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91. In Fig. FE-8, what is the slope-intercept equation of line M, considering x as the independent variable and y as the dependent variable (a) y = ( 5/4)x 2 (b) y = (5/4)x + 3/2 (c) y = (4/5)x + 3 (d) y = ( 4/5)x 8/5 (e) More information is necessary to answer this 92. In Fig. FE-8, what is the slope-intercept equation of line L, considering y as the independent variable and x as the dependent variable (a) x = (2/3)y 2 (b) x = ( 2/3)y 2 (c) x = (3/2)y + 3 (d) x = ( 3/2)y 3 (e) More information is necessary to answer this 93. In Fig. FE-8, what is the slope-intercept equation of line M, considering y as the independent variable and x as the dependent variable (a) x = (4/5)y 2 (b) x = (4/5)y + 2

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The res directory is where your in project resources are held and compiled into your application. When you create a new Android project, the res directory contains three subdirectories: drawable, layout, and values. You will use the drawable and layout directories in many of your projects to hold and display images and layouts respectively, whereas the values directory holds string globals that can be used throughout your application.

The typical syndrome consists of partial deafness, facial palsy, dysphagia, and unilateral atrophy of the tongue combined with a vascular polyp in the external auditory meatus and a palpable mass below and anterior to the mastoid eminence, occasionally with a.

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positive and the reaction still happens, we know that the entropy contribution must be in the favorable direction (and positive). Otherwise, G couldn t be negative. In this case, we would say that the reaction is entropically driven (i.e., the reaction occurs because of the increase in entropy increased disorder that accompanies the reaction). Driving force can also be used to denote the physical interaction that provides the most negative free energy to an overall reaction. For example, the driving force for the folding of proteins is the hydrophobic interaction. Other forces contribute to a favorable protein-folding reaction; however, the largest contribution comes from the packing of the hydrophobic residues into the interior of the protein. To make it more meaningful, let s take the reaction for the formation of a hydrogen bond in water: C O % HOH H2O % H N R R C O % HN R H2O % HOH

inducing antigen in EAE is known, whereas the putative antigen in MS is not Also incorporated into most theories of the immune pathogenesis is an alteration of the blood-brain barrier, represented by adhesion of lymphocytes to endothelial cells Whether this is an active interaction or a passive event triggered by antigenic attraction is not clear; nonetheless, these cell-vascular interactions have been incorporated into pathogenic theories and is the basis of newer treatments for MS As matters now stand, the focus of attention is on the pathogenic role of speci c subsets of T lymphocytes, which regulate humoral immune responses either as potentiators (T-helper cells) or as inhibitors (T-suppressor cells) of immunoglobulin production by the B lymphocytes So-called helper (CD41) T cells are found in abundance within MS plaques and surrounding venules (perivascular cuf ng).

It has been demonstrated that T-cell receptors respond to antigens presented by (major histocompatibility complex, or MHC) class II molecules on macrophages and astrocytes This interaction is thought to stimulate T-cell proliferation and a cascade of related cellular events, including the activation of B cells and macrophages and the secretion of cytokines (one of which is IFN- and another IFN- ; see further on) These cellular events are accompanied by a breakdown of the blood-brain barrier and, if suf ciently intense, by destruction of myelin (see review by French-Constant) A reduction in T cells, both helper and suppressor subsets, or an increase in the ratio of helper-suppressor cells, may precede an acute attack and appears to be associated with increasing disability in patients with MS Always in the background is the element of genetic susceptibility, presumably making certain individuals prone to these immunologic events.

The foregoing data notwithstanding, it must be added that the immune mechanisms in MS are not fully speci ed and the autoimmune hypothesis is not beyond challenge It is noteworthy that the prevalence of other diseases of presumed autoimmune origin is no higher in MS patients than in the general population (De Keyser) Moreover, the course of MS has been altered only inconsistently by the administration of any of the nonspeci c immunosuppressive therapies (Goodkin et al, 1992) Also worthy of comment is the relatively ineffective remyelination of the MS plaque When remyelination of denuded axons occurs, thinly myelinated bers are produced, creating areas of socalled shadow plaques Histologic evidence suggests that some of the oligodendrocytes are destroyed in areas of active demyelination but also that some of the remaining ones have little ability to proliferate.

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