Precise radial velocities of giant stars XIII. A second Jupiter orbiting in 4:3 resonance in the 7 CMa system

We report the discovery of a second planet orbiting the K giant star 7 CMa based on 166 high-precision radial velocities obtained with Lick, HARPS, UCLES and SONG. The periodogram analysis reveals two periodic signals of approximately 745 and 980 d, associated to planetary companions. A double-Keplerian orbital fit of the data reveals two Jupiter-like planets with minimum masses $m_b\sin i \sim 1.9 \,\mathrm{M_{J}}$ and $m_c\sin i \sim 0.9 \,\mathrm{M_{J}}$, orbiting at semi-major axes of $a_b \sim 1.75\,\mathrm{au}$ and $a_c \sim 2.15\,\mathrm{au}$, respectively. Given the small orbital separation and the large minimum masses of the planets close encounters may occur within the time baseline of the observations, thus, a more accurate N-body dynamical modeling of the available data is performed. The dynamical best-fit solution leads to collision of the planets and we explore the long-term stable configuration of the system in a Bayesian framework, confirming that 13% of the posterior samples are stable for at least 10 Myr. The result from the stability analysis indicates that the two-planets are trapped in a low-eccentricity 4:3 mean-motion resonance. This is only the third discovered system to be inside a 4:3 resonance, making it very valuable for planet formation and orbital evolution models.Comment: Accepted in A&

Disturbed Clockwork Resetting in Sharp-1 and Sharp-2 Single and Double Mutant Mice

BACKGROUND: The circadian system provides the basis to anticipate and cope with daily recurrent challenges to maintain the organisms' homeostasis. De-synchronization of circadian feedback oscillators in humans causes 'jet lag', likely contributes to sleep-, psychiatric-, metabolic disorders and even cancer. However, the molecular mechanisms leading to the disintegration of tissue-specific clocks are complex and not well understood. METHODOLOGY/PRINCIPAL FINDINGS: Based on their circadian expression and cell culture experiments, the basic Helix-Loop-Helix (bHLH) transcription factors SHARP-1(Dec2) and SHARP-2(Stra13/Dec1) were proposed as novel negative regulators of the molecular clock. To address their function in vivo, we generated Sharp-1 and Sharp-2 single and double mutant mice. Our experiments reveal critical roles for both factors in regulating period length, tissue-specific control of clock gene expression and entrainment to external cues. Light-pulse experiments and rapid delays of the light-dark cycle (experimental jet lag) unravel complementary functions for SHARP-1 and SHARP-2 in controlling activity phase resetting kinetics. Moreover, we show that SHARP-1 and 2 can serve dual functions as repressors and co-activators of mammalian clock gene expression in a context-specific manner. This correlates with increased amplitudes of Per2 expression in the cortex and liver and a decrease in the suprachiasmatic nucleus (SCN) of double mutant mice. CONCLUSIONS/SIGNIFICANCE: The existence of separate mechanisms regulating phase of entrainment, rhythm amplitude and period length has been postulated before. The differential effects of Sharp-deficiency on rhythmicity and behavioral re-entrainment, coupled to tissue-dependent regulatory functions, provide a new mechanistic basis to further understand the complex process of clock synchronizations

Excitons, biexcitons, and phonons in ultrathin CdSe/ZnSe quantum structures

The optical properties of CdSe nanostructures grown by migration-enhanced epitaxy of CdSe on ZnSe are studied by time-, energy-, and temperature-dependent photoluminescence and excitation spectroscopy, as well as by polarization-dependent four-wave mixing and two-photon absorption experiments. The nanostructures consist of a coherently strained Zn1−xCdxSe/ZnSe quantum well with embedded islands of higher Cd content with sizes of a few nanometer due to strain-induced CdSe accumulation. The local increase in CdSe concentration results in a strong localization of the excitonic wave function, in an increase in radiative lifetime, and a decrease of the dephasing rate. Local LO-phonon modes caused by the strong modulation of the Cd concentration profile are found in phonon-assisted relaxation processes. Confined biexcitons with large binding energies between 20 and 24 meV are observed, indicating the important role of biexcitons even at room temperature

Transient four-wave mixing in T-shaped GaAs quantum wires

The binding energy of excitons and biexcitons and the exciton dephasing in T-shaped GaAs quantum wires is investigated by transient four-wave mixing. The T-shaped structure is fabricated by cleaved-edge overgrowth, and its geometry is engineered to optimize the one-dimensional confinement. In this wire of 6.6×24 nm2 size, we find a one-dimensional confinement of more than 20 meV, an inhomogeneous broadening of 3.4 meV, an exciton binding energy of 12 meV, and a biexciton binding energy of 2.0 meV. A dispersion of the homogeneous linewidth within the inhomogeneous broadening due to phonon-assisted relaxation is observed. The exciton acoustic-phonon-scattering coefficient of 6.1±0.5 μeV/K is larger than in comparable quantum-well structures

Capsaicin-Induced Changes in LTP in the Lateral Amygdala Are Mediated by TRPV1

The transient receptor potential vanilloid type 1 (TRPV1) channel is a well recognized polymodal signal detector that is activated by painful stimuli such as capsaicin. Here, we show that TRPV1 is expressed in the lateral nucleus of the amygdala (LA). Despite the fact that the central amygdala displays the highest neuronal density, the highest density of TRPV1 labeled neurons was found within the nuclei of the basolateral complex of the amygdala. Capsaicin specifically changed the magnitude of long-term potentiation (LTP) in the LA in brain slices of mice depending on the anesthetic (ether, isoflurane) used before euthanasia. After ether anesthesia, capsaicin had a suppressive effect on LA-LTP both in patch clamp and in extracellular recordings. The capsaicin-induced reduction of LTP was completely blocked by the nitric oxide synthase (NOS) inhibitor L-NAME and was absent in neuronal NOS as well as in TRPV1 deficient mice. The specific antagonist of cannabinoid receptor type 1 (CB1), AM 251, was also able to reduce the inhibitory effect of capsaicin on LA-LTP, suggesting that stimulation of TRPV1 provokes the generation of anandamide in the brain which seems to inhibit NO synthesis. After isoflurane anesthesia before euthanasia capsaicin caused a TRPV1-mediated increase in the magnitude of LA-LTP. Therefore, our results also indicate that the appropriate choice of the anesthetics used is an important consideration when brain plasticity and the action of endovanilloids will be evaluated. In summary, our results demonstrate that TRPV1 may be involved in the amygdala control of learning mechanisms

Differences in numbers of isolated and proliferating PSC cells.

<p>A. Number of isolated PSCs from pancreas of WT and KO mice (n = 10). PSCs were counted immediately after isolation in 5 separate areas of the dish. B. Difference in proliferation of WT and KO PSC following isolation and cell culture, as measured daily with Cell Counting Kit 8. (n = 3–5). Significant difference (P<0.05) between WT and KO (*) is indicated.</p

PSC phenotype.

<p>A. Nile red lipid staining at day 2. B. αSMA antibody staining at day 7. C. GFAP antibody staining at day 7. Secondary antibody was conjugated to Alexa 488 (green) and nuclear stain was DAPI (blue). Representative images of 3 independent experiments. Scale bars are 50 µm.</p

Expression of the P2X7 receptor in PSCs.

<p>A. PCR results from PSCs isolated from WT and KO mice illustrate the presence of all isoforms A–D and K; mRNA transcripts are also present in KO. The area disrupted by homologous recombination (In) is, however, absent. Similarly, the area spanning the disrupted area (Sp) is missing. B. Immunostaining of PSCs with primary antibody for the extracellular domain of the P2X7 receptor. Scale bar is 10 µM. C. Western blots on whole cell lysate with antibody against an extracellular domain (ex-dom) and the C-terminal part of P2X7 (C-term) in reducing (r) and non-reducing conditions. The loading control was αSMA and this blot was exposed for shorter times. Representative of 3 independent experiments.</p