The pacemaker and AV canal are the most temperature-sensitive segments of the embryonic heart. We suggest that the critical point for conduction is the connection of the ventricular trabecular network to the AV canal.

Remodeling of nanoscopic structures is not just crucial for cell biology, but it is also at the core of bioinspired materials. While the microtubule cytoskeleton in cells undergoes fast adaptation, adaptive materials still face this remodeling challenge. Moreover, the guided reorganization of the microtubule network and the correction of its abnormalities is still a major aim. This work reports new findings for externally triggered microtubule network remodeling by nanosecond electropulses (nsEPs). At first, a wide range of nsEP parameters, applied in a low conductivity buffer, is explored to find out the minimal nsEP dosage needed to disturb microtubules in various cell types. The time course of apoptosis and microtubule recovery in the culture medium is thereafter assessed. Application of nsEPs to cells in culture media result in modulation of microtubule binding properties to end‐binding (EB1) protein, quantified by newly developed image processing techniques. The microtubules in nsEP‐treated cells in the culture medium have longer EB1 comets but their density is lower than that of the control. The nsEP treatment represents a strategy for microtubule remodeling‐based nano‐biotechnological applications, such as engineering of self‐healing materials, and as a manipulation tool for the evaluation of microtubule remodeling mechanisms during various biological processes in health and disease.

Prevalence of cardiac arrhythmias increases gradually with age; however, specific rhythm disturbances can appear even prior to birth and markedly affect foetal development. Relatively little is known about these disorders, chiefly because of their relative rarity and difficulty in diagnosis. In this review, we cover the most common forms found in human pathology, specifically congenital heart block, pre-excitation, extrasystoles and long QT syndrome. In addition, we cover pertinent literature data from prenatal animal models, providing a glimpse into pathogenesis of arrhythmias and possible strategies for treatment.

Nanosecond pulsed electric field offers novel opportunities in bionanotechnology and biomedicine enabling ultrafast physical control of membrane, and protein‐based processes for the development of novel bionanomaterials and biomedical theranostic methods. However, the mechanisms of nanosecond pulsed electric field action at the nano‐ and molecular scale are not fully understood due to lack of appropriate research tools. In order to overcome this challenge, a technological platform for the exploration of these mechanisms in live biological samples is provided here. This paper describes step by step the proposed chip platform, including the design, fabrication, installation, and testing of the chip. The developed chip is capable of delivering hundreds of volts of nanosecond electric pulses compared to conventional chips using few volts. Moreover, the chip is fully integrated into a super‐resolution microscope. Later on, the chip function is demonstrated by affecting microtubule architecture in living cells. Therefore, the chip‐based technological advancement enables the assessment of pulsed electric field effects on bionanostructures and observing their effects in real‐time. The results contribute to the chip‐based high‐frequency bioelectronics technology for modulating the function of biological matter at the nanoscale level.

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The function of the embryonic heart is strongly affected by temperature. Changes in the kinetics of ion channels are crucial for generation and propagation of electricity. We set to analyze in detail the effects of temperature changes on electrical activity of the embryonic chick heart using in vitro high‐speed calcium imaging and in ovo video microscopy.In embryonic day 4 hearts we found that a decrease in temperature from 37 °C to 34 °C lead in vitro to a 22 % drop of the intrinsic heart rate and unchanged amplitude of Ca2+ transients, compared to a 25% deceleration between 37 °C and 34 °C in ovo. Increase in temperature from 37 °C to 40 °C lead in vivo to 23% and in ovo to 20 % acceleration of the intrinsic heart rate, and a significant decrease in amplitude of Ca2+ transients (atrium ‐35%, ventricle ‐38%). Hyperthermia in vitro increased the incidence of complete atrioventricular (AV) blocks, while no complete AV block was observed in hypothermia. Similar situation was recorded in ovo. Electrical stimulation experiments in ovo suggested that the AV blocks were caused by hypoxia a not by the tachycardia per se. Activation maps placed the location of the AV block at the inner curvature and the AV canal‐ventricular boundary along the outer curvature.Temperature is thus an important epigenetic factor influencing the function of the developing cardiac conduction system. Increased temperature augments the metabolic requirements of the myocardium, resulting in a relative hypoxia and AV conduction disturbances.Supported by GACR P302/11/1308 (DS) and GAUK 716214 (FV).

The rhythmic and synchronized contraction of atria and ventricles is essential for efficient pumping of blood throughout the body. This process relies on the proper generation and conduction of the cardiac electrical impulse. Electrophysiological properties differ in various regions of the heart, revealing intrinsic heterogeneities rooted, at least in part, in regional differences in expression of ion channel and gap junction subunit genes. A causal relation between transcription factors and such regionalized gene expression has been established. Abnormal cardiac electrical function and arrhythmias in the postnatal heart may stem from a developmental changes in gene regulation. Genome-wide association studies have provided strong evidence that common genetic variation at developmental gene loci modulates electrocardiographic indices of conduction and repolarization and susceptibility to arrhythmia. Functional aspects are illustrated by description of selected prenatally occurring arrhythmias and their possible mechanisms. We also discuss recent findings and provide background insight into these complex mechanisms.