Wavelengths and oscillator strengths of Xe II from the UVES spectra of four HgMn stars

In spite of large overabundances of Xe II observed in numerous mercury-manganese (HgMn) stars, Xe II oscillator strengths are only available for a very limited number of transitions. As a consequence, several unidentified lines in the spectra of HgMn stars could be due to Xe II. In addition, some predicted Xe II lines are redshifted by about 0.1 A from stellar unidentified lines, raising the question about the wavelength accuracy of the Xe II line data available in the literature. For these reasons we investigated the Xe II lines lying in the 3900-4521 A, 4769-7542 A, and 7660-8000 A spectral ranges of four well-studied HgMn stars. We compared the Xe II wavelengths listed in the NIST database with the position of the lines observed in the high-resolution UVES spectrum of the xenon-overabundant, slowly rotating HgMn stars HR 6000, and we modified them when needed. We derived astrophysical oscillator strengths for all the Xe II observed lines and compared them with the literature values, when available. In this framework, we performed a complete abundance analysis of HD 71066, while we relied on our previous works for the other stars. We find that all the lines with wavelengths related to the 6d and 7s energy levels have a corresponding unidentified spectral line, blueshifted by the same quantity of about 0.1 A in all the four stars, so that we identified these lines as coming from Xe II and modified their NIST wavelength value according to the observed stellar value. We find that the Xe II stellar oscillator strengths may differ from one star to another from 0.0 dex to 0.3 dex. We adopted the average of the oscillator strengths derived from the four stars as final astrophysical oscillator strength.Comment: Paper was accepted by A&A for publicatio

Carbon deficiencies in the primaries of some classical Algols

The equivalent widths of C II $\lambda$ 4267 \AA line were measured for the mass-gaining primary stars of the 18 Algol-type binary systems. The comparison of the EWs of the gainers with those of the single standard stars having the same effective temperature and luminosity class clearly indicates that they are systematically smaller than those of the standard stars. The primary components of the classical Algols, located in the main-sequence band of the HR diagram, appear to be C poor stars. We estimate $[N_{C} /N_{tot}]$ relative to the Sun as -1.91 for GT Cep, -1.88 for AU Mon and -1.41 for TU Mon, indicating poorer C abundance. An average differential carbon abundance has been estimated to be -0.82 dex relative to the Sun and -0.54 dex relative to the main-sequence standard stars. This result is taken to be an indication of the transferring material from the evolved less-massive secondary components to the gainers such that the CNO cycle processed material changed the original abundance of the gainers. There appear to be relationships between the EWs of C II $\lambda$ 4267 \AA line and the rates orbital period increase and mass transfer in some Algols. As the mass transfer rate increases the EW of the C II line decreases, which indicates that accreted material has not been completely mixed yet in the surface layers of the gainers. This result supports the idea of mixing as an efficient process to remove the abundance anomaly built up by accretion. Chemical evolution of the classical Algol-type systems may lead to constrains on the initial masses of the less massive, evolved, mass-losing stars.Comment: 10 pages, 4 figures, accepted in MNRA

The conserved C-terminus of the PcrA/UvrD helicase interacts directly with RNA polymerase

Copyright: © 2013 Gwynn et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: This work was supported by a Wellcome Trust project grant to MD (Reference: 077368), an ERC starting grant to MD (Acronym: SM-DNA-REPAIR) and a BBSRC project grant to PM, NS and MD (Reference: BB/I003142/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

Transcription-replication conflicts: How they occur and how they are resolved

The frequent occurrence of transcription and DNA replication in cells results in many encounters, and thus conflicts, between the transcription and replication machineries. These conflicts constitute a major intrinsic source of genome instability, which is a hallmark of cancer cells. How the replication machinery progresses along a DNA molecule occupied by an RNA polymerase is an old question. Here we review recent data on the biological relevance of transcription-replication conflicts, and the factors and mechanisms that are involved in either preventing or resolving them, mainly in eukaryotes. On the basis of these data, we provide our current view of how transcription can generate obstacles to replication, including torsional stress and non-B DNA structures, and of the different cellular processes that have evolved to solve them

XRN2 Links Transcription Termination to DNA Damage and Replication Stress

We thank the Proteomics Core Facility. We thank Dr. Robert J. Crouch for providing us with GFP- and GFP-RNase H expression plasmids. We also thank Dr. Stephen H. Leppla for providing us with antibodies directed against RNA:DNA hybrids (R loops) (S9.6). We thank Novus Biologicals for generously providing XRN2 and Rrp45 antibodies. We also thank the members of the Boothman lab for critical reading of this manuscript.Author Summary Genomic instability is one of the primary causes of disease states, in particular cancer. One major cause of genomic instability is the formation of DNA double strand breaks (DSBs), which are one of the most dangerous types of DNA lesions the cell can encounter. If not repaired in a timely manner, one DSB can lead not only to cell death. If misrepaired, one DSB can lead to a hazardous chromosomal aberration, such as a translocation, that can eventually lead to cancer. The cell encounters and repairs DSBs that arise from naturally occurring cellular processes on a daily basis. A number of studies have demonstrated that aberrant structures that form during transcription under certain circumstances, in particular RNA:DNA hybrids (R loops), can lead to DSB formation and genomic instability, especially during DNA synthesis. Thus, it is important to understand how the cell responds and repairs transcription-mediated DNA damage in general and R loop-related DNA damage in particular. This paper both demonstrates that the XRN transcription termination factor links transcription and DNA damage, but also provides a better understanding of how the cell prevents transcription-related DNA damage.Yeshttp://www.plosgenetics.org/static/editorial#pee

C9orf72 Expansion Disrupts ATM-mediated Chromosomal Break Repair

A hexanucleotide repeat expansion represents the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the mechanisms by which the expansion cause neurodegeneration are poorly understood. We report elevated levels of DNA/RNA hybrids (R-loops) and double-strand breaks (DSBs) in rodent neurons, human cells, and in C9orf72-ALS patient spinal cord tissues. Accumulation of endogenous DNA damage is concomitant with defective ATM-mediated DNA repair signalling and accumulation of protein-linked DNA breaks. We further reveal that defective ATM-mediated DNA repair is a consequence of p62 accumulation, which impairs H2A ubiquitylation and perturbs ATM signalling. Adeno-associated virus- mediated expression of C9orf72-related RNA and dipeptide repeats in the murine central nervous system causes elevated DSBs, ATM defects, and triggers neurodegeneration. These findings identify R-Loops, DSBs, and defective ATM-mediated repair as pathological consequences of C9orf72 expansions, and suggest that C9orf72-linked neurodegeneration is driven, at least in part, by genomic instability

On the Properties of B and A Type Supergiants

We review the literature of high dispersion studies of late B and early A type supergiants to assess the importance of non-LTE abundance calculations for them. Practically we are interested in learning which elements and species have such calculations been performed and then which of these should be implemented in calculations with plane-parallel LTE model atmospheres. The techniques available for the quantitative modeling of these atmospheres are outlined and some recent results are discussed

Rectal dexmedetomidine in rats: Evaluation of sedative and mucosal effects [Dexmedetomidina retal em ratos: Avaliação dos efeitos sedativos e sobre a mucosa]

Background and objectives: In this study, we investigated the anesthetic and mucosal effects of the rectal application of dexmedetomidine to rats. Methods: Male Wistar albino rats weighing 250-300g were divided into four groups: Group S (n=8) was a sham group that served as a baseline for the normal basal values; Group C (n=8) consisted of rats that received the rectal application of saline alone; Group IPDex (n=8) included rats that received the intraperitoneal application of dexmedetomidine (100 µg kg-1); and Group RecDex (n=8) included rats that received the rectal application of dexmedetomidine (100 µg kg-1). For the rectal drug administration, we used 22G intravenous cannulas with the stylets removed. We administered the drugs by advancing the cannula 1cm into the rectum, and the rectal administration volume was 1mL for all the rats. The latency and anesthesia time (min) were measured. Two hours after rectal administration, 75 mg kg-1 ketamine was administered for intraperitoneal anesthesia in all the groups, followed by the removal of the rats' rectums to a distal distance of 3cm via an abdominoperineal surgical procedure. We histopathologically examined and scored the rectums. Results: Anesthesia was achieved in all the rats in the Group RecDex following the administration of dexmedetomidine. The onset of anesthesia in the Group RecDex was significantly later and of a shorter duration than in the Group IPDEx (p < 0.05). In the Group RecDex, the administration of dexmedetomidine induced mild-moderate losses of mucosal architecture in the colon and rectum, 2 h after rectal inoculation. Conclusion: Although 100µgkg-1 dexmedetomidine administered rectally to rats achieved a significantly longer duration of anesthesia compared with the rectal administration of saline, our histopathological evaluations showed that the rectal administration of 100µgkg-1 dexmedetomidine led to mild-moderate damage to the mucosal structure of the rectum. © 2013 Sociedade Brasileira de Anestesiologia