New method for the quantum ground states in one dimension

A simple, general and practically exact method is developed to calculate the ground states of 1D macroscopic quantum systems with translational symmetry. Applied to the Hubbard model, a modest calculation reproduces the Bethe Ansatz results

New method for the 3D Ising model

A simple, general and practically exact method is developed for the equilibrium properties of the macroscopic physical systems with translational symmetry. Applied to the Ising model in two and three dimension, a modest calculation gives the spontaneous magnetization and the specific heat to less than 1% error

Entanglement perturbation theory for the quantum ground states in two dimensions

A simple, general and practically exact method, Entanglement Perturbation Theory (EPT), is formulated to calculate the ground states of 2D macroscopic quantum systems with translational symmetry. An emphasis will be placed on the applicability of EPT to fermions. We will discuss some preliminary evidences which indicate a potential of EPT

Symmetry Algebras of Large-N Matrix Models for Open Strings

We have discovered that the gauge invariant observables of matrix models invariant under U($N$) form a Lie algebra, in the planar large-N limit. These models include Quantum Chromodynamics and the M(atrix)-Theory of strings. We study here the gauge invariant states corresponding to open strings (`mesons'). We find that the algebra is an extension of a remarkable new Lie algebra ${\cal V}_{\Lambda}$ by a product of more well-known algebras such as $gl_{\infty}$ and the Cuntz algebra. ${\cal V}_{\Lambda}$ appears to be a generalization of the Lie algebra of vector fields on the circle to non-commutative geometry. We also use a representation of our Lie algebra to establish an isomorphism between certain matrix models (those that preserve `gluon number') and open quantum spin chains. Using known results on quantum spin chains, we are able to identify some exactly solvable matrix models. Finally, the Hamiltonian of a dimensionally reduced QCD model is expressed explicitly as an element of our Lie algebra.Comment: 44 pages, 8 eps figures, 3 tables, LaTeX2.09; this is the published versio

Transcriptional regulation of the AP-1 and Nrf2 target gene sulfiredoxin

“Two-cysteine” peroxiredoxins are antioxidant enzymes that exert a cytoprotective effect in many models of oxidative stress. However, under highly oxidizing conditions they can be inactivated through hyperoxidation of their peroxidatic active site cysteine residue. Sulfiredoxin can reverse this hyperoxidation, thus, reactivating peroxiredoxins. Here we review recent investigations that have shed further light on sulfiredoxin’s role and regulation. Studies have revealed sulfiredoxin to be a dynamically regulated gene whose transcription is induced by a variety of signals and stimuli. Sulfiredoxin expression is regulated by the transcription factor AP-1, which mediates its up-regulation by synaptic activity in neurons, resulting in protection against oxidative stress. Furthermore, sulfiredoxin has been identified as a new member of the family of genes regulated by Nuclear factor erythroid 2-related factor (Nrf2) via a conserved cis-acting antioxidant response element (ARE). As such, sulfiredoxin is likely to contribute to the net antioxidative effect of small molecule activators of Nrf2. As discussed here. the proximal AP-1 site of the sulfiredoxin promoter is embedded within the ARE, as is common with Nrf2 target genes. Other recent studies have shown that sulfiredoxin induction via Nrf2 may form an important part of the protective response to oxidative stress in the lung, preventing peroxiredoxin hyperoxidation and, in certain cases, subsequent degradation. We illustrate here that sulfiredoxin can be rapidly induced in vivo by administration of CDDO-TFEA, a synthetic triterpenoid inducer of endogenous Nrf2, which may offer a way of reversing peroxiredoxin hyperoxidation in vivo following chronic or acute oxidative stress

New System for the Acceleration of the Airflow in Wind Turbines

Background: This patent is based on the wind industry technology called Diffuser Augmented Wind Turbines (DAWTs). This technology consists of a horizontal axis wind turbine, which is housed inside a duct with diverging section in the direction of the free air stream. In this paper, a review of preceding patents related to this technology is carried out. Objective: This paper presents an innovative patent to improve the performance of horizontal axis wind turbines. In particular, this system is aimed at improving the performance of those turbines that otherwise might not be installed due to the low wind resource existing at certain locations. Methods: The most innovative elements of this patent are: (1) the semi-spherical grooves, which are mechanized on the surface of the two diffusers in order to guarantee a more energetic boundary layer; (2) the coaxial diffuser, which is located downwind following the first diffuser in order to increase the suction effect on the air mass close to the inlet; (3) the coaxial rings located around the first diffuser outlet, which are used to deflect the external airflow toward the turbine wake; and (4), the selforientating system to orientate the system by the prevailing wind direction. Results: An application of the patent for increasing the power generated by a horizontal axis wind turbine with three blades is presented. The patent is designed and its performance is evaluated by using a Computational Fluid Dynamics code. The numerical results show that this system rises the airflow going through the rotor of the turbine. Conclusion: The patented device is an original contribution aimed at enabling a more profitable installation of wind turbines in places where the wind resource is insufficient because of the wind shear caused both by the proximity of the earth and the obstacles on the earth surface.This work was supported by the OASIS Research Project that was cofinanced by CDTI (Spanish Science and Innovation Ministry) and developed with the Spanish companies: Iridium, OHL Concesiones, Abertis, Sice, Indra, Dragados, OHL, Geocisa, GMV, Asfaltos Augusta, Hidrofersa, Eipsa, PyG, CPS, AEC and Torre de Comares Arquitectos S.L and 16 research centres. The authors also acknowledge the partial funding with FEDER funds under the Research Project FC-15-GRUPIN14-004. Finally, we also thank Swanson Analysis Inc. for the use of ANSYS University Research programs as well as the Workbench simulation environment

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease