[Adaptation to hypoxia, as opposed to adaptation to stress, does not protect the isolated heart from reperfusion after total ischemia. A nuclear magnetic resonance study].
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PrPSc is a specific protein marker for slow infectious diseases known as the transmissible subacute spongiform encephalopathies. Although PrPSc is closely associated with infectivity, it is not known if it is the infectious agent itself, a component of the agent or merely adventitiously associated with infectivity. In the present study we demonstrate that the resistance of PrPSc to partial denaturation and of infectivity to inactivation differs markedly for two scrapie strains. Proteinase K treatment or electrophoretic analysis of partially denatured PrPSc preparations reveal a dissociation between infectivity and demonstrable PrPSc. Our findings support other evidence that not all PrPSc is required for infectivity. Our studies combined with previous biological analyses suggest that PrPSc cannot be the sole component associated with the infectious agent.
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The innate immune system senses pathogens largely through signals initiated by a collection of phylogenetically related proteins known as "Toll-like receptors" (TLRs), of which 10 representatives are encoded in the human genome. Our understanding of the sensing role played by the TLRs began with the positional cloning of a spontaneous mutation (Lps(d)) in the gene encoding the mammalian lipopolysaccharide (LPS) receptor. Other key innate immunity proteins have been disclosed by germline mutagenesis, and are discussed in the present review.
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