Accelerating Quantum Decay by Multiple Tunneling Barriers

A quantum particle constrained between two high potential barriers provides a paradigmatic example of a system sustaining quasi-bound (or resonance) states. When the system is prepared in one of such quasi-bound states, the wave function approximately maintains its shape but decays in time in a nearly exponential manner radiating into the surrounding space, the lifetime being of the order of the reciprocal of the width of the resonance peak in the transmission spectrum. Naively, one could think that adding more lateral barriers would preferentially slow down or prevent the quantum decay since tunneling is expected to become less probable and due to quantum backflow induced by multiple scattering processes. However, this is not always the case and in the early stage of the dynamics quantum decay can be accelerated (rather than decelerated) by additional lateral barriers, even when the barrier heights are arbitrarily large. The decay acceleration originates from resonant tunneling effects and is associated to large deviations from an exponential decay law. We discuss such a counterintuitive phenomenon by considering the hopping dynamics of a quantum particle on a tight-binding lattice with on-site potential barriers

Anyonic PT\mathcal{PT} symmetry, drifting potentials and non-Hermitian delocalization

We consider wave dynamics for a Schr\"odinger equation with a non-Hermitian Hamiltonian $\mathcal{H}$ satisfying the generalized (anyonic) parity-time symmetry $\mathcal{PT H}= \exp(2 i \varphi) \mathcal{HPT}$, where $\mathcal{P}$ and $\mathcal{T}$ are the parity and time-reversal operators. For a stationary potential, the anyonic phase $\varphi$ just rotates the energy spectrum of $\mathcal{H}$ in complex plane, however for a drifting potential the energy spectrum is deformed and the scattering and localization properties of the potential show intriguing behaviors arising from the breakdown of the Galilean invariance when $\varphi \neq 0$. In particular, in the unbroken $\mathcal{PT}$ phase the drift makes a scattering potential barrier reflectionless, whereas for a potential well the number of bound states decreases as the drift velocity increases because of a non-Hermitian delocalization transition.Comment: 7 pages, 5 figure

Sarcopenia: What a Surgeon Should Know

Sarcopenia is an increasingly frequent syndrome characterized by generalized and progressive loss of muscle mass, reduction in muscle strength, and resultant functional impairment. This condition is associated with increased risk of falls and fractures, disability, and increased risk of death. When a sarcopenic patient undergoes major surgery, it has a higher risk of complications and postoperative mortality because of less resistance to surgical stress. It is not easy to recognize a sarcopenic patient preoperatively, but this is essential to evaluate the correct risk to benefit ratio. The role of sarcopenia in surgical patients has been studied for both oncological and non-oncological surgery. For correct surgical planning, data about sarcopenia are essential to design a correct tailored treatment

Gorgias y Platón sobre lógos, persuasión y engaño

In Sophist 234b-c Plato characterizes the sophist as a maker of “spoken images”. In order to clarify this art of the sophist, an analogy is proposed between painting and sophistry. This analogy has been criticized as involving an illegitimate assimilation between visual and spoken images, or between the objects of seeing and statements/beliefs. I argue in this paper for a different interpretation. Plato deals with mímesis as a kind of making something (poiésis) rather than as a kind of acquiring something (ktêsis) that is or has already come into being. He focuses on the making prior to the product.En Sofista 234b-c, Platón caracteriza al sofista como fabricante de “imágenes habladas” (eídola legómena). Para esclarecer la arte que pratica, una analogía es propuesta entre el pintor y el sofista, pero esa analogía ha sido criticada por envolver una asimilación ilegítima entre imágenes visuales e habladas, o entre lo que es visto y lo dicho o creído. Intentaré mostrar en este texto, una interpretación diferente. Platón se refiere a la mímesis como una forma de producción (poíesis), a diferencia de la adquisición (ktêsis) de algo que ya es o que ha llegado a ser dirigiendo la atención al producir antes que al producto

ALGUNOS ASPECTOS DE LA CRÍTICA PLATÓNICA AL ARTE IMITATIVO – LA ANALOGÍA ENTRE EL SOFISTA Y EL PINTOR

In the Sophist 234b-c, Plato attempts to characterize the sophist as a maker of "spoken images". This analogy between painting and sophistry, which the dialogue proposes in order to clarify the art practiced by sophists, has been criticized as involving an illegitimate assimilation of visual to spoken images, or of the objects of seeing to those of stating/believing. However, as I try to demonstrate in this paper, a different interpretation is possible.No Sofista, 234b-c, Platão descreve o sofista como um criador de “imagens faladas”. Para esclarecer essa arte, é proposta uma analogia entre a pintura e a sofística. A analogia tem sido criticada por implicar assimilação ilegítima entre imagens visuais e faladas, ou entre objetos da visão e do enunciado/crença. De qualquer forma, tento demonstrar neste artigo que é possível uma interpretação diferente

Time lag between metamorphism and crystallization of anatectic granites (Córdoba, Argentina)

SHRIMP and LA-ICP-MS analyses carried out on zircons from the Río de los Sauces granite revealed their metamorphic and igneous nature. The metamorphic zircons yielded an age of 537±4.8 (2σ)Ma that probably predates the onset of the anatexis during the Pampean orogeny. By contrast, the igneous zircons yielded a younger age of 529±6 (2σ)Ma and reflected its crystallization age. These data point to a short time lag of ca. 8Myr between the High Temperature (HT) metamorphic peak and the subsequent crystallization age of the granite. Concordia age of 534±3.8 (2σ)Ma, for both types of zircon populations, can be considered as the mean age of the Pampean HT metamorphism in the Sierras de Córdoba

Broadband Printed Antenna for Radiofrequency Energy Harvesting

In this work a broadband UHF antenna with high inductive input impedance for radiofrequency energy harvesting is presented. It consists of a small feeding loop and a biconical radiating dipole. A prototype has been fabricated on a FR4 substrate and tested. Experimental results show a - 3dB power transmission bandwidth of about 135MHz (840MHz−975MHz)

Time lag between metamorphism and crystallization of anatectic granites (Córdoba, Argentina)

SHRIMP and LA-ICP-MS analyses carried out on zircons from the Río de los Sauces granite revealed their metamorphic and igneous nature. The metamorphic zircons yielded an age of 537±4.8 (2σ)Ma that probably predates the onset of the anatexis during the Pampean orogeny. By contrast, the igneous zircons yielded a younger age of 529±6 (2σ)Ma and reflected its crystallization age. These data point to a short time lag of ca. 8Myr between the High Temperature (HT) metamorphic peak and the subsequent crystallization age of the granite. Concordia age of 534±3.8 (2σ)Ma, for both types of zircon populations, can be considered as the mean age of the Pampean HT metamorphism in the Sierras de Córdoba

Counteracting the Common Shwachman–Diamond Syndrome-Causing SBDS c.258+2T>C Mutation by RNA Therapeutics and Base/Prime Editing

Shwachman-Diamond syndrome (SDS) represents one of the most common inherited bone marrow failure syndromes and is mainly caused by SBDS gene mutations. Only supportive treatments are available, with hematopoietic cell transplantation required when marrow failure occurs. Among all causative mutations, the SBDS c.258+2T>C variant at the 5 ' splice site (ss) of exon 2 is one of the most frequent. Here, we investigated the molecular mechanisms underlying aberrant SBDS splicing and showed that SBDS exon 2 is dense in splicing regulatory elements and cryptic splice sites, complicating proper 5 ' ss selection. Studies ex vivo and in vitro demonstrated that the mutation alters splicing, but it is also compatible with tiny amounts of correct transcripts, which would explain the survival of SDS patients. Moreover, for the first time for SDS, we explored a panel of correction approaches at the RNA and DNA levels and provided experimental evidence that the mutation effect can be partially counteracted by engineered U1snRNA, trans-splicing, and base/prime editors, ultimately leading to correctly spliced transcripts (from barely detectable to 2.5-5.5%). Among them, we propose DNA editors that, by stably reverting the mutation and potentially conferring positive selection to bone-marrow cells, could lead to the development of an innovative SDS therapy

Tailoring the CRISPR system to transactivate coagulation gene promoters in normal and mutated contexts

Engineered transcription factors (TF)have expanded our ability to modulate gene expression and hold great promise as bio-therapeutics. The first-generation TF, based on Zinc Fingers or Transcription-Activator-like Effectors (TALE), required complex and time-consuming assembly protocols, and were indeed replaced in recent years by the CRISPR activation (CRISPRa)technology. Here, with coagulation F7/F8 gene promoters as models, we exploited a CRISPRa system based on deactivated (d)Cas9, fused with a transcriptional activator (VPR), which is driven to its target by a single guide (sg)RNA. Reporter gene assays in hepatoma cells identified a sgRNA (sgRNA F7.5 )triggering a ~35-fold increase in the activity of F7 promoter, either wild-type, or defective due to the c.-61T>G mutation. The effect was higher (~15-fold)than that of an engineered TALE-TF (TF4)targeting the same promoter region. Noticeably, when challenged on the endogenous F7 gene, the dCas9-VPR/sgRNA F7.5 combination was more efficient (~6.5-fold)in promoting factor VII (FVII)protein secretion/activity than TF4 (~3.8-fold). The approach was translated to the promoter of F8, whose reduced expression causes hemophilia A. Reporter gene assays in hepatic and endothelial cells identified sgRNAs that, respectively, appreciably increased F8 promoter activity (sgRNA F8.1 , ~8-fold and 3-fold; sgRNA F8.2 , ~19-fold and 2-fold)with synergistic effects (~38-fold and 2.7-fold). Since modest increases in F7/F8 expression would ameliorate patients' phenotype, the CRISPRa-mediated transactivation extent might approach the low therapeutic threshold. Through this pioneer study we demonstrated that the CRISPRa system is easily tailorable to increase expression, or rescue disease-causing mutations, of different promoters, with potential intriguing implications for human disease models