Novelty Induces Behavioural And Glucocorticoid Responses In A Songbird Artificially Selected For Divergent Personalities

Stress physiology is thought to contribute to individual differences in behaviour. In part this reflects the fact that canonical personality measures consist of responses to challenges, including novel objects and environments. Exposure to novelty is typically assumed to induce a moderate increase in glucocorticoids (CORT), although this has rarely been tested. We tested this assumption using great tits, Parus major, selected for divergent personalities (bold-fast and shy-slow explorers), predicting that the shy birds would exhibit higher CORT following exposure to a novel object. We also scored behavioural responses to the novel object, predicting that bold birds would more frequently approach the novel object and exhibit more abnormal repetitive behaviours. We found that the presence of a novel object did induce a moderate CORT response, but selection lines did not differ in the magnitude of this response. Furthermore, although both selection lines showed a robust CORT elevation to a subsequent restraint stressor, the CORT response was stronger in bold birds and this effect was specific to novel object exposure. Shy birds showed a strong positive phenotypic correlation between CORT concentrations following the novel object exposure and the subsequent restraint stress. Behaviourally, the selection lines differed in their response during novel object exposure: as predicted, bold birds more frequently approached the novel object and shy birds more strongly decreased overall locomotion during the novel object trial, but birds from both selection lines showed significant and similar frequencies of abnormal repetitive behaviours during novel object exposure. Our findings support the hypothesis that personality emerges as a result of correlated selection on behaviour and underlying endocrine mechanisms and suggest that the relationship between endocrine stress physiology and personality is context dependent

How limiting is optical follow-up for fast radio burst applications? Forecasts for radio and optical surveys

Fast radio bursts (FRBs) are the first cosmological radio sources that vary on millisecond timescales, which makes them a unique probe of the Universe. Many proposed applications of FRBs require associated redshifts. These can only be obtained by localizing FRBs to their host galaxies and subsequently measuring their redshifts. Upcoming FRB surveys will provide arcsecond localization for many FRBs, not all of which can be followed up with dedicated optical observations. We aim to estimate the fraction of FRB hosts that will be catalogued with redshifts by existing and future optical surveys. We use the population synthesis code frbpoppy to simulate several FRB surveys, and the semi-analytical galaxy formation code GALFORM to simulate their host galaxies. We obtain redshift distributions for the simulated FRBs and the fraction with host galaxies in a survey. Depending on whether FRBs follow the cosmic star formation rate or stellar mass, 20 to 40 per cent of CHIME FRB hosts will be observed in an SDSS-like survey, all at $z<0.5$. The deeper DELVE survey will detect 63 to 85 per cent of ASKAP FRBs found in its coherent search mode. CHIME FRBs will reach $z\sim 3$, SKA1-Mid FRBs $z\sim 5$, but ground based follow-up is limited to $z\lesssim 1.5$. We discuss consequences for several FRB applications. If $\sim1/2$ of ASKAP FRBs have measured redshifts, 1000 detected FRBs can be used to constrain $\Omega_\text{b} h_{70}$ to within $\sim10$ per cent at 95 per cent credibility. We provide strategies for optimized follow-up, when building on data from existing surveys. Data and codes are made available.Comment: 18 pages, 16 figures, 4 tables, accepted for publication in MNRAS. Code available at https://github.com/JoschaJ/mockFRBhost

A Look At Three Different Scenarios for Bulge Formation

In this paper, we present three qualitatively different scenarios for bulge formation: a secular evolution model in which bulges form after disks and undergo several central starbursts, a primordial collapse model in which bulges and disks form simultaneously, and an early bulge formation model in which bulges form prior to disks. We normalize our models to the local z=0 observations of de Jong & van der Kruit (1994) and Peletier & Balcells (1996) and make comparisons with high redshift observations. We consider model predictions relating directly to bulge-to-disk properties. As expected, smaller bulge-to-disk ratios and bluer bulge colors are predicted by the secular evolution model at all redshifts, although uncertainties in the data are currently too large to differentiate strongly between the models.Comment: 19 pages, 6 figures, accepted for publication in the Astrophysical Journa

Faint Lyman-Break galaxies as a crucial test for galaxy formation models

It has recently been shown that galaxy formation models within the LambdaCDM cosmology predict that, compared to the observed population, small galaxies (with stellar masses < 10^{11} M_sun) form too early, are too passive since z ~ 3 and host too old stellar populations at z=0. We then expect an overproduction of small galaxies at z > 4 that should be visible as an excess of faint Lyman-break galaxies. To check whether this excess is present, we use the MORGANA galaxy formation model and GRASIL spectro-photometric + radiative transfer code to generate mock catalogues of deep fields observed with HST-ACS. We add observational noise and the effect of Lyman-alpha emission, and perform color-color selections to identify Lyman-break galaxies. The resulting mock candidates have plausible properties that closely resemble those of observed galaxies. We are able to reproduce the evolution of the bright tail of the luminosity function of Lyman-break galaxies (with a possible underestimate of the number of the brightest i-dropouts), but uncertainties and degeneracies in dust absorption parameters do not allow to give strong constraints to the model. Besides, our model shows a clear excess with respect to observations of faint Lyman-break galaxies, especially of z_{850} ~ 27 V-dropouts at z ~ 5. We quantify the properties of these "excess" galaxies and discuss the implications: these galaxies are hosted in dark matter halos with circular velocities in excess of 100 km s^{-1}, and their suppression may require a deep re-thinking of stellar feedback processes taking place in galaxy formation.Comment: 17 pages, 13 figures, 1 table; accepted for publication by MNRA

Serum APE1 as a predictive marker for platinum-based chemotherapy of non-small cell lung cancer patients

Purpose: To define the role of the DNA repair protein apurinic/apyrimidinic endonuclease 1 (APE1) in predicting the prognosis and chemotherapeutic response of non-small cell lung cancer patients receiving platinum-containing chemotherapy. Results: Our investigations found that serum APE1 level was significantly elevated in 229 of 412 NSCLC patients and correlated with its level in tissue (r2 = 0.639, p < 0.001). The elevated APE1 level in both tissue and serum of patients prior to chemotherapy was associated with worse progression-free survival (HR: 2.165, p < 0.001, HR: 1.421, p = 0.012), but not with overall survival. After 6 cycles of chemotherapy, a low APE1 serum level was associated with better overall survival (HR: 0.497, p = 0.010). Experimental Design: We measured APE1 protein levels in biopsy tissue from 172 NSCLC patients and sera of 412 NSCLC patients receiving platinum-based chemotherapy by immunohistochemistry and a newly established sensitive and specific enzyme-linked immunosorbent assay, respectively. APE1 levels in sera of 523 healthy donors were also determined as control. Conclusions: Our studies indicate that APE1 is a biomarker for predicting prognosis and therapeutic efficacy in NSCLC. The chemotherapy-na\uefve serum APE1 level, which correlated with its tissue level inversely associated with progressionfree survival of platinum-containing doublet chemotherapy, whereas post-treatment serum APE1 level was inversely associated with overall survival

Overlapping effector interfaces define the multiple functions of the HIV-1 Nef polyproline helix

Background: HIV-1 Nef is a multifunctional protein required for full pathogenicity of the virus. As Nef has no known enzymatic activity, it necessarily functions through protein-protein interaction interfaces. A critical Nef protein interaction interface is centered on its polyproline segment (P69VRPQVPLRP78) which contains the helical SH3 domain binding protein motif, PXXPXR. We hypothesized that any Nef-SH3 domain interactions would be lost upon mutation of the prolines or arginine of PXXPXR. Further, mutation of the non-motif “X” residues, (Q73, V74, and L75) would give altered patterns of inhibition for different Nef/SH3 domain protein interactions. Results: We found that mutations of either of the prolines or the arginine of PXXPXR are defective for Nef-Hck binding, Nef/activated PAK2 complex formation and enhancement of virion infectivity (EVI). Mutation of the non-motif “X” residues (Q, V and L) gave similar patterns of inhibition for Nef/activated PAK2 complex formation and EVI which were distinct from the pattern for Hck binding. These results implicate an SH3 domain containing protein other than Hck for Nef/activated PAK2 complex formation and EVI. We have also mutated Nef residues at the N-and C-terminal ends of the polyproline segment to explore interactions outside of PXXPXR. We discovered a new locus GFP/F (G67, F68, P69 and F90) that is required for Nef/activated PAK2 complex formation and EVI. MHC Class I (MHCI) downregulation was only partially inhibited by mutating the PXXPXR motif residues, but was fully inhibited by mutating the C-terminal P78. Further, we observed that MHCI downregulation strictly requires G67 and F68. Our mutational analysis confirms the recently reported structure of the complex between Nef, AP-1 μ1 and the cytoplasmic tail of MHCI, but does not support involvement of an SH3 domain protein in MHCI downregulation. Conclusion: Nef has evolved to be dependent on interactions with multiple SH3 domain proteins. To the N- and C- terminal sides of the polyproline helix are multifunctional protein interaction sites. The polyproline segment is also adapted to downregulate MHCI with a non-canonical binding surface. Our results demonstrate that Nef polyproline helix is highly adapted to directly interact with multiple host cell proteins