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Your initial focus should be on making sure that all of the standard business content (SBC) that needs to be migrated is activated. This is not that hard, and if you re used to activation of the SBC within BW, you will be able to very quickly collect these objects and then activate them. The following illustrations show some of this content in the display process within the SBC activation process. You can find the majority of the required SBC under the header BEx Web Template and of course this is the 7.0 version, not the 3.x version, which is clearly marked on the SBC activation screen. To access these, go to the Administration Workbench and use the button on the left side of the screen BI Content. Then using the option for Object Types you can see the Web Templates and Items for both the 3.x and 7.0 versions.
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of the limbs predominantly and is only slowly progressive. It was rst clearly separated from other forms of motor system disease and from muscular dystrophy by Wohlfart and by Kugelberg and Welander in the mid-1950s. In about one-third of the cases, the onset is before 2 years of age, and in half, between 3 and 18 years. Males predominate, especially among patients with juvenile and adult onset. The usual form of transmission is by an autosomal recessive pattern; most cases result from mutations in the SMN gene. Families with dominant and sex-linked inheritance have also been described. The disease begins insidiously, with weakness and atrophy of the pelvic girdle and proximal leg muscles, followed by involvement of the shoulder girdle and upper arm muscles. Unlike the sporadic form of spinal muscular atrophy, the Wohlfart-KugelbergWelander variety (also listed in other books and monographs as Kugelberg-Welander disease) is bilaterally symmetrical from the beginning, and fasciculations are observed in only half the cases. Ultimately the distal limb muscles are involved and tendon re exes are lost. Bulbar musculature and corticospinal tracts are spared, although Babinski signs and an associated ophthalmoplegia (presumably neural) have been reported in rare instances. The presence of fasciculations and the EMG and muscle biopsy ndings all of which show the characteristic abnormalities of neural atrophy permit distinction from muscular dystrophy. Cases that have been examined postmortem have shown loss and degeneration of the anterior horn cells. The disease progresses very slowly, and some patients survive to old age without serious disability. In general, the earlier the onset, the less favorable the prognosis; however, even the most severely affected patients retain the ability to walk for at least 10 years after the onset. Admittedly, it is dif cult to make a sharp distinction between these cases of Wohlfart-Kugelberg-Welander disease and certain milder instances of Werdnig-Hoffmann disease with onset in late infancy and early childhood and prolonged survival (Byers and Banker). Kennedy Syndrome (X-Linked Bulbospinal Muscular Atrophy) An unusual pattern of distal muscular atrophy with prominent bulbar signs and, less often, ocular palsies was rst described by Kennedy. The time of onset has varied from childhood to adult age, but most patients have been in their third decade when neurologic symptoms arose. Most cases have shown an X-linked pattern of inheritance and a lesser number an autosomal dominant pattern. The proximal shoulder and hip musculature are involved rst by weakness and atrophy, followed in about half of patients by dysarthria and dysphagia. Often muscle cramps or twitching precede weakness. Facial fasciculations and mild weakness are also characteristic and may be striking. The tendon re exes become depressed and may be absent; a mild sensory neuropathy is almost universal. In the family described by Kaeser, in which 12 members in ve generations were affected, the pattern of weakness was shoulder-shank, i.e., scapuloperoneal; it may therefore be mistaken for muscular dystrophy. The muscular atrophy is associated in twothirds of patients with gynecomastia, a feature that may rst identify affected men in a kindred. Oligospermia and diabetes are frequent associations. The CK level is elevated, sometimes tenfold, and physiologic studies reveal denervation and reinnervation as well as indications of a mild sensory neuropathy. As in Huntington disease and certain of the spinocerebellar atrophies, the genetic defect is a CAG expansion, in this case in the gene that codes for the androgen receptor on the short arm of
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As mentioned, BI systems often bring together an organization s most important data and present it in an analytically friendly way. This data consolidation is great for people who are supposed to have access to the data, but if the data is not properly secured, people can exploit data they shouldn t be allowed to access. We look at ways to provide both coarse- and finegrained data protection. Coarse permissions are fairly easy to define ( only group A should have access to a certain type of data ), so we focus most of our attention on the fine-grained securing of data, including both row- and column-level security. We will consider two methods of providing row-level security and will compare and contrast these methods. Next, we look at how web catalog content can be protected. We focus on the mechanisms in Oracle BI used to organize and secure all BI content (dashboards, reports, ad hoc requests, and alerts). Protection means controlling who has access to the definitions of these objects and who can manipulate these definitions. NOTE In order for a user to run a report successfully, that user must have access both to the definition of the report and the data presented in the report. Finally, we look at the privileges that need to be granted to different users of the system. We focus on privileges that require specific care. Oracle BI offers some advanced features that should be granted only after careful consideration. Users should have access to these features only if they have been trained in how to use them. Some of these features allow users to impact data and functionality for other users. It is important that you know exactly what you are allowing users to do when you give them access to a specific feature.
Figure 11-14
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