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Cell death is a mystery in various forms. Whichever type of cell death, this is always accompanied by active or passive molecules release. The recent years marked the renaissance of the study of these molecules showing they can signal to and communicate with recipient cells and regulate physio- or pathological events. This review summarizes the defined forms of messages cells could spread while dying, the effects of these signals on the target tissue/cells, and how these types of communications regulate physio- or pathological processes. By doing so, this review hopes to identify major unresolved questions in the field, formulate new hypothesis worthy of further investigation, and when possible, provide references for the search of novel diagnostic/therapeutics agents. Du_P5Mc2hRRCD81pS52mbL Video abstract [ABSTRACT FROM AUTHOR]

Delayed cerebral ischemia (DCI) and vasospasm are two complications of subarachnoid hemorrhages (SAHs) which entail high risks of morbidity and mortality. However, it is unknown why only some patients who suffer SAHs will experience DCI and vasospasm. The purpose of this review is to describe the main genetic single nucleotide polymorphisms (SNPs) that have demonstrated a relationship with these complications. The SNP of the nitric oxide endothelial synthase (eNOS) has been related to the size and rupture of an aneurysm, as well as to DCI, vasospasm, and poor neurological outcome. The SNPs responsible for the asymmetric dimetilarginine and the high-mobility group box 1 have also been associated with DCI. An association between vasospasm and the SNPs of the eNOS, the haptoglobin, and the endothelin-1 receptor has been found. The SNPs of the angiotensin-converting enzyme have been related to DCI and poor neurological outcome. Studies on the SNPs of the Ryanodine Receptor yielded varying results regarding their association with vasospasm. [ABSTRACT FROM AUTHOR]

DNA replication is a tightly regulated fundamental process allowing the correct duplication and transfer of the genetic information from the parental cell to the progeny. It involves the coordinated assembly of several proteins and protein complexes resulting in replication fork licensing, firing and progression. However, the DNA replication pathway is strewn with hurdles that affect replication fork progression during S phase. As a result, cells have adapted several mechanisms ensuring replication completion before entry into mitosis and segregating chromosomes with minimal, if any, abnormalities. In this review, we describe the possible obstacles that a replication fork might encounter and how the cell manages to protect DNA replication from S to the next G1. [ABSTRACT FROM AUTHOR]

In the recent years a considerable effort has been devoted to foster the understanding of the basic mechanisms underlying the dynamical arrest that is involved in glass forming in supercooled liquids and in the sol-gel transition. The elucidation of the nature of such processes represents one of the most challenging unsolved problems in the field of material science. In this context, two important theories have contributed significantly to the interpretation of these phenomena: the Mode-Coupling theory (MCT) and the Percolation theory (PT). These theories are rooted on the two pillars of statistical physics, universality and scale laws, and their original formulations have been subsequently modified to account for the fundamental concepts of Energy Landscape (EL) and of the universality of the fragile to strong dynamical crossover (FSC). In this review, we discuss experimental and theoretical results, including Molecular Dynamics (MD) simulations, reported in the literature for colloidal and polymer systems displaying both glass and sol-gel transitions. Special focus is dedicated to the analysis of the interferences between these transitions and on the possible interplay between MCT and PT. By reviewing recent theoretical developments, we show that such interplay between sol-gel and glass transitions may be interpreted in terms of the extended F13 MCT model that describes these processes based on the presence of a glass-glass transition line terminating in an A3 cusp-like singularity (near which the logarithmic decay of the density correlator is observed). This transition line originates from the presence of two different amorphous structures, one generated by the inter-particle attraction and the other by the pure repulsion characteristic of hard spheres. We show here, combining literature results with some new results, that such a situation can be generated, and therefore experimentally studied, by considering colloidal-like particles interacting via a hard core plus an attractive square well potential. In the final part of this review, scaling laws associated both to MCT and PT are applied to describe, by means of these two theories, the specific viscoelastic properties of some systems. [ABSTRACT FROM AUTHOR]

Dyspnea or breathlessness is a symptom occurring in multiple acute and chronic illnesses, however, the understanding of the neural mechanisms underlying its subjective experience is limited. In this topical review, we propose neural oscillatory dynamics and cross‐frequency coupling as viable candidates for a neural mechanism underlying respiratory perception, and a technique warranting more attention in respiration research. With the evidence for the potential of neural oscillations in the study of normal and disordered breathing coming from disparate research fields with a limited history of interdisciplinary collaboration, the main objective of the review was to converge the existing research and suggest future directions. The existing findings show that distinct limbic and cortical activations, as measured by hemodynamic responses, underlie dyspnea, however, the time‐scale of these activations is not well understood. The recent findings of oscillatory neural activity coupled with the respiratory rhythm could provide the solution to this problem, however, more research with a focus on dyspnea is needed. We also touch on the findings of distinct spectral patterns underlying the changes in breathing due to experimental manipulations, meditation and disease. Subsequently, we suggest general research directions and specific research designs to supplement the current knowledge using neural oscillation techniques. We argue for the benefits of interdisciplinary collaboration and the converging of neuroimaging and behavioral methods to best explain the emergence of the subjective and aversive individual experience of dyspnea. Breathlessness or dyspnea is rarely studied using temporally precise spectral EEG/MEG techniques. In this review, we argue that understanding oscillatory neural dynamics of normal and disordered breathing can help us more efficiently assess and treat dyspnea. We review existing literature and suggest specific directions for future studies. [ABSTRACT FROM AUTHOR]

The damage and repair of DNA is a continuous process required to maintain genomic integrity. DNA double-strand breaks (DSBs) are the most lethal type of DNA damage and require timely repair by dedicated machinery. DSB repair is uniquely important to nondividing, post-mitotic cells of the central nervous system (CNS). These long-lived cells must rely on the intact genome for a lifetime while maintaining high metabolic activity. When these mechanisms fail, the loss of certain neuronal populations upset delicate neural networks required for higher cognition and disrupt vital motor functions. Mammalian cells engage with several different strategies to recognize and repair chromosomal DSBs based on the cellular context and cell cycle phase, including homologous recombination (HR)/homology-directed repair (HDR), microhomology-mediated end-joining (MMEJ), and the classic non-homologous end-joining (NHEJ). In addition to these repair pathways, a growing body of evidence has emphasized the importance of DNA damage response (DDR) signaling, and the involvement of heterogeneous nuclear ribonucleoprotein (hnRNP) family proteins in the repair of neuronal DSBs, many of which are linked to age-associated neurological disorders. In this review, we describe contemporary research characterizing the mechanistic roles of these non-canonical proteins in neuronal DSB repair, as well as their contributions to the etiopathogenesis of selected common neurological diseases. [ABSTRACT FROM AUTHOR]