Synthetic recovery of impulse propagation in myocardial infarction via silicon carbide semiconductive nanowires

Myocardial infarction causes 7.3 million deaths worldwide, mostly for fibrillation that electrically originates from the damaged areas of the left ventricle. Conventional cardiac bypass graft and percutaneous coronary interventions allow reperfusion of the downstream tissue but do not counteract the bioelectrical alteration originated from the infarct area. Genetic, cellular, and tissue engineering therapies are promising avenues but require days/months for permitting proper functional tissue regeneration. Here we engineered biocompatible silicon carbide semiconductive nanowires that synthetically couple, via membrane nanobridge formations, isolated beating cardiomyocytes over distance, restoring physiological cell-cell conductance, thereby permitting the synchronization of bioelectrical activity in otherwise uncoupled cells. Local in-situ multiple injections of nanowires in the left ventricular infarcted regions allow rapid reinstatement of impulse propagation across damaged areas and recover electrogram parameters and conduction velocity. Here we propose this nanomedical intervention as a strategy for reducing ventricular arrhythmia after acute myocardial infarction.

Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5

Oligodendrocytes facilitate rapid impulse propagation along the axons they myelinate and support their long-term integrity. However, the functional relevance of many myelin proteins has remained unknown. Here we find that expression of the tetraspan-transmembrane protein CMTM5 (Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5) is highly enriched in oligodendrocytes and CNS myelin. Genetic disruption of the Cmtm5-gene in oligodendrocytes of mice does not impair the development or ultrastructure of CNS myelin. However, oligodendroglial Cmtm5-deficiency causes an early-onset progressive axonopathy, which we also observe in global and in tamoxifen-induced oligodendroglial Cmtm5-mutants. Presence of the Wlds mutation ameliorates the axonopathy, implying a Wallerian degeneration-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis.

Using of the Ultrasonic Method for Alkali-Silica Reaction Detection in the Cement Mortar

The alkali–silica reaction (ASR) causes internal corrosion of concrete. The aim of this work is to verify the possibility of ultrasonic method in detection of concrete internal structure changes, which were initiated by the alkali-silica reaction. For this purpose, we prepared samples that contained aggregates of two types, namely one with 98% of SiO2 content and one with a greywacke. The dependence of ultrasonic impulse propagation velocity on the changes in the structure of mortars containing aggregates from these rocks was researched. The results of this work are not unambiguous yet and therefore it is necessary to carry out more extensive investigation with using of other methods that will allow to examine changes in the internal structure of composites more detailed.

Impulse Propagation in Compositions and Words

We consider compositions of n represented as bargraphs and subject these to repeated impulses which start from the left at the top level and destroy horizontally connected parts. This is repeated while moving to the right first and then downwards to the next row and the statistic of interest is the number of impulses needed to annihilate the whole composition. We achieve this by conceptualizing a generating function that tracks compositions as well as the number of impulses used. This conceptualization is repeated for words (over a finite alphabet) represented by bargraphs.

Ionic Mechanisms of Impulse Propagation Failure in the FHF2-Deficient Heart

Rationale: FHFs (fibroblast growth factor homologous factors) are key regulators of sodium channel (Na V ) inactivation. Mutations in these critical proteins have been implicated in human diseases including Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy. The underlying ionic mechanisms by which reduced Na v availability in Fhf2 knockout ( Fhf2 KO ) mice predisposes to abnormal excitability at the tissue level are not well defined. Objective: Using animal models and theoretical multicellular linear strands, we examined how FHF2 orchestrates the interdependency of sodium, calcium, and gap junctional conductances to safeguard cardiac conduction. Methods and Results: Fhf2 KO mice were challenged by reducing calcium conductance (gCa V ) using verapamil or by reducing gap junctional conductance (Gj) using carbenoxolone or by backcrossing into a cardiomyocyte-specific Cx43 (connexin 43) heterozygous background. All conditions produced conduction block in Fhf2 KO mice, with Fhf2 wild-type ( Fhf2 WT ) mice showing normal impulse propagation. To explore the ionic mechanisms of block in Fhf2 KO hearts, multicellular linear strand models incorporating FHF2-deficient Na v inactivation properties were constructed and faithfully recapitulated conduction abnormalities seen in mutant hearts. The mechanisms of conduction block in mutant strands with reduced gCa V or diminished Gj are very different. Enhanced Na v inactivation due to FHF2 deficiency shifts dependence onto calcium current (I Ca ) to sustain electrotonic driving force, axial current flow, and action potential (AP) generation from cell-to-cell. In the setting of diminished Gj, slower charging time from upstream cells conspires with accelerated Na v inactivation in mutant strands to prevent sufficient downstream cell charging for AP propagation. Conclusions: FHF2-dependent effects on Na v inactivation ensure adequate sodium current (I Na ) reserve to safeguard against numerous threats to reliable cardiac impulse propagation.