Amyloid and amyloidosis by Gilles Grateau, Robert A. Kyle, Martha Skinner PDF

By Gilles Grateau, Robert A. Kyle, Martha Skinner

ISBN-10: 0849335345

ISBN-13: 9780849335341

This authoritative quantity includes 179 chapters by means of overseas specialists on fresh advancements in our realizing of amyloid proteins, protein folding issues, and new and proposed medical trials in amyloidosis. themes comprise detection and characterization options; organic features; genetics; problems, analysis, and coverings, together with organ transplants and drug treatments; effects from broad scientific experiences; and epidemiology. it is a necessary source for clinicians who deal with sufferers with systemic and localized kinds of amyloidosis, and for researchers in biochemistry, neurobiology, and phone biology.

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All lipid peaks were identified according to their m/z (Fig. 1). 8 ng. The molecular species of lipids present in amyloid deposits are given in table 1. The relative peak intensities were distinguished in 3 categories: ++ denotes high intensity, + moderate and 0 indicates just detectable amounts of lipids. 15 16 Amyloid and Amyloidosis Table 1. Membrane lipid classes and their molecular species found in ex vivo amyloid fibrils AA1 GC SU PE PS PC SM 18:0 18:1 20:1 22:0 22:1 22:2 22:4 24:0 24:1 24:2 26:0 26:1 26:2 26:3 26:4 24: 0 24:3 26:6 18:0/20:4 18:0/22:4 18:0/22:6 18:0/24:3 (p)18:0/18:2 (p)18:0/20:4 PI 16:0/22:4 18:0/20:4 18:1/20:4 18:1/22:6 16:0/16:1 16:1/18:1 16:1/18:2 16:0/20:2 16:0/22:0 18:0/18:1 18:0/20:4 18:0/22:0 18:0/22:4 18:0/22:6 18:1/18:2 (p)20:0/22:1 (p)20:0/22:2 16:0/16:0 16:0/18:1 16:0/20:4 18:0/20:4 18:1/20:4 18:0 18:1 22:0 24:0 24:1 24:2 AA2 AA3 AL1 AL2 AL3 AL4 AL5 AL6 + + + ++ + + ++ ++ 0 ++ ++ 0 ++ + + ++ ++ + + ++ + ++ + + + ++ + + ++ ++ + + ++ + + + + + + + ++ + + ++ ++ ++ + ++ + + ++ ++ 0 ++ ++ 0 ++ ++ ++ + + ++ ++ + + ++ ++ + ++ + + + + ++ 0 + ++ ++ + 0 ++ ++ + + + + ++ ++ ++ + ++ + 0 ++ + + ++ + ++ ++ + Our analyses revealed that the lipid composition of amyloid fibrils is distinct from healthy tissue in that it is particularly rich in cholesterol and sphingolipids and contain only very rare amounts of those phospholipids, PE and PC, that occur in undiseased tissues in very high amounts (Fig.

The most exposed part in lipids are unsaturated fatty acids. Since fatty acid double bonds are highly unstable [6], their loss reflects the Amyloid Fibrillogenesis 17 extent of degradation. This points out against a strong oxidative or hydrolytic damage of the lipid classes that could have occurred while purifying the amyloid deposits or during lipid analysis. CONCLUSION: The method is suitable for analysis of small quantities of lipids present in purified amyloid deposits. The lipids possess a typical pattern that is rich in sphingolipids and cholesterol.

Our in vitro study on stefin B site specific mutant G4R and the two variants, rec-stB and wt-stB shows that order of stability and the propensity to fibrillise differ; there is no correlation. The order of stability is : wt-stB >= G4R mutant >> rec-stB and propensity to fibrillise : wt-stB > rec-stB > G4R mutant. It can be seen that wt-stB forms fibrils after the lowest lag phase of about 100 hours and to the largest extent (judged by final ThT fluorescence). The rec-stB starts fibril growth after a lag phase of 200 hours, even though, this variant is less stable than wt-stB.

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Amyloid and amyloidosis by Gilles Grateau, Robert A. Kyle, Martha Skinner

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