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- BookGary D Lopaschuk and Naranjan S. Shalla, editors.Contents:
Part I. Control of Energy Metabolism
A Primer on Carbohydrate Metabolism in the Heart / Heinrich Taegtmeyer
Lipoproteins: A Source of Cardiac Lipids / Konstantinos Drosatos and Ira J. Goldberg
Role of Lipoprotein Lipase in Fatty Acid Delivery to the Heart / Andrea Wan and Brian Rodrigues
Control of Myocardial Fatty Acid Uptake / Jan F. C. Glatz and Joost J. F. P. Luiken
Cardiac Energy Metabolism in Heart Failure Associated with Obesity and Diabetes / Gary D. Lopaschuk
Transcriptional Control of Mitochondrial Biogenesis and Maturation / Rick B. Vega , Teresa C. Leone , and Daniel P. Kelly
Relationship Between Substrate Metabolism and Cardiac Efficiency / Ellen Aasum
Acetylation in the Control of Mitochondrial Metabolism and Integrity / Michael N. Sack
Part II. Alteration in Energy Metabolism
Adrenergic Control of Cardiac Fatty Acid Oxidation in Diabetes / Vijay Sharma and John H. McNeill
The Myocardial Creatine Kinase System in the Normal, Ischaemic and Failing Heart / Craig A. Lygate and Stefan Neubauer
Fuel Metabolism Plasticity in Pathological Cardiac Hypertrophy and Failure / Stephen C. Kolwicz and Rong Tian
Defects in Mitochondrial Oxidative Phosphorylation in Hearts Subjected to Ischemia-Reperfusion Injury / Vijayan Elimban , Paramjit S. Tappia , and Naranjan S. Dhalla
The Role of AMPK in the Control of Cardiac Hypertrophy / Nikole J. Byrne, Miranda M. Sung, and Jason R. B. Dyck
The Role of Incomplete Fatty Acid β-Oxidation in the Development of Cardiac Insulin Resistance / John R. Ussher
Part III. Optimization of Energy Metabolism
Metabolic Therapy for the Ischemic Heart / Giacinta Guarini , Alda Huqi , and Mario Marzilli
Inhibition of Fatty Acid Oxidation to Treat Heart Failure in Patients / Rui Yan , Jin Wei , and Dengfeng Gao
Cardiac Metabolic Protection for the Newborn Heart / J. Carter Ralphe and Thomas D. Scholz
Targeting Transcriptional Control of Fatty Acid Oxidation to Treat Heart Disease / Michael A. Portman and Aaron K. Olson.Digital Access Springer 2014 - ArticleMoore A, Ross GD, Nachman RL.J Clin Invest. 1978 Nov;62(5):1053-60.The agglutination of human platelets by ristocetin and von Willebrand factor was inhibited by aggregated immunoglobulin (Ig)G and by Fc fragments of IgG, but not by Fab, F(ab')(2) or pFc fragments of IgG. Because this inhibition occurred with formalin-fixed platelets as well as with normal platelets, a generalized aggregation of fluid membrane components by Fc fragments was not responsible for this inhibition of ristocetin and von Willebrand factor-induced agglutination. Reciprocal inhibition of platelet Fc receptors was produced by prior incubation of platelets with von Willebrand factor and ristocetin. Sucrose density gradient ultracentrifugation studies demonstrated that aggregated IgG did not form fluid-phase complexes with von Willebrand factor and ristocetin. Furthermore, passage of von Willebrand factor and ristocetin through a column of immobilized heat-aggregated IgG did not alter platelet agglutinating activity which indicates that aggregated IgG did not inactivate von Willebrand factor or ristocetin. Thus, it was likely that the IgG-mediated interference with platelet agglutination by ristocetin and von Willebrand factor did not occur in the fluid phase but at the platelet surface. These studies suggest that the platelet membrane Fc receptor may be either a part of, or sterically related to, the membrane glycoprotein I complex that interacts with von Willebrand factor, and that occupation of one of these surface components blocks the availability of the other.