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Search Results: 1 - 10 of 11157 matches for " Enrique Fernandez-Borja "
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Black hole state degeneracy in Loop Quantum Gravity
Ivan Agullo,Jacobo Diaz-Polo,Enrique Fernandez-Borja
Physics , 2008, DOI: 10.1103/PhysRevD.77.104024
Abstract: The combinatorial problem of counting the black hole quantum states within the Isolated Horizon framework in Loop Quantum Gravity is analyzed. A qualitative understanding of the origin of the band structure shown by the degeneracy spectrum, which is responsible for the black hole entropy quantization, is reached. Even when motivated by simple considerations, this picture allows to obtain analytical expressions for the most relevant quantities associated to this effect.
Black hole entropy quantization
Alejandro Corichi,Jacobo Diaz-Polo,Enrique Fernandez-Borja
Physics , 2006, DOI: 10.1103/PhysRevLett.98.181301
Abstract: Ever since the pioneer works of Bekenstein and Hawking, black hole entropy has been known to have a quantum origin. Furthermore, it has long been argued by Bekenstein that entropy should be quantized in discrete (equidistant) steps given its identification with horizon area in (semi-)classical general relativity and the properties of area as an adiabatic invariant. This lead to the suggestion that black hole area should also be quantized in equidistant steps to account for the discrete black hole entropy. Here we shall show that loop quantum gravity, in which area is {\it not} quantized in equidistant steps can nevertheless be consistent with Bekenstein's equidistant entropy proposal in a subtle way. For that we perform a detailed analysis of the number of microstates compatible with a given area and show consistency with the Bekenstein framework when an oscillatory behavior in the entropy-area relation is properly interpreted.
Loop quantum gravity and Planck-size black hole entropy
Alejandro Corichi,Jacobo Diaz-Polo,Enrique Fernandez-Borja
Physics , 2007, DOI: 10.1088/1742-6596/68/1/012031
Abstract: The Loop Quantum Gravity (LQG) program is briefly reviewed and one of its main applications, namely the counting of black hole entropy within the framework is considered. In particular, recent results for Planck size black holes are reviewed. These results are consistent with an asymptotic linear relation (that fixes uniquely a free parameter of the theory) and a logarithmic correction with a coefficient equal to -1/2. The account is tailored as an introduction to the subject for non-experts.
Quantum geometry and microscopic black hole entropy
Alejandro Corichi,Jacobo Diaz-Polo,Enrique Fernandez-Borja
Physics , 2006, DOI: 10.1088/0264-9381/24/1/013
Abstract: Quantum black holes within the loop quantum gravity (LQG) framework are considered. The number of microscopic states that are consistent with a black hole of a given horizon area $A_0$ are counted and the statistical entropy, as a function of the area, is obtained for $A_0$ up to $550 l^2_{\rm Pl}$. The results are consistent with an asymptotic linear relation and a logarithmic correction with a coefficient equal to -1/2. The Barbero-Immirzi parameter that yields the asymptotic linear relation compatible with the Bekenstein-Hawking entropy is shown to coincide with a value close to $\gamma=0.274$, which has been previously obtained analytically. However, a new and oscillatory functional form for the entropy is found for small, Planck size, black holes that calls for a physical interpretation.
Black hole radiation spectrum in LQG: Isolated Horizon framework
Jacobo Diaz-Polo,Enrique Fernandez-Borja
Physics , 2007, DOI: 10.1088/0264-9381/25/10/105007
Abstract: Recent detailed analysis within the Loop Quantum Gravity calculation of black hole entropy shows a stair-like structure in the behavior of entropy as a function of horizon area. The non-trivial distribution of the degeneracy of the black hole horizon area eigenstates is at the origin of this behavior. This degeneracy distribution is analyzed and a phenomenological model is put forward to study the implications of this distribution in the black hole radiation spectrum. Some qualitative quantum effects are obtained within the isolated horizon framework. This result provides us with a possible observational test of this model for quantum black holes.
Black hole state counting in Loop Quantum Gravity: A number theoretical approach
Ivan Agullo,J. Fernando Barbero G.,Jacobo Diaz-Polo,Enrique Fernandez-Borja,Eduardo J. S. Villase?or
Physics , 2008, DOI: 10.1103/PhysRevLett.100.211301
Abstract: We give a practical method to exactly compute black hole entropy in the framework of Loop Quantum Gravity. Along the way we provide a complete characterization of the relevant sector of the spectrum of the area operator, including degeneracies, and determine the number of solutions to the projection constraint analytically. We use a computer implementation of the proposed algorithm to confirm and extend previous results on the detailed structure of the black hole degeneracy spectrum.
The Small GTPase RhoB Regulates TNFα Signaling in Endothelial Cells
Jeffrey Kroon, Simon Tol, Sven van Amstel, Judith A. Elias, Mar Fernandez-Borja
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0075031
Abstract: The inflammatory response of endothelial cells triggered by cytokines such as TNFα and IL1β plays a pivotal role in innate immunity. Upon pro-inflammatory cytokine stimulation, endothelial cells produce chemokines and cytokines that attract and activate leukocytes, and express high levels of leukocyte adhesion molecules. This process is mediated by intracellular signaling cascades triggered by activation of e.g. the TNFα receptor (TNFR) that lead to the activation of the NFκB transcription factor and of MAP kinases, which in turn activate inflammatory gene transcription. We found that the small GTPase RhoB was strongly and rapidly upregulated in primary human endothelial cells by TNFα, IL1β and LPS. We subsequently investigated the role of RhoB in the regulation of TNFR signaling in endothelial cells by silencing RhoB expression with siRNA. We provide evidence that the TNFα-induced activation of p38 MAP kinase is strongly dependent on RhoB, but not on RhoA, while JNK activation is regulated by both RhoB and RhoA. Consistent with the important role of p38 MAP kinase in inflammation, we demonstrate that loss of RhoB impairs TNFα-induced ICAM-1 expression and reduces cell production of IL6 and IL8. In addition, we show that RhoB silencing alters the intracellular traffic of TNFα after endocytosis. Since RhoB is a known regulator of the intracellular traffic of membrane receptors, our data suggest that RhoB controls TNFα signaling through the regulation of the TNFR traffic.
The Shear Stress-Induced Transcription Factor KLF2 Affects Dynamics and Angiopoietin-2 Content of Weibel-Palade Bodies
Ellen L. van Agtmaal, Ruben Bierings, Bieuwke S. Dragt, Thomas A. Leyen, Mar Fernandez-Borja, Anton J. G. Horrevoets, Jan Voorberg
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038399
Abstract: Background The shear-stress induced transcription factor KLF2 has been shown to induce an atheroprotective phenotype in endothelial cells (EC) that are exposed to prolonged laminar shear. In this study we characterized the effect of the shear stress-induced transcription factor KLF2 on regulation and composition of Weibel-Palade bodies (WPBs) using peripheral blood derived ECs. Methodology and Principal Findings Lentiviral expression of KLF2 resulted in a 4.5 fold increase in the number of WPBs per cell when compared to mock-transduced endothelial cells. Unexpectedly, the average length of WPBs was significantly reduced: in mock-transduced endothelial cells WPBs had an average length of 1.7 μm versus 1.3 μm in KLF2 expressing cells. Expression of KLF2 abolished the perinuclear clustering of WPBs observed following stimulation with cAMP-raising agonists such as epinephrine. Immunocytochemistry revealed that WPBs of KLF2 expressing ECs were positive for IL-6 and IL-8 (after their upregulation with IL-1β) but lacked angiopoietin-2 (Ang2), a regular component of WPBs. Stimulus-induced secretion of Ang2 in KLF2 expressing ECs was greatly reduced and IL-8 secretion was significantly lower. Conclusions and Significance These data suggest that KLF2 expression leads to a change in size and composition of the regulated secretory compartment of endothelial cells and alters its response to physiological stimuli.
The Human Minor Histocompatibility Antigen1 Is a RhoGAP
Bart-Jan de Kreuk, Antje Schaefer, Eloise C. Anthony, Simon Tol, Mar Fernandez-Borja, Dirk Geerts, Jos Pool, Lothar Hambach, Els Goulmy, Peter L. Hordijk
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0073962
Abstract: The human minor Histocompatibility Antigen HMHA-1 is a major target of immune responses after allogeneic stem cell transplantation applied for the treatment of leukemia and solid tumors. The restriction of its expression to hematopoietic cells and many solid tumors raised questions regarding its cellular functions. Sequence analysis of the HMHA-1 encoding HMHA1 protein revealed the presence of a possible C-terminal RhoGTPase Activating Protein (GAP) domain and an N-terminal BAR domain. Rho-family GTPases, including Rac1, Cdc42, and RhoA are key regulators of the actin cytoskeleton and control cell spreading and migration. RhoGTPase activity is under tight control as aberrant signaling can lead to pathology, including inflammation and cancer. Whereas Guanine nucleotide Exchange Factors (GEFs) mediate the exchange of GDP for GTP resulting in RhoGTPase activation, GAPs catalyze the low intrinsic GTPase activity of active RhoGTPases, resulting in inactivation. Here we identify the HMHA1 protein as a novel RhoGAP. We show that HMHA1 constructs, lacking the N-terminal region, negatively regulate the actin cytoskeleton as well as cell spreading. Furthermore, we show that HMHA1 regulates RhoGTPase activity in vitro and in vivo. Finally, we demonstrate that the HMHA1 N-terminal BAR domain is auto-inhibitory as HMHA1 mutants lacking this region, but not full-length HMHA1, showed GAP activity towards RhoGTPases. In conclusion, this study shows that HMHA1 acts as a RhoGAP to regulate GTPase activity, cytoskeletal remodeling and cell spreading, which are crucial functions in normal hematopoietic and cancer cells.
Sphingosine-1-Phosphate Receptor 3 Mediates Sphingosine-1-Phosphate Induced Release of Weibel-Palade Bodies from Endothelial Cells
Kathinka W. E. M. van Hooren, Léon J. A. Spijkers, Dorothee van Breevoort, Mar Fernandez-Borja, Ruben Bierings, Jaap D. van Buul, Astrid E. Alewijnse, Stephan L. M. Peters, Jan Voorberg
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0091346
Abstract: Sphingosine-1-phosphate (S1P) is an agonist for five distinct G-protein coupled receptors, that is released by platelets, mast cells, erythrocytes and endothelial cells. S1P promotes endothelial cell barrier function and induces release of endothelial cell-specific storage-organelles designated Weibel-Palade bodies (WPBs). S1P-mediated enhancement of endothelial cell barrier function is dependent on S1P receptor 1 (S1PR1) mediated signaling events that result in the activation of the small GTPase Rac1. Recently, we have reported that Rac1 regulates epinephrine-induced WPB exocytosis following its activation by phosphatidylinositol-3,4,5-triphosphate-?dependentRac exchange factor 1 (PREX1). S1P has also been described to induce WPB exocytosis. Here, we confirm that S1P induces release of WPBs using von Willebrand factor (VWF) as a marker. Using siRNA mediated knockdown of gene expression we show that S1PR1 is not involved in S1P-mediated release of WPBs. In contrast depletion of the S1PR3 greatly reduced S1P-induced release of VWF. S1P-mediated enhancement of endothelial barrier function was not affected by S1PR3-depletion whereas it was greatly impaired in cells lacking S1PR1. The Rho kinase inhibitor Y27632 completely abrogated S1P-mediated release of VWF. Also, the calcium chelator BAPTA-AM significantly reduced S1P-induced release of VWF. Our findings indicate that S1P-induced release of haemostatic, inflammatory and angiogenic components stored within WPBs depends on the S1PR3.
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