The 15-43 GHz parsec-scale circular polarization of 41 active galactic nuclei

We present the results of parsec-scale circular-polarization measurements based on Very Long Baseline Array data for a number of radio-bright, core-dominated active galactic nuclei obtained simultaneously at 15, 22 and 43 GHz. The degrees of circular polarization m(c) for the Very Long Baseline Interferometry (VLBI) core region at 15 GHz are similar to the values reported earlier at this wavelength, with typical values of a few tenths of a per cent. We find that mc as often rises as falls with increasing frequency between 15 and 22 GHz, while the degree of circular polarization at 43 GHz is in all cases higher than at 22 and 15 GHz. This behaviour seems contrary to expectations, since the degree of circular polarization from both synchrotron radiation and the Faraday conversion of linear to circular polarization - the two main mechanisms considered thus far in the literature - should decrease towards higher frequencies if the source is homogeneous. The increase in mc at 43 GHz may be due to the presence of regions of both positive and negative circular polarization with different frequency dependences ( but decreasing with increasing frequency) on small scales within the core region; alternatively, it may be associated with the intrinsic inhomogeneity of a Blandford-Konigl like jet. In several objects, the detected circular polarization appears to be near, but not coincident with, the core, although further observations are needed to confirm this. We find several cases of changes in sign with frequency, most often between 22 and 43 GHz. We find tentative evidence for transverse structure in the circular polarization of 1055+018 and 1334-127, that is consistent with their being generated by either the synchrotron mechanism or the Faraday conversion in a helical magnetic field. Our results confirm the earlier finding that the sign of the circular polarization at a given observing frequency is generally consistent across epochs separated by several years or more, suggesting stability of the magnetic-field orientation in the innermost jets

Volume-preserving normal forms of Hopf-zero singularity

A practical method is described for computing the unique generator of the algebra of first integrals associated with a large class of Hopf-zero singularity. The set of all volume-preserving classical normal forms of this singularity is introduced via a Lie algebra description. This is a maximal vector space of classical normal forms with first integral; this is whence our approach works. Systems with a non-zero condition on their quadratic parts are considered. The algebra of all first integrals for any such system has a unique (modulo scalar multiplication) generator. The infinite level volume-preserving parametric normal forms of any non-degenerate perturbation within the Lie algebra of any such system is computed, where it can have rich dynamics. The associated unique generator of the algebra of first integrals are derived. The symmetry group of the infinite level normal forms are also discussed. Some necessary formulas are derived and applied to appropriately modified R\"{o}ssler and generalized Kuramoto--Sivashinsky equations to demonstrate the applicability of our theoretical results. An approach (introduced by Iooss and Lombardi) is applied to find an optimal truncation for the first level normal forms of these examples with exponentially small remainders. The numerically suggested radius of convergence (for the first integral) associated with a hypernormalization step is discussed for the truncated first level normal forms of the examples. This is achieved by an efficient implementation of the results using Maple

Intracellular Trafficking and Persistence of Acinetobacter baumannii Requires Transcription Factor EB

Acinetobacter baumannii is a significant human pathogen associated with hospital-acquired infections. While adhesion, an initial and important step in A. baumannii infection, is well characterized, the intracellular trafficking of this pathogen inside host cells remains poorly studied. Here, we demonstrate that transcription factor EB (TFEB) is activated after A. baumannii infection of human lung epithelial cells (A549). We also show that TFEB is required for the invasion and persistence inside A549 cells. Consequently, lysosomal biogenesis and autophagy activation were observed after TFEB activation which could increase the death of A549 cells. In addition, using the Caenorhabditis elegans infection model by A. baumannii, the TFEB orthologue HLH-30 was required for survival of the nematode to infection, although nuclear translocation of HLH-30 was not required. These results identify TFEB as a conserved key factor in the pathogenesis of A. baumannii.Consejería de Innovación, Ciencia y EmpresaInstituto de Salud Carlos IIIMinisterio de Economía, Industria y Competitividad. Subdirección General de Redes y Centros de Investigación CooperativaSpanish Ministry of Economy and Competitivenes

Impacto de la modificación de la respuesta inmunitaria por la lisofosfatidilcolina en la eficacia de la terapia antibiótica en un modelo experimental de sepsis peritoneal y de neumonía por Pseudomonas aeruginosa

Introduction: Immune response stimulation may be an adjuvant to antimicrobial treatment. Here, we evaluated the impact of immune response modification by lysophosphatidylcholine (LPC), combined with imipenem or ceftazidime, in murine models of peritoneal sepsis (PS) and pneumonia induced by Pseudomonas aeruginosa. Methods: The imipenem and ceftazidime-susceptible strain (Pa39) and imipenem and ceftazidime- resistant strain (Pa238) were used. Ceftazidime pharmacokinetic and pharmacodynamic parameters were determined. The therapeutic efficacy and TNF- and IL-10 levels were determined in murine mod- els of PS and pneumonia induced by Pa39 and Pa238 and treated with LPC, imipenem or ceftazidime, alone or in combination. Results: In the PS model, LPC+ceftazidime reduced spleen and lung Pa238 concentrations (−3.45 and −3.56 log10 CFU/g; P < 0.05) to a greater extent than ceftazidime monotherapy, while LPC + imipenem maintained the imipenem efficacy (−1.66 and −1.45 log10 CFU/g; P > 0.05). In the pneumonia model, LPC + ceftazidime or LPC + imipenem reduced the lung Pa238 concentrations (−2.37 log10 CFU/g, P = 0.1, or −1.35 log10 CFU/g, P = 0.75). For Pa39, no statistically significant difference was observed in the PS and pneumonia models between combined therapy and monotherapy. Moreover, LPC + imipenem and LPC+ceftazidime significantly decreased and increased the TNF- and IL-10 levels, respectively, in com- parison with the untreated controls and monotherapies. Conclusions: These results demonstrate the impact of immune response modification by LPC plus antibiotics on the prognosis of infections induced by ceftazidime-resistant P. aeruginosa.introducción: La estimulación de la respuesta inmunitaria podría ser adyuvante al tratamiento antimi- crobiano. En este estudio, hemos evaluado el impacto de la modificación de la respuesta inmunitaria por la lisofosfatidilcolina (LPC), combinada con imipenem ó ceftazidima, en modelos murinos de sepsis peritoneal (SP) y de neumonía por Pseudomonas aeruginosa (P. aeruginosa).Métodos: La cepa sensible a imipenem y ceftazidima (Pa39) y la cepa resistente a ambos antibióticos (Pa238) fueron usadas. Los parámetros farmacocinéticos/farmacodinámicos de ceftazidima fueron deter- minados. La eficacia terapéutica y los niveles de TNF- and IL-10 fueron determinados en los modelos murinos de SP y de neumonía por Pa39 y Pa238 y tratados con LPC, imipenem o ceftazidima, en monoter- apia ó en combinación. Resultados: En el modelo de SP, LPC + ceftazidima redujo la concentración de Pa238 en el bazo y el pulmón (–3,45 y –3,56 log10 UFC/g; p < 0,05) en comparación con ceftazidima, mientras LPC + impenem mantuvo la eficacia de imipenem (–1,66 y –1,45 log10 UFC/g; p > 0,05). En el modelo de neumonía, LPC + ceftazidima o LPC + imipenem redujo la concentración de Pa238 en pulmón (–2,37 log10 UFC/g, p = 0,1 o –1,35 log10 UFC/g, p = 0,75). Para Pa39, no se observó diferencia estadística significativa entre la terapia combinada y la monoterapia en los modelos de SP y de neumonía. Además, LPC + imipenem y LPC + ceftazidime redujeron y aumentaron los niveles de TNF- y IL-10, respectivamente, en comparación con los controles no tratados y las monoterapias. Conclusiones: Estos resultados demuestran el impacto de la modificación de la respuesta inmunitaria por LPC en combinación con antibióticos en el pronóstico de las infecciones por P. aeruginosa ceftazidima- resistente