Retired galaxies: not to be forgotten in the quest of the star formation -- AGN connection

We propose a fresh look at the Main Galaxy Sample of the Sloan Digital Sky Survey by packing the galaxies in stellar mass and redshift bins. We show how important it is to consider the emission-line equivalent widths, in addition to the commonly used emission-line ratios, to properly identify retired galaxies (i.e. galaxies that have stopped forming stars and are ionized by their old stellar populations) and not mistake them for galaxies with low-level nuclear activity. We find that the proportion of star-forming galaxies decreases with decreasing redshift in each mass bin, while that of retired galaxies increases. Galaxies with $M_\star > 10^{11.5} M_\odot$ have formed all their stars at redshift larger than 0.4. The population of AGN hosts is never dominant for galaxy masses larger than $10^{10} M_\odot$. We warn about the effects of stacking galaxy spectra to discuss galaxy properties. We estimate the lifetimes of active galactic nuclei (AGN) relying entirely on demographic arguments --- i.e. without any assumption on the AGN radiative properties. We find upper-limit lifetimes of about 1--5 Gyr for detectable AGN in galaxies with masses between $10^{10}$--$10^{12} M_\odot$. The lifetimes of the AGN-dominated phases are a few $10^8$ yr. Finally, we compare the star-formation histories of star-forming, AGN and retired galaxies as obtained by the spectral synthesis code STARLIGHT. Once the AGN is turned on it inhibits star formation for the next $\sim$ 0.1 Gyr in galaxies with masses around $10^{10} M_\odot$, $\sim$ 1 Gyr in galaxies with masses around $10^{11} M_\odot$.Comment: accepted for MNRAS figure resolution has been degraded with respect to what will be published in MNRA

Cloning and expression of a human kinesin heavy chain gene: interaction of the COOH-terminal domain with cytoplasmic microtubules in transfected CV-1 cells.

To understand the interactions between the microtubule-based motor protein kinesin and intracellular components, we have expressed the kinesin heavy chain and its different domains in CV-1 monkey kidney epithelial cells and examined their distributions by immunofluorescence microscopy. For this study, we cloned and sequenced cDNAs encoding a kinesin heavy chain from a human placental library. The human kinesin heavy chain exhibits a high level of sequence identity to the previously cloned invertebrate kinesin heavy chains; homologies between the COOH-terminal domain of human and invertebrate kinesins and the nonmotor domain of the Aspergillus kinesin-like protein bimC were also found. The gene encoding the human kinesin heavy chain also contains a small upstream open reading frame in a G-C rich 5' untranslated region, features that are associated with translational regulation in certain mRNAs. After transient expression in CV-1 cells, the kinesin heavy chain showed both a diffuse distribution and a filamentous staining pattern that coaligned with microtubules but not vimentin intermediate filaments. Altering the number and distribution of microtubules with taxol or nocodazole produced corresponding changes in the localization of the expressed kinesin heavy chain. The expressed NH2-terminal motor and the COOH-terminal tail domains, but not the alpha-helical coiled coil rod domain, also colocalized with microtubules. The finding that both the kinesin motor and tail domains can interact with cytoplasmic microtubules raises the possibility that kinesin could crossbridge and induce sliding between microtubules under certain circumstances

Use of strategies to improve retention in primary care randomised trials: a qualitative study with in-depth interviews

Objective To explore the strategies used to improve retention in primary care randomised trials.<p></p> Design Qualitative in-depth interviews and thematic analysis.<p></p> Participants 29 UK primary care chief and principal investigators, trial managers and research nurses.<p></p> Methods In-depth face-to-face interviews.<p></p> Results Primary care researchers use incentive and communication strategies to improve retention in trials, but were unsure of their effect. Small monetary incentives were used to increase response to postal questionnaires. Non-monetary incentives were used although there was scepticism about the impact of these on retention. Nurses routinely used telephone communication to encourage participants to return for trial follow-up. Trial managers used first class post, shorter questionnaires and improved questionnaire designs with the aim of improving questionnaire response. Interviewees thought an open trial design could lead to biased results and were negative about using behavioural strategies to improve retention. There was consensus among the interviewees that effective communication and rapport with participants, participant altruism, respect for participant's time, flexibility of trial personnel and appointment schedules and trial information improve retention. Interviewees noted particular challenges with retention in mental health trials and those involving teenagers.<p></p> Conclusions The findings of this qualitative study have allowed us to reflect on research practice around retention and highlight a gap between such practice and current evidence. Interviewees describe acting from experience without evidence from the literature, which supports the use of small monetary incentives to improve the questionnaire response. No such evidence exists for non-monetary incentives or first class post, use of which may need reconsideration. An exploration of barriers and facilitators to retention in other research contexts may be justified.<p></p&gt