This is great however I've noticed that my Ipaq seems drop the connection to ActiveSync after being connected for a short while, any idea's why it would be doing this?? Also does anyone know whether it's possible to use GPRS whilst the device is synced?? Mainly because this would allow me to use MSN from my keyboard and mouse despite my work proxy blocking the ports. Thanks for your help, Adam. Hello, I have an Ipaq HW6910 with WM5and have recently installed ActiveSync 4.5 on my PC, I have a hand bit of software that allows me to use my Ipaq as if it's another monitor so I can control just by moving my mouse off the screen. This is great however I've noticed that my Ipaq seems drop the connection to ActiveSync after being connected for a short while, any idea's why it would be doing this?? Also does anyone know whether it's possible to use GPRS whilst the device is synced?? Mainly because this would allow me to use MSN from my keyboard and mouse despite my work proxy blocking the ports. Thanks for your help, Adam. Found this interesting answer from CA955182: Re: h5450 -- SIM card reader? -- PocketPC Phone Edition?Post Options04:07 PM When HP developed the 545x, they were also developing a 5600 series iPAQ which they decided not to market before it ever came to market. The difference between the 5400 and the 5600 was that the 5600 had a tri-band cellular module in place of the 5400's WiFi module. The body of the 5400 and 5600 are identical so the 5400 has what looks like a SIM slot, but it isn't connected to any cellular hardware. In the earliest units (the ones that have Phone Edition on the back sticker) inserting a SIM card in the slot would produce the cellular icon on the status bar, but nothing else. In later units, the connectors aren't even there. The ROM software never included any SIM functionality.So, there isn't any way to give the 545x phone functions or to make any effective use of phone SIM cards even.However I can't confirm that it also applies to the h5500. In looking through specs for the h5500, though, I do not find anything about a SIM card.Hope this helps somewhat.aricari. Hi All, I have an O2 6230i which I'd like to be able to use to connect my PDA (Psion Netpad Windows CE 4.11) to the Internet with when / GPRS isn't available. I enter all the ISP details on the PDA and try to connect to the 6230i via the Infrared port. All seems to go well, and the phone dials the number, but as soon as the call is connected, it is disconnected and the PDA displays a message 'Cannot Detect Carrier'. I've tried the same thing from my Laptop with much the same results. I'm certain the ISP details are correct on the PDA as using a Nokia 6310i on Vodafone with the same details works correctly. These leads me to several conclusions: 1. The 6230i doesn't have an analouge modem in it. O2 are somehow blocking my attempts at phoning the number. I'm missing a setting somewhere in the phone that needs to tweaked. If this continues, I may loose what little sanity I have left Could anyone offer me some guidance and/or things to try? Thanks, Martin. Hi All, I have an O2 6230i which I'd like to be able to use to connect my PDA (Psion Netpad Windows CE 4.11) to the Internet with when / GPRS isn't available. I enter all the ISP details on the PDA and try to connect to the 6230i via the Infrared port. All seems to go well, and the phone dials the number, but as soon as the call is connected, it is disconnected and the PDA displays a message 'Cannot Detect Carrier'. I've tried the same thing from my Laptop with much the same results. I'm certain the ISP details are correct on the PDA as using a Nokia 6310i on Vodafone with the same details works correctly. These leads me to several conclusions: 1. The 6230i doesn't have an analouge modem in it. O2 are somehow blocking my attempts at phoning the number. I'm missing a setting somewhere in the phone that needs to tweaked. If this continues, I may loose what little sanity I have left Could anyone offer me some guidance and/or things to try? Thanks, Martin. Hi, Just received a new 6230i and I have been unable to connect my laptop to the internet using GPRS. I am on the Orange UK network and the phone seems set up ok. (I can connect to WAP ok and the data GPRS is enabled). I have the latest PC Suite installed (6.8) and the phone connects to my pc using a bluetooth device running the widcomm drivers. PC Suite can see my phone and it connects automatically. It transfers data and syncronises contacts without problems. Unlike my previous SE, no modems were set up automatically for the phone (although if I connect using irda a modem was set up). I have tried manually setting up a bluetooth modem using the downloaded nokia drivers. When I click on the connect to internet it attempts to use the Nokia 6230i Bluetooth modem I set up and attempts to connect although my phone is just not interested. I have tried both manual and automatic settings. Each time I try and connect the system confirms 'Failed to connect to the network! One Touch Access could not connect to the selected device.' Can someone help me get online and hopefully confirm what I am doing wrong. Kind Regards Si. The backup software on old Ipaqs like the h2210 was encoded into the operating system and privately branded by Sprite for HP. There is no update for this backup software. If you want a more current backup software, you'll need to purchase an application for your Ipaq. Unfortunately the h2210 is pretty old and the version of the windows mobile OS that runs on it is pretty ancient. I doubt you'll find a version of Sprite Backup software that can be purchased and that is compatible with the OS that is running on your Ipaq. Hi, i just recently purchased a 6300. I also have a N70 and the 6230i. Their GPRS works like a charm with Gmaill, Google Map, and Opera Mini. However, the 6300 seems to be a pain. I've gotten the configurations from Tmobile. I've even set up the GPRS in the Personal config. My Email system and Nokia web browser works fine. However, when i start to use the applications that i've downloaded, it seems to just break down. This is what i get when i try to access my GPRS. A tiny capital E on the upper right hand corner in a BOX. Thats about it. The program usually says 'loading' for about 2 minutes and then it pops up and error saying various messages like connection was not made etc etc. I looked in the manual/guide for the phone and it shows that the capital E stands for EGPRS. Isn't that ENHANCED GPRS? I'm not sure if TMOBILE USA has that. Might this be the reason why my applications are not connecting? PLEASE PLEASE HELP ME. I've spent hours and hours trying to figure this out. Hi, I am developing a Java application for Windows Mobile 2003 phone edition (Pocket PC) which as to communicate with a J2EE Server. On CLDC MIDP devices this works very good, just having to invoke Connector.open(xx) and even if the phone is not connected to the internet via GPRS, the connection is opened by the underlying j2me implementation/phone os. Now on a ipaq 6510 for example, if there is NO GPRS or Wi-Fi connection enabled, the Java app just doesn't get a connection. I can see that native windows mobile apps actively invoke/open a GPRS connection if needed - how can that be done in Java? Any Ideas - e.g. Regards, Hans. Hi, I am developing a Java application for Windows Mobile 2003 phone edition (Pocket PC) which as to communicate with a J2EE Server. On CLDC MIDP devices this works very good, just having to invoke Connector.open(xx) and even if the phone is not connected to the internet via GPRS, the connection is opened by the underlying j2me implementation/phone os. Now on a ipaq 6510 for example, if there is NO GPRS or Wi-Fi connection enabled, the Java app just doesn't get a connection. I can see that native windows mobile apps actively invoke/open a GPRS connection if needed - how can that be done in Java? Any Ideas - e.g. Regards, Hans. I don't think there's a list available of which is the most recent version for each network. Sadly lol Are you in the UK? The bits about the shipping are relevent only to the UK lol Assuming your warranty is intact, and there is an update available for your handset, yes, it should be updated for free, and yes, they do allow you to post them, though I'm not sure if that's all the Nokia Service Centres, or a select few - best to get in touch before sending it. Also, you should send it Special Delivery so it's insurred, and ask about this first, but you'll probably have to pay for the costs of return too - so I'd pay for that to be special delivery too lol. (Special Delivery items are insured for £500. Which is nice in the event of them going missing. Which does happen occasionally. Believe me, after ebay, I know! Haha ) Nokia History: 3110, 5110, 7110, 7110, 3510i, 6210, 6310i, 5210, 6100, 6610, 7250, 7250i, 6650, 6230, 6230i, 6260, N70, N70, 5300, N95, N95, E71, E72 Android History: HTC Desire, SE Xperia Arc, HTC Sensation, Sensation XE, One X+, Google Nexus 5. • • • From our current account that likes to thank you as you spend, to our travel money delivered wherever it's most convenient for you, we aim to give you banking the way you want it. • • • • • • • • • • • • • • Whether it's to help manage your spending, spreading the costs of a one-off purchase, or the serious business of buying a house, we've got it covered. • • • • • • • • • • • • • • • • • • • • • • • • • • Our range of savings accounts can give you competitive rates and easy access, while our ISAs offer tax free saving for you and your children. • • • • • • • • • • • • • • • • Whether you're protecting your car, your pets, your house, or just want to be safe on your travels, we have a comprehensive range of insurances with options that let you tailor your cover to your lifestyle. • • • • • • • • • • • • • • • • • • • • • • • • • • Calculators and comparison tables, jargon busters and top tips - our selection of tools and helpful information can help you get to grips with our products. • • • • • • • • • • • • • • • • • • • • • Help • If you're already banking or have insurance with us and you've got a question, need some help, or want to know what's available to you, you've come to the right place. • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •. 0% interest on purchases for up to 29 months Some things can’t wait, but the cost of them can. Help spread the cost of your spending as this card has our longest 0% interest period on purchases. ![]() • No interest to pay on purchases for up to 29 months from account opening. We may offer you a 0% interest period of 23 or 17 months instead depending on your individual circumstances • Collect even more Tesco Clubcard points when you spend • 0% interest on balance transfers for the first 3 months with a balance transfer fee of 2.9%. ![]() What you need to know about your new Tesco Clubcard. Do I need to activate the new card? The same place you would tap or enter your bank or credit card when. Mar 31, 2016. You must have your debit card before this can be activated and you can find out how to activate your card here: You can also call our Current Account team on 0345 835 3353 to activate your card. To earn 3% AER credit interest on balances up to £3,000 until 1 April 2019, simply pay in at least £750 and pay at least three Direct Debits each statement month. All of your existing payments in and out are automatically transferred to your new account; Once your debit card is activated, switching takes just seven working. You can transfer up to 95% of your available credit limit. • To benefit from these 0% interest periods you must make your minimum repayments on time and in full. 0% balance transfer fee No fee to transfer your balance and no interest to pay on the amount you transfer for up to 22 months from account opening. • 0% interest on balance transfers for up to 22 months from account opening. 0% balance transfer fee. We may offer you a 0% interest period of 18 or 14 months instead depending on your individual circumstances. ![]() Help to get you started with your new phone or tablet Pay. Activate your phone. 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Tesco Bank Credit Cards are provided by: Tesco Bank, PO Box 27028, Glasgow, G2 9FT. How to collect points with your Tesco Bank Credit Card It’s simple: use your credit card wherever you see the Mastercard logo. You’ll collect points on almost everything you buy. With the Premium Credit Card you collect 1 point for every £1 spent (£1 minimum) in Tesco and 1 point for every £4 spent (£4 minimum) outside Tesco in each purchase transaction. For all our other credit cards you collect 1 point for every £4 spent (£4 minimum) in Tesco and 1 point for every £8 spent (£8 minimum) outside Tesco in each purchase transaction. There are some products at Tesco you can't collect points on. Find out more about collecting points at the Tesco Clubcard website. Clubcard points also can’t be collected on Tesco Travel Money purchases. Points collection rates are subject to change. You must have available credit. The Tesco Clubcard Scheme is administered by Tesco Stores Limited, Tesco House, Shire Park, Kestrel Way, Welwyn Garden City, AL7 1GA, who are responsible for fulfilling points. Travel Insurance Tesco Bank Premium Credit Card Travel Insurance is included if you (the primary cardholder) are aged under 70. It also covers your immediate family members under the age of 70. You’ll be insured for as many trips of up to 31 days as you like and the policy also includes 17 days winter sports cover each year as standard. Immediate family means the primary cardholder’s spouse, co-habiting partner or civil partner and their dependent children, including grandchildren, step-children and foster children under the age of 18. No add-ons are available and the policy does not cover pre-existing medical conditions. Tesco Bank Premium Credit Card Travel Insurance is provided by Ageas Insurance Limited. PDF, 86kb 5,000 Clubcard points bonus If you spend £5,000 on your Premium Credit Card in Tesco in any year you will collect 5,000 bonus Clubcard points. Qualifying spend includes any purchase transactions in Tesco Stores UK (excluding Tesco Opticians, Tesco Mobile and Tesco Travel Money), Tesco.com (UK only), Tesco Direct, F&F Clothing, Tesco Wine by the Case and Tesco Petrol Filling Stations (UK only, excludes Esso). A year begins on the date the account was opened and each anniversary of that date, and ends 12 months later. Any refunds that you receive for returned items will be deducted from your total spend in that year. These points will be added to your Tesco Clubcard account within 45 days of the end of the relevant year and will be included in your next Tesco Clubcard statement after that. The Tesco Clubcard Scheme is administered by Tesco Stores Limited, Tesco House, Shire Park, Kestrel Way, Welwyn Garden City, AL7 1GA, who are responsible for fulfilling points. 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Its interface is more or less the same. ![]() ![]() ![]() Official Symbol PLAT provided by Official Full Name plasminogen activator, tissue type provided by Primary source See related Gene type protein coding RefSeq status REVIEWED Organism Lineage Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo Also known as TPA; T-PA Summary This gene encodes tissue-type plasminogen activator, a secreted serine protease that converts the proenzyme plasminogen to plasmin, a fibrinolytic enzyme. The encoded preproprotein is proteolytically processed by plasmin or trypsin to generate heavy and light chains. These chains associate via disulfide linkages to form the heterodimeric enzyme. This enzyme plays a role in cell migration and tissue remodeling. Increased enzymatic activity causes hyperfibrinolysis, which manifests as excessive bleeding, while decreased activity leads to hypofibrinolysis, which can result in thrombosis or embolism. ![]() Read the side effects of tissue plasminogen activator (tPA) therapy to fully understand the risks of this treatment before it is medically necessary. Define tissue plasminogen activator: a clot-dissolving enzyme with an affinity for fibrin that is produced naturally in blood vessel linings and is. Alternative splicing of this gene results in multiple transcript variants, at least one of which encodes an isoform that is proteolytically processed. [provided by RefSeq, Jan 2016] Expression Broad expression in urinary bladder (RPKM 61.1), placenta (RPKM 41.3) and 18 other tissues Orthologs. These reference sequences exist independently of genome builds. These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in above. Genomic • NG_023264.1 RefSeqGene Range 5001.37959 Download,,, mRNA and Protein(s) • → tissue-type plasminogen activator isoform 1 preproprotein Status: REVIEWED Description Transcript Variant: This variant (1) represents the longest transcript and encodes the longest isoform (1). Source sequence(s) Consensus CDS UniProtKB/Swiss-Prot Related,,, Conserved Domains (4) Location: 41 → 83 FN1; Fibronectin type 1 domain Location: 125 → 209 KR; Kringle domain; Kringle domains are believed to play a role in binding mediators, such as peptides, other proteins, membranes, or phospholipids. They are autonomous structural domains, found in a varying number of copies, in blood clotting and. Location: 313 → 559 Tryp_SPc; Trypsin-like serine protease; Many of these are synthesized as inactive precursor zymogens that are cleaved during limited proteolysis to generate their active forms. Alignment contains also inactive enzymes that have substitutions of the catalytic triad. Location: 215 → 296 Kringle; Kringle domain • → tissue-type plasminogen activator isoform 4 precursor Status: REVIEWED Description Transcript Variant: This variant (4) lacks two alternate in-frame exons in the 5' coding region compared to variant 1. The encoded isoform (4) is shorter than isoform 1. This isoform (4) may undergo proteolytic processing similar to isoform 1. Source sequence(s) Consensus CDS UniProtKB/Swiss-Prot UniProtKB/TrEMBL Related,,, Conserved Domains (4) Location: 221 → 467 Tryp_SPc; Trypsin-like serine protease Location: 41 → 83 FN1; Fibronectin type 1 domain Location: 224 → 470 Tryp_SPc; Trypsin-like serine protease; Many of these are synthesized as inactive precursor zymogens that are cleaved during limited proteolysis to generate their active forms. Alignment contains also inactive enzymes that have substitutions of the catalytic triad. Location: 126 → 207 Kringle; Kringle domain • → tissue-type plasminogen activator isoform 3 precursor Status: REVIEWED Description Transcript Variant: This variant (3) lacks an alternate in-frame exon in the 5' coding region compared to variant 1. The encoded isoform (3) is shorter than isoform 1. This isoform (3) may undergo proteolytic processing similar to isoform 1. ![]() Source sequence(s) Consensus CDS UniProtKB/Swiss-Prot Related,,, Conserved Domains (4) Location: 264 → 510 Tryp_SPc; Trypsin-like serine protease Location: 79 → 163 KR; Kringle domain; Kringle domains are believed to play a role in binding mediators, such as peptides, other proteins, membranes, or phospholipids. They are autonomous structural domains, found in a varying number of copies, in blood clotting and. Location: 267 → 513 Tryp_SPc; Trypsin-like serine protease; Many of these are synthesized as inactive precursor zymogens that are cleaved during limited proteolysis to generate their active forms. Alignment contains also inactive enzymes that have substitutions of the catalytic triad. Location: 169 → 250 Kringle; Kringle domain. The following sections contain reference sequences that belong to a specific genome build. This section includes genomic Reference Sequences (RefSeqs) from all assemblies on which this gene is annotated, such as RefSeqs for chromosomes and scaffolds (contigs) from both reference and alternate assemblies. Model RNAs and proteins are also reported here. ![]() Reference GRCh38.p7 Primary Assembly Genomic • NC_000008.11 Reference GRCh38.p7 Primary Assembly Range 4217724 complement Download,, Alternate CHM1_1.1 Genomic • NC_018919.2 Alternate CHM1_1.1 Range 4203859 complement Download. Plasminogen activator inhibitor type-1 (PAI-1) is a multi-functional protein. It is a fast acting inhibitor of plasminogen activators; urokinase-plasminogen activator and tissue type plasminogen activator, and also plays an important role in regulating cell proliferation, adhesion, migration, and signal transduction pathways. These biological events are important processes during angiogenesis and restenosis. PAI-1 has been shown to regulate proliferation, migration, and apoptosis of vascular smooth muscle cells and endothelial cells. ![]() The ability of PAI-1 to regulate cellular proliferation and migration has been attributed to its ability to control plasmin production, modify signaling pathways, and its inherent multifactorial ability to bind to vitronectin and lipoprotein receptor-related protein. However, the mechanism by which PAI-1 regulates the apoptotic pathway is not well understood. Evidence from the literature suggests that PAI-1 or its deficiency alters key signaling pathways, such as the PI3-k/Akt and the Jak/STAT pathways, and is involved in maintaining endothelial cell integrity thereby regulating cell death. Other investigators have demonstrated that PAI-1 directly binds to caspases as a mechanism of PAI-1-mediated cellular apoptosis. Moreover, results from studies assessing the role of PAI-1 in apoptosis have suggested that PAI-1 can exert pathogenic or protective effects, which may be related to the disease model or type of injury employed. Introduction Programmable cell death or apoptosis of vascular cells is an important process that occurs during blood vessel remodeling under both physiological and pathological conditions and is an important determinant in the fate of tumor growth (–), as well as in the formation of an atherosclerotic plaque (–). In vascular smooth muscle cells (VSMC), both apoptosis and anoikis, which is detachment of the cell from the extracellular matrix (ECM), significantly affects the development of atherothrombosis, plaque rupture, and aneurysm formation (,). Vascular cell apoptosis also occurs during neonatal vascular remodeling, where the VSMC and endothelial cells (EC) are subject to dramatic hemodynamic changes at birth (). Components of the plasminogen-plasminogen activator system have been implicated in playing an important role in these processes by facilitating ECM remodeling. Both VSMC and EC exhibit considerable fibrinolytic activity, whereby inactive plasminogen is converted to active plasmin by urokinase-plasminogen activator (uPA) and tissue type plasminogen activator (tPA). ![]() It has been demonstrated by in vitro and ex vivo studies utilizing VSMC, that tPA-mediated plasmin generation induced fibronectin fragmentation leading to cell detachment or anoikis (). In an Alzheimer’s disease model it was observed that activation of plasminogen by uPA or tPA was accompanied by increased viability of cerebrovascular smooth muscle cells due to degradation of the pathogenic amyloid-beta protein. Thus the plasmin-generating cascade serves a neuro-protective role. However, chronic expression of uPA and plasminogen activation led to significant cell detachment (). It was observed that increased PAI-1 expression in the hippocampus and amygdala regions of the brain specifically reduced tPA activity and clearance of the amyloid-beta protein (). In certain acute neuronal insults, such as ischemia microglial activation, tPA synthesis increases triggering neuronal death. This effect could be prevented by the presence of PAI-1 (). It thus appears that not only tight control of plasmin generation is important, but the neuroprotective effect of PAI-1 may surface during specific acute injuries, as in an ischemic attack. However, chronically increased levels of PAI-1 that inhibit plasmin generation promotes accumulation of the toxic amyloid-beta protein. Apart from the perspicuous functional capability of uPA and its cognate receptor (uPAR) in playing a dominant role in matrix degradation, migration, proliferation, and cytoskeleton changes (–), all hallmark events in cellular transformation; an emerging role in apoptosis is evolving. Blocking interaction of uPA to uPAR, or down-regulation of both uPA and uPAR resulted in decreased tumor cell invasion, and increased apoptotic cell death in prostate cancer (,) and breast cancer cell lines (). Pre-exposure of nontransformed human retinal pigment epithelial cells to uPA diminished anoikis and UV-induced apoptosis, which were mechanistically attributed to up-regulation of the anti-apoptotic factor Bcl-xL via the MEK/ERK and PI3-k pathway. The protective anti-apoptotic effect was eliminated when uPA/uPAR expression was down-regulated by RNAi (). TNF-α-induced apoptosis in monocytes could be inhibited by plasmin with concomitant reduction in the levels of active caspase-3, -8, and -9 (). Although it has been established that tPA, uPA, uPAR, and plasmin are involved in regulating apoptosis, plasminogen activator inhibitor-1 (PAI-1), which is the primary inhibitor of the uPA/tPA-plasmin axis, is also known to regulate cellular apoptosis. This review focuses on the role of PAI-1 in apoptosis and a number of possible mechanisms are discussed herein. The Paradoxical PAI-1: To Be Apoptotic or Not To Be PAI-1 is a rapid and most physiologically-relevant inhibitor of uPA and tPA. Several investigations have detailed a positive correlation between high levels of uPA and uPAR with poor prognosis and unfavorable clinical outcome in several types of cancers (, –). It would appear logical that PAI-1, by virtue of its ability to inhibit activation of plasminogen by uPA or tPA, would effectively inhibit tumor angiogenesis and growth. However, increased levels of PAI-1 are indicators of poor prognosis for cancer patient survival (–). The role of PAI-1 in angiogenesis is controversial, where it has been documented to be pro-angiogenic (–), anti-angiogenic (–), or indifferent (). These observations were found to be dependent on the experimental setting, stage of cancer progression, and the origin of the cells. Furthermore, angiogenic effects of PAI-1 have also been found to be dose-dependent (, ). In these studies, physiological concentrations (nanomolar) of PAI-1 promoted angiogenesis through its anti-proteolytic activity, whereas high concentrations (micromolar) of PAI-1 were anti-angiogenic attributed to its vitronectin binding function (). PAI-1 has been proposed to act as a molecular switch, and at high concentrations it dissociates EC uPAR from vitronectin promoting a migratory phenotype followed by correct presentation of integrins to matrix ligands that allows for EC adhesion (, ), thus promoting angiogenesis. Poor prognosis may be related to the source of PAI-1. Observations leading to poor prognosis correlated to high PAI-1 levels in the surgical samples (–) or in the patient’s plasma (, ). However, when tumor cell lines were transfected with PAI-1, the aggressiveness of tumor growth and metastasis was diminished in HT-1080 fibrosarcoma cells (), murine melanoma (), PC-3 prostate cancer cell lines (), and in malignant keratinocytes (). From these early studies emerged the tenet that PAI-1 may play a role in apoptosis. Subsequently other studies followed that corroborated the novel role of PAI-1 in regulating apoptosis. PAI-1 and apoptosis in neovascularization Tumor progression and dissemination are dependent on neovascularization or formation of new blood vessels, which involves tipping the pro-angiogenic and anti-angiogenic balance in favor of the former. Though this process involves a large number of proteases and extensive remodeling of the ECM promoting tumor invasiveness, investigations on mediating tumor cell apoptosis and its mechanism are significantly scrutinized as a means of controlling tumor growth. Neovascularization is also manifested during atherosclerotic plaque formation typically characterized by accumulation of smooth muscle cells and inflammatory cells in the media and sub-endothelial spaces. The role and mechanism of apoptosis in defined cell lineages, such as VSMC, EC, and macrophages during plaque formation would provide novel therapeutic insights for drug design in atherosclerosis. This section highlights the role of PAI-1 in apoptosis in pathophysiological settings of tumors and atherosclerosis. When the human prostate cancer cell line PC-3, and the human promyelocytic leukemia cell line HL-60 were treated with recombinant wild-type (WT) PAI-1, induced and spontaneous apoptosis were diminished. This inhibition of apoptosis by PAI-1 was reversed by the presence of a neutralizing antibody that accelerated the conformational change of active PAI-1 to inactive PAI-1. Similarly, treatment of cells with latent PAI-1 did not inhibit apoptosis, thus suggesting that the reactive site loop may be required for the apoptosis inhibiting function. Furthermore, inhibition of apoptosis by PAI-1 is independent of the PAI-1:uPA complex, signaling through uPAR, or binding to vitronectin. Inhibition of apoptosis by an exogenous source of PAI-1 could very well mimic the tumor environment where PAI-1 is secreted in the tumor vasculature by surrounding stromal cells, and potentially increasing the aggressiveness of the tumor, thus giving credence to the reported observations of PAI-1 as a prognostic marker of poor overall survival (). In contrast, tumor cells transfected to express high levels of PAI-1, acting as tumor-host PAI-1, behave differently, conferring anti-angiogenic properties (,, ). The differential effect of PAI-1 expressed by normal and cancerous cells on apoptosis has been documented by Lademann et al (2005), who have observed that fibrosarcomas obtained through spontaneous transformation in WT mice showed decreased cellular sensitivity to chemotherapy-induced apoptosis compared to fibrosarcomas obtained from PAI-1 −/− mice. Whereas, WT and PAI-1 −/− mice display similar sensitivity to etoposide exposure, clearly underlining that PAI-1 expressed by cancer cells behaves differently than PAI-1 expressed by normal cells on apoptosis, and that inhibiting PAI-1 may be beneficial for encouraging chemotherapy-induced apoptosis (). Another study from the same group highlighting the anti-apoptotic potential of PAI-1 demonstrated that fibrosarcoma cell lines established from PAI-1 −/− mice took significantly longer to grow and develop tumors when injected in WT or PAI-1 −/− mice compared to fibrosarcoma cell lines established in WT mice. Also, the PAI-1 −/− fibrosarcoma cells were more susceptible to TNF-α-induced apoptosis accompanied by increased levels of caspase-3 activity compared to the WT fibrosarcoma cells (). These differences in PAI-1 expressing and PAI-1-deficient fibrosarcoma cells have been attributed to differences in cell proliferation, and that PAI-1 expressed by the tumor cells protects the tumors from apoptosis. Since exogenous PAI-1 could also inhibit apoptosis in non-tumor cells, such as HUVEC and the benign human breast epithelial MCF-10A cell lines, it is thought that regulation of apoptosis by PAI-1 could also have physiological implications (). The inconsistent nature of PAI-1 surfaced when rPAI-1 did not induce apoptotic death or, control the growth and metastasis of implanted human colon cancer xenografts in nude mice. On the other hand, intraperitoneal infusion of rPAI-2 diminished the size of the primary tumor and enhanced the tumor apoptotic index (). A similar anti-cancer activity of PAI-2 was observed due to enhanced apoptosis in metastatic prostate cancer cells (). However, stable transfection of the human prostate cancer PC3 cells that conditionally expressed active PAI-1 regulated by doxycycline resulted in dramatic inhibition of angiogenesis as observed by CD31 staining, when these cells were injected in nude mice. The PAI-1-induced diminished angiogenesis was ascribed to an early wave of apoptosis in tumor EC with a concomitant decrease in cell proliferation. The induction of EC apoptosis by PAI-1 was found to be vitronectin-dependent, which served as an adhesion matrix during angiogenesis (). PAI-1 induces EC apoptosis by preventing the interaction of EC integrins, α vβ 3, to the RGD binding site of vitronectin resulting in disruption of integrin-mediated signaling and hence triggering anoikis (). At the time of a pathological condition, such as cancer progression, PAI-1 levels are dramatically increased. Studies initiated with different cell lines, such as PC3 or malignant PDVA keratinocytes stably transfected with PAI-1 cDNAs express approximately 9–18-fold elevated levels of secreted PAI-1 antigen (,, ). Tumorigenicity and angiogenic phenotype of these transfected cell lines were observed when injected in either WT or PAI-1 deficient mice to allow investigation on the effect of PAI-1 on newly established tumor vasculature in early stages of tumor progression. It is possible that these high levels of PAI-1 present during pathological conditions are sufficient to compete and displace the binding of EC integrins α vβ 3, to the RGD binding sites of vitronectin. Furthermore, recapitulation of PAI-1 inducing EC apoptosis, which is dependent on vitronectin, was observed in vitro when microvascular EC co-cultured with PC3 cells, stably transfected to express PAI-1 exclusively, underwent apoptosis when plated in the presence of vitronectin (). Similarly, PAI-1 could inhibit EC tube formation in the presence of vitronectin but not in the presence of fibronectin (). These in vitro experiments were performed utilizing rPAI-1 at high concentrations of 40–100 nM. However, it should be noted that this mechanism of PAI-1-mediated tumor apoptosis by a vitronectin-dependent mechanism might be possible in an environment where the tumor is established and angiogenesis is still active. In such a scenario the EC detach and launch to re-adhere to vitronectin, which is inhibited due to the presence of high levels of PAI-1 in the tumor microenvironment. Since tumor growth is dependent on neovascularization, this would result in an inability of the tumor to sustain further growth. A similar anti-adhesive property of PAI-1, the result of a 2–3-fold increase in apoptosis, was documented in EC and VSMC, and found to be vitronectin-dependent. Induction of apoptosis was mediated by the caspase-3 pathway and the apoptotic cells were associated with foam cells as observed in atherosclerotic vessel sections, thus re-enforcing the importance of apoptotic and anti-adhesive mechanism in tissue remodeling during neointima formation (). In contrast PAI-1 did not induce apoptosis of human brain microvascular EC even though it inhibited α vβ 3 integrin-mediated adhesions to vitronectin. Instead it stimulated migration of EC from vitronectin towards fibronectin, promoting cell migration away from the vitronectin-rich perivascular spaces towards fibronectin-rich tumor tissues. Thus, a lack of adhesion alone is not sufficient to induce apoptosis by PAI-1 suggesting that other mechanisms may be involved (). Tumor growth of T241 fibrocarcoma cells was significantly suppressed in PAI-1 −/− mice accompanied by decreased proliferation and increased apoptosis in tumors from these deficient mice compared to WT mice (). In this case, lack of host PAI-1 did not sustain tumor growth and survival potentially due to a lack of the ability to disrupt EC adhesion from the surrounding vitronectin and promote motility, thereby preventing neovascularization. EC isolated from aortas of PAI-1 −/− mice exhibit increased proliferative phenotype associated with hyperactivation of the Akt molecule required to maintain cell survival and integrity. The increased levels of Akt(P-Ser473) were responsible for increased levels of inactive caspase-9(P-Thr163) and hence lower levels of active caspase-3 in the PAI-1 −/− cells compared to WT cells. Spontaneous apoptosis was also decreased in PAI-1 −/− EC relative to WT cells. Treatment of PAI-1 −/− EC with recombinant PAI-1 induced a WT proliferative phenotype, and also increased the levels and activity of caspase-3 which increased spontaneous apoptosis, establishing a novel role for PAI-1 in regulating apoptosis via the Akt signaling pathway. It was determined that interaction of PAI-1 with the endocytic receptor lipoprotein receptor-related protein (LRP) was essential for PAI-1 to negatively regulate cell proliferation, since the mutant R76E[PAI-1], which has diminished ability to bind to LRP, was unable to regulate cell proliferation of PAI-1 −/− cells (, ). It appears from the studies of Balsara et, 2006 () and Chen et al, 2008 () that either an exogenous source of PAI-1, in case of in vitro EC studies or tumor cells overexpressing PAI-1 is effectively able to induce apoptosis and control growth of tumor vasculature. Conversely, a complete deficiency of host PAI-1 also does not support tumor growth by induction of apoptosis as observed when PAI-1 −/− mice were injected with the T241 fibrosarcoma cells (), and these observations could reflect that the source of PAI-1 is an important determinant for deciding the fate of a tumor. Increased proliferation and decreased apoptosis of VSMC is a distinguishing hallmark of restenosis (–) accompanied by increased synthesis of PAI-1 in patients with type 1 diabetes (–) suggesting that increased PAI-1 expression could affect VSMC apoptosis. It has been observed by Chen et al (2004) () that VSMC from SM22-PAI-1 + mice, which overexpress PAI-1 by 2-fold, were approximately 20% less apoptotic than control WT cells when stimulated with tissue necrotic factor and/or phorbol myristate acetate. These findings are in consonance with the fibrosarcoma studies of Romer et al (2005) described earlier (). Decreased apoptosis was due to a decrease in caspase-3 activity, and when exogenous PAI-1 was added to VSMC lysates or directly to recombinant caspase-3, inhibition of caspase-3 activity was observed. Solid phase binding assays demonstrated that PAI-1 could bind to caspase-3 with an apparent Kd of ~3 nM. The proteolytically inactive PAI-1 (H190L-H191L) could neither bind to caspase-3 nor inhibit caspase-3 activity suggesting that the inhibitory activity of PAI-1 is essential for its anti-apoptotic activity (). The high affinity interaction, in vitro, of PAI-1 with caspase-3 to form a complex is not considered stable as the 1:1 stoichiometric complex formed between PAI-1 and uPA or tPA. The PAI-1/caspase-3 complex is dissociable under reducing conditions. Analogous interactions between other inhibitory proteinases of the serpin superfamily and caspases have been documented typically described as “cross-class” interaction, in which a serpin inhibits a non-serpin proteinase (, ). The serpin CrmA (Cytokine Response Modifier A) binds to caspase-1 modulating host inflammatory responses (), and the PI9 (Proteinase Inhibitor 9) serpin interacts with caspases-1, -4, and -8 (). While binding of CrmA to capase-1 is rapid with a second-order rate constant of 2 × 10 7 M −1s −1 (), the second-order rate constant for PI9 and caspase-1 is 700 M −1s −1 (). This could have significant physiological implications where CrmA could be required to completely inhibit an inflammatory response. In contrast, inhibition of caspase activity in a more controlled manner would be beneficial. Though not much is known about inhibition of caspase-3 activity by interaction with PAI-1 it is possible that intracellular PAI-1 can bind to caspase-3 or pro-caspase-3 attenuating apoptosis. It is also possible that internalization of secreted PAI-1 by the uPA/uPAR/PAI-1 tri-complex could bind and inhibit caspase-3, thereby serving as an anti-apoptotic agent. Further consequences of increased PAI-1 levels in the SM22-PAI-1 + VSMC resulted in increased proliferation due to increased expression and activity of FLICE-like inhibitory protein (FLIP) which in turn induces NFκ-B and ERK signaling to promote proliferation. Additionally, the levels of dichotomous cleaved caspase-8 that can cleave caspase-3 or cleave FLIP to generate p43 that promotes proliferation, was increased in the SM22-PAI-1 + VSMC favoring proliferation compared to littermate control VSMC. Inhibition of NFκ-B and ERK signaling effectively diminished cell proliferation of SM22-PAI-1 + VSMC indicating that PAI-1-mediated cell proliferation in these cells is through both of these pathways (). Conversely, plasminogen-induced apoptotic index was high in VSMC from PAI-1 −/− mice compared to VSMC from WT, uPA −/−, and tPA −/− mice. The pro-apopotic index paralleled the generation of plasmin activity, which was higher in PAI-1 −/− VSMC, and the PAI-1-deficient cells showed morphological alterations reminiscent of apoptosis, such as cell shrinkage and nuclear fragmentation (). In fact, the apoptotic index of VSMC in atherosclerotic aortas from ApoE −/−:PAI-1 −/− mice was higher accompanied with enhanced in vivo levels of plasmin, and active caspase-3, consequently leading to a decrease in VSMC density relative to the ApoE −/− littermates (). Fibroblasts and myofibroblasts are key cells involved in wound closure and reepithelialization and undergo physiologic apoptosis during wound repair, the absence of which could cause tissue fibrosis (, ). Plasminogen-induced apoptosis of fibroblasts, which is accompanied with fibronectin proteolysis and anoikis of fibroblasts, could be inhibited by TGFβ-1 due to TGFβ-1-mediated upregulation of PAI-1, and subsequent inhibition of plasminogen activation. Furthermore, TGFβ-1 was unable to protect the cells from apoptosis when lung fibroblasts from PAI-1 −/− mice were treated with plasminogen. PAI-1 −/− fibroblasts demonstrated increased plasminogen-induced apoptosis, which was reversed when the deficient cells were reconstituted with exogenous PAI-1 (). High levels of PAI-1 prevented extracellular proteolysis resulting in accumulation of extracellular matrix components, such as fibronectin, thereby promoting progressive tissue fibrosis. Although the precise mechanism as to how PAI-1 regulates apoptosis in fibroblast cells is unknown, it has been shown to be associated with pericellular proteolysis of fibronectin. Therefore, PAI-1 plays a central role in protecting cells against plasminogen-induced apoptosis. There is strong evidence suggesting a role for PAI-1, and in general the plasminogen/plasmin system, in VSMC apoptosis which is a major process that determines atherosclerotic plaque vulnerability (, ). The significance of these findings allows for mechanistic insights regarding the pivotal role of PAI-1 in vascular remodeling, whereby increased expression of PAI-1 in diabetic patients may promote increased accumulation of VSMC in response to a vessel wall injury. However, neointima formation was attenuated following an arterial copper cuff injury () or carotid artery ligation () in PAI-1 −/− mice compared to control mice with no differences observed in proliferation of PAI-1 −/− VSMC. This highlights the conflicting effects of PAI-1, which may be a reflection of variation in experimental scenarios that may be dependent on cell types and the challenge models that are employed. PAI-1 and apoptosis in the central nervous system In the central nervous system the tPA-plasmin system has been known to play a significant role in synaptic plasticity, remodeling (, ), and in regulation of neuronal survival in response to excitoxicity (, ). However, PAI-1 although secreted by astrocytes does not behave as the prototypic inhibitor of the neural protease cascade but rather functions as a neuroprotective agent (, ), and high levels of PAI-1 in cerebrospinal fluids (, ), and the central nervous system could also serve as an index of neurological diseases (–). There is some evidence of a role for PAI-1 in regulating neuronal apoptosis. When PC-12 neurons were grown in medium containing PAI-1 obtained from astrocyte-derived conditioned medium, the neurons maintained their morphology and survived. However, when the neurons were cultured in medium deficient of PAI-1, neuron survival decreased by 50% and the cells exhibited typical apoptotic characteristics of a rounded morphology and DNA fragmentation. The mechanism by which a PAI-1 deficiency promotes apoptosis is through stimulating the release of mitochondrial cytochrome c, and decreasing mRNA levels of anti-apoptotic Bcl-2 and Bcl-X L genes with a concomitant increase in pro-apoptotic Bcl-X S and Bax mRNA (). Eventually, the formation of the apoptosome composed of cytochrome c, Apaf-1, and procaspase-9 results in upregulation of caspase-3 activity. Similar results were observed when an anti-PAI-1 neutralizing antibody was added to the neuronal medium. Anti-apoptotic characteristics were restored to the neurons when recombinant PAI-1 was added to the culture medium. Interestingly, neural plasminogen activation activity was not affected by the presence or absence of PAI-1. Thus reinforcing that PAI-1 is not the primary inhibitor of the neural plasminogen system, and that it plays an important role in regulating survival of neurons (). The anti-apoptotic or pro-survival function of PAI-1 on neurons was demonstrated in PC12 cells where PAI-1 promoted neurite outgrowth and survival. These phenotypic observations were reversed in the absence of PAI-1 when the PC12 cells exhibited a typical apoptotic/necrotic phenotype. The pro-survival function of PAI-1 was found to be due to activation of c-jun and ERK pathways, which was preceded by the activation of the nerve growth factor receptor, Trk A (). Summarizes the pro- and anti-apoptotic activities of PAI-1 in different cell types. Effect of PAI-1 on apoptosis on some select cell lines In other studies of N-methyl-D-aspatate (NMDA)-induced excitotoxicity of co-cultures of neurons and astrocytes, transforming growth factor-α and -β (TGF-α/β) -mediated neuroprotection against apoptotic cell death was attributed to increased expression of PAI-1 by astrocytes via two different signaling pathways. TGF-α-mediated increase in PAI-1 expression was through activation of the ERK pathway, whereas TGF-β-mediated increase in PAI-1 expression was through the Smad-3-dependent signaling pathway. This neuroprotection was not observed when neurons were co-cultured with PAI-1 −/− astrocytes, thus highlighting the role of PAI-1 in controlling excitotoxic neuronal death stimulated by the glutamatergic agonist NMDA (, ). This is in consonance with earlier studies where the cerebral ischemic infarct size was significantly enlarged in PAI-1 −/− mice compared to WT mice and this was reversed when the PAI-1 −/− mice were injected with recombinant adenovirus encoding PAI-1 protein (). However, in primary cortical neurons, blocking of the serine protease HtrA1 (high temperature responsive antigen 1), which is known to regulate several pathologies, such as Alzheimer’s disease, macular degeneration, and osteoarthritis, led to overexpression of neuronal PAI-1 mediated by TGF-β1 signaling and eventually to neuronal death (). This observation is in contrast to the neuroprotective effect of PAI-1 against NMDA-induced excitoxicity (, ). However it is possible that HtrA1-mediated TGF-β signaling effect on PAI-1 expression could play a central role in neuronal maturation during brain development. Conclusion It is evident that PAI-1 is a functionally promiscuous protein, not only acting as a primary inhibitor of uPA and tPA, but also involved in modulating cell proliferation, migration, and apoptosis (,,,, ). PAI-1 expression is tightly regulated and under normal conditions PAI-1 is present as a trace protein in plasma. However, during a pathological condition, such as cancer, atherosclerosis, diabetes, and severe obesity PAI-1 levels are dramatically elevated(). The involvement of PAI-1 in angiogenesis is controversial and not fully understood. It regulates this process through binding of PAI-1 to vitronectin () or through inhibition of uPA and tPA where excess plasmin activity is abrogated leading to vessel stabilization (, ). Components of the plasminogen activators-plasmin system are also known to regulate apoptosis, however PAI-1 can be pro-apoptotic (,, ), and anti-apoptotic (,,, ). Increased levels of PAI-1 in tumor pathologies prove to be beneficial to the tumor as it down-regulates apoptosis promoting a more aggressive phenotype and supporting the paradox that elevated PAI-1 levels correlate with poor patient prognosis. Indeed, addition of exogenous PAI-1 to HL-60 and PC-3 cells could inhibit apoptosis that required the inhibitory activity of PAI-1, but was not necessarily via the uPA/uPAR-signaling axis (). Another advantage for cancer cells producing high levels of endogenous PAI-1 may be that they are less sensitive to chemotherapy treatment. Church and colleagues () demonstrated that MDA-MB-435 breast cancer cells expressing WT PAI-1 had an increased recovery compared to MDA-MB-435 cells expressing inactive PAI-1 after treatment with paclitaxel. Hence, up-regulation of PAI-1 in cancer cells foster tumor growth and spread. Furthermore, by cDNA microarray analysis it was demonstrated that MDA-MB-435 cells expressing WT PAI-1 down-regulated genes, such as follistatin, which is an inhibitor of anti-proliferation (). Similarly, fibrosarcoma fibroblasts established from PAI-1 −/− mice were more sensitive to apoptotic stimuli and had a longer lag-phase before they could establish tumors when injected in mice (). From the above investigations it appears that down-regulation of PAI-1 would be beneficial for killing tumorigenic growth. Absence of PAI-1 in VSMC, an important component of an atherosclerotic plaque, increases the apoptotic index, which may be beneficial in preventing atherosclerotic plaque formation or restenosis. Increased expression of PAI-1 or addition of exogenous PAI-1 controlled VSMC apoptosis by inhibiting caspase-3 (). Addition of plasminogen to PAI-1 −/− VSMC induced an increase in apoptosis compared to WT, tPA −/−, or uPA −/− VSMC, indicating that plasminogen-mediated apoptosis is dependent on plasmin generated by tPA or uPA and is dampened by PAI-1 (, ). These data provide mechanistic insights in terms of the pathogenic or protective role of PAI-1 in vascular remodeling. Schematically portrays the possible mechanisms by which PAI-1 could be regulating apoptosis. Alhough PAI-1 is a secreted protein, any intracellular events occurring after PAI-1 is internalized and is able to interact with caspases or other apoptotic proteins should not be discounted. Besides, interaction of PAI-1 with LRP may elicit recruitment of signaling intermediates that could regulate apoptosis via an unknown mechanism. There is a high probability that such a mechanism is possible when PAI-1 is added exogenously. We have demonstrated that r-PAI-1 could effectively diminish the hyperactivation of Akt in PAI-1 −/− EC with downstream consequences of increasing levels of active caspase-3 thereby increasing spontaneous apoptosis (). Excess PAI-1 synthesized in a diseased state is known to compete for binding with vitronectin causing detachment of EC. It is also possible that PAI-1 could be controlling apoptosis by two different mechanisms simultaneously. PAI-1-mediated apoptosis Another mechanism by which PAI-1 can control proliferation is by controlling key cell cycle progression proteins. It has been reported that mouse embryonic fibroblasts (MEFs) from PAI-1 −/− mice display an uncontrolled proliferative phenotype compared to PAI-1 expressing MEFs mediated by a senescence bypass mechanism. As observed in primary murine aortic PAI-1 −/− EC (), the PAI-1 −/− MEFs also exhibited sustained activation of Akt(P-Ser473) accompanied by nuclear retention of cyclin D1 and increased inactivation of GSK3-β was sufficient to bypass senescence (103). Thus PAI-1 acts as an inhibitor of proliferation. In pathological conditions where PAI-1 over expression promotes accumulation of VSMC, as in the increased incidence of restenosis after percutaneous coronary interventions or renders tumor cells resistant to chemotherapeutic agents, decreasing PAI-1 levels would be beneficial. 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See sky.ie for more details and our Usage Policies. Eircom compatible phone line required. Sky Q Hub: Inclusive for new Sky Broadband customers with Sky Q TV (otherwise €50 if joining without Sky Q TV or €10 if upgrading from Sky TV taking Sky Broadband for the first time). €99 for existing Sky Broadband customers who choose to upgrade or downgrade. Standard broadband activation fee of €5-€10 depending upon product choice. #Sky Talk Freetime: Inclusive evening and weekend calls of up to an hour to the Republic of Ireland local and national landline numbers only (excludes calls to Directory Enquiries, indirect access, dial-up Internet numbers, mobile, and 0700 numbers) and then calls are charged at rate of 6.90c per minute (evening) and 1.40c per minute (weekend). Evening – Monday to Friday, after 7pm and before 7am. Weekend - between midnight on Friday and midnight on Sunday. Fair Use Policy applies (see contracts for details). Eircom compatible phone line required. 12 month minimum subscription. Set up costs may apply. Sky Talk Line Rental required. **Sky Talk Anytime: Anytime calls of up to an hour to the Republic of Ireland and Northern Ireland local and national landline numbers only (excludes calls to Directory Enquiries, indirect access, dial-up Internet numbers and 0700 numbers) and then charged at 6.90c per minute (daytime & evening) and 1.40c per minute (weekend). Anytime international geographic landline calls of up to an hour to 20 countries (Austria, Australia, Belgium, Canada, Czech Republic, Denmark, France, Germany, Greece, Hungary, Italy, Luxembourg, Netherlands, New Zealand, Norway, Spain, Sweden, Switzerland, UK and USA (also includes calls to mobiles in Canada and USA). Fair Use Policy applies (see contracts for details). Eircom compatible phone line required. 12 month minimum subscription. Set up costs may apply. Sky Talk Line Rental required. Mobile Hotspots and Tablets are only compatible with Straight Talk Data Service Plans. Straight Talk Unlimited Plans and All You Need Plans will not work with these devices. Service Plans are not refundable or returnable. For Mobile Hotspot devices: A single connected device will experience optimal speeds. Performance will be reduced if multiple devices access data through the hotspot simultaneously. Actual speed, availability and coverage will vary based on device, usage, and network availability. Straight Talk Mobile Hotspot original settings will allow any Wi-Fi® capable device to connect unless connection is secured. You can change the security settings in the Wi-Fi® tab. For more information please refer to the Services Guide included in the package. When using this App, standard data rates may apply. Information may be transmitted with a delay and may not reflect actual balances. ††Based on a comparison of the average cost of the $45 Straight Talk Service Plan plus average sales tax and fees when purchased in Walmart and the average total monthly cost reported by top two carriers’ postpaid customers on a 2-year service contract individual plan with unlimited talk, text and comparable high speed data. Plan costs include all taxes, fees and overage charges. Source: Nationwide survey conducted February 2016. When you purchase, activate, or use a Straight Talk product or Straight Talk Wireless services, you agree to comply with the latest, which are subject to change from time to time without notice. Straight Talk is a registered trademark of TracFone Wireless, Inc. All other trademarks, service marks and trade names referenced in this site are the property of their respective owners. ©2017 TracFone Wireless, Inc. 9700 NW 112th Avenue, Miami, FL 33178. All rights reserved. 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I got access to adobe licensing site, where they gave me a serial number and I downloaded the media, but the serial key doestn work. ![]() I tricked the MSI into trial mode and got Adobe to install, but it asks to activate over the net. We cant allow that due to security policy so I had to activate by phone. Activation key for Acrobat 8 Professional has stopped working. I uninstalled Acrobat 8 Professional in the process of finding why it would not print pdf documents received over the internet (prints garbage). Adobe.Acrobat.8.0.Professional-Patch CiM keygen and crack were successfully generated. Download it now for free and unlock the software. I was able to activate on one computer but each other computer requires a unique activation code. Any one know how to incorporate licensing into the package? Where does adobe store the license info once a machine has been activated? Attention, Internet Explorer User Announcement: Jive has discontinued support for Internet Explorer 7 and below. In order to provide the best platform for continued innovation, Jive no longer supports Internet Explorer 7. Jive will not function with this version of Internet Explorer. Please consider upgrading to a more recent version of Internet Explorer, or trying another browser such as Firefox, Safari, or Google Chrome. (Please remember to honor your company's IT policies before installing new software!) • • • •. ![]() Lebara mobile might seem attractive, but they are a nightmare to deal with - especially if you're travelling from overseas into the UK. I bought a Lebara SIM because I had used Lebara in, and it was very easy. But, in the UK, it chewed up all my credit in just a few days. And then, when I tried to top-up my credit, I ran into the ridiculous problem of Lebara ONLY accepting UK credit cards. What kind of company that wants to attract travellers only accepts UK credit cards????? The stupidity of this defies belief. What was even more painful, is that when you try and recharge online they don't tell you this. You just keep on getting error messages without explanation. Lebara help page explaining how to Topup online in simple easy steps. Topup online and enjoy Lebara mobile UK's cheap call rates! Lebara Mobile UK offers cheap international calls, national & data plans. Order your free PAYG sim or Topup online today! How to order free Lebara SIM card from. Activate the SIM card. Create 'my Lebara. Lebara France mailed me a SIM card right away, but Lebara UK said they only. When I did call (and sat on hold for 10 mins), they finally explained that international credit cards aren't accepted. Extraordinarily stupid. (Even more stupid, when I used my international credit card just fine in Spain to recharge my Spanish Lebara Sim) The only solution they provide is to hunt-down an on-street seller of Lebara credit. This is doable, but it would be good if they simply advised on their website they don't accept international credit cards. Many UK phone networks only allow online topup to UK registered cards. Probably an anti-fraud measure. UK and Spanish financial laws are different. Finding a store that sells Lebara top-up is hardly difficult though. Any shop displaying the green Top-up symbol where you'd top-up any other network, Payzone, Paypoint, Post Office, Phones4U, Carphone Warehouse, Asda, Morrisons, Tesco, Sainsburys. It's not like it's some strange small company where you can only top up at 3 places in London and they're all in Hounslow. I'd definitely agree-DO NOT buy a Lebara sim. We got them at the airport and they seemed ok, really cheap calls to Australia and free messages to Lebara, as well as data for maps etc. However, once the data is expired there's no way to opt out and renew again or get a different pass. If you run out of data after 20 days, you are stuck for 10 days not being able to get a new pass, you can 'recharge' credit but not the data or pass, and you are stuck being charged an exorbitant amount for data (ours lasted 2 days with this option-10 pound down the drain). After calling customer service and spending about half an hour on the phone were told you can only have one active pass, and even if you opt out, you can't get a new one before 30 days (no where in terms and conditions does it say anything about that). Furious about the situation. Try t mobile or anyone else. I bought Lebara sim card, added Data Plus 500 Pass for 15 GBP. They declared: 'Mobile Data: Unlimited'. After 5 days they cancelled my Data Plus pass without prior notice and switched my sim card to pay-as-you-go tariff, 1 GBP for 0.2 Mb, after that all my Lebara balance was withdrawn in 10 minutes. I called them to find out what happened. They said that they applied their amendment: 'UNLIMITED data (subject to no naughty abuse of our offer terms and fair use policy)'. So, I downloaded 3 Gb of data and they considered that it is not 'fair'. Beware of this tricky company called Lebara. I totally agree. DO NOT buy a Lebara SIM. Their customer services are simply appalling to deal with. They actually made it impossible for me to switch my old mobile number over to them. Part way through the procedure, the call was cut off. When I called back, I had to repeat all the PUK and PAC codes (understandably) and answer how much credit I had. Since it was a new card I just had the £10 but they said as I got a security question wrong (how much credit) they would not deal with me. I later discovered that the original call had taken 10pence off my credit which I did not realise so gave the wrong answer. I have binned the SIM! • What about Power Converters and Adapters? • 'Staying in touch' while travelling? So many questions! • More Questions about Luggage • Packing Tips? • Mobile / cell phone questions? • Bring an unlocked phone or buy a Prepaid phone in USA / Canada? • Digital camera? Photo storage media? • Tips regarding internet use when traveling? • Take a lap-top or net-book? • What is a good tablet / e-reader to choose for travel? • What apps are good for tablets? • The Wish List; & Top Ten (10), or less, Gadgets and/or Gear? Roaming - Use Your Phone Abroad If you travel abroad you can still use your Lebara Mobile SIM card. All you have to do is log on to your MyLebara account and for roaming, we will then activate roaming on your number within a few minutes. Signing Up for Roaming: • To sign up for roaming you must have a CPR-number and a current Danish address. • You must be 18 years or older. • Lebara Mobile approves the roaming application after validation of your credit rating. We reserve the right to reject a roaming application due to your credit rating. • You must have a valid bank card (Dankort, Visa, Visa Electron, Mastercard). • Roaming will be charged regularly from your bank card, provided you have used your phone abroad. • Signing up for roaming costs 49 kr. Using Your Phone Abroad: • Lebara Mobile follows the roaming rates set by Telenor. • When you use your mobile phone abroad, you are using one of the local mobile operators with which Telenor has a roaming agreement. In any country where Telenor has more than one partner operator, you can choose which operator you want to use. When you are abroad, you will see the name of the foreign operator on the display of your phone. You can find out how to select operator manually in your phone’s user guide. • Please note: Telenor does not have roaming agreements with all operators in all countries. • To be able to use your phone abroad, particularly when travelling to a different continent, you must make sure that your mobile can use the frequency of network used in that country. If you have a smartphone you should not experience any issues but if your phone is a few years old or is a basic model you may wish to check this beforehand. If you travel outside Europe the minimum requirement should be a so-called ‘triband’ phone. Roaming Rates: • When using your phone abroad you must pay to make and receive calls. • When you receive calls abroad, you pay the international part of the conversation, i.e. From Denmark to the country that you are in. The person calling you pays normal rate for calling a Danish mobile. • It is free of charge to receive SMS but you must pay to send an SMS. • Mobile data is generally expensive to use abroad and you should not have an active data connection unless you need it. When you use Data in EU: You will have 2GB per month if you have 2GB left in you active package. Hereafter you will be charged per MB. To avoid a high data usage we will always send you an SMS when you have spent 450 kr. On data within 1 calendar month when travelling in the EU, and we will block any further data usage unless you request to have data enabled again. • You can see the current roaming rates. A bba H air S pray A lternative H air P roducts. Com||||||||||||: Finish your hair styles with Abba Hair Spray. Abba offers four different types of hairspray to meet every hair need. Whether you need protection from heat styling or you need to set your curly hair in place, Abba has what you need. 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January 2018
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