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More about the selection theory: Jerne meant that the Socratic idea of learning was a fitting analogy for 'the logical basis of the selective theories of antibody formation': Can the truth (the capability to synthesize an antibody) be learned? If so, it must be assumed not to pre-exist; to be learned, it must be acquired. We are thus confronted with the difficulty to which Socrates calls attention in Meno [ ... ] namely, that it makes as little sense to search for what one does not know as to search for what one knows; what one knows, one cannot search for, since one knows it already, and what one does not know, one cannot search for, since one does not even know what to search for. Socrates resolves this difficulty by postulating that learning is nothing but recollection. The truth (the capability to synthesize an antibody) cannot be brought in, but was already inherent.

Niels Kaj Jerne
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I am a child of the poisonous wind that copulated with the East River on an oil-slick, garbage infested midnight. I turn about on my own parentage. I inoculate against those very biles that brought me to light. I am a serum born of venoms. I am the antibody of all Time. I am the Cure. You do of the City, do you not? Manhattan is your punisher, let me be you shield.

Ray Bradbury, Long After Midnight
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The researchers looked deeper into these observations, in hopes of gaining insight into the mechanisms underlying the high evolutionary rate and extraordinary immunologic plasticity of influenza HA. They probed in more detail the precise codons that are used by the virus to encode the influenza HA1 protein. The discriminated between codons on the basis of volatility. Each three-nucleotide codon is related by a single nucleotide change to nine 'mutational neighbours.' Of those nine mutations, some proportion change the codon to a synonymous codon and some change it to a nonsynonymous one, which directs the incorporation of a different amino acid into the protein. More volatile codons are those for which a larger proportion of those nine mutational neighbours encode an amino acid change. The use of particular codons in a gene at a frequency that is disproportionate to their random selection for encoding a chosen amino acid is termed codon bias. Such bias is common and is influenced by many factors, but here the collaborators found strong evidence for codon bias that was particular for and restricted to the amino acids making up the HA1 epitopes. Remarkably, they observed that influenza employs a disproportionate number of volatile codons in its epitope-coding sequences. There was a bias for the use of codons that had the fewest synonymous mutational neighbours. In other words, influenza HA1 appears to have optimized the speed with which it can change amino acids in its epitopes. Amino acid changes can arise from fewer mutational events. The antibody combining regions are optimized to use codons that have a greater likelihood to undergo nonsynonymous single nucleotide substitutions : they are optimized for rapid evolution.

Michael G Cordingley, Viruses: Agents of Evolutionary Invention
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