My hp pavillion broke just yesterday, so i took my hard drive out and put it in a toshiba satelite, while looking threw my things i notice it says ' 2 days until automatic activation' something about the product key, whats does this mean and what will i have to do in 2 days? Also will i have problems. My hp pavillion broke just yesterday, so i took my hard drive out and put it in a toshiba satelite, while looking threw my things i notice it says ' 2 days until automatic activation' something about the product key, whats does this mean and what will i have to do in 2 days? Also will i have problems cause its not a hp mother board? Best Answer: Your laptop has OEM license so it works only in one computer. You have transferred your HDD to other system and you OS things that system is changed as it is asking you for activation. Simply try to activate windows because OEM licensed support approx 5 activation in-case you format your system or you have any hardware failure.If you cant activate with Same key came with HP then try other activation option that is Phone activation same you find when you get error while activating windows on Toshiba.Then after call Microsoft on toll free number and provide them your Installation ID and as per your installation ID they will provide you activation ID from that you can activate your windows. • Tell us some more • Upload in Progress • Upload failed. Please upload a file larger than 100x100 pixels • We are experiencing some problems, please try again. • You can only upload files of type PNG, JPG, or JPEG. • You can only upload files of type 3GP, 3GPP, MP4, MOV, AVI, MPG, MPEG, or RM. • You can only upload photos smaller than 5 MB. • You can only upload videos smaller than 600MB. • You can only upload a photo (png, jpg, jpeg) or a video (3gp, 3gpp, mp4, mov, avi, mpg, mpeg, rm). • You can only upload a photo or a video. • Video should be smaller than 600mb/5 minutes • Photo should be smaller than 5mb •. ![]() ![]() ![]() Learn how to legally use Windows without activating, for 360 days. 0: Specifies that the. Disable Automatic Activation Feature in Windows 10/8/7. Apr 18, 2017 This step-by-step article describes how to enable and disable Auto-activation feature in. 0 = Allow Auto-activation. Automatic activation begins. I've just put in my windows 7 disc and it says 3 days until automatic activation. Could someone please tell me what this means. This article describes how to use Multiple Activation Key. Volume Activation Management Tool (VAMT) 2.0 Tool. '3 days until automatic activation.
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Below we will look at two programs in Excel VBA. One program loops through all charts on a sheet and changes each chart to a pie chart. The other program changes some. Below we will look at two programs in Excel VBA. One program loops through all charts on a sheet and changes each chart to a pie chart. The other program changes some properties of the first chart. See solution in other versions of Excel: • • • • • How to open the VBA environment You can access the VBA environment in Excel 2007 by opening the Microsoft Visual Basic window. First, be sure that the Developer tab is visible in the toolbar in Excel. The Developer tab is the toolbar that has the buttons to open the VBA editor and create Form/ActiveX Controls like buttons, checkboxes, etc. To display the Developer tab, click on the Microsoft Office button in the top left of the Excel window and then click on the Excel Options button. When the Excel Options window appears, click on the Popular option on the left. Select the option called ' Show Developer tab in the Ribbon'. Then click on the OK button. Select the Developer tab from the toolbar at the top of the screen. Then click on the Visual Basic option in the Code group. Now the Microsoft Visual Basic editor should appear and you can view your VBA code. ||| Books at Amazon.com Quick Excel Chart VBA Examples The use of VBA in Microsoft Excel charting is a topic that would fill a large volume. The examples here are straightforward illustrations of easy techniques to create charts, add and remove series, and move and resize charts using VBA. ![]() ![]() ![]() ![]() ![]() ACTIVATION WINDOWS 7 ULTIMATE ON DELL LATITUDE D820 CAN BE DONE I came here to find out how to INSTALL WINDOWS ULTIMATE 32 BIT for my 3 YEARS OLD DELL LATITUDE D820. After so many activation attempts, I FINALLY GOT IT LICENSED AS IT SHOULD BE. ( very proud ). I decided to write this article for DELL LATITUDE OWNERS out there who wants to upgrade to WINDOWS 7 ULTIMATE but do not want to do much digging around. PREPARATION: • DOWNLOAD WINDOWS 7 ULTIMATE RTM BUILD 7600.16385.x86fre.win7_rtm.0. This is the lastest and final from MICROSOFT TO THIS DATE. I've been fighting this problem for months. Around 2008-2009, I purchased a refurb'd Studio 1735 laptop directly from Dell. It came with Vista Home Premium OEMAct factory installed. There was some special deal at the time that included a Windows 7 upgrade. When I received the product, it came with the. I am building a computer, and I was wondering if I could use a good friends Windows 7 Re-installation CD from dell on the brand new computer. We've used the disk. I do not know any other versions will work with this activation process. • DOWNLOAD the modified version D820_A09_SLIC of the BIOS. This version will have SLIC 2.1 required for 7LOADER. Dell released SLIC 2.0 version on their web site, this will not allow you to active your WINDOWS 7. This is the file name which I found somewhere in this awesome forum 'DELL_Latitude_D820-DELL-A09.rar' Search for it boys. I don't want to go back to get the link • DOWNLOAD Windows 7Loader By Orbit30 & Hazar Build 1.4 (Released August 12, 2009). ![]() The file name is '7Loader 1.4.exe' I attached the screenshot of the software below. STEPS TO ACTIVATE: • YOU need to flash your bios with the program D820_A09_SLIC.EXE. Dell DO NOT ALLOW to flash without BATTERY so go to find your battery and plug it in. After you run the flash program, the laptop will restart automatically. SIT AND WAIT FOR PC TO RESTART. You might see short time of BLACK OUT. • THEN You can pop your WIN7 DVD in and happily install your WINDOWS 7 ULTIMATE. ACTIVATION WINDOWS 7 ULTIMATE ON DELL LATITUDE D820 CAN BE DONE I came here to find out how to INSTALL WINDOWS ULTIMATE 32 BIT for my 3 YEARS OLD. They all usually start from the security block and the creative bug from the source shifts their paradigm to a vision of freedom. You wonder what would be the answer if you asked the CEO of Microsoft, Bill Gates or Dell Computer's CEO Michael Dell which one have they always wanted, security or freedom. I'm certain of this,. Put ultimate productivity back in your hands. Maximize the performance of your OptiPlex with Dell-recommended essential accessories. SKIP THE SERIAL KEY PART, JUST CARRY ON. YOU DON'T HAVE TO PUT ANYTHING THERE • After complete installation. Run '7Loader 1.4.exe' and • CLICK ON SLIC 2.1 IN BIOS. WAIT TO SELECT 'DELL' CERTIFICATE. THE FIRST DELL. ![]() THERE ARE 2 DELL CERTIFICATE IN THERE. • THEN CLICK ON 'Install 7 Loader' and wait for a few minutes. YOU SHOULD BE ABLE TO SEE YOUR LICENSE KEY POP UP • YOU CAN CHECK 'ACTIVATION STATUS' AFTER ALL TO SEE YOUR RESULT • FINALLY INSTALL YOUR VISTA DRIVERS. ![]() XP DRIVERS WON'T WORK ON WIN 7. YOU CAN DOWNLOAD FROM DELL WEBSITE. MOST DRIVERS WE NEED COME WITH WINDOWS 7 EXCEPT GRAPHIC DRIVER. ENJOY YOUR WINDOWS 7. MICROSOFT, I LIKE YOU SO MUCH. If you need any help, drop me a line. Kratki pogled na windows 7. Isprika radi snimke,snimano je mobitelom. Excuse for the recording, recorded a mobile phone. Windows 7 Ultimate is the most versatile and powerful edition of Windows 7. It combines remarkable ease-of-use with the entertainment features of Home Premium and the business capabilities of Professional, including the ability to run many Windows XP productivity programs in Windows XP Mode. For added security, you can encrypt your data with BitLocker and BitLocker-To-Go. And for extra flexibility, you can work in any of 35 languages. Get it all with Windows 7 Ultimate. Whenever we send an email to the other person, we generally hope that the email will be opened and they will reply us with some response. Unfortunately, hope doesn’t necessarily mean that it will be done. In fact, there will be times when we are in desperate need to know if the receiving party has even opened the sent email. ![]() After all, most of us hate to be ignored. Gmail users doesn’t have any built-in feature to request read receipts or to get email open notifications. That said, there are traditional methods to track email opens like using images, Google scripts, link shorteners, etc. These methods are time consuming and are not easily accessible for all users due to all the technical details. Here is an easy way that doesn’t require any technical knowledge to request Gmail read receipts and to get email open notifications. ![]() Jul 31, 2013 Overview of how to send a read receipt in GMail. A lot of people consider Read Receipt Confirmation a. How to send Request Read Receipts in Gmail? How to activate/enable Read Receipts for Google Apps. Of course, the method shown below is not foolproof. Note: The tip shown here works even when you are using Google apps. Gmail Read Receipts and Email Open Notifications The workaround here to track email opens is to use a free web application called Yesware. The working of Yesware is real simple and uses the traditional approach, i.e. This web application inserts a tracking pixel (1 x 1 transparent image) into the email you are sending. That said, Yesware does all the heavy lifting like tracking those pixels and maintaining a record of all the notifications. To get started, head to, scroll down and then click on “add yesware to Gmail” button. This action will install an extension or addon depending on the browser you are using (Firefox or Chrome). Once you have installed the extension, Yesware automatically opens your Gmail account. Enter your Gmail account password, if needed. Once your Gmail account is opened, Yesware will show you a pop-up where you have to click the “Activate now” button to activate Yesware for that specific account. As soon as you click the “activate now” button, Yesware will open another window where you have to accept for the requested permissions. Go through all the permissions and click on the “Accept” button to continue. Once you have accepted the requested permissions, Yesware will display another pop-up asking whether you would like to connect a salesforce account. As this is not available for free accounts, just click on the “I don’t use salesforce” button to continue. Of course, if you want to integrate Yesware with your salesforce account, you can do so. After finishing the installation process, you’ll see a small ribbon on the top of your inbox displaying various menu items like events, emails, schedule, etc. Now to track any email you are sending, just select the checkbox “track” and then send the message to the intended recipient. Once the recipient opens the email you have sent, the event is logged and you will receive a notification that looks something like this. Along with the notification, all the events are logged under the event tab located on top of the inbox. The content displayed in the Cylex Business Directory consists of information from third parties, among others from publicly accessible sources, or from customers, who have a presentation page in our directory. Cylex cannot be held responsible or liable for the accuracy, correctness, usefulness or reliability of the data. The brand names, logos, images and texts are the property of these third parties and their respective owners. If you have any questions or suggestions regarding this matter, you are welcome to contact our customer support team. What Is It Really Like to Follow Jesus? Ben Fagerland Series: You Asked for It 2017. Find opening hours, phone number, address and more info of best Churches in Maroondah. St Pauls Anglican Church Ringwood; Activate Church. ![]() ![]() Activate Church is passionate to see people come together under the name of Jesus. Our heart is to build faith, love people and raise disciples of Jesus. The Activate Church app keeps you up to date with key information about Activate Church. It allows you to register easily for upcoming events, join a life group, submit a prayer request and even give financially. SPECIAL FEATURES: * Podcast: Listen to the latest sermon or lookup a previous one in the podcast library. * Digital Bible: Enter in the passage you want or use quick keys to go directly to the passage you desire to read. ![]() ![]() ![]() * Free Audio Bible: Click listen and you are instantly listening to the daily devotional plan. You can also look up any passage you want, the listen tab is in the bottom right hand corner at all times. SOCIAL INTEGRATION: Share content with your friends via Twitter, Facebook, or email. * Facebook: You can share a Bible passage, journal entry or anything in the app with one click. * Twitter: You can tweet a Bible passage, reading plan, journal entry or just a note with easy. PURSUE JOURNAL: * Daily Bible Reading Plan: The Pursue Bible reading plan takes you through the Old Testament once a year and through the New Testament twice a year. Average reading or listening time is 15 minutes a day. * Free Customizable Journal: The Pursue Journal is designed to give you the freedom to journal whenever and however you desire. Entries are fully secure for your privacy, yet at any time you can share them via Facebook, twitter or email. * Cloud Based Journal: Your Pursue Journal is accessible online anytime at www.PursueJournal.com. This allows you to be able to add entries anywhere, anytime and they are automatically linked to your Activate Church app. For more information about Activate Church, please visit: For more information about Pursue Journal, please visit: The Activate Church app was created by “Custom Church Apps TM” Web: www.customchurchapps.com Email. ![]() What are neurons? They are tiny cells that are in charge of participating in the functions related to the nervous system. In our brain, there are millions of neurons, scientists calculate that we have about 80 million when we are born. As we grow, this number decreases. After 80 years-old, we will have lost 30% of our neurons. Throughout our life, we constantly lose and regenerate neurons. By our neurons' regeneration process, new connections are made which produces a process called neurogenesis. This process allows for the birth of new neurons through a person's life. Scientists know that the active areas of the brain use more energy, and thus use more oxygen and glucose. Femur (thigh bone) Gastrocremius muscle Patela (knee cap) Posterior Anterior Achilles I Visualize some exercises that would be good for strengthening your bones. Deteriorate At the end of the second sentence is a synonym for this word. What does deteriorate mean? Hunched Use your logic to determine the meaning. Center for Regenerative Medicine at Mayo Clinic: Exploring neuroregeneration to repair damage or disease in the brain and central nervous system. ![]() ![]() This way, more blood is brought to these areas with the intention of satisfying the active neurons' demands. As you activate your brain, blood runs to the working brain cells. MRI images are used to understand blood flow in the brain. These images have shown that our brain cells, also known as neurons, are very dependent from the oxygen supply. The more we use our brain and activate the neurons, the more blood supply they receive. On the other hand, an inactive brain cell receives less and less blood until it ultimately dies. * CogniFit assessments are intended as a screening tools for detecting cognitive decline or alterations in an effort to allow physician directed therapeutic intervention to occur. In a clinical setting, the CogniFit results (when interpreted by a qualified healthcare provider), may be used as a screening aid to assist in determining whether or not a particular individual should be referred for further neuropsychological evaluation (e.g., a complete neuropsychological exam). CogniFit does not directly offer a medical diagnosis of any type. A diagnosis of ADHD, dyslexia, dementia, or similar disease can only be made by a qualified physician or psychologist considering a wide range of potential contributing factors. Consistent with this stated intended use, CogniFit assessments tools have no indication that are or should be considered a Medical Device by the FDA. The product may also be used for research purposes for any range of cognitive related assessments. If used for research purposes, all use of the product must be in compliance with appropriate human subjects' procedures as they exist within the researchers' institution and will be the researcher's obligation. All such human subject protections will under no circumstances be less than those required to be afforded to research subjects under the provisions of Section 45 CFR 46 of the Code of Federal Regulations. ![]() Mastercard offers a wide range of debit cards, whether you need a debit card for your everyday purchases or a debit card for your world travel. ![]() • Tell us some more • Upload in Progress • Upload failed. Please upload a file larger than 100x100 pixels • We are experiencing some problems, please try again. • You can only upload files of type PNG, JPG, or JPEG. • You can only upload files of type 3GP, 3GPP, MP4, MOV, AVI, MPG, MPEG, or RM. • You can only upload photos smaller than 5 MB. • You can only upload videos smaller than 600MB. • You can only upload a photo (png, jpg, jpeg) or a video (3gp, 3gpp, mp4, mov, avi, mpg, mpeg, rm). • You can only upload a photo or a video. • Video should be smaller than 600mb/5 minutes • Photo should be smaller than 5mb •. Ack1 Tyrosine Kinase Activation Correlates With Pancreatic Cancer Progression - Download Free Apps2/26/2018 TNK2 gene encodes a non-receptor tyrosine kinase, ACK1. The activation of ACK1 has been observed in. Pancreatic, lung and ovarian cancer cells. Activation of Tyrosine Kinases in Cancer. Of targeted tyrosine kinase (TK) inhibitors for cancer treatment. Drives cancer progression. Kiran Mahajan, PhD Academic. LIneberger Comprehensive Cancer Center. Ack1 tyrosine kinase activation correlates with pancreatic cancer progression. ![]() ![]() TNK2 Available structures Ortholog search: List of PDB id codes,,,,,,,,, Identifiers, ACK, ACK-1, ACK1, p21cdc42Hs, tyrosine kinase non receptor 2 External IDs Targeted by Drug Molecular function • • • • • • • • • • • • • • • Cellular component • • • • • • • • • • • • • Biological process • • • • • • • • • • • • • • Sources: / pattern Orthologs Species Human Mouse RefSeq (mRNA) RefSeq (protein) Location (UCSC) search Activated CDC42 kinase 1, also known as ACK1, is an that in humans is encoded by the TNK2. TNK2 gene encodes a non-receptor tyrosine kinase, ACK1, that binds to multiple receptor tyrosine kinases e.g. EGFR, MERTK, AXL, HER2 and insulin receptor (IR). ACK1 also interacts with Cdc42Hs in its GTP-bound form and inhibits both the intrinsic and GTPase-activating protein (GAP)-stimulated GTPase activity of Cdc42Hs. This binding is mediated by a unique sequence of 47 amino acids C-terminal to an SH3 domain. The protein may be involved in a regulatory mechanism that sustains the GTP-bound active form of Cdc42Hs and which is directly linked to a tyrosine phosphorylation signal transduction pathway. Several alternatively spliced transcript variants have been identified from this gene, but the full-length nature of only two transcript variants has been determined. Interactions ACK1 or TNK2 has been shown to with, Androgen receptor or, a tumor suppressor, and. ACK1 interaction with its substrates resulted in their phosphorylation at specific tyrosine residues. ACK1 has been shown to directly phosphorylate AKT at tyrosine 176, AR at Tyrosine 267 and 363, and WWOX at tyrosine 287 residues, respectively. ACK1-AR signaling has also been reported to regulate levels, Clinical relevance ACK1 is a survival kinase and shown to be associated with tumor cell survival, proliferation, hormone-resistance and radiation resistance. The activation of ACK1 has been observed in prostate, breast, pancreatic, lung and ovarian cancer cells. ACK1 transgenic mice, expressing activated ACK1 specifically in prostate gland has been reported; these mice develop prostatic intraepithelial neoplasia (PINs). ACK1 inhibitors Ack1 has emerged as a new cancer target and multiple small molecule inhibitors have been reported. All of these inhibitors are currently in the pre-clinical stage. • Maruyama K, Sugano S (1994). 'Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides'. 138 (1–2): 171–4... • Satoh T, Kato J, Nishida K, Kaziro Y (1996). 'Tyrosine phosphorylation of ACK in response to temperature shift-down, hyperosmotic shock, and epidermal growth factor stimulation'. 386 (2–3): 230–4... • Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, et al. 'Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library'. 200 (1–2): 149–56... • Mott HR, Owen D, Nietlispach D, et al. 'Structure of the small G protein Cdc42 bound to the GTPase-binding domain of ACK'. 399 (6734): 384–8... • Eisenmann KM, McCarthy JB, Simpson MA, et al. 'Melanoma chondroitin sulphate proteoglycan regulates cell spreading through Cdc42, Ack-1 and p130cas'. 1 (8): 507–13... • Kato J, Kaziro Y, Satoh T (2000). 'Activation of the guanine nucleotide exchange factor Dbl following ACK1-dependent tyrosine phosphorylation'. 268 (1): 141–7... • Owen D, Mott HR, Laue ED, Lowe PN (2000). 'Residues in Cdc42 that specify binding to individual CRIB effector proteins'. 39 (6): 1243–50... • Kiyono M, Kato J, Kataoka T, et al. 'Stimulation of Ras guanine nucleotide exchange activity of Ras-GRF1/CDC25(Mm) upon tyrosine phosphorylation by the Cdc42-regulated kinase ACK1'. 275 (38): 29788–93... • Linseman DA, Heidenreich KA, Fisher SK (2001). 'Stimulation of M3 muscarinic receptors induces phosphorylation of the Cdc42 effector activated Cdc42Hs-associated kinase-1 via a Fyn tyrosine kinase signaling pathway'. 276 (8): 5622–8... • Teo M, Tan L, Lim L, Manser E (2001). 'The tyrosine kinase ACK1 associates with clathrin-coated vesicles through a binding motif shared by arrestin and other adaptors'. 276 (21): 18392–8... • Kato-Stankiewicz J, Ueda S, Kataoka T, et al. 'Epidermal growth factor stimulation of the ACK1/Dbl pathway in a Cdc42 and Grb2-dependent manner'. 284 (2): 470–7... • Oda T, Muramatsu MA, Isogai T, et al. 'HSH2: a novel SH2 domain-containing adapter protein involved in tyrosine kinase signaling in hematopoietic cells'. 288 (5): 1078–86... • Strausberg RL, Feingold EA, Grouse LH, et al. 99 (26): 16899–903.... • Salomon AR, Ficarro SB, Brill LM, et al. 100 (2): 443–8.... • Ahmed I, Calle Y, Sayed MA, et al. 'Cdc42-dependent nuclear translocation of non-receptor tyrosine kinase, ACK'. 314 (2): 571–9... • Gu Y, Lin Q, Childress C, Yang W (2004). 'Identification of the region in Cdc42 that confers the binding specificity to activated Cdc42-associated kinase'. 279 (29): 30507–13... • Brandenberger R, Wei H, Zhang S, et al. 'Transcriptome characterization elucidates signaling networks that control human ES cell growth and differentiation'. 22 (6): 707–16... • Lougheed JC, Chen RH, Mak P, Stout TJ (2004). 'Crystal structures of the phosphorylated and unphosphorylated kinase domains of the Cdc42-associated tyrosine kinase ACK1'. 279 (42): 44039–45... External links • human gene location in the. • human gene details in the. Abstract Receptor and nonreceptor tyrosine kinases (TKs) have emerged as clinically useful drug target molecules for treating certain types of cancer. Epidermal growth factor receptor (EGFR)-TK is a transmembrane receptor TK that is overexpressed or aberrantly activated in the most common solid tumors, including non-small cell lung cancer and cancers of the breast, prostate, and colon. Activation of the EGFR-TK enzyme results in autophosphorylation, which drives signal transduction pathways leading to tumor growth and malignant progression. Randomized clinical trials of the EGFR-TK inhibitor gefitinib have demonstrated clinical benefits in patients with advanced non-small cell lung cancer whose disease had previously progressed on platinum- and docetaxel-based chemotherapy regimens. Bcr-Abl is a constitutively activated nonreceptor TK enzyme found in the cytoplasm of Philadelphia chromosome-positive leukemia cells. STI571 (imatinib mesylate) inhibits the Bcr-Abl TK, blocks the growth of these leukemia cells, and induces apoptosis. STI571 also inhibits other TKs, including the receptor TK c-kit, which is expressed in gastrointestinal stromal tumors. As TK inhibitors become available for clinical use, new challenges include predicting which patients are most likely to respond to these targeted TK inhibitors. Additional clinical trials are needed to develop the full potential of receptor and nonreceptor TK inhibitors for cancer treatment. I ntroduction The clinical development of targeted tyrosine kinase (TK) inhibitors for cancer treatment represents a breakthrough in the understanding of the molecular mechanisms of disease, and a challenge in reevaluating existing intervention strategies. Small-molecule TK inhibitors, such as STI571 (imatinib mesylate, Gleevec ™; Novartis Pharmaceuticals Corporation; East Hanover, NJ), gefitinib (Iressa ®; AstraZeneca Pharmaceuticals LP; Wilmington, DE), and OSI-774 (erlotinib, Tarceva ™; OSI Pharmaceuticals; Melville, NY/Genentech; South San Francisco, CA), are different from antibody-based therapies in that they enter tumor cells and directly interfere with TK enzymes that are aberrantly activated in tumor cells and are critical to the growth of the tumor. Oral bioavailability and good tolerability profiles also distinguish these agents from conventional cytotoxic chemotherapies. It is important to understand this new approach to cancer treatment in order to identify how it best fits with current treatment practices and to maximize its potential. TK s as T argets for A ntitumor T herapy TKs are enzymes that transfer γ-phosphate groups from ATP to the hydroxyl group of tyrosine residues on signal transduction molecules []. Phosphorylation of signal transduction molecules is a major activating event that leads to dramatic changes in tumor growth. Some TKs, such as epidermal growth factor receptor (EGFR)-TK, can autophosphorylate when activated, as well as phosphorylating other signaling molecules []. The resulting phosphotyrosine residues in the EGFR-TK cytoplasmic domain serve to further activate the TK activity of the receptor and to act as docking sites for cytoplasmic signal transduction molecules containing Src homology or phosphotyrosine binding motifs []. Tyrosine kinases play a central role in signal transduction, acting as relay points for a complex network of interdependent signaling molecules that ultimately affect gene transcription within the nucleus. Strict regulation of TK activity controls the most fundamental processes of cells, such as the cell cycle, proliferation, differentiation, motility, and cell death or survival [, ]. In tumor cells, it is common that key TKs are no longer adequately controlled, and excessive phosphorylation sustains signal transduction pathways in an activated state. Approximately 90 TKs have been identified, 58 of which are the transmembrane receptor type and 32 the cytoplasmic nonreceptor type []. TK receptors transduce signals from both outside and inside the cell and function as relay points for signaling pathways inside the cell. The nonreceptor TKs are found in the cytoplasm; they lack a transmembrane segment and generally function downstream of the receptor TKs. The Bcr-Abl fusion protein and c-Src are examples of nonreceptor TKs that transduce signals inside the cell []. Many of both types of TKs are regularly found to be mutated or expressed at high levels in human malignancies [, ]. In addition, the ability to transform normal cells or affect tumor cell processes in vitro has been reported for many different TKs. However, clinical agents to inhibit the activity of these molecules have been developed for only a few of these TKs. Examples of clinically targeted transmembrane receptor TKs include the EGFR, the closely related HER-2 (ErbB-2/Neu), platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF) receptor, and c-kit/stem cell factor receptor [, ]. These new targeted therapies are designed to take advantage of the molecular differences specific to tumor cells compared with normal tissues. The goal is to achieve tumor responses with better safety profiles than those associated with cytotoxic chemotherapies. EGFR-TK in C ancer Abnormally elevated EGFR-TK activity is associated with the most common human solid tumors, including non-small cell lung cancer (NSCLC), colorectal adenocarcinoma, glioblastoma, squamous cell carcinoma of the head and neck, and gastric, pancreatic, breast, ovarian, cervical, and prostate cancers (Table 1) [, ]. From precancerous lesions to malignant tumors, elevated EGFR-TK activity has been detected at all stages of tumor progression [, ]. Oncogenic activation of EGFR-TK can occur by multiple mechanisms: excess ligand expression or high expression of EGFR, activating mutation, failure of inactivation mechanisms, or transactivation through receptor dimerization [,, ]. There are four members of the EGFR family of receptor TKs including ErbB-1 (EGFR), ErbB-2 (HER-2), ErbB-3, and ErbB-4. Ligand binding induces receptor homodimerization or heterodimerization. While ErbB-2 is the preferred binding partner for all other ErbB family members, the actual dimers formed follow a hierarchy of likely binding partners, which is dictated by various factors including the ligand (EGF, NRG-1, BTC) and cell type [, ]. Homodimers of ErbB-3 are the only known inactive dimer combination, due to impaired kinase activity. However, heterodimers containing ErbB-3 are able to activate intracellular signaling. The various dimer combinations allow for both signal amplification and diversity. Each EGFR family member is able to recruit a variety of specific signaling molecules that bind to specific phosphotyrosine residues in the intracellular portion of the receptor []. Dimerization partners may not only affect the activation of specific signaling pathways but may also affect responses to various ErbB family inhibitors. For example, it is possible that combining inhibitors of EGFR and ErbB-2/HER-2 may synergistically inhibit the growth of some tumor types and reduce resistance. Alternatively, certain binding combinations may reduce the efficacy of some inhibitors if the binding partner is able to robustly activate signaling pathways independently. EGFR-TK activity plays a key role in numerous processes that affect tumor growth and progression, including proliferation, dedifferentiation, inhibition of apoptosis, metastasis (through effects on cell migration, invasiveness, and lack of adhesion dependence), and angiogenesis [,, ]. Signaling through EGFR-TK is pleiotropic both in terms of the multiple signaling pathways that are activated and in terms of the biologic downstream effects, as shown in Figure 1 [,,, ]. Phosphorylated tyrosine residues in the EGFR serve as binding sites for the Grb2/Sos complex, thus activating the Ras/Raf/mitogen-activated protein kinase (MAPK) signaling cascade, which, in turn, influences cell proliferation, migration, and differentiation [,, ]. Recruitment of a second signaling pathway, the phosphatidylinositol 3-kinase pathway (PI3K), results in inhibition of apoptosis mechanisms in tumor cells []. Other key downstream signaling molecules that are influenced by EGFR-TK activity include phospholipase C, Ca 2+/calmodulin-dependent kinases, and the Janus kinase/signal transducer and activator of transcription pathway []. Activity of EGFR-TK also influences tumor angiogenesis by upregulating expression of VEGF and interleukin-8 []. Furthermore, crosstalk with other signaling molecules, such as G-protein-coupled receptors and integrins, increases the range of impact of EGFR-TK []. Activity of EGFR-TK is, therefore, an attractive drug target for inhibiting cancer because of its central role in multiple, fundamental tumor biology processes. Other kinases may be less promising drug targets due to redundancy or compensatory mechanisms in the cell. For example, the activity of only one of the nine known Src family kinases (at least three of which are expressed in most cell types) is needed for intracellular signaling and expression of its function []. Thus, agents that block only one of these Src kinases would not be expected to inhibit Src-mediated cell functions. Inhibitors of EGFR-TK Activity There are several small-molecule EGFR-TK inhibitors approved or in clinical development (Table 2). Some are selective for the EGFR, others inhibit several members of the ErbB family. All act by competing for occupation of the ATP-binding site on the TK domain of the receptor. Two EGFR-TK inhibitors, OSI-774 and gefitinib, have been investigated in phase I, II, and III clinical trials; several other EGFR-TK inhibitors, such as CI-1033 (Pfizer Inc.; New York, NY) and GW572016 (GlaxoSmithKline; Research Triangle Park, NC) are undergoing phase I and II testing []. OSI-774 is a quinazoline EGFR-TK inhibitor in clinical development. In phase I trials, the maximum-tolerated dose of OSI-774 was established at 150 mg/day []. In a randomized phase II trial of 57 patients with stage IIIB or IV NSCLC, OSI-774 was investigated as monotherapy at 150 mg/day []. Patients were required to have tumors in which more than 10% of cells were EGFR positive by immunohistochemistry. In that study population, the majority of patients (42%) had received two prior chemotherapies including a platinum agent. The tumor response rate was 12%, and 34% of treated patients experienced stable disease. The most common adverse events were grade 1 or 2 rash and diarrhea. Further studies of OSI-774 as monotherapy or as combination therapy for advanced NSCLC are ongoing []. Gefitinib was recently approved for use in the U.S., Australia, and Japan for the treatment of advanced NSCLC after prior chemotherapy and has undergone the most extensive clinical investigation of all the EGFR-TK inhibitors. Phase I trials established the maximum-tolerated dose for gefitinib as 700–800 mg/day, with diarrhea as the dose-limiting toxicity [, ]. Tumor responses in a variety of common human solid tumors, including NSCLC and prostate, head and neck, colorectal, and ovarian cancers, were also observed in these heavily pretreated patients [–]. The phase II trials, Iressa Dose Evaluation in Advanced Lung Cancer (IDEAL)-1 and IDEAL-2, compared gefitinib as monotherapy at 250 mg/day with a 500-mg/day dose for previously treated patients with advanced NSCLC. IDEAL-1 ( n = 210) required that patients had received one or two prior chemotherapies including a platinum agent. IDEAL-2 ( n = 216) required that patients had received two or more prior chemotherapies including a platinum agent and docetaxel. Testing for EGFR expression in tumors was not required for entry in these trials [–]. Objective response rates in the IDEAL-1 trial were 18% and 19%, at 250 mg/day and 500 mg/day, respectively, and were 12% and 9%, respectively, in the IDEAL-2 trial. One-quarter to one-third of patients achieved stable disease, and many patients in these monotherapy trials experienced relief of lung-cancer-related symptoms such as breathlessness, coughing, and chest pain. The most frequent drug-related adverse events were grade 1 or 2 skin rash and diarrhea. In the adult, EGFR-TK activity plays a restricted role in skin and gastrointestinal tract cancers, suggesting an EGFR inhibition mechanism for such effects [–]. These adverse effects may be common to the EGFR-TK inhibitor class of agents []. Based on the distribution and role of the EGFR-TK target molecule in human tumors, EGFR-TK inhibitors, such as gefitinib and OSI-774, have the potential to inhibit other common solid tumors in addition to lung cancer, including colon, breast, prostate, cervical and ovarian cancers, squamous cell carcinomas of the head and neck, melanomas, and glioblastomas []. This potential is being explored in clinical trials in many common solid tumor types and across all stages of neoplastic progression. Additional studies are ongoing to evaluate EGFR-TK inhibitors as monotherapy or in combination with chemotherapy or radiation therapy. B cr-A bl TK: R ole in C ancer and E ffects of TK I nhibition An example of a nonreceptor TK with clinical relevance is Bcr-Abl. It is a fusion protein created by the t(9;22) chromosomal translocation, which generates the distinctive Philadelphia (Ph) chromosome found in some forms of leukemia, including most cases of chronic myelogenous leukemia (CML) and many cases of adult acute lymphoblastic leukemia (ALL) []. This translocation juxtaposes the c- abl nonreceptor TK gene on chromosome 9 with a breakpoint cluster region ( bcr) gene on chromosome 22. The resulting fusion protein, Bcr-Abl, is a constitutively activated form of the Abl TK that drives uncontrolled growth of Ph + cells. Whereas Abl can translocate to the nucleus, in which it has a role in DNA-damage-induced apoptosis, Bcr-Abl is retained in the cytoplasm in association with the cytoskeleton, where its lack of proapoptotic activity contributes to its oncogenic properties [, ]. The 2-phenylaminopyrimidine STI571 is a small-molecule TK inhibitor for the treatment of CML. It inhibits c-Abl and Bcr-Abl, blocking the growth of Bcr-Abl-transformed leukemic cells and inducing apoptosis (Fig. Drug-related adverse effects include nausea, vomiting, myalgias, edema, diarrhea, and, less commonly, anemia, thrombocytopenia, neutropenia, and myelosuppression [, ]. In at least the initial stages of treatment, STI571 has been very effective in inhibiting progression of CML and Ph + adult ALL [, ]. The ability of this Bcr-Abl inhibitor to act alone is evidence that, in the early stages of disease, this TK is the sole or principal driver of growth in leukemic cells. However, most patients in the advanced stages of disease relapse with STI571-resistant tumor cell variants []. CML has a long initial chronic phase, which lasts an average of 3 to 4 years, followed by an accelerated blast phase during which additional mutations accumulate [, ]. In a phase I study of patients in blast crisis, 55% of CML patients and 70% of ALL patients initially responded to STI571, but 70% of the first responding group and 100% of the second group relapsed within 6 months []. By contrast, patients treated in the earlier, chronic phase of the disease developed drug resistance only rarely and often demonstrated prolonged remissions []. These findings suggest that, in early CML, the t(9;22) translocation may be the only genetic alteration responsible for cancer growth. Thus, STI571 is highly effective for early-stage disease. At later stages of the disease, however, other mutations may arise that bypass the inhibition of Bcr-Abl TK, and the control of leukemic progression is less effective. STI571 is not specific for the Bcr-Abl TK, and its action extends to the c-kit and PDGFR TKs []. The c-kit TK is important in a number of cell types, including hematopoietic stem cells, mast cells, intraepithelial lymphocytes, melanocytes, and gametocytes []. Mutations leading to ligand-independent, constitutive activation of c-kit are associated with some rare human cancers, including gastrointestinal stromal tumors (GISTs) and mast cell/myeloid leukemia []. An autocrine growth loop involving c-kit and its ligand, stem cell factor, also appears to characterize approximately 70% of SCLCs []. STI571 was recently approved for the treatment of c-kit-positive advanced and/or surgically unresectable GISTs and is undergoing trials for the treatment of SCLC. Autocrine PDGFR stimulation is found in several human tumor types, including dermatofibrosarcoma protuberans, giant cell fibroblastoma, and glioblastoma, each of which responds to STI571 with growth inhibition or apoptosis in vitro and in xenograft models [, ]. Chronic myelomonocytic leukemia is characterized by a translocation that yields a Tel-PDGFR fusion protein with constitutive TK activity. These tumor cells are also growth inhibited in vitro by STI571 []. In addition, approximately 50%–60% of resected NSCLC specimens express PDGFR [, ]. Signaling through PDGFR was shown to increase interstitial fluid pressure that subsequently leads to interstitial hypertension and a poor uptake of anticancer drugs. It has been shown that inhibition of PDGFR with STI571 decreased the interstitial hypertension and increased capillary to interstitium transport of 51Cr-EDTA []. These data suggest that STI571 may be applicable as a lung cancer treatment, as a novel strategy to increase the uptake of chemotherapeutic agents. P otential for TK-T argeted T herapies A cross T umor T ypes and S tages Of the TKs known to drive growth and progression of tumor cells, some (e.g., Bcr-Abl) are restricted to specific types of cancer, whereas others (e.g., EGFR-TK) have transforming capacity in most common types of solid tumors and across tumor stages. In contrast to the situation in CML, in which one gene mutation drives cancer progression, most solid tumors are thought to be the result of several genetic alterations []. In this respect, the EGFR may not be the only molecule driving tumor growth. While many common solid tumors may express EGFR, these tumors may result from multiple genetic changes leading to the expression of additional receptor and nonreceptor TKs that play roles in tumor growth. For example, while a tumor expresses EGFR, treatment with an EGFR-TK inhibitor may not necessarily inhibit tumor growth since mutations in other molecules may lead to the activation of several EGFR-dependent and EGFR-independent signaling pathways and subsequent tumor growth. A tumor may express additional TKs, such as Ras or PTEN, that are overexpressed or genetically mutated and are capable of activating downstream signaling. There may not, therefore, be a direct or straightforward correlation between EGFR expression and tumor response. However, as TK activity plays a key role in so many tumorigenic processes, from increased proliferation, invasion, angiogenesis, and metastasis to decreased apoptosis, inhibiting TK activity is likely to have an antitumor effect across the spectrum of disease stages in solid tumors. More research is needed to evaluate the contributions of other TKs and downstream effector molecules to tumor cell growth. In addition, future studies will investigate combinations of targeted agents designed to inhibit multiple mechanisms of tumor growth. The inhibition of Bcr-Abl TK blocks the progression of a large percentage of Ph + tumors. However, the incidences of Ph + CML and adult ALL are very low. Inhibition of EGFR-TK activity has the potential to benefit a much larger number of cancer patients. For example, it is estimated that 171,900 individuals will be diagnosed with lung cancer in the U.S. In 2003, with NSCLC as the histologic diagnosis in more than 80% of those patients []. Most cases of NSCLC are locally advanced or metastatic at initial presentation []. Based on the results of the IDEAL-1 and IDEAL-2 trials, many patients with advanced NSCLC could potentially benefit from gefitinib monotherapy. In addition, EGFR-TK is expressed in large numbers in the most common solid tumors. Whereas STI571 may be useful for different tumor types by inhibiting multiple TKs, EGFR-TK inhibitors may have broad applicability in cancer therapy due to the expression and activation of the EGFR-TK target molecule across solid tumor types. Although it is known that SCLC cell lines and tumor tissue express c-kit, it is unclear what the therapeutic role of STI571 might be in this disease. In vitro studies showed that STI571 inhibits the growth of SCLC cell lines []. A phase I clinical trial of standard cisplatin/etoposide with daily STI571 for newly diagnosed SCLC is testing the hypothesis that STI571 (by inhibition of proliferation, induction of apoptosis, and promotion of drug delivery) will enhance the cytotoxic effect of chemotherapy. Another study investigated the cytotoxic effects of STI571 in combination with commonly used antileukemic agents in several Ph + leukemia cell lines. Different combinations of drugs were variously additive, antagonistic, or synergistic in some or all of the cell lines. Interestingly, simultaneous exposure to STI571 and vincristine (a vinca alkaloid) produced synergistic effects in all four cell lines, suggesting that this drug combination might be active against CML in lymphoid crisis and Ph + ALL []. The reasoning behind this observation was that mitotic inhibitors, such as vinca alkaloids and taxanes, have been shown to induce phosphorylation of Bcl-2 family proteins, including Bcl-2 and Bcl-x, which is accompanied by loss of function and apoptosis. Oetzel et al. Reported that STI571 induced apoptosis in bcr-abl-transfected cell lines by downregulating Bcl-x []. The synergistic effect of STI571 and vincristine may be attributable to their effects on Bcl-x. These findings may provide clues as to new treatment combinations for STI571 with chemotherapy for SCLC. By potentiating the apoptotic effect of the antimicrotubule agents (taxanes and vinca alkaloids), STI571 could represent an important addition to SCLC treatment regimens. In vitro testing is ongoing for cytotoxicity of STI571 combined with different chemotherapeutic agents on SCLC and NSCLC cell lines. Other potential applications for TK inhibitors might be in the adjuvant setting, or for chemoprevention. About 50% of patients with stage I NSCLC, despite complete surgical resection, die from recurrent disease within 5 years []. Seventy percent of recurrences occur outside the chest, indicating that submicroscopic dissemination of cancer cells occurs early in the course of NSCLC []. Recent evidence suggests that chemotherapy administered after surgery results in significantly better overall survival and disease-free survival rates [, ]. These recent results with cisplatin and uracil and tegafur (UFT) chemotherapy contradict prior data that showed no survival benefit with adjuvant chemotherapy [–]. It has been proposed that TK inhibitors may improve adjuvant treatment for stage I NSCLC and lead to improved overall survival. Additionally, a phase IIB/III clinical trial is investigating the effect of the EGFR-TK inhibitor gefitinib on molecular changes in premalignant bronchial lesions in former smokers []. The presence of aberrant EGFR-TK activity in all disease stages, combined with the low toxicity and oral administration of EGFR-TK inhibitors, raises the possibility that EGFR-TK inhibitors may have utility for chronic or long-term treatment settings, such as high-risk situations or maintenance after chemotherapy [, ]. F uture D irections As TK inhibitors become available for use in clinical practice, it will be important to identify which patients will respond to these therapies. In the case of Bcr-Abl TK inhibition, the presence of Ph + cells is a good indication of potential responders, although native or acquired resistance can be confounding. The identification of potential responders to EGFR-TK inhibition is not as straightforward, as demonstrated by results of preclinical data with small molecule inhibitors, the complex nature of EGFR-TK activation, and the lack of a standardized assay for measuring EGFR-TK levels or activity in tumors. In the OSI-774 trial, overexpression of the EGFR was required for enrollment, whereas patients in the gefitinib IDEAL trials were enrolled regardless of EGFR expression levels in their tumors. This strategy was based on the high frequency of EGFR expression observed in NSCLC specimens (up to 80%) []. Continued investigation is needed to identify useful clinical or diagnostic predictors of responsiveness to EGFR-TK inhibitors, since EGFR expression may not be solely predictive of tumor response. Several ongoing studies with EGFR-TK inhibitors are measuring expression and activation of EGFR and other downstream signaling molecules such as PI3K, Akt, and MAPK in tumor tissue using immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). The objective of those studies is to establish a profile of potential responders. To date, most studies have shown no correlation between EGFR expression and tumor responses to EGFR-TK inhibitors [–]. While EGFR levels may not correlate with response, studies are ongoing to compare the levels of phosphorylated, activated EGFR with tumor responses. In addition, downstream signaling molecules may play an important role in tumor growth and response to targeted agents. Techniques such as IHC and FISH that are able to assess genetic mutations, expression levels, and phosphorylation/activation of various signaling molecules will be valuable in defining subsets of patients who may potentially respond to targeted therapy. Nevertheless, the manageable side-effect profiles of EGFR-TK inhibitors like gefitinib make it possible to try this new approach in patients who have a chance of responding. Continued clinical studies with TK inhibitors are needed to define those patients who are most likely to respond and to provide insight into how TK inhibition can be integrated into current treatment strategies for lung cancer and other common solid tumors. • © AlphaMed Press. Use User Exit 14 is a screen enhancement that allows you to design a reserved part of the contract data screen yourself. In this area, which appears as a tab page, you can define your own company-specific functional fields for each product type. You also have the option of adding an append structure to the table VDARL that will allow you to enter or change additional master data in the tab page. You use the append structure to add additional master data fields that are not available in the table VDARL.You can then enter data in this tab or display additional information. Activities • Choose Tools ABAP Workbench Utilities Enhancements Definition. The SAP Enhancements screen appears. Test User-exit without creating a project. This tip will show us how to test user-exit from SMOD without. Now go back to the test screen and press activate. Nov 24, 2017. In this SAP tutorial you will learn: What is Customer Exits and User Exit?, Types of Customer Exits, Examples of Customer Exits (CAT2, SE38 ), Locating Customer(SMOD, SE81 ) Exits, Create a Customer Exit (CMOD). Jun 25, 2012. USER EXITS IBM Global Services Objectives The participants will be able to: Discuss the procedure of modifying SAP Standard program t. IBM Global Services Activating Function-Exit You do not actually activate a single function IBM Global Services User-Exit Transactions CMOD: This. In the Enhancement field, enter the screen enhancement F67A0014 (Screen Enhancement in Loans Syndicated Data). You can display the attributes, the components and the documentation for User Exit 14. • In order to be able to use User Exit 14, you must create and activate a project. In the application, choose Tools ABAP Workbench Utilities Enhancements Project Management. For more information, see. ![]() ![]() ![]() ![]() ![]() You can host your users’ desktops and line-of-business (LOB) applications by using Terminal Services. This makes it easier for you to maintain, monitor, and update the applications that keep your business running, that save it money, and that extend the life of your desktop hardware. You can add Terminal Services to your network by using either of the following methods: • Add an additional server and configure it for Terminal Services. • Use a single server, which is running the Windows® Small Business Server 2003 (Windows SBS) R2 server software, and run Terminal Services within a virtual machine on it. The first method involves adding a server to your network that is running Windows Server 2003 R2 and that is configured to run Terminal Services (see Figure 1). When you deploy an additional server that is configured with Terminal Services, you reduce the risk that a single hardware failure can disrupt your business. You can also add capacity to the server without disrupting other services on your network that Windows SBS 2003 R2 manages. For nearly all businesses that want to manage user desktops or user applications, this is the recommended method for adding Terminal Services to your network. Method 2: Use Virtual Server. The second method involves installing Virtual Server 2005 R2 on your server that is running Windows SBS 2003 R2, and then running Windows Server 2003 R2 configured with Terminal Services within a virtual machine (see Figure 2). This way, you can combine all of the services that you need onto a single piece of hardware and avoid investing in a second server. However, this method cannot easily grow to meet user or application demand. If your business has only a few employees and cannot afford the cost of an additional server, you can use Virtual Server 2005 R2 to host desktops without investing in additional hardware. But if you plan to host more than 15 user desktops, or if you plan to run CPU or disk-intensive applications, this solution is not recommended for your network. The recommended method is to add an additional server because it provides more flexibility for your customer and provides room for future growth. Before you begin. The capacity that Terminal Services requires depends on the number of users, the configuration of the server and the network, and the applications that you are hosting. For adequate performance, Terminal Services requires a minimum of 512 megabytes (MB) of RAM, plus additional RAM for each user who is running applications. You can maximize the availability of the CPU if you have multiple processors. In general, the processor and memory requirements scale linearly. You can support nearly double the number of users on a multi-processor system if you double the number of processors and the amount of memory. For this reason, you should buy a system that supports multiple processors. Use the following guidelines to determine how much capacity your server should have: • User demand. The capacity that Terminal Services needs depends on the application features, how often the application is used, and how much work it performs. • Application considerations. Carefully check the system requirements for each application that you plan to install on your server, and consider that RAM and CPU requirements increase according to the number of people who use Terminal Services simultaneously. Because Terminal Services shares executable resources among individual users, the memory requirements for additional users who are running the same program are typically less than the requirements for the first user who loads the application. Monitor the server load after deployment to ensure that your server has adequate capacity. Plan hardware requirements for the virtual machine configuration. This method uses several server applications on a single computer. Because the server applications share one set of physical resources, it is important to plan for your hardware requirements, software requirements, licenses, and server installation. This solution has been tested by using the following assumptions: • Information worker scenario. Users are engaged in casual use of office applications such as e-mail, word processing, Web browsers, or spreadsheets. These users are not engaged in heavy computation tasks such as computer-aided drafting or computer-aided manufacturing (CAD/CAM) applications or running complex merges and joins against a database. • Five to fifteen concurrent users. Five to fifteen concurrent users may be supported by this configuration. A significant percentage of small businesses have this number of casual users. Important The information worker scenario was tested in accordance with Gartner Group recommendations. However, your actual applications, features, and data sets used will be different than the laboratory conditions used for this configuration. Your real-world deployment may differ by orders of magnitude due to the impact of specific applications, feature configurations, usage patterns, and workload spikes. Microsoft cannot provide any assurance that this configuration will be acceptable in your environment, or that it will meet your application performance or user experience requirements. Table 1 lists the minimum hardware requirements for this solution. As you test your configuration for your unique environment, you may find that additional resources are required. Table 1 Minimum hardware requirements for running Terminal Services, Virtual Server, and Windows SBS 2003 R2 on one computer Hardware Recommended CPU 2 CPUs @ 3 gigahertz (GHz) RAM 2 gigabytes (GB) Hard drive 1 160-GB fast Serial ATA (SATA) or small computer system interface (SCSI) hard drive Because Virtual Server 2005 R2 draws upon the server's hardware to load and manage virtual machines, selecting appropriate hardware is a balancing act between CPU power and available RAM. Consider the following: • Virtual Server 2005 R2 requires some operating overhead to dynamically change disk sizes and to save the contents of the virtual machine memory when the system shuts down. • Each operating system and application that you install has its own requirements which contribute to the total requirements for physical RAM and disk space. For example, when running Windows Server 2003 R2 within a virtual machine, you will need to configure the virtual machine to have the RAM necessary to support the server and its software. When the server is configured for Terminal Services, each user session requires at least 12 MB of RAM, plus the RAM necessary to support the shared applications. See the single-server capacity planning worksheet below (Table 2) to help you calculate the hardware capacity required for your virtual machine. Application requirements may also vary depending on user demand, features being used, or specific hardware or software requirements listed by the application manufacturer. To deploy this solution, you need five types of licenses: • Windows SBS 2003 R2 Standard Edition or Premium Edition license • Windows SBS 2003 R2 client access licenses (CALs), Per User or Per Device • Windows Server 2003 R2 Standard Edition license • Terminal Services client access licenses (TS CALs), Per User or Per Device • Application licenses for your shared applications The Windows SBS 2003 R2 and Windows Server 2003 R2 licenses are required to run your server software in your business. The Windows SBS 2003 R2 CALs allow users or devices to connect to other Windows servers on your network, but they do not cover the use of Terminal Services, which requires TS CALs. Table 3 lists the licenses and retail cost per license for your solution. Table 3 Product licenses required and retail cost in U.S. Dollars Product licenses required Retail list price (U.S. Dollars)* Windows SBS 2003 R2 Standard or Premium Edition (Premium Edition can only be used in a multiple-server scenario) Premium $1,299 with 5 CALs Standard $599 with 5 CALs Windows SBS 2003 R2 CALs, Per Device or Per User $489 5-pack CAL $1,929 20-pack CAL Windows Server 2003 R2 Standard Edition $999 with 5 CALs TS CALs, Per Device or Per User $149 per CAL Application licenses Varies by application *Prices on this page are stated in U.S. Dollars and reflect pricing for purchases within the United States and Canada. The prices listed are estimated prices; reseller pricing may vary. To find the Microsoft Web site for your country/region, visit the worldwide sites page. As with Windows SBS 2003 R2 CALs, there are two types of TS CALs: Per Device and Per User. A TS Per Device CAL provides each client computer the right to access Windows Server 2003 R2 configured to provide Terminal Services. The TS Per Device CAL is stored locally and presented to the server each time the client computer connects to the server. ![]() What changes are being introduced with the licensing of Microsoft Windows® Terminal Server for Microsoft Windows Server™ 2003. Scenario 1: Windows XP Professional licenses acquired through volume licensing – Using the “Install Licenses” function of the Terminal Server Licensing administration tool, a customer. ![]() Per Device licensing is a good choice for: • Hosting a user’s primary desktop for devices that you own or control. • Thin clients or computers that use Terminal Services for a large percentage of the working day. • Devices or computers that are used by several people throughout the day, such as computers on a manufacturing floor or computers shared by workers on different shifts. With Per User licensing, you must have one license for every user that connects to the server. With Per User licensing, one user can access Terminal Services from an unlimited number of devices, and thus only needs one TS Per User CAL rather than a TS Per Device CAL for each device. Per User licensing is a good choice in the following situations: • Providing access for roaming users or users who log on from different computers at work throughout the day. • Providing access for users who use more than one device, for example, a desktop at work and a laptop at home. • Providing ease of management for organizations that track access to the network by user rather than by computer. Which TS CALs you choose depends on how you plan to use the product. You can serve both license types from the same license server. For more information about Terminal Server Licensing, see the Terminal Server Licensing page on the Windows Server 2003 TechCenter (). Terminal Services also requires the installation of a Terminal Server license server on your network. A Terminal Server license server on your network manages the TS CALs and tracks the license tokens that have been issued to clients. This white paper shows you how to set up Windows SBS 2003 R2 to perform this role so that all your organization's licensing information is maintained in one location. For ease of administration, it is recommended that you purchase the same type of CALs for both Windows SBS 2003 R2 and Terminal Services. License management can be extremely flexible, but it can also become complex. If your Windows SBS 2003 R2 users access the network with Per User CALs, purchase the appropriate number of TS Per User CALs for users who will need access to the shared applications. Each application that is accessed by using Terminal Services must be licensed appropriately. Microsoft Office Small Business 2007 is licensed per device for use with Terminal Services; for more information, see the Microsoft Web site (). Most license agreements do not permit concurrent licensing (where you purchase licenses for the number of concurrent connections), so applications will need to be licensed for the number of users or devices. As part of your pre-installation license planning, check the product documentation, Microsoft Software License Terms, or any other document that specifies product usage rights so that you can determine which license methods are available to you and how many licenses you need to purchase. Plan for printers. When the user logs on to Terminal Services, the server detects the client’s local printer and installs the appropriate printer driver on the remote computer. If multiple printers are connected to the client computer, Terminal Services defaults to routing all print jobs to the client computer’s default printer. Only printers whose drivers are available on the Windows client computer appear as available in a Remote Desktop session for local redirected printers (server-side printers are always available). If the driver for your printer is not included with the client operating system, you must manually install it on the server. Software requirements. Table 4 lists the software needed to deploy a single-server solution. Table 4 Software required for running Terminal Services, Virtual Server, and Windows Small Business Server on one computer Software required Notes Windows Small Business Server 2003 R2 Standard Edition Consider increasing the server RAM to 3 GB Virtual Server 2005 R2 Enterprise Edition Download from the Microsoft Web site () Windows Server 2003 R2 Standard Edition Can also use Windows Server 2003 R2 Enterprise Edition Prepare your server. After you verify that your hardware and software requirements are met, do the following: • Complete a full backup of your server that is running Windows SBS 2003 R2, including data files and configurations. For instructions about how to back up your server, see 'Backing Up and Restoring Windows Small Business Server 2003' on the Microsoft Web site (). • If you are installing Virtual Server on your server running Windows SBS 2003 R2, verify that Microsoft Internet Information Services (IIS) is operating. By default, IIS is installed and turned on when you install Windows SBS 2003 R2. To check the status, click Start, Administrative Tools, and then Services. Scroll to World Wide Web Publishing Service. If it is not started, right-click the service and then click Start. Steps to deploy Terminal Services on a Windows SBS 2003 R2 network. The following sections describe how to deploy Terminal Services on your Windows Small Business Server 2003 R2 network, how to prepare it to run your applications, and how to install those applications. The steps are as follows: • Step 1: Add your server account to Windows SBS 2003 R2. You must add the server name to Windows SBS 2003 R2 before you can connect it to the domain. If you are adding a member server to the network, skip to step 6. • Step 2: Install Virtual Server 2005 R2. Install Virtual Server 2005 R2 on the server running Windows Small Business Server 2003 R2. • Step 3: Create a virtual machine. Configure a virtual machine for Windows Server 2003 R2 and its applications. • Step 4: Install Windows Server 2003 R2 on the virtual machine. Install the Windows Server 2003 R2 operating system on the virtual machine to run your applications. • Step 5: Install virtual machine additions. Install the additions that make it easier for you to manage the virtual machine. • Step 6: Install Windows Server 2003 R2 on the member server. Install the Windows Server 2003 R2 operating system on the member server to run your applications. • Step 7: Join the member server to the domain. Join the server running within the virtual machine to your domain. This automatically configures it with the permissions needed to function with Windows SBS 2003 R2. • Step 8: Add the Terminal Services role to Windows Server 2003 R2. After the server is installed, you must configure it for Terminal Services on the network. • Step 9: Configure Terminal Services Licensing. Configure Windows SBS 2003 R2 as a Terminal Server license server to manage your TS CALs. • Step 10: Activate the Terminal Server license server and add client access licenses. The license server must be activated and client access licenses added before your users can connect to Terminal Services. • Step 11: Install client applications. Install your desired client applications on the virtual machine. • Step 12: Configure client computers. Install the Remote Desktop Connection (RDC) client on your computers so that they can connect to Terminal Services. Step 1: Add your server account to Windows SBS 2003 R2. Caution When you add a server account to Windows SBS 2003 R2, you should use all lowercase letters for the account name. Otherwise, you might encounter name and addressing issues when you are setting up the server. For more information about uppercase letters in server names, see the Microsoft Web site (). To add your server account to Windows SBS 2003 R2 • Open the Server Management console in Windows SBS 2003 R2. To do so, click Start, and then click Server Management. • In the console tree, click Server Computers. • In the details pane, click Set Up Server Computers. • When the Set Up Server Wizard begins, click Next. • In the Server Name box, type the server name. The server name must follow standard naming conventions: no more than 15 alphanumeric characters and no spaces or other reserved characters. Create a name that other users can recognize. For example, acctsrv is a great name for a server that will be running your accounting software. • In the IP Address Configuration dialog box, select Use the following static IP address and enter the static address for the new server. This address will be automatically added to the DHCP exclusion list. • Review the Completing the Set Up Server Wizard page. It contains a summary of the configuration of your new server, including a link to the Connect Computer Wizard on the Windows SBS 2003 R2 Web site. To print, save, or e-mail the configuration details, click the link at the bottom of the page. • After you have recorded the information about the new server, click Finish. If you are adding a member server to your network, complete steps 6 through 12. If you are installing the single-server solution, continue with the rest of the steps. Step 2: Install Virtual Server 2005 R2. After you install Virtual Server 2005 R2, you can create virtual machines and install additional operating systems and applications on them. To install Virtual Server 2005 R2 • Log on to the server that is running Windows SBS 2003 R2 as an administrator. • Insert the CD or DVD for Virtual Server 2005 R2. If you have downloaded Virtual Server 2005 R2 from Microsoft, double-click Setup.exe. The Virtual Server 2005 Setup Wizard starts automatically. • On the Microsoft Virtual Server 2005 R2 Setup page, click Install Microsoft Virtual Server 2005 R2. Proceed through the wizard until you reach the Setup Type page. • On the Setup Type page, select Complete to install Virtual Server in its default configuration, and then click Next. • On the Configure Components page, accept the default Web site port value of 1024. Accept the default setting Configure the Administration Website to always run as the authenticated user, and then click Next. • On the second Configure Components page, clear the Enable Virtual Server exceptions in Windows Firewall option, and then click Next. • On the Ready to Install page, click Install. • After the installation is finished, the Setup Complete page appears. Click Finish to close the page and exit the Setup Wizard. You can read the information on the Installation Summary page, and then close Internet Explorer. Step 3: Create a virtual machine. After Virtual Server 2005 R2 is installed, you need to configure a virtual machine. You first must create the virtual machine with the name, RAM, hard drive, and network adapter information. Next you must configure physical drives for the machine, set the machine to automatically restart, and then start the virtual machine so that you can install Windows Server 2003 R2. To create a virtual machine • Click Start, click All Programs, click Microsoft Virtual Server, and then click Virtual Server Administration Website. • In the navigation pane, under Virtual Machines, click Create. The page refreshes with options to configure your new virtual machine. • In the Virtual Machine Name box, type a descriptive name for the virtual machine so that users can easily identify it. The best name is the one that you used when you set up the server in Windows SBS 2003 R2; for example, acctsrv. • In the Virtual machine memory box, allocate memory for the virtual machine by using the amount of RAM that you calculated in the 'Before you begin' section earlier in this document. Note that Virtual Server suggests a range with a recommended maximum; if the memory that you need is larger than the RAM that you can allocate in Virtual Server, you will need to purchase additional RAM for your server or reduce the amount of users or application features that you will run on your application server. • In the Virtual hard disk section, select Create a new virtual hard disk. In the Size box, type the size of the virtual hard disk, and then in the Units list, select either MB for megabytes or GB for gigabytes. • In the Virtual network adapter section, select the physical network interface card that is connected to your LAN. This allows the virtual machine to communicate with other computers on your network. While Virtual Server labels all physical adapters as 'External,' only one of them is connected to the server local area connection. If you don't know which one is the LAN adapter, click Start, click Run, type ncpa.cpl and then click OK. You can identify which adapter is your Server Local Area Connection and then select the correct adapter in Virtual Server. • Click Create. Virtual Server 2005 R2 creates the virtual machine. It also creates a pane on the Administration Web site where you can start or stop your virtual machine, monitor the status, and change its configuration. Next, you need to configure a physical CD-ROM drive and a physical floppy disk for the virtual machine. This captures the physical drives on the server running Windows SBS 2003 R2 for use by the virtual machine, enabling you to install an operating system on the virtual machine. After you configure the physical drives for use by the virtual machine, Windows SBS 2003 R2 can still access and use the drives. To configure physical drives • Scroll to the VirtualMachineName Configuration pane. • Click CD/DVD. • On the VirtualMachineName CD/DVD Drive Properties page, select Physical CD/DVD drive. • Select the appropriate physical drive from the list, and then click OK. The physical drive is mapped to the virtual machine. • In the VirtualMachineName Configuration pane, click Floppy drive. • Click Physical floppy drive. Select the appropriate physical floppy drive from the list. If you do not capture a physical floppy drive, the virtual machine may hang during the installation process due to the default boot sequence in the emulated BIOS. If you want your virtual machine to restart automatically, you must configure it to run by using a user's credentials. A best practice is to create a user account in the domain, such as TermServ, and then add the user to the Domain Users group. If you use the Add Users Wizard to do this, you do not need to specify a computer or a mailbox for this user account. To automatically restart the virtual machine • Scroll to the VirtualMachineName Configuration pane. • Click General Properties. • On the VirtualMachineName General Properties page, select Run virtual machine under the following user account. • Type the name and password of a user account in the fields provided. • In the Action when Virtual Server starts list, select the appropriate action, for example, Automatically turn on virtual machine if it was running when Virtual Server stopped. You can now start the virtual machine and install Windows Server 2003 R2 on the virtual machine. To start the virtual machine • In the Status pane, click the thumbnail image. • —OR— • Place your cursor over the small arrow that is next to your virtual machine name, and then on the menu, click Turn On. Your virtual machine is now running, and you are ready to install the operating system. Step 4: Install Windows Server 2003 R2 on the virtual machine. After you have configured Virtual Server 2005 R2, you can install Windows Server 2003 R2 on the virtual machine that you have created. When you do so, you need to make four configuration choices during the Setup process: • Configure licensing. You must do this so that Windows SBS 2003 R2 client access licenses (CALs) can be used to access the new server. Windows SBS 2003 R2 CALs allow users to access any additional Windows–based servers on your network. Other applications must be licensed separately, such as line-of-business applications or anti-virus software. • Configure the additional server computer name. You must use the name that you added to Windows SBS 2003 R2. • Configure the IP addressing method. Set up Windows Server 2003 R2 to use a static IP address. • Connect to a workgroup. This is an intermediate step until you join the server to the Windows SBS 2003 R2 domain in a later task. To install Windows Server 2003 R2 on the virtual machine • Confirm that your virtual machine is running by checking its status on its configuration page on the Virtual Server Administration Web site. To open the Virtual Server Administration Web site, click Start, All Programs, Microsoft Virtual Server, and then Virtual Server Administration Website. If your virtual machine is not running, start the virtual machine as described in Step 2 of this document. • Under Status, double click the virtual-machine thumbnail to enter the Virtual Machine Remote Control (VMRC) window. This window provides the desktop view of the virtual machine; this is the same view that you would see if you were installing an operating system on a physical computer. Note You may be prompted with an error message stating that VMRC server must be enabled before you can remotely control a virtual machine. Select the Enable check box, and then click OK. You may then be prompted with another message asking you to install the ActiveX control in your browser. Click Install, and then click OK. • To use mouse and keyboard commands in the VMRC window, do the following: • Move your cursor into the VMRC window. The cursor changes from your default cursor to a small square. Click in the VMRC window to make your cursor change back to your default. The virtual machine now captures your mouse and keyboard input. • To return control to the host machine, press the Host Key. By default, this is mapped to the right ALT key. The active cursor changes again to a small square, and the arrow becomes static. When you move the cursor outside the VMRC window, the cursor changes back to your default. • To emulate the CTRL+ALT+DELETE combination while operating within the VMRC window, press ALT+DELETE. • Place the Windows Server 2003 R2 CD in the drive. The installation process begins. • On the Licensing Modes page, select Per Device or Per User, and then click Next. • On the Computer Name and Administrator Password page, in the Computer name box, type the name of the server. You must use the same name that you added to the Manage Server Computers dialog box in Windows SBS 2003 R2. Click Next to continue with the setup process. • On the Network Settings page, select Custom settings and then click Next. Select Internet Protocol (TCP/IP) and then click Properties. On the General tab, select Use the following IP address. Type the static IP address you reserved when setting up your server in Windows SBS 2003 R2. Select Use the following DNS server addresses and then type the internal IP address for your server running Windows SBS 2003 R2. This configures your server to use a static IP address on your network. • On the Workgroup or Computer Domain page, click Workgroup. In a later step you will use the Windows SBS 2003 R2 Connect Computer Wizard to join your server to the domain. This will make the necessary changes to Active Directory Domain Services on both computers, and ensures that your server is properly configured for the network. • Continue with the rest of the setup process. Step 5: Install virtual machine additions. Virtual machine additions improve many aspects of your experience when you are using Virtual Server. For example, you can move the pointer freely between the virtual machine window and the host operating system when you are using Virtual Machine Remote Control (VMRC). To install virtual machine additions • Open the Virtual Server Administration Web site. To open the Virtual Server Administration Web site, click Start, All Programs, Microsoft Virtual Server, and then Virtual Server Administration Website. • Start the virtual machine and then log on to Windows Server 2003 R2 as an administrator. • After the operating system is loaded, press the right ALT keyto release the mouse pointer, and then, in Navigation, click Configure VirtualMachineName. • In VirtualMachineName Configuration, click Virtual Machine Additions, select Install Virtual Machine Additions, and then click OK. • Under Status, point to the virtual machine name, and then click Remote Control. • Click in the Remote Control window to return to the guest operating system. The Virtual Machine Additions Installation Wizard starts. Proceed through the wizard. • After the wizard is finished, when you are prompted to, restart the server to complete the installation. After you have installed the Virtual Server machine additions, it is recommended that you log on to your server and run Windows Update to install any needed service packs, product updates, or hotfixes that are available. As you have already installed a member server on a virtual machine, skip step 6 and continue with step 7. Step 6: Install Windows Server 2003 R2 on the member server. If you perform a clean installation of Windows Server 2003 R2 on a member server, you need to make four configuration choices during the Setup process: • Configure licensing. You must configure licensing so that Windows SBS 2003 R2 client access licenses (CALs) can be used to access the new server. Windows SBS 2003 R2 CALs allow users to access any additional Windows–based servers on your network. Other applications must be licensed separately, such as line-of-business applications or anti-virus software. • Configure the member server computer name. You must use the name for your member server that you added to Windows SBS 2003 R2 in the previous step. • Configure the IP addressing method. Set up Windows Server 2003 R2 to use a static IP address. • Connect to a workgroup. This is an intermediate step until you join the server to the Windows SBS 2003 R2 domain in a later task. If you have purchased a new server with Windows Server 2003 R2 pre-installed, when you run the mini-setup process, make the appropriate selections as listed above. To install Windows Server 2003 R2 on the member server • Place the Windows Server 2003 R2 CD in the drive. The installation process begins. • On the Licensing Modes page, select Per Device or Per User, and then click Next. • On the Computer Name and Administrator Password page, in the Computer name box, type the name of the member server. You must use the same name that you added to the Manage Server Computers dialog box in Windows SBS 2003 R2. Click Next to continue with the setup process. • On the Network Settings page, select Custom settings and then click Next. Select Internet Protocol (TCP/IP) and then click Properties. On the General tab, select Use the following IP address. Type the static IP address you reserved when setting up your server in Windows SBS 2003 R2. Select Use the following DNS server addresses and then type the internal IP address for your server running Windows SBS 2003 R2. This configures your server to use a static IP address on your network. • On the Workgroup or Computer Domain page, click Workgroup. In the next step you will use the Windows SBS 2003 R2 Connect Computer Wizard to join your server to the domain. This will make the necessary changes to Active Directory Domain Services on both computers, and ensures that your server is properly configured for the network. • Continue with the rest of the setup process. Step 7: Join the member server to the domain. Next, you need to join the member server to the domain. After you join the member server to your domain, you may interact with your new server as you would with any other server on the network: sharing folders, copying files, and performing other network activities. To join the member server to the domain • Log on as an administrator to Windows Server 2003 R2. • Open Internet Explorer. Type WindowsSBSMachineName/ConnectComputer and then press ENTER. • On the Network Configuration page, click Connect to the network now. If you receive a security warning, click Add to add the Windows SBS 2003 R2 Web site to the Trusted sites list, click Add again, and then click Close. • When the security warning appears, click Yes. The Small Business Server Network Configuration Wizard starts. • On the User Account and Password Information page, type the name and password of an account that has permission to join computers to the domain. This will typically be the administrator name and password. • On the Computer Name page, select the server name that you set up in Windows SBS 2003 R2; for example, acctsrv, and then click Next. • On the Completing the Network Configuration Wizard page, click Finish. The server restarts twice to configure and apply the new settings. Step 8: Add the Terminal Services role to Windows Server 2003 R2. After you add your server to the domain, you can configure it for Terminal Services. The Manage Your Server console allows you to add and remove roles to Windows Server 2003 R2. To add the Terminal Services role to Windows Server 2003 R2 • Log on to Windows Server 2003 R2 as an administrator. • On the Manage Your Server console, click Add or remove a role. If the console doesn't appear automatically when you log on, click Start and then click Manage Your Server. The Configure Your Server Wizard starts. • On the Preliminary Steps page, review the information, and then click Next. • On the Server Role page, select Terminal Server, and then click Next. • On the Summary of Selections page, click Next. A warning message appears, notifying you that the server will restart during the configuration process. Close any open applications, and then click OK. • After the server restarts, log on as an administrator. On the Configure Your Server Wizard page, click Finish. • The Windows Server 2003 R2 Help file opens to the section on Terminal Services. Review any information that you need, and when you are finished, close the Help file. Step 9: Configure Terminal Server Licensing. After you have added the Terminal Services role to Windows Server 2003 R2, you must configure the server running Windows SBS 2003 R2 to provide licensing services for your server. You must have a Terminal Server license server on your network, or Terminal Services will stop accepting unlicensed connections after 120 days. For more information about Terminal Server Licensing, see the Terminal Server Licensing page on the Windows Server 2003 TechCenter (). To configure Terminal Server Licensing • On the server running Windows SBS 2003 R2, click Start, click Control Panel, and then click Add or Remove Programs. • Click Add/Remove Windows Components. • In the Components dialog box, click Terminal Server Licensing, and then click Next. • On the Terminal Server Licensing Setup page, click Next to accept the default on that page. When the Terminal Server license server is activated, it becomes the repository for Terminal Services client access licenses (TS CALs). If you do not activate the Terminal Server license server, it can issue temporary licenses for clients that will allow use of terminal servers for up to 120 days from the date of the first client logon. After this evaluation period ends, the terminal server can no longer allow clients to connect unless it locates an activated Terminal Server license server to issue TS CALs. To activate the license server • On the server running Windows SBS 2003 R2, click Start, click Administrative Tools, and then click Terminal Server Licensing. • In the console tree, right-click the Terminal Server license server that you want to activate, and then click Activate Server to start the Terminal Server License Server Activation Wizard. • On the Activation method page, select Automatic connection (recommended), and then click Next. Follow the instructions in the wizard. You must purchase a client access license (CAL) for each client computer that connects to the terminal server and install the licenses on the license server. For more information about Terminal Server Licensing, see the Terminal Server Licensing page on the Windows Server 2003 TechCenter (). Note By default, Terminal Server Licensing is set to Per Device licensing mode. To change to Per User licensing mode, click Start, click Control Panel, click Administrative Tools, and then click Terminal Services Configuration. In the console tree, click Server Settings. In the details pane, double-click Licensing. In the Licensing Mode dialog box click Per User, and then click OK. To add client access licenses • On the terminal server, click Start, click Control Panel, click Administrative Tools, and then click Terminal Server Licensing. • Verify that the installation method for the Terminal Server license server is set to Automatic by right-clicking the Terminal Server license server for which you want to install key packs, and then clicking Properties. On the Installation Method tab, change the installation method if necessary. • In the console tree, right-click the Terminal Server license server for which you want to install key packs, click Install Licenses to start the terminal server CAL Installation Wizard, and then click Next. Steps 1 through 3 are not necessary if the Terminal Server CAL Installation Wizard is already started. • In Program and Client License Information, provide the required information for your licensing program to receive your key packs, and then click Next. The Microsoft Clearinghouse processes your request, and installs the encrypted client license key pack on your Terminal Server license server. • Click Finish to complete the process. • The Terminal Server license server can now issue licenses to clients that connect to the terminal server. Step 11: Install client applications. Note Before beginning this procedure, ensure that Applauncher.exe has completed running on the server that is running Windows Server 2003 R2. To check the status of Applauncher.exe, press CTRL+ALT+DELETE, and then click Task Manager. On the Processes tab, ensure that Applauncher.exe does not appear. To install Microsoft Office Outlook 2003 • On the terminal server, log on by using the domain administrator account. • Click Start, click Run, and then type WindowsSBSMachineName. • Double-click ClientApps, and then double-click Outlook2003. • Double-click Setup.exe, and then follow the setup instructions. • After installation, to close Outlook Setup, click Next, and then click Finish. Ensure that you close the wizard that launches along with Setup. Note You do not need to configure Outlook for each terminal server user. When the user logs on for the first time, Client Setup automatically configures Outlook. Also, for terminal server users, Cached Exchange Mode is not available. You can also install other client applications directly on the terminal server, such as Microsoft Office 2003 Small Business Edition. You can install most applications without additional configuration on the server, and they will be available to users connecting via terminal server. Note For more information about installing and running applications with Terminal Services, see the Terminal Services page on the Windows Server 2003 TechCenter (). For more information about installing Microsoft Office 2003 in a Terminal Services environment, see the white paper 'Deploying Office 2003 in a Windows Terminal Services Environment' on the Microsoft Web site (). To install line-of-business applications • Insert your application media in the appropriate CD or DVD drive, or connect to it through the network. • Install the application, following the procedure described in the documentation for your application. If you install applications that require access to Microsoft SQL Server, which is included with Windows SBS 2003 R2 Premium Edition, remember to set your network path configurations to point to the SQL Server installation in Windows SBS 2003 R2, or to another server running SQL Server on your network that contains your application data. Step 12: Configure client computers. Note The Remote Desktop Connection client is installed by default when you install Windows Server 2003 R2, Windows XP, and most versions of Windows CE. On earlier versions of Windows and Pocket PC, you have to manually install Remote Desktop Connection. To install Remote Desktop Connection on client computers • From the client computer, click Start, click Run, and then type WindowsSBSMachineName ClientApps. • Click tsclient. • Double-click the Win32 folder, and then double-click Setup.exe. • Complete the Remote Desktop Connection - InstallShield Wizard. You can now share user desktops and applications from the terminal server. Improve your virtual environment performance. You can improve your virtual environment performance by following the tips in article 903748 in the Microsoft Knowledge Base (). One of the best suggestions is to place your virtual hard disks (VHDs) on a separate physical disk than the one used by the host operating system. You can also improve performance by converting your virtual hard drive to a fixed-size virtual hard disk; this reduces the management cycles spent resizing the virtual disk. See the article for instructions on how to do these tasks. It is also recommended that you schedule a task to defragment your virtual hard drives every night and defragment your physical drives every week. For more information about scheduling tasks, click Start, click Help and Support, and then search for 'Schedule a task.' Additional references. |
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March 2018
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