Each year, the Editors-in-Chief and the editorial board members of the ASME Journal of Biomechanical Engineering identify the most meritorious papers published in the journal in the previous calendar year, and an external committee selects the top paper of the year from that list. The authors of this paper are the recipients of the Richard Skalak Award, named after an early leader within the ASME Bioengineering community. Richard Skalak (1923–1997) played a leadership role in the formative decades of the discipline of biomedical engineering through his technical contributions in biomechanics, his educational influence on students, and his service to many developing societies and journals. Richard Skalak believed in several central approaches to bioengineering and several central values in working with people. In bioengineering, these were: (1) the useful combination of mathematical and computational modeling with experimental results, to better inform the new biological understanding that is derived and (2) the inclusion of both microscale and macroscale phenomena in understanding complex biological systems. In terms of mentoring students and collaborating with colleagues, these were: (1) share ideas freely, (2) listen to ideas of others and integrate the best into new developments, and (3) show tolerance and respect for others at all times. These tenets help guide us as a community and as a journal, and we are honored by the opportunity to contribute to Richard Skalak's legacy by giving an award bearing his name. The Editors thank the 2015 Skalak Award committee: Jimmy Moore (chair), Michael Sacks, Jeff Weiss, and Lori Setton.
The Skalak Award winner for 2015 was “Bending of the Looping Heart: Differential Growth Revisited” by Yunfei Shi, Jiang Yao, Gang Xu, and Larry A. Taber. The paper was published in J. Biomech. Eng., 136(8), p. 081002.
ABSTRACT: In the early embryo, the primitive heart tube (HT) undergoes the morphogenetic process of c-looping as it bends and twists into a c-shaped tube. Despite intensive study for nearly a century, the physical forces that drive looping remain poorly understood. This is especially true for the bending component, which is the focus of this paper. For decades, experimental measurements of mitotic rates had seemingly eliminated differential growth as the cause of HT bending, as it has commonly been thought that the heart grows almost exclusively via hyperplasia before birth and hypertrophy after birth. Recently published data, however, suggest that hypertrophic growth may play a role in looping. To test this idea, we developed finite-element models that include regionally measured changes in myocardial volume over the HT. First, models based on idealized cylindrical geometry were used to simulate the bending process in isolated hearts, which bend without the complicating effects of external loads. With the number of free parameters in the model reduced to the extent possible, stress and strain distributions were compared to those measured in embryonic chick hearts that were isolated and cultured for 24 hrs. The results show that differential growth alone yields results that agree reasonably well with the trends in our data, but adding active changes in myocardial cell shape provides closer quantitative agreement with stress measurements. Next, the estimated parameters were extrapolated to a model based on realistic 3D geometry reconstructed from images of an actual chick heart. This model yields similar results and captures quite well the basic morphology of the looped heart. Overall, our study suggests that differential hypertrophic growth in the myocardium (MY) is the primary cause of the bending component of c-looping, with other mechanisms possibly playing lesser roles.
