By Martin Morad, Yuichiro J. Suzuki (auth.), Samuel Sideman, Rafael Beyar (eds.)
The 10th Henry Goldberg Workshop is a superb get together to remember our pursuits and rejoice a few of our humble achievements. imaginative and prescient and love of our fellow guy are mixed the following to: 1) Foster interdisciplinary interplay among major international scientists and scientific cardiologists with a purpose to establish lacking wisdom and catalyze new study principles; 2) relate easy microscale, molecular and subcellular phenomena to the worldwide clinically manifested cardiac functionality; three) practice conceptual modelling and quantitative research to raised discover, describe, and comprehend cardiac body structure; four) interpret to be had scientific facts and layout new revealing experiments; and five) increase overseas cooperation within the never-ending look for the secrets and techniques of existence and their implication on cardiac pathophysiology. the 1st Goldberg Workshop, held in Haifa, in 1984, explored the interplay of mechanics, electric activation, perfusion and metabolism, emphasizing imaging within the scientific setting. the second one Workshop, in 1985, mentioned an identical parameters with a slant in the direction of the regulate points. The 3rd Goldberg Workshop, held within the united states at Rutgers collage, in 1986, highlighted the transformation of the microscale activation phenomena to macro scale task and function, concerning electrophysiology, power metabolism and cardiac mechanics. The fourth Goldberg Workshop endured the hassle to clarify some of the parameters affecting cardiac functionality, with emphasis at the ischemic middle. The 5th Workshop targeting the impression of the inhomogeneity of the cardiac muscle on its functionality. The 6th Workshop highlighted new imaging options which enable perception into the neighborhood and international cardiac performance.
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Extra info for Analytical and Quantitative Cardiology
Dr. N. Westerhof: Pre-stretching of filled blood vessels could explain the negative elasticity too. Dr. H. ter Keurs: The perfused blood vessels prestretched in these experiments were without perfusion. Dr. N. Westerhof: But they might be prestretched; even vessels like the aorta are prestretched in the body. If you take it out it shortens considerably. It is a negative type of elasticity. Dr. H. ter Keurs: That is a possible thought. Dr. A. McCuUoch: Your interpretation of your model suggests that there is a calcium dependent critical buckling length for titin that changes during diastole.
I have measured it in a guinea pig ventricle at about 10 pA/pF vs 1 pNpF and I am amazed at the difference between the two. I am amazed at the level of problem that HERG channel causes clinically, since it has such a spotty expression in the heart. How do you explain this? How do you fit all of this together? Dr. H. Strauss: The question of current density is somewhat complicated because most of these studies were done in the atrium where the cell capacitance is smaller. But the current is still small raising concern about its overall contribution to repolarization.
30 I I ... 120nm ~~ 500ms Figure 4. A) The time course of the modulus of stiffness (MOD) and phase shift (cI» during diastole in the presence of 1 mM (circles) and 2 mM (squares) of [Ca2+ lo' The results are expressed as mean±sem; n=173, 18 muscles. 05. The time scale is expressed in % of diastolic interval. B) shows the time courses of SL of a muscle representative of Panel A, showing slight spontaneous motions of the sarcomeres (arrowhead) at 1 mM (upper trace) and 2 mM [Ca2+ lo (lower trace) during two consecutive diastoles.
Analytical and Quantitative Cardiology by Martin Morad, Yuichiro J. Suzuki (auth.), Samuel Sideman, Rafael Beyar (eds.)