Specialized Mutual Funds in Software

Encoder EAN-13 Supplement 2 in Software Specialized Mutual Funds

44 Natural Numbers and Integers
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Parameter Internal Display Menu (MENU_ELEMENT_L1) (continued)
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file format Add this parameter if you want to control the file format Excel uses for the workbook usually a good idea. If you omit the file format parameter, Excel uses the format selected in the Save Files In This Format pop-up menu in the Compatibility Preferences. Table 15-1 explains the most useful of Excel s many file formats. add to most recently used list Add this optional parameter and set it to true if you want the workbook to appear on the Recent Documents list for example, so that the user can reopen the workbook quickly from the File menu. If you don t want the workbook to appear on the Recent Documents list, either set this parameter to false or simply omit it the default value is false. create backup Add this optional parameter set to with create backup to make Excel create a backup copy of the file.
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Two: Identifying Components
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Once your information is authenticated, you should see the screen shown in the following illustration. Notice that there is no Return button here; just click the Home key on the Emulator to return to the main screen.
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LYSIS T (thymic) lymphocyte scout Antigen antibody reaction Transforms
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the more so as the degree of malignancy increases. (Anaplasia refers to the more primitive undifferentiated state of the constituent cells.) However, it is currently thought that many tumors arise from more primitive elements, speci cally stem cells, and it may be that the ostensible dedifferentiation is an artifact of the histologic appearance of tumors. The factor of age is also important in the biology of brain tumors. Medulloblastomas, polar spongioblastomas, optic nerve gliomas, and pinealomas occur mainly before the age of 20 years, and meningiomas and glioblastomas are most frequent in the sixth decade. Heredity gures importantly in the genesis of certain tumors, particularly retinoblastomas, neuro bromas, and hemangioblastomas. The rare familial disorders of multiple endocrine neoplasia and multiple hamartomas are associated with an increased incidence of anterior pituitary tumors and meningiomas, respectively. Glioblastomas and cerebral astrocytomas have also been reported occasionally in more than one member of a family, but the study of such families has not disclosed the operation of an identi able genetic factor. Only in the gliomas associated with neuro bromatosis and tuberous sclerosis and in the cerebellar hemangioblastoma of von Hippel-Lindau is there signi cant evidence of a hereditary determinant. Although there is no direct evidence for an association between viruses and primary tumors of the nervous system, epidemiologic and experimental data drawn from studies of the human papillomavirus and the hepatitis B, Epstein-Barr, and human T-lymphotropic viruses indicate that they may be a risk factor in certain human cancers. In transgenic mice, certain viruses are capable of inducing olfactory neuroblastomas and neuro bromas. Each of these viruses possesses a small number of genes that are incorporated in a cellular component of the nervous system (usually a dividing cell such as an astrocyte, oligodendrocyte, ependymocyte, endothelial cell, or lymphocyte). The virus is believed to thrive on the high levels of nucleotides and amino acid precursors and at the same time acts to force the cell from of its normal reproductive cycle into an unrestrained replicative cycle (Levine). Because of this capacity to transform the cellular genome, the virus product is called an oncogene; such oncogenes are capable of immortalizing, so to speak, the stimulated cell to form a tumor. Molecular and Genetic Features of Brain Tumors All of the above ideas have been expanded greatly by studies of the human genome, which have led to the identi cation of certain chromosomal aberrations linked to tumors of the nervous system. What has emerged from these studies is the view that the biogenesis and progression of brain tumors are a consequence of defects in the control of the cell cycle. Some molecular defects predispose to tumor genesis; others underlie subsequent progression and accelerated malignant transformation. In effect, this model presupposes the acquisition of multiple defects over time. In some instances, the initial predisposition is a genetic defect that is inherited by germline transmission and that the additional events arise as somatic genetic lesions. For example, mutations in genes that normally suppress cell proliferation may set the stage for tumor development. Typically, these inherited mutations affect only one of two copies of the tumor suppressor or gene. By itself, such a mutation does not cause cancer. However, if the second copy of the gene acquires a mutation (e.g., from a chemical toxin or irradiation), the tumor suppression function of the gene is lost and cancerous transformation of the cell becomes likely. These notions are consistent with the observation that many of the gene defects that predispose to cancer are dominantly inherited.
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Icon view List view Column view Cover Flow view
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The solution to this problem is presented with a detailed example in Section 8.2.2. The computed pseudoranges are functions of the computed satellite po sitions pi while the measured ranges are functions of the actual satellite positions. Therefore, the estimated value of x will be a ected by the error pi pi . To make this dependence explicit in the model of the pseudorange, we manipulate eqn. (8.3) as shown below to obtain the L1 C/A pseudorange model of eqn. (8.6): i r = (x, pi ) + (x, pi ) (x, pi ) + c ti + = (x, pi ) + E i + c ti + f2 i i i i I + T r + M + f1 r (8.6)
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