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There are also directives for intradatabase allocations, which further divide the I/O bandwidth Consumer group 1 gets 50 percent of the I/O for Database 1, which works out to 21 percent of the overall I/O available 50 percent (the intradatabase percentage) of the 42 percent available for Database 1 in the High category Consumer group 5, which gets 75 percent of the allocation for Database 1 in the Low category, ends up with 135 percent, 75 percent of the 18 percent for that category and database You can start to see how flexible I/O Resource Management can be, especially when you couple it with the fact that resource plans can be dynamically changed But you may be wondering how the Exadata Storage Server Software is able to implement these potentially complex scenarios It really is not that hard, as you can see in Figure 3-7 You can see that the end of the line is a simple queue used to grab I/O requests The disk simply takes requests off the disk queue Upstream from this queue are a number of separate queues, one for each consumer group The percentage allocations assigned by the different directives in the plan are used to control which queue is used by IORM next So if a queue for consumer group 1 calls for the group to get 80 percent of the requests for Database 1, IORM would go to that queue first 80 percent of the time At the end of the line, the plan directs the I/O Resource Manager how to prioritize requests for each database IORM, like other aspects of the Exadata Storage Server Software stack, also makes sure that essential operations proceed without interruption Write operations for the redo log, essential in completing write operations with integrity, and control file I/Os always take top priority, regardless of the resource plan You can either assign DBWR (database writer) operations to a specific consumer group or leave them in a default group You can also.

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This disease, estimated to occur once in every 100,000 births, is inherited as an autosomal recessive trait It has its onset in the neonatal period or early infancy and as a rule leads to death within a few months Motor inactivity and hypotonia, dysmorphic alterations of the skull and face (high forehead, shallow orbits, hypertelorism, high arched palate, abnormal helices of ears, retrognathia), poor visual xation, multifocal seizures, swallowing dif culties, xed exion posture of the limbs, cataracts, abnormal retinal pigmentation, optic atrophy, cloudy corneas, hepatomegaly, and hepatic dysfunction are the usual manifestations Stippled, irregular calci cations of the patellae and greater trochanters are highly characteristic Pathologically, there is dysgenesis of the cerebral cortex and degeneration of white matter as well as a number of visceral abnormalities cortical renal cysts, hepatic brosis, intrahepatic biliary dysgenesis, agenesis of the thymus, and iron storage in the reticuloendothelial system As to the biochemical abnormality, A B Moser and coworkers have demonstrated a vefold increase of very-long-chain fatty acids, particularly hexacosanoic acid, in the plasma and cultured skin broblasts from 35 patients with Zellweger disease A similar abnormality was found in cultured amniocytes of women at risk of bearing a child with Zellweger disease, thus permitting prenatal diagnosis The ndings of Moser and colleagues are in keeping with current notions about the basic abnormality in Zellweger syndrome namely, that it is due to a lack of liver peroxisomes (oxidase-containing, membrane-bound cytoplasmic organelles), in which the very-long-chain fatty acids are normally oxidized (Gold scher et al) Currently, a spectrum of at least 12 disorders of peroxisomal function is recognized, all of them characterized by de ciencies in the peroxisomal enzyme of fatty-acid oxidation a veritable peroxisomal assembly The most widely recognized are neonatal adrenoleukodystrophy and infantile Refsum disease, but the Zellweger cerebrohepatorenal syndrome can be considered the prototype Each variant can be identi ed by its characteristic pro le of elevated longand very-long-chain fatty acids, and the speci c diagnosis can be con rmed by enzymology of cultured broblasts or amniocytes Several of them become manifest at a later age and are discussed further on For an authoritative discussion of peroxisomal biogenesis, the reader is referred to the article by Gould and Valle.

Menkes Disease (Kinky- or Steely-Hair Disease; Trichopoliodystrophy)

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