By Golder Wilson

ISBN-10: 0071471839

ISBN-13: 9780071471831

This one of a kind attempt prep consultant lets you attempt your wisdom of crucial biochemistry and genetics thoughts for the USMLE Step 1; perform with 500 USMLE Step 1-style questions with referenced solutions; evaluate causes for correct and mistaken solutions; and construct self belief, talents, and information.

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Additional info for Biochemistry and Genetics, 2007, p.514

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Glucose, fructose, and galactose are the main carbohydrates absorbed from dietary starch, sucrose, and lactose, respectively; fructose and galactose are converted to glucose in liver (mainly) and deficiencies in their conversion cause essential fructosemia and galactosemia. • Glycolysis (Fig. 12) is the main path of glucose metabolism (and of dietary fructose or galactose), producing lactate in anaerobic tissues (brain, muscle, gastrointestinal tract, retina, skin, and erythrocytes with no mitochondria).

CO2 (as bicarbonate), ammonium ion, ornithine, and citrulline enter the mitochondrial matrix via specific carriers (see heavy dots) present in the inner membrane of liver mitochondria. (Reproduced with permission, from Murray RK, Granner DK, Mayes PA, Rodwell VW: Harper’s Biochemistry. 26/e. , glutamate derivatives). • Catabolism of amino acid carbon chains often yields acetyl CoA; enzyme deficiencies in the degradation pathways for phenylalanine (phenylketonuria), tyrosine (tyrosinemia, alkaptonuria), branched chain amino acids (maple syrup urine disease), and tryptophan (Hartnup disease) cause specific metabolic diseases.

The reciprocal Lineweaver-Burk plot constructed by measuring enzyme velocities with and without inhibitor distinguishes competitive inhibition from noncompetitive inhibition (Fig. 10). A competitive inhibitor will have similar structure to the substrate and compete for enzyme catalytic sites, changing the effective Km but not the Vmax (Fig. 10A). A simple noncompetitive inhibitor does not resemble substrate in structure and will not compete for its binding at the enzyme catalytic site—thus changing Vmax but not Km (Fig.

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Biochemistry and Genetics, 2007, p.514 by Golder Wilson


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