Thermalization and Cooling of Plasmon-Exciton Polaritons: Towards Quantum Condensation

We present indications of thermalization and cooling of quasi-particles, a precursor for quantum condensation, in a plasmonic nanoparticle array. We investigate a periodic array of metallic nanorods covered by a polymer layer doped with an organic dye at room temperature. Surface lattice resonances of the array---hybridized plasmonic/photonic modes---couple strongly to excitons in the dye, and bosonic quasi-particles which we call plasmon-exciton-polaritons (PEPs) are formed. By increasing the PEP density through optical pumping, we observe thermalization and cooling of the strongly coupled PEP band in the light emission dispersion diagram. For increased pumping, we observe saturation of the strong coupling and emission in a new weakly coupled band, which again shows signatures of thermalization and cooling.Comment: 8 pages, 5 figures including supplemental material. The newest version includes new measurements and corrections to the interpretation of the result

Leibniz algebras with associated Lie algebras sl_2\dot{+} R (dim R=2)

From the theory of finite dimensional Lie algebras it is known that every finite dimensional Lie algebra is decomposed into a semidirect sum of semisimple subalgebra and solvable radical. Moreover, due to work of Mal'cev the study of solvable Lie algebras is reduced to the study of nilpotent ones. For the finite dimensional Leibniz algebras the analogues of the mentioned results are not proved yet. In order to get some idea how to establish the results we examine the Leibniz algebra for which the quotient algebra with respect to the ideal generated by squares elements of the algebra (denoted by $I$) is a semidirect sum of semisimple Lie algebra and the maximal solvable ideal. In this paper the class of complex Leibniz algebras, for which quotient algebras by the ideal $I$ are isomorphic to the semidirect sum of the algebra $sl_2$ and two-dimensional solvable ideal $R$, are described.Comment: 11 page

Evidence of internal rotation and a helical magnetic field in the jet of the quasar NRAO 150

The source NRAO 150 is a very prominent millimeter to radio emitting quasar at redshift z = 1.52 for which previous millimeter VLBI observations revealed a fast counterclockwise rotation of the innermost regions of the jet. Here we present new polarimetric multi-epoch VLBI-imaging observations of NRAO 150 performed at 8, 15, 22, 43, and 86 GHz with the Very Long Baseline Array (VLBA), and the Global Millimeter VLBI Array (GMVA) between 2006 and 2010. All new and previous observational evidence - i.e., spectral index maps, multi-epoch image cross-correlation, and low level of linear polarization degree in optically thin regions - are consistent with an interpretation of the source behavior where the jet is seen at an extremely small angle to the line of sight, and the high frequency emitting regions in NRAO 150 rotate at high speeds on the plane of the sky with respect to a reference point that does not need to be related to any particularly prominent jet feature. The observed polarization angle distribution at 22, 43, and 86 GHz during observing epochs with high polarization degree suggests that we have detected the toroidal component of the magnetic field threading the innermost jet plasma regions. This is also consistent with the lower degree of polarization detected at progressively poorer angular resolutions, where the integrated polarization intensity produced by the toroidal field is explained by polarization cancellation inside the observing beam. All this evidence is fully consistent with a kinematic scenario where the main kinematic and polarization properties of the 43 GHz emitting structure of NRAO 150 are explained by the internal rotation of such emission regions around the jet axis when the jet is seen almost face on. A simplified model developed to fit helical trajectories to the observed kinematics of the 43GHz features fully supports this hypothesis. This explains the kinematics of the innermost regions of the jet in NRAO 150 in terms of internal jet rotation

DRAFT 03

DRAFT 03, a magazine published about work and thoughts of students and staff of Interiors

ALMA full polarization observations of PKS 1830−211 during its record-breaking flare of 2019

We report Atacama Large Millimeter Array (ALMA) Band 6 full-polarization observations of the lensed blazar PKS 1830−211 during its record-breaking radio and gamma-ray flare in the spring of 2019. The observations were taken close to the peak of the gamma activity and show a clear difference in polarization state between the two time-delayed images. The leading image has a fractional polarization about three times lower than the trailing image, implying that significant depolarization occurred during the flare. In addition, we observe clear intra-hour variability of the polarization properties between the two lensed images, with a quasi-linear increase in the differential electric-vector position angle at a rate of about two degrees per hour, associated with changes in the relative fractional polarization of ∼10%. This variability, combined with the lower polarization close to the peak of gamma activity, is in agreement with models of magnetic turbulence to explain polarization variability in blazar jets. Finally, the comparison of results from the full and differential polarization analysis confirms that the differential polarization technique (Martí-Vidal et al. 2016, A&A, 593, A61) can provide useful information on the polarization state of sources like gravitationally lensed radio-loud quasars.Accepted manuscrip

Lipocalin prostaglandin D synthase and PPARγ2 coordinate to regulate carbohydrate and lipid metabolism in vivo

Mice lacking Peroxisome Proliferator-Activated Receptor γ2 (PPARγ2) have unexpectedly normal glucose tolerance and mild insulin resistance. Mice lacking PPARγ2 were found to have elevated levels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose tissue (WAT). To determine if induction of L-PGDS was compensating for a lack of PPARγ2, we crossed L-PGDS KO mice to PPARγ2 KO mice to generate Double Knock Out mice (DKO). Using DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) function. In scWAT, DKO mice had reduced expression of thermogenic genes, the de novo lipogenic program and the lipases ATGL and HSL. Despite the reduction in markers of lipolysis in scWAT, DKO mice had a normal metabolic rate and elevated serum FFA levels compared to L-PGDS KO alone. Analysis of intra-abdominal white adipose tissue (epididymal WAT) showed elevated expression of mRNA and protein markers of lipolysis in DKO mice, suggesting that DKO mice may become more reliant on intra-abdominal WAT to supply lipid for oxidation. This switch in depot utilisation from subcutaneous to epididymal white adipose tissue was associated with a worsening of whole organism metabolic function, with DKO mice being glucose intolerant, and having elevated serum triglyceride levels compared to any other genotype. Overall, L-PGDS and PPARγ2 coordinate to regulate carbohydrate and lipid metabolism

PPAR gamma 2 Prevents Lipotoxicity by Controlling Adipose Tissue Expandability and Peripheral Lipid Metabolism

Peroxisome proliferator activated receptor gamma 2 (PPARg2) is the nutritionally regulated isoform of PPARg. Ablation of PPARg2 in the ob/ob background, PPARg2(−/−) Lep(ob)/Lep(ob) (POKO mouse), resulted in decreased fat mass, severe insulin resistance, β-cell failure, and dyslipidaemia. Our results indicate that the PPARg2 isoform plays an important role, mediating adipose tissue expansion in response to positive energy balance. Lipidomic analyses suggest that PPARg2 plays an important antilipotoxic role when induced ectopically in liver and muscle by facilitating deposition of fat as relatively harmless triacylglycerol species and thus preventing accumulation of reactive lipid species. Our data also indicate that PPARg2 may be required for the β-cell hypertrophic adaptive response to insulin resistance. In summary, the PPARg2 isoform prevents lipotoxicity by (a) promoting adipose tissue expansion, (b) increasing the lipid-buffering capacity of peripheral organs, and (c) facilitating the adaptive proliferative response of β-cells to insulin resistance