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No other sequence of numbers has been studied as extensively, or applied to more elds: biology, demography, art, architecture, music, to name just a few. And, together with the powers of 2, it is computer science s favorite sequence. In fact, the Fibonacci numbers grow almost as fast as the powers of 2: for example, F 30 is over a million, and F100 is already 21 digits long! In general, F n 20.694n (see Exercise 0.3). But what is the precise value of F100 , or of F200 Fibonacci himself would surely have wanted to know such things. To answer, we need an algorithm for computing the nth Fibonacci number. An exponential algorithm One idea is to slavishly implement the recursive de nition of F n . Here is the resulting algorithm, in the pseudocode notation used throughout this book: function fib1(n) if n = 0: return 0 if n = 1: return 1 return fib1(n 1) + fib1(n 2)

3. I

Step 2 of the process enables you to choose the settings for the Display dropdown box, as shown next. The options are Show Drop Down Box, which allows the user to see the different data providers that are available to pick from; Sort Alphabetical, which generates a list in alphabetical order; and Keep Filter Values, which allows the data provider (normally a query) to keep any filters that have been defaulted into the definition.

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As you can see, the SYSTEM account has privileges not only to read or write the Sales History data using privileges such as SELECT ANY TABLE and UPDATE ANY TABLE, but the account can modify the structures in which the data is stored using a privilege such as ALTER ANY TABLE. The same types of system ANY privileges are usually granted to named database administrator accounts, providing the same unbounded access to application data. We must introduce a DBV realm around the SH and HR schemas to enforce the separation of duty and mitigate compliance concerns over unprotected access to PII or the integrity of financial numbers used in an audit.

STOMACH COLON (LARGE INTESTINE)

The McGraw Hill Companies, 2010

(b) Show that if N is an odd prime, there are exactly (N +1)/2 quadratic residues in {0, 1, . . . , N 1}.

by The first iteration is completecl substitutingthe calculatedvaluesfor 'rt and'r: into to E q .( E 1 2 . 1 . 3 ) y i e l d

The angiomas of this disease may form in either the spinal cord or brain, where they can produce apoplectic syndromes; or as in one of our patients, there may be an intermittently progressive focal thalamic syndrome resulting from enlargement of the vascular lesions (or possibly from a succession of small hemorrhages) An unexplained gastrointestinal, genitourinary, intracranial, or intraspinal hemorrhage warrants a search for small cutaneous lesions, which are easily overlooked Satellite lesions tend to form after obliteration of an angioma To date, two mutant genes have been identi ed as causes of this disease: endoglin and novel kinase von Hippel-Lindau Disease (See also page 568) This is a genetic disease of multiple neoplasms, speci cally identi ed by the presence of a hemangioblastoma, sometimes multiple (these are discussed with other cerebral tumors in Chap 31).

The tumor is situated in the cerebellum in most cases but may also arise in the brainstem or spinal cord In addition to the characteristic cerebellar tumor with its nodule within a cyst, half of these patients have retinal hemangioblastomas and somewhat fewer develop renal cell cancer; an even smaller number have a pheochromocytoma, pancreatic tumors or cysts, or cystadenomas Polycythemia vera is an interesting feature in a few cases The cerebellar hemangioblastoma typically develops in the fourth decade and causes symptoms of ataxia and headache On imaging studies, the lesions have a striking appearance of a cyst with a nodule contained in its wall, and angiography demonstrates the highly vascular nature of the nodule, which represents the actual neoplasm (Fig 31-13) The other identifying features of the disease, retinal hemangiomas, are indistinguishable histologically from the craniospinal ones.

They are multiple and bilateral, usually appearing earlier than the cerebellar lesions but remaining asymptomatic until they become extensive (retinal detachment is one feature) Their diagnosis is made by funduscopy, by which a large feeding vessel leading to an irregularly shaped ovoid tumor in the retina can usually be appreciated Imaging studies of the cranium that use dye enhancement will reveal this as well Inheritance is autosomal dominant with variable but high penetrance by older age The causative mutation is in the so-called VHL gene located on chromosome 3 This is a tumor suppressor gene that is inactivated by the mutation and may induce oncogenesis by increasing the expression of vascular mitogenic factors such as vascular endothelial growth factor (VEGF); the precise mechanisms are not known.

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