Suboptimal Health." 1985.Manuscript Notes and Typescripts"Difference in Electrophoretic Behavior of Sickle Cell Hemoglobin and Normal Human Hemoglobin." April 27, 1949."Molecular Disease." 1950s.Notes re: "Abnormality of Hemoglobin Molecules in Hereditary Hemolytic Anemias." April 29, 1954."The Structure and Biological Properties of Molecules." November 1954."Molecular Disease and Evolution." September 16, 1963."The Advancement of Knowledge - Orthomolecular Psychiatry." February 25, 1969."The Impact of Molecular Information on Disease." January 20, 1972."The Genesis of the Concept of Molecular Disease." 1973."Ascorbic Acid and Cancer." February 14, 1976.Quotes"It appears, therefore, that while some of the details of this picture of the sickling process are as yet conjectural, the proposed mechanism is consistent with experimental observations at hand and offers a chemical and physical basis for many of them. Furthermore, if it is correct, it supplies a direct link between the existence of defective hemoglobin molecules and the pathological consequences of sickle cell disease."Linus Pauling. "Sickle Cell Anemia, a Molecular Disease." Science 110: 543-548. April 1949."The demonstration that sickle cell hemoglobin differs in electrophoretic mobility from normal hemoglobin led to the entitled inference: 'Sickle cell anemia, a molecular disease.' This astonishingly simple concept is of fundamental importance to medicine for the ultimate understanding of the origins of sickness, and to biology for the insight into what genes do. In the author's words, 'This investigation...reveals a clear case of a change produced in a protein molecule by an allelic change in a single gene involved in synthesis.'"Samuel H. Boyer IV. Introduction to "Sickle Cell Anemia, a Molecular Disease." Papers on Human Genetics, 115-25. 1963."In 1949, application of methods of physical chemistry directly to the study of a protein produced by a mutated gene led Pauling, Itano, Singer and Wells to identify the specific change in the protein brought about by the gene. The discovery of the first of the abnormal human hemoglobins which they described as causing a 'molecular disease' -- sickle cell anemia -- was followed the identification of a large number of other proteins, each of which owed its difference from normal structure to a mutated gene. Ingram then showed that the change due to the mutation, in the case of each of two abnormal hemoglobins, was confined to a single amino acid residue at one point in one of the polypeptide chains composing the globin. There could be no doubt that genes controlled protein structure by specifying the sequence of amino acid residues in the polypeptide chains. The assumed basic functional correspondence was then altered from 'one gene-one enzyme' to 'one gene-one polypeptide.'"L. C. Dunn. "Old and New in Genetics." Bulletin of the New York Academy of Medicine, 40(5): 325-333, 329. May 1964.Audio Clips"Men and Molecules: Molecular Medicine" February 26, 1962.The Definition of Molecular Disease. (1:10) Drs. Pauling and Castle: "The Evolution of Molecular Biology." 1969.Itano's Work on Sickle Cell Anemia. (2:18) "Molecular Disease Lectures" November 1970.Itano, Singer and Wells' Work on Sickle Cell Anemia. (2:18) Henney Kilowatt O Henney Kilowatt foi o primeiro veiculo eletrico regulado por transistores; foi comercializado em 1959, e produziram-se 47 unidades, vendidas entre 1959 e 1962. De elas, ainda existem menos de uma