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Coordinated cell interactions are required to accomplish several complex and dynamic tasks observed in several tissues. Cell function may be coordinated by cell-to-cell communication through gap junctions channels (GJCs). These channels are formed by the serial docking of two hemichannels, which in turn are formed by six protein subunits called connexins (Cxs). It is well known that GJCs are involved in several functions, such as intercellular propagation of calcium waves, spread of electrotonic potentials and spatial buffering of ions and metabolites. On the other hand, undocked hemichannels, which are not forming GJCs, can also serve other functions as “free hemichannels”. Currently, it is recognized that undocked hemichannels may have functional relevance in cell physiology allowing diffusional exchange of ions and small molecules between intra- and extra-cellular compartments. Additionally, another family of proteins calls pannexins (Panx) also forms functional hemichannels at the plasma membrane. Recently, Panxhemichannels have been involved in both pathological and physiological processes. Controlled hemichannel opening allows the release of small signaling molecules including ATP, glutamate, NAD+, adenosine, cyclic nucleotides, PGE2. They also allow uptake of relevant signaling molecules (e.g., cADPR) and metabolites (e.g., glucose). Additionally, a growing body of evidence shows that hemichannels are involved in important processes, such glucose detection in tanicytes, activation of the inflammasome, memory consolidation in the basolateral amygdala, potentiation of muscle contraction and release of nitric oxide from endothelial cells, among others. However, hemichannels can also play an important role in the homeostatic imbalance observed in diverse chronic diseases. In fact, massive and/or uncontrolled hemichannel opening induces or accelerates cell death in several pathological conditions including Charcot-Marie-Tooth disease, ischemia, oculodentodigital dysplasia, hydrotic ectodermic dysplasia, inflammatory responses, and deafness. Hemichannel-mediated cell death is due mainly to an entry of Ca+2. The latter activates proteases, nucleases and lipases, causing irreversible cell damage. An increasing amount of evidence demonstrates that blockade of uncontrolled hemichannel opening greatly reduces the cellular damage observed in several chronic diseases models. Therefore, Cx and Panx-hemichannels appear as promising drug targets for clinical treatment of human chronic diseases. Therefore, pharmacological tools are urgently needed to further elucidate hemichannels functions and to validate them as drug targets for the development of novel therapies for connexin-based diseases. Thus, understanding the role of Cx and Panx-hemichannels under physiological conditions and recognizing the molecular mechanisms controlling them, may provide us with a better picture of the hemichannels participation in some diseases and of the signals underlying their malfunctioning.

Gap junctions (Cell biology) --- Connexins. --- Junctions, Gap (Cell biology) --- Nexus (Cell biology) --- Cell junctions --- Connexins --- Membrane proteins --- redox regulation --- posttranslational modifications --- gap junction channels --- pannexins --- hemichannels

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The current book entitled Heterojunctions and Nanostructures is divided into two sections. In Section 1, the chapters are related to topological insulators where their theoretical aspects, their current experiments, and their applications are presented. A few presented topics are, among others, the topological phases of matter, band topology of insulators and also of Weyl semimetals, transport properties of 3D topological insulator quantum wires and the influence of disorder, transport properties of quasi-1D (and 2D) topological surface states, quantum coherence, and topological insulator thin-film Hall bar device. In Section 2, the chapters are related to light devices such as laser diodes and their fabrication techniques. This section includes, among others, topics such as semiconductor quantum nanowire laser diodes, solutions of Schrodinger equation in nanostructures, numerical methods, light-to-electricity conversion devices, photoexcited carrier transportation process in quantum wells and quantum dots, growth mode and characterization of heterostructure of large lattice mismatch, and photoionization cross section.

Heterojunctions. --- Nanostructures. --- Nanoscience --- Physics --- Heterostructures --- Semiconductors --- Junctions --- Solid-State Physics --- Physical Sciences --- Engineering and Technology --- Materials Science --- Semiconductor

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The effective management of cardiac arrhythmias, either of atrial or of ventricular origin, remains a major challenge. Sudden cardiac death due to ventricular tachyarrhythmias remains the leading cause of death in industrialized countries while atrial fibrillation is the most common rhythm disorder; an arrhythmia that’s prevalence is increasing and accounts for nearly one quarter of ischemic stokes the elderly population. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising antiarrhythmic agents were found to increase rather than decrease mortality in patients recovering from myocardial infarction. The question then is what went wrong, why have these interventions proven to be so ineffective? An obvious answer is the drugs were designed to attack the wrong therapeutic target. Clearly, targeting single ion channels (using either isolated ion channels or single myocytes preparations) has proven to be less than effective. What then is the appropriate target? It is well established that cardiac electrical properties can vary substantially between single cells and intact preparations. One obvious example is the observation that action potential duration is much longer in isolated cells as compared to multi-cellular preparations or intact hearts. Due to the low electrical resistance between adjacent myocytes, the cells act in coordinated fashion producing “electrotonic interdependence” between neighboring cells. Myocardial infarction and/or acute ischemia provoke profound changes in the passive electrical properties of cardiac muscle. In particular, electrotonic uncoupling of the myocytes disrupts the coordinated activation and repolarization of cardiac tissue. The resulting compensatory changes in ionic currents decrease cardiac electrical stability increasing the risk for life-threatening changes in the cardiac rhythm. Thus, the electrical properties of myocardial cells must be considered as a unit rather than in isolation. It is the purpose of this Research Topic to evaluate the largely neglected relationship between changes in passive electrical properties of cardiac muscle and arrhythmia formation.

Gap Junctions --- Myocardial Infarction --- computer modeling --- arrhythmias --- Fibrosis --- electrotonic coupling --- cable theory --- sino-atrial node --- Ventricular Fibrillation --- Atrial Fibrillation

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This is a Special Issue on Molecular Electronics which provides an overview of the field and will be useful for both theoreticians and experimentalists. Topics include protein-based electronics, field-induced trans-to-cis isomerisation, phonon thermal conductance, spin-dependent transport, attenuation factors, HOMO-LUMO gap corrections and nanofabrication techniques.

molecular electronics --- self-assembly films --- Langmuir-Blodgett films --- electrografting --- top-contact electrode --- molecular junctions --- attenuation factor --- density functional theory --- graphene --- single molecule junctions --- metal/molecule interface --- energy level alignment --- conductance --- electron transport --- DFT + Σ --- thermoelectricity --- phonon --- thermal conductance --- OPE3 --- anchor groups --- pyridyl --- thiol --- methyl sulphide --- carbodithioate --- spin polarization --- magnetic chain with AAH modulation --- light irradiation --- single-molecule junctions --- STM break-junction --- in-situ isomerisation --- carotenoids --- azurin --- solid-state junction --- biomolecular electronics --- electronic transport --- molecular dynamics --- n/a

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Cell adhesion --- Cell migration --- Cell interaction --- Cell-cell interaction --- Cell communication --- Cellular communication (Biology) --- Cellular interaction --- Intercellular communication --- Migration of cells --- Adherence, Cell --- Cell adherence --- Cell adhesion. --- Cell interaction. --- Cell migration. --- Cell Adhesion --- Cell Movement --- Cell Migration --- Locomotion, Cell --- Migration, Cell --- Motility, Cell --- Movement, Cell --- Cell Locomotion --- Cell Motility --- Cell Movements --- Movements, Cell --- Adhesion, Cell --- Adhesions, Cell --- Cell Adhesions --- Cellular control mechanisms --- Cytology --- Adhesion --- Membrane fusion --- Junctional complexes (Epithelium) --- Cell Tracking --- Cell-Matrix Junctions --- Focal Adhesions --- Life Sciences --- Biology --- cell biology --- cell-cell interactions --- cell-matrix interactions --- cell biomechanics --- cell fusion --- cell adhesion complexes --- Histology. Cytology --- Cell Adhesion. --- Cell Movement. --- Cellules --- Adhésivité --- Migration --- Interaction