Publishing In The Accounting Journals: Is There A Gender Bias?

To publish or not to publish?… that is the question (adapted from William Shakespeare).  In the world of academe, the answer is short and sweet… publish or get out.  This rule holds true for both male and female faculty members, yet it is sometimes postulated that there may be some inconsistencies on how this rule applies across the genders.  This study focuses on whether male and female accounting academics have distinctive patterns of representation as authors in top ranked accounting journals. Archival data, consisting of author information and article information was collected for two journals, The Accounting Review and Journal Accounting Research.  Consistent with previous research findings, preliminary results suggest that females represent a disproportionately small minority of authors in both of these two top accounting journals

Concentrated Perchlorate at the Mars Phoenix Landing Site: Evidence for Thin Film Liquid Water on Mars

NASA\u27s Phoenix mission, which landed on the northern plains of Mars in 2008, returned evidence of the perchlorate anion distributed evenly throughout the soil column at the landing site. Here, we use spectral data from Phoenix\u27s Surface Stereo Imager to map the distribution of perchlorate salts at the Phoenix landing site, and find that perchlorate salt has been locally concentrated into subsurface patches, similar to salt patches that result from aqueous dissolution and redistribution on Earth. We propose that thin films of liquid water are responsible for translocating perchlorate from the surface to the subsurface, and for concentrating it in patches. The thin films are interpreted to result from melting of minor ice covers related to seasonal and long-term obliquity cycles

Neuronspecific expression of the rat gonadotropin-releasing hormone gene is conferred by interactions of a defined promoter element with the enhancer in GT1–7 cells

Neuroendocrine control of the reproductive cascade is mediated by GnRH, which in mammals is produced by a subset of neurons scattered throughout the hypothalamus and forebrain. Utilizing a cultured cell model of GnRH neurons (GT1-7 cells), two regulatory regions in the rat GnRH 5 flanking DNA were identified as essential for cell-type specificity: a 300-bp enhancer and a 173-bp conserved proximal promoter. Using transient transfections to compare expression in GT1-7 cells to a non-GnRH-expressing cell type (NIH 3T3), we show that the GnRH enhancer and the proximal promoter each play roles in conferring this specificity. Deletion of footprint 2 (FP2; ؊26 to ؊76) from the promoter when coupled to the GnRH enhancer diminishes reporter activity in GT1-7 cells more strongly than in NIH 3T3 cells. Furthermore, deletion of FP2 from the promoter when coupled to the heterologous Rous sarcoma virus 5-long terminal repeat promoter abolishes the difference in reporter activity between GT1-7 and NIH 3T3 cells, suggesting that FP2 of the GnRH promoter is necessary for cell-specific expression. In addition, FP2 alone is sufficient to confer cell-specific expression and can interact with the GnRH enhancer to augment reporter gene expression specifically in GT1-7 cells. Finally, a 31-bp sequence from within FP2 (؊63 to ؊33) synergistically activates transcription when coupled with the GnRH enhancer in GT1-7 cells but not in NIH 3T3 cells. Thus, this 31-bp region contains elements necessary for interaction between the GnRH enhancer and promoter. We show that two of five protein complexes that bind to the ؊63 to ؊33 region are GT1-7 cell specific, and both of them appear to be homeodomain proteins. The identification of a cell-specific element in the GnRH proximal promoter significantly advances our understanding of the transcriptional basis for neuron-specific GnRH gene expression. (Molecular Endocrinology 14: 1509-1522, 2000

Controlling the motor activity of a transcription-repair coupling factor: autoinhibition and the role of RNA polymerase

Motor proteins that couple ATP hydrolysis to movement along nucleic acids play a variety of essential roles in DNA metabolism. Often these enzymes function as components of macromolecular complexes, and DNA translocation by the motor protein drives movement of other components of the complex. In order to understand how the activity of motor proteins is regulated within multi-protein complexes we have studied the bacterial transcription-repair coupling factor, Mfd, which is a helicase superfamily 2 member that binds to RNA polymerase (RNAP) and removes stalled transcription complexes from DNA. Using an oligonucleotide displacement assay that monitors protein movement on double-stranded DNA we show that Mfd has little motor activity in isolation, but exhibits efficient oligonucleotide displacement activity when bound to a stalled transcription complex. Deletion of the C-terminal domain of Mfd increases the ATPase activity of the protein and allows efficient oligo-displacement in the absence of RNAP. Our results suggest that an autoinhibitory domain ensures the motor activity of Mfd is only functional within the correct macromolecular context: recruitment of Mfd to a stalled transcription complex relieves the autoinhibition and unmasks the motor activity

Determining Segment and Network Traffic Volumes from Video Imagery Obtained from Transit Buses in Regular Service: Developments and Evaluation of Approaches for Ongoing Use across Urban Networks

69A3551747111Transit agencies around the world are increasingly mounting video cameras inside and outside their buses for liability, safety, and security reasons. Some of the cameras provide fields of view that allow observation of vehicles traveling on the surrounding roadways. Such video imagery could conceivably be used to estimate traffic volumes on roadway segments traversed by the transit buses. Transit buses are attractive platforms for acquiring the information that leads to traffic volume estimates, since a fleet of transit buses collectively covers most major surface streets in an urban area and the buses regularly and repeatedly cover the same roadway segments, which would allow for multiple, independent estimates of roadway segment flows across days and by time of day. Since the video cameras are already installed for other purposes, the costs of estimating traffic flows from video obtained from transit buses in regular service would be minimal. Therefore, traffic flows could be estimated with much greater geographic coverage, with much greater frequency, and with much lower cost than is presently available from existing traffic volume observation methods

MutLα heterodimers modify the molecular phenotype of Friedreich ataxia

This article has been made available through the Brunel Open Access Publishing Fund.Background: Friedreich ataxia (FRDA), the most common autosomal recessive ataxia disorder, is caused by a dynamic GAA repeat expansion mutation within intron 1 of FXN gene, resulting in down-regulation of frataxin expression. Studies of cell and mouse models have revealed a role for the mismatch repair (MMR) MutS-heterodimer complexes and the PMS2 component of the MutLα complex in the dynamics of intergenerational and somatic GAA repeat expansions: MSH2, MSH3 and MSH6 promote GAA repeat expansions, while PMS2 inhibits GAA repeat expansions. Methodology/Principal Findings: To determine the potential role of the other component of the MutLα complex, MLH1, in GAA repeat instability in FRDA, we have analyzed intergenerational and somatic GAA repeat expansions from FXN transgenic mice that have been crossed with Mlh1 deficient mice. We find that loss of Mlh1 activity reduces both intergenerational and somatic GAA repeat expansions. However, we also find that loss of either Mlh1 or Pms2 reduces FXN transcription, suggesting different mechanisms of action for Mlh1 and Pms2 on GAA repeat expansion dynamics and regulation of FXN transcription. Conclusions/Significance: Both MutLα components, PMS2 and MLH1, have now been shown to modify the molecular phenotype of FRDA. We propose that upregulation of MLH1 or PMS2 could be potential FRDA therapeutic approaches to increase FXN transcription. © 2014 Ezzatizadeh et al.This article has been made available through the Brunel Open Access Publishing Fund