Before submitting your abstract, you need to create an account on the conference website using this link: https://bgrssb.icgbio.ru/2022/wa_registration/

Since abstracts will only be published online, we have increased the maximum abstract size to two pages. Abstract may include any necessary sections, see the template below.

Every participant who already sent the abstract can update it if necessary.

Abstract template (docx)

The abstracts must be submitted online before April, 25, 2022.

  • The abstracts, including the full title of the report, full name of the authors, their place of work, e-mail address of the speaker, key words and the text of the abstract should not exceed two pages.
  • The title of the report should be in bold 14 Times New Roman.
  • Authors‘ names separated by commas in 11 Times New Roman.
  • Place of work of the authors in italic font 9 Times New Roman.
  • e-mail of the author-speaker in italic font 9 Times New Roman.
  • Key words in regular font 9 Times New Roman.
  • The text of the abstracts in regular font 11 Times New Roman. Latin names of species and gene designations are italicized.
  • References section (if required) in regular font 9 Times New Roman.

You can use the template as an example or base of your abstract.

The information about figures in the abstract:

Figures must be inserted in the abstract file and additionally uploaded as separate file. Formats: EPS, JPEG, PNG, TIFF with a resolution of 300 dpi. Figures used in the article, protected by copyright law, must be accompanied by written permission from the copyright holders for their publication. Figures will not be edited. Tables are accepted with a standard (black and white) color scheme.

Sample:

DOI 10.18699/SBB-2021-000

Cardiac mechanics, calcium overload and arrhythmogenesis

Ivanov A.1*, Petrov O.1, 2, Sidorov L.3
1 Institute of Cytology and Genetics, SB RAS, Novosibirsk, Russia
2 Kurchatov Genomic Center of the Institute of Cytology and Genetics, SB RAS, Novosibirsk, Russia
3 Siberian Research Institute of Plant Production and Breeding – Branch of the Institute of Cytology and Genetics, SB RAS, Novosibirsk, Russia
* ivanov@gmail.com

Key words: calcium overload, rhythm disturbances, cardiac mechanics

Motivation and Aim: It is well-known that Ca2+ overload may cause cardiac arrhythmia. However, possible contribution of the mechanical factors to the arrhythmia development in Ca2+-overloaded cardiomyocytes has been insufficiently addressed. Earlier we have developed a mathematical model of cardiomyocyte electro-mechanical function [1] that predicted a significant role of the intra- and extracellular mechanical factors in arrhythmogenesys. Model prediction was verified in experiments on papillary muscles from the right ventricle of guinea pigs overloaded with calcium [2].

Methods and Algorithms: We utilized the cellular model to study effects of the electromechanical coupling between cardiomyocytes in a 1D heterogeneous muscle strand formed of 90% of normal (N) cardiomyocytes and 10% of sub-critical (SC) cardiomyocytes with decreased Na+-K+ pump activity. Single SC‑cardiomyocytes did not demonstrate spontaneous activity during isometric contractions at a reference length. Regular fiber twitches at the reference initial cell length were induced by 1 bps electrical stimulation applied at an edge of the strand. Excitation spread along the tissue via electro-diffusional cell coupling followed by cell contractions and force development in the fiber.

Results: Mechanical interactions between N- and SC-cells in the tissue resulted in the spontaneous activity emerged in the SC‑zone between the regular stimuli. If the excitation wave spread from SC- to N-region, the SC-cells developed delayed after-dеpolarizations (DAD) that caused a slowly developing beat-to-beat decrease in the force of fiber contraction. If the excitation spread in opposite direction, DAD in the SC-cells induced reflected downward excitation waves capturing the normal region and followed by extrasystoles in the whole fiber.

Conclusion: The results obtained in the model suggest that ectopic activity may emerge in a sub-critical myocardial region, e.g. comprising cardiomyocytes with moderately depressed N+-K+ pump, due to its mechanical interactions in the myocardial tissue. Moreover, such ectopic zone may expand by capturing normal regions in myocardium via the electro-mechanical coupling between cardiomyocytes.

Acknowledgements: The study is supported by the Kurchatov Genomic Centre of the Institute of Cytology and Genetics, SB RAS (075-15-2019-1662).

References

  1. Katsnelson L.B. et al. Contribution of mechanical factors to arrhythmogenesis in calcium overloaded cardiomyocytes: Model predictions and experiments. Progress in Biophysics and Molecular Biology. 2011;107(1):81-89.
  2. Lashin S.A., Matushkin Yu.G. Haploid evolutionary constructor: new features and further challenges. In Silico. Biol. 2012;11(3):125-135.