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The direct close contact between the SWCNT and bacteria is proposed to cause bacterial cell death [105].
More recently, epimutations have also been proposed to cause at least one such syndrome, hereditary non-polyposis colorectal cancer (HNPCC).
The development of neointimal hyperplasia with subsequent atherosclerotic deposition has been proposed to cause most late vein graft failures.
LVs are associated with diabetes and myocarditis in bank voles and have been proposed to cause disease in humans.
Impaired renal blood flow, acute tubular necrosis, glomerular micro-thrombi and apoptosis have all been proposed to cause this renal dysfunction [1,2].
A main obstacle in chronic hepatitis B, however, is the high load of viral antigens expressed and secreted, which has been proposed to cause antigen-specific immune tolerance.
We will additionally highlight points of contact between the biology and the pathophysiology that has been proposed to cause a clinical disorder of scene construction – spatial hemineglect.
Two mechanisms are proposed to cause FXTAS: RNA gain-of-function, where CGG RNA sequesters specific proteins, and translation of CGG repeats into a polyglycine-containing protein, FMRpolyG.
A closer or further location of the aromatic rings to the peptide backbone in the mutants relative to F13 is proposed to cause a drop in activity.
Diffusion and microstructural sintering at the particle-particle interfaces were proposed to cause the change in bonding mechanism from mechanical interlocking to metallurgical bonding and lead to the ductile characteristics of these samples.
Dilatancy leads to strain localisation in dilatant shear bands shortly after crystal impingement and is proposed to cause the initiation of cracks in the expanding regions between crystals at higher solid fraction.
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