Spontaneously broken symmetry restoration of quantum fields in the vicinity of neutral and electrically charged black holes

We consider the restoration of a spontaneously broken symmetry of an interacting quantum scalar field around neutral, i.e., Schwarzschild, and electrically charged, i.e., Reissner-Nordstr\"om, black holes in four dimensions. This is done through a semiclassical self-consistent procedure, by solving the system of non-linear coupled equations describing the dynamics of the background field and the vacuum polarization. The black hole at its own horizon generates an indefinitely high temperature which decreases to the Hawking temperature at infinity. Due to the high temperature in its vicinity, there forms a bubble around the black hole in which the scalar field can only assume a value equal to zero, a minimum of energy. Thus, in this region the symmetry of the energy and the field is preserved. At the bubble radius, there is a phase transition in the value of the scalar field due to a spontaneous symmetry breaking mechanism. Indeed, outside the bubble radius the temperature is low enough such that the scalar field settles with a nonzero value in a new energy minimum, indicating a breaking of the symmetry in this outer region. Conversely, there is symmetry restoration from the outer region to the inner bubble close to the horizon. Specific properties that emerge from different black hole electric charges are also noteworthy. It is found that colder black holes, i.e., more charged ones, have a smaller bubble length of restored symmetry. In the extremal case the bubble has zero length, i.e., there is no bubble. Additionally, for colder black holes, it becomes harder to excite the quantum field modes, so the vacuum polarization has smaller values. In the extremal case, the black hole temperature is zero and the vacuum polarization is never excited.Comment: 16 pages, 4 figure

Entropy of an extremal electrically charged thin shell and the extremal black hole

There is a debate as to what is the value of the the entropy $S$ of extremal black holes. There are approaches that yield zero entropy $S=0$, while there are others that yield the Bekenstein-Hawking entropy $S=A_+/4$, in Planck units. There are still other approaches that give that $S$ is proportional to $r_+$ or even that $S$ is a generic well-behaved function of $r_+$. Here $r_+$ is the black hole horizon radius and $A_+=4\pi r_+^2$ is its horizon area. Using a spherically symmetric thin matter shell with extremal electric charge, we find the entropy expression for the extremal thin shell spacetime. When the shell's radius approaches its own gravitational radius, and thus turns into an extremal black hole, we encounter that the entropy is $S=S(r_+)$, i.e., the entropy of an extremal black hole is a function of $r_+$ alone. We speculate that the range of values for an extremal black hole is $0\leq S(r_+) \leq A_+/4$.Comment: 11 pages, minor changes, added references, matches the published versio

Qubit Picture of Virtual Particles

We show that virtual particles, despite being unobservable, can be described by quantum operators which can be interpreted under certain conditions as valid qubit quantum states. For a single virtual fermion, we prove that such a state is a separable mixed 2-qubit state with a well-defined finite temperature. For spin-1 virtual bosons, we find them to be associated to 4-qubit operators which can be interpreted as quantum states for some gauges. We also study the creation of virtual pairs of fermions, where the pair is shown to be associated to an entangled 4-qubit operator, and show the corresponding quantum circuit. Finally, we prove that renormalization does not structurally affect these results. These findings represent new connections between quantum field theory, quantum information and quantum thermodynamics.Comment: Published version in PRA. The paper was restructured with new sections added. The spin 1 boson and fermionic pair creation cases were introduce

Molecular mechanisms of salamander limb regeneration

Salamanders, like newts and axolotls, stand out among adult vertebrates for their outstanding capacity to regenerate whole body parts and restore complex structures upon injury. One of the best-known examples is their ability to fully regenerate a functional limb. Despite the important progress in the field, our understanding of the molecular cues that control limb regeneration is still limited. In this thesis, I focus on the mechanisms by which skeletal muscle stimulates limb regeneration. Skeletal muscle is particularly interesting because, in newts, it contributes to limb regeneration by dedifferentiation. This unique process is characterized by fragmentation of the multinucleated myofiber and subsequent cell cycle reentry by the derived mononucleate progeny. In Paper I, we sequenced and edited the ~20 Gigabases genome of the Iberian ribbed newt Pleurodeles waltl, a commonly used species for regeneration studies in salamanders. Using CRISPR/Cas9 technology we perturbed two key transcription factors (Pax3 and Pax7) that are involved in skeletal muscle development and regeneration in vertebrates. We found that contrary to mammals, in which Pax7 expression by skeletal muscle stem cells is indispensable for regeneration, muscle regeneration was not altered when Pax7 gene was mutated in newts. Moreover, we observed that embryonic stem cell-specific microRNAs (mir-93b and mir-427), as well as Harbinger DNA transposons carrying the Myb-like proto-oncogene have expanded dramatically in the Pleurodeles waltl genome and are co-expressed during limb regeneration. This study provides a foundation for comparative genomic studies that could improve our understanding of the uneven distribution of regenerative capacities among vertebrates. In Paper II, we identified a microRNA, miR-10b-5p, which is highly abundant in muscle tissue across species and downregulated during early limb regeneration in newts. In contrast, miR-10b-5p displayed the opposite regulation in mammalian cultured myotubes, when these were induced to dedifferentiate. To investigate a possible function of miR-10b-5p in newt limb regeneration, we overexpressed it by mimic injection. We found that such manipulation of miR-10b-5p levels during the initial stages of regeneration slowed down the regeneration process. Moreover, we observed that overexpression of miR-10b-5p decreased the number of cycling cells and counteracted blastema growth. The identification of miR-10b-5p targets will be an important task for future studies. In Paper III, we showed that blood clotting proteases cleaved and activated bloodderived bone morphogenetic proteins (BMPs) to promote BMP signaling-dependent cell cycle re-entry by myofiber progeny. In particular, we found that protease-activated BMP4/7 heterodimers which were present in serum, strongly induced myotube cell cycle re-entry, with protease cleavage yielding a 30-fold potency increase of BMP4/7 compared with canonical BMP4/7. Additionally, we observed that inhibition of BMP signaling, via muscle-specific dominant-negative receptor expression, reduced cell cycle re-entry in vitro and in vivo. Furthermore, in vivo inhibition of serine protease activity depressed cell cycle re-entry, which in turn could be rescued by cleavedmimic BMP. This work provides a new molecular mechanism for the reversal of the differentiated state in muscle. In Paper IV, we carried out a comparative analysis of centrosome dynamics in mouse and newt muscle cells. We showed, through a detailed characterization of different centrosome components, that centrosomes were gradually disassembled during muscle differentiation in mammals. We also provided new insights into the underlying mechanisms and variations in gene expression during that inactivation process. On the other hand, we found that salamanders retained several centrosome components even in mature myofibers. Moreover, we observed that not only the centrosomes were maintained in salamander muscle, but they also appeared to be active as microtubule organizing centers. This study has elucidated fundamental differences between vertebrates at cellular level, which might help us to understand why species differ in their ability to produce regenerative progenitor cells