Lady and the accounts: Missing from accounting history?

Amanda Vickery\u27s, The Gentleman\u27s Daughter: Women\u27s Lives in Georgian England, [1998] provides a challenging and controversial account of the lives of genteel women in provincial England. In this review essay, we consider the implications of her insights and revelations for accounting history research. We argue that her work raises a number of issues concerning what and where accounting took place in the 18th century. In particular, it is suggested that the detailed accounts\u27 contained within genteel women\u27s pocket books were a means by which they came to know\u27 their household in order to manage their duties and responsibilities. Accounting historians are encouraged to consider these private\u27 records as a potentially illuminating source of material on accounting within and without the 18th-century household

a case study of the implementation of the EU eigth directive in Denmark 1984-2003

This paper analyses the complex process through which EU's Eighth Company Law Directive on the qualification of statutory auditors (1984) was implemented in Denmark. The Directive envisaged one group of ‘statutory auditors’ in each member state. However, in Denmark there were two groups of auditors: the state authorised auditors who had a long education and high status, and the registered auditors who had a shorter education, lower status and whose clients were mainly medium and small sized businesses. An exemption was made in the Directive to allow the registered auditors to continue to audit despite that they did not have the required ‘university level’ education. This made the issue of education central to the long-term survival of the registered auditors and it consequently became the object of a long conflict between the parties with an interest in auditor education and qualifications: the profession, the state and the educational institutions. This case illustrates the processes of audit regulation in a small European state with a highly developed economy where auditors are approved and regulated by the state but through processes heavily influenced by the profession. It provides an interesting contrast to other studies carried out on the implementation of this Directive, e.g. in the UK (Cooper et al, 1996) and in Greece (Caramanis, 1999), and perhaps some insight into the difficulties which may be encountered in implementing the new Eighth Directive proposed by the Commission in May 2003. Key Words: EU; Eighth Directive; accounting profession; Denmark; harmonisation; regulation

iRNA-seq: computational method for genome-wide assessment of acute transcriptional regulation from total RNA-seq data

RNA-seq is a sensitive and accurate technique to compare steady-state levels of RNA between different cellular states. However, as it does not provide an account of transcriptional activity per se, other technologies are needed to more precisely determine acute transcriptional responses. Here, we have developed an easy, sensitive and accurate novel computational method, iRNA-seq, for genome-wide assessment of transcriptional activity based on analysis of intron coverage from total RNA-seq data. Comparison of the results derived from iRNA-seq analyses with parallel results derived using current methods for genome-wide determination of transcriptional activity, i.e. global run-on (GRO)-seq and RNA polymerase II (RNAPII) ChIP-seq, demonstrate that iRNA-seq provides similar results in terms of number of regulated genes and their fold change. However, unlike the current methods that are all very labor-intensive and demanding in terms of sample material and technologies, iRNA-seq is cheap and easy and requires very little sample material. In conclusion, iRNA-seq offers an attractive novel alternative to current methods for determination of changes in transcriptional activity at a genome-wide level

Loss of TLE3 promotes the mitochondrial program in beige adipocytes and improves glucose metabolism.

Prolonged cold exposure stimulates the recruitment of beige adipocytes within white adipose tissue. Beige adipocytes depend on mitochondrial oxidative phosphorylation to drive thermogenesis. The transcriptional mechanisms that promote remodeling in adipose tissue during the cold are not well understood. Here we demonstrate that the transcriptional coregulator transducin-like enhancer of split 3 (TLE3) inhibits mitochondrial gene expression in beige adipocytes. Conditional deletion of TLE3 in adipocytes promotes mitochondrial oxidative metabolism and increases energy expenditure, thereby improving glucose control. Using chromatin immunoprecipitation and deep sequencing, we found that TLE3 occupies distal enhancers in proximity to nuclear-encoded mitochondrial genes and that many of these binding sites are also enriched for early B-cell factor (EBF) transcription factors. TLE3 interacts with EBF2 and blocks its ability to promote the thermogenic transcriptional program. Collectively, these studies demonstrate that TLE3 regulates thermogenic gene expression in beige adipocytes through inhibition of EBF2 transcriptional activity. Inhibition of TLE3 may provide a novel therapeutic approach for obesity and diabetes

Extensive chromatin remodelling and establishment of transcription factor 'hotspots' during early adipogenesis

Adipogenesis is tightly controlled by a complex network of transcription factors acting at different stages of differentiation. Peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein (C/EBP) family members are key regulators of this process. We have employed DNase I hypersensitive site analysis to investigate the genome-wide changes in chromatin structure that accompany the binding of adipogenic transcription factors. These analyses revealed a dramatic and dynamic modulation of the chromatin landscape during the first hours of adipocyte differentiation that coincides with cooperative binding of multiple early transcription factors (including glucocorticoid receptor, retinoid X receptor, Stat5a, C/EBPβ and -δ) to transcription factor ‘hotspots'. Our results demonstrate that C/EBPβ marks a large number of these transcription factor ‘hotspots' before induction of differentiation and chromatin remodelling and is required for their establishment. Furthermore, a subset of early remodelled C/EBP-binding sites persists throughout differentiation and is later occupied by PPARγ, indicating that early C/EBP family members, in addition to their well-established role in activation of PPARγ transcription, may act as pioneering factors for PPARγ binding

Lack of acute phase response in the livers of mice exposed to diesel exhaust particles or carbon black by inhalation

<p>Abstract</p> <p>Background</p> <p>Epidemiologic and animal studies have shown that particulate air pollution is associated with increased risk of lung and cardiovascular diseases. Although the exact mechanisms by which particles induce cardiovascular diseases are not known, studies suggest involvement of systemic acute phase responses, including C-reactive protein (CRP) and serum amyloid A (SAA) in humans. In this study we test the hypothesis that diesel exhaust particles (DEP) – or carbon black (CB)-induced lung inflammation initiates an acute phase response in the liver.</p> <p>Results</p> <p>Mice were exposed to filtered air, 20 mg/m³DEP or CB by inhalation for 90 minutes/day for four consecutive days; we have previously shown that these mice exhibit pulmonary inflammation (Saber AT, Bornholdt J, Dybdahl M, Sharma AK, Loft S, Vogel U, Wallin H. Tumor necrosis factor is not required for particle-induced genotoxicity and pulmonary inflammation., Arch. Toxicol. 79 (2005) 177–182). As a positive control for the induction of an acute phase response, mice were exposed to 12.5 mg/kg of lipopolysaccharide (LPS) intraperitoneally. Quantitative real time RT-PCR was used to examine the hepatic mRNA expression of acute phase proteins, serum amyloid P (<it>Sap</it>) (the murine homologue of <it>Crp</it>) and <it>Saa1 </it>and <it>Saa3</it>. While significant increases in the hepatic expression of <it>Sap, Saa1 </it>and <it>Saa3 </it>were observed in response to LPS, their levels did not change in response to DEP or CB. In a comprehensive search for markers of an acute phase response, we analyzed liver tissue from these mice using high density DNA microarrays. Globally, 28 genes were found to be significantly differentially expressed in response to DEP or CB. The mRNA expression of three of the genes (serine (or cysteine) proteinase inhibitor, clade A, member 3C, apolipoprotein E and transmembrane emp24 domain containing 3) responded to both exposures. However, these changes were very subtle and were not confirmed by real time RT-PCR.</p> <p>Conclusion</p> <p>Our findings collectively suggest that <it>Sap, Saa1 </it>and <it>Saa3 </it>are not induced in livers of mice exposed to DEP or CB. Despite pulmonary inflammation in these mice, global transcriptional profiling of liver did not reveal any hepatic response following exposure by inhalation.</p

Feasibility of simultaneous PET/MR of the carotid artery: first clinical experience and comparison to PET/CT

The study aimed at comparing PET/MR to PET/CT for imaging the carotid arteries in patients with known increased risk of atherosclerosis. Six HIV-positive men underwent sequential PET/MR and PET/CT of the carotid arteries after injection of 400 MBq of (18)F-FDG. PET/MR was performed a median of 131 min after injection. Subsequently,PET/CT was performed. Regions of interest (ROI) were drawn slice by slice to include the carotid arteries and standardized uptake values (SUV) were calculated from both datasets independently. Quantitative comparison of (18)F-FDG uptake revealed a high congruence between PET data acquired using the PET/MR system compared to the PET/CT system. The mean difference for SUV(mean) was -0.18 (p < 0.001) and -0.14 for SUV(max) (p < 0.001) indicating a small but significant bias towards lower values using the PET/MR system. The 95% limits of agreement were -0.55 to 0.20 for SUV(mean) and -0.93 to 0.65 for SUV(max). The image quality of the PET/MR allowed for delineation of the carotid vessel wall. The correlations between (18)F-FDG uptake from ROI including both vessel wall and vessel lumen to ROI including only the wall were strong (r = 0.98 for SUV(mean) and r = 1.00 for SUV(max)) indicating that the luminal (18)F-FDG content had minimal influence on the values. The study shows for the first time that simultaneous PET/MR of the carotid arteries is feasible in patients with increased risk of atherosclerosis. Quantification of (18)F-FDG uptake correlated well between PET/MR and PET/CT despite difference in method of PET attenuation correction, reconstruction algorithm, and detector technology

Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2

<p>Abstract</p> <p>Background</p> <p>There is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease.</p> <p>Methods</p> <p>We investigated plaque progression and vasodilatory function in apolipoprotein E knockout (<it>ApoE</it>^-/-) mice exposed to TiO₂. <it>ApoE</it>^-/-mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine TiO₂(fTiO₂, 288 nm), photocatalytic 92/8 anatase/rutile TiO₂(pTiO₂, 12 nm), or rutile nano TiO₂(nTiO₂, 21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. The progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized TiO₂(0.5 mg/kg bodyweight) once a week for 4 weeks. We measured mRNA levels of <it>Mcp-1</it>, <it>Mip-2</it>, <it>Vcam-1</it>, <it>Icam-1 </it>and <it>Vegf </it>in lung tissue to assess pulmonary inflammation and vascular function. TiO₂-induced alterations in nitric oxide (NO) production were assessed in human umbilical vein endothelial cells (HUVECs).</p> <p>Results</p> <p>The exposure to nTiO₂was associated with a modest increase in plaque progression in aorta, whereas there were unaltered vasodilatory function and expression levels of <it>Mcp-1</it>, <it>Mip-2</it>, <it>Vcam-1</it>, <it>Icam-1 </it>and <it>Vegf </it>in lung tissue. The <it>ApoE^-/-</it>mice exposed to fine and photocatalytic TiO₂had unaltered vasodilatory function and lung tissue inflammatory gene expression. The unaltered NO-dependent vasodilatory function was supported by observations in HUVECs where the NO production was only increased by exposure to nTiO₂.</p> <p>Conclusion</p> <p>Repeated exposure to nanosized TiO₂particles was associated with modest plaque progression in <it>ApoE^-/-</it>mice. There were no associations between the pulmonary TiO₂exposure and inflammation or vasodilatory dysfunction.</p