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Plaque structure

Figure 17.5. The precursor molecule APP and the three different proteases a, (i, y secretase that are involved in the processing of APPto fS-amyloid peptide. The aberrant processing of the amyloid precursor protein (APP) leads to accumulation of beta-amyloid fragments, first as protofibrils and then as fibers that aggregate in the senile plaque structures. (See color insert.)... Figure 17.5. The precursor molecule APP and the three different proteases a, (i, y secretase that are involved in the processing of APPto fS-amyloid peptide. The aberrant processing of the amyloid precursor protein (APP) leads to accumulation of beta-amyloid fragments, first as protofibrils and then as fibers that aggregate in the senile plaque structures. (See color insert.)...
HF coils and optimized MR sequences a characterization of plaque structure can successfully be performed that possibly could help to predict the risk of plaque rupture (Figs. 5.8, 5.9) (Yuan et al. 2001). [Pg.83]

First, we describe the chemical composition of plaque fluid in relation to caries, then the role of plaque structure. Next, we discuss the influence of F retained in plaque, including site-to-site differences, followed by the effect of treatments that seek to deposit plaque calcium (Ca) and/or inorganic phosphate (Pi). A combination of small sample volumes and low constituent concentrations typically leads to high measurement variability that results, in turn, with authors often having difficulty in discriminating between subject groups. [Pg.132]

In the context of a chapter on plaque as a reservoir for active ingredients, plaque structure has an important influence on the penetration and clearance of such materials and also of various other species involved in the caries process. We have discussed in previous sections the thermodynamic approach to caries susceptibility adopted by Margolis et al. [1,4-5] that focuses on calculations of the DS of the plaque fluid with respect to dental enamel based on extensive chemical analyses of plaque samples. Dawes, Dibdin and their co-workers [12-19], on the other hand, have modelled essentially the kinetics of the saliva-plaque system to compute Stephan curves within plaque and at the enamel surface following sucrose exposure. Sucrose (and related highly water-soluble species such as glucose) strictly speaking are not retained in plaque, but are either rapidly cleared from the mouth by saliva or converted to other molecules by plaque bacteria. The H+ ions that determine pH are one product of such conversion processes and are retained to an extent. [Pg.137]

Half of the products of oncogenes are protein kinases, mostly of the tyrosine type. This finding was of fundamental importance because it revealed that abnormal phosphorylation of a number of proteins could explain, at least in part, various effects of transformation. The critical cell proteins whose abnormal phosphorylation presumably leads to transformation are still to be defined. However, they include vinculin, which is a protein found in focal adhesion plaques (structures involved in intercellular adhesions). The abnormal phosphorylation of vinculin in focal adhesion plaques could explain the tendency of cells to become round and... [Pg.206]

Fig. 16.3a-d. Hypothetical density of lumen versus plaque on representative cross-sections, a The coronary lumen (filled with an iodine contrast agent at 400 HU) is surrounded by soft plaque and epicardial fat. The problem zone in this situation is the delineation of soft plaque versus epicardial fat b Part of the soft plaque structures are densely calcified. The calcified plaque with a density of 700 HU is oversized due to partial volrnne averaging, but delineation against the lumen is not compromised by contrast issues, c For a hypothetical plaque structure at an initial stage of calcification (Hounsfield units... [Pg.214]

Bacterial catabolism of oral food residue is probably responsible for a higher [NHj] in the oral cavity than in the rest of the respiratory tract.Ammonia, the by-product of oral bacterial protein catabolism and subsequent ureolysis, desorbs from the fluid lining the oral cavity to the airstream.. Saliva, gingival crevicular fluids, and dental plaque supply urea to oral bacteria and may themselves be sites of bacterial NH3 production, based on the presence of urease in each of these materials.Consequently, oral cavity fNTi3)4 is controlled by factors that influence bacterial protein catabolism and ureolysis. Such factors may include the pH of the surface lining fluid, bacterial nutrient sources (food residue on teeth or on buccal surfaces), saliva production, saliva pH, and the effects of oral surface temperature on bacterial metabolism and wall blood flow. The role of teeth, as structures that facilitate bacterial colonization and food entrapment, in augmenting [NH3J4 is unknown. [Pg.220]

A number of rare genetic diseases involve collagen abnormalities, including Marfan s syndrome and the Ehlers-Danlos syndromes, which result in hyperextensible joints and skin. The formation of atheroselerotie plaques, which cause arterial blockages in advanced stages, is due in part to the abnormal formation of collagenous structures in blood vessels. [Pg.178]

HDL and VLDL are assembled primarily in the endoplasmic reticulum of the liver (with smaller amounts produced in the intestine), whereas chylomicrons form in the intestine. LDL is not synthesized directly, but is made from VLDL. LDL appears to be the major circulatory complex for cholesterol and cholesterol esters. The primary task of chylomicrons is to transport triacylglycerols. Despite all this, it is extremely important to note that each of these lipoprotein classes contains some of each type of lipid. The relative amounts of HDL and LDL are important in the disposition of cholesterol in the body and in the development of arterial plaques (Figure 25.36). The structures of the various... [Pg.841]

Just like in coiled-coils, p-sheet secondary structure (Fig. 2) is ubiquitous in natural examples and in proteins and biomaterials. Alzheimer s disease is characterized by fibrillar amyloid plaques in the cerebral parenchyma. The insoluble amyloid fibrils are predominantly formed upon conformational switching of the 42 amino acid... [Pg.146]

The most definitive diagnosis of AD is a postmortem examination of the brain for the presence of two characteristic lesions the neuritic plaque (NP) and the neurofibrillary tangle. Both structures were originally described in 1906 by Alois Alzheimer using silver-based histological stains. The discovery of NPs was hailed as a watershed moment in the history of neurological disease as it helped shift society s perception of age-related dementia from social stigma to physical disease [2]. [Pg.316]


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See also in sourсe #XX -- [ Pg.83 ]




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Cell structure, adhesion plaques

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