Non-technical skills and students' overconfidence in accounting

Purpose: Despite the institutional calls to include the development of non-technical skills as objectives in accounting curriculum and the attempts to do so, a gap between the level of skills exhibited by graduates and those needed to succeed as a professional is still perceived. One of the possible causes could be students' overconfidence, defined as a very optimistic assessment of their own abilities. The main objective of the paper is to assess the existence of overconfidence. Design/methodology/approach: Two samples, students and employers were surveyed regarding the exhibited level of accounting graduates in a set of 22 non-technical skills, highlighted as relevant in the literature. This enabled a comparison of the opinions of employers with the perceptions of students concerning the demonstrated level of such skills. Findings: The results of this study support the existence of students' overconfidence. In all the skills students score their ability higher than employers do with those differences being statistically significant in 21 out of 22 skills. Employers who are in closer contact with entry level accountants perceive even lower exhibited skills levels in graduates. Research limitations/implications: Overconfident students would be less motivated to actively participate in activities designed to improve skills resulting in underachievement and in lower performance. This low performance in highly valued skills could potentially harm their employability. Originality/value: Although the literature focussing on non-technical skills in accounting is prolific there are few papers comparing the views of employers and students, and there are no previous studies focussing on overconfidence

Evidence for the association of the SLC22A4 and SLC22A5 genes with Type 1 Diabetes: a case control study

BACKGROUND: Type 1 diabetes (T1D) is a chronic, autoimmune and multifactorial disease characterized by abnormal metabolism of carbohydrate and fat. Diminished carnitine plasma levels have been previously reported in T1D patients and carnitine increases the sensitivity of the cells to insulin. Polymorphisms in the carnitine transporters, encoded by the SLC22A4 and SLC22A5 genes, have been involved in susceptibility to two other autoimmune diseases, rheumatoid arthritis and Crohn's disease. For these reasons, we investigated for the first time the association with T1D of six single nucleotide polymorphisms (SNPs) mapping to these candidate genes: slc2F2, slc2F11, T306I, L503F, OCTN2-promoter and OCTN2-intron. METHODS: A case-control study was performed in the Spanish population with 295 T1D patients and 508 healthy control subjects. Maximum-likelihood haplotype frequencies were estimated by applying the Expectation-Maximization (EM) algorithm implemented by the Arlequin software. RESULTS: When independently analyzed, one of the tested polymorphisms in the SLC22A4 gene at 1672 showed significant association with T1D in our Spanish cohort. The overall comparison of the inferred haplotypes was significantly different between patients and controls (χ(2 )= 10.43; p = 0.034) with one of the haplotypes showing a protective effect for T1D (rs3792876/rs1050152/rs2631367/rs274559, CCGA: OR = 0.62 (0.41–0.93); p = 0.02). CONCLUSION: The haplotype distribution in the carnitine transporter locus seems to be significantly different between T1D patients and controls; however, additional studies in independent populations would allow to confirm the role of these genes in T1D risk

Defining the Role of the MHC in Autoimmunity: A Review and Pooled Analysis

The major histocompatibility complex (MHC) is one of the most extensively studied regions in the human genome because of the association of variants at this locus with autoimmune, infectious, and inflammatory diseases. However, identification of causal variants within the MHC for the majority of these diseases has remained difficult due to the great variability and extensive linkage disequilibrium (LD) that exists among alleles throughout this locus, coupled with inadequate study design whereby only a limited subset of about 20 from a total of approximately 250 genes have been studied in small cohorts of predominantly European origin. We have performed a review and pooled analysis of the past 30 years of research on the role of the MHC in six genetically complex disease traits – multiple sclerosis (MS), type 1 diabetes (T1D), systemic lupus erythematosus (SLE), ulcerative colitis (UC), Crohn's disease (CD), and rheumatoid arthritis (RA) – in order to consolidate and evaluate the current literature regarding MHC genetics in these common autoimmune and inflammatory diseases. We corroborate established MHC disease associations and identify predisposing variants that previously have not been appreciated. Furthermore, we find a number of interesting commonalities and differences across diseases that implicate both general and disease-specific pathogenetic mechanisms in autoimmunity

Complex haplotypic structure of the central MHC region flanking TNF in a West African population.

TNF polymorphisms have been associated with susceptibility to malaria and other infectious and inflammatory conditions. We investigated a sample of 150 West African chromosomes to determine linkage disequilibrium (LD) between 25 SNP markers located in an 80 kb segment of the MHC Class III region encompassing TNF and eight neighbouring genes. We observed 45 haplotypes, and 22 of them comprise 80% of the sample. The pattern of LD is remarkably patchy, such that many markers show no LD with adjacent markers but high LD with markers that are much further away. We introduce a method of examining the implications of LD data for disease association studies based on sample size considerations: this shows that certain TNF polymorphisms would be likely to yield positive associations if the true disease allele resided in LTA or BAT1. We conclude that detailed marker maps are needed to resolve the causal origin of disease associations observed at the TNF locus

ISSLS Prize in clinical science 2018: Longitudinal analysis of inflammatory, psychological, and sleep-related factors following an acute low back pain episode-the good, the bad, and the ugly

Prospective longitudinal study.To determine whether systemic cytokines and C-reactive protein (CRP) during an acute episode of low back pain (LBP) differ between individuals who did and did not recover by 6\ua0months and to identify sub-groups based on patterns of inflammatory, psychological, and sleep features associated with recovery/non-recovery. Systemic inflammation is observed in chronic LBP and may contribute to the transition from acute to persistent LBP. Longitudinal studies are required to determine whether changes present early or develop over time. Psychological and/or sleep-related factors may be related.Individuals within 2\ua0weeks of onset of acute LBP (N\ua0=\ua0109) and pain-free controls (N\ua0=\ua055) provided blood for assessment of CRP, tumor necrosis factor (TNF), interleukin-6 (IL-6) and interleukin-1β, and completed questionnaires related to pain, disability, sleep, and psychological status. LBP participants repeated measurements at 6 months. Biomarkers were compared between LBP and control participants at baseline, and in longitudinal (baseline/6 months) analysis, between unrecovered (≥pain and disability), partially recovered (reduced pain and/or disability) and recovered (no pain and disability) participants at 6 months. We assessed baseline patterns of inflammatory, psychological, sleep, and pain data using hierarchical clustering and related the clusters to recovery (% change in pain) at 6 months.CRP was higher in acute LBP than controls at baseline. In LBP, baseline CRP was higher in the recovered than non-recovered groups. Conversely, TNF was higher at both time-points in the non-recovered than recovered groups. Two sub-groups were identified that associated with more ("inflammatory/poor sleep") or less ("high TNF/depression") recovery.This is the first evidence of a relationship between an "acute-phase" systemic inflammatory response and recovery at 6 months. High inflammation (CRP/IL-6) was associated with good recovery, but specific elevation of TNF, along with depressive symptoms, was associated with bad recovery. Depression and TNF may have a two-way relationship. These slides can be retrieved under Electronic Supplementary Material

Photosynthesis in poor nutrient soils, in compacted soils, and under drought

Plants require the uptake of nutrients (in most cases via roots) and their incorporation into plant organs for growth. In non-woody species, 83% of fresh weight is water, 7% is carbon, 5% is oxygen, with the remaining 5% including hydrogen and such nutrients. In natural ecosystems, availability of nutrients in soils is heterogeneous, and many species often adapt their growth to the amount of nutrients that roots can take up by exploring the available soil volume. In agricultural areas, the lack of some nutrients is frequent. In both cases, plants must also face periods of drought and soil compaction. These environmental stresses are therefore not uncommon in natural ecosystems and crops, and the stressed plants often experience a decrease in photosynthetic CO2 fixation. In this chapter, we review changes observed in photosynthesis in response to nutrient deficiencies, soil compaction, and drought. The current knowledge on photosynthesis in carnivorous plants, as a special case of plant species growing in nutrient poor soils, is also included. Pigment limitations (chlorosis and/or necrosis), stomatal limitations, ultrastructural effects and mesophyll conductance limitations, photochemistry (primary reactions), carboxylation and Calvin-cycle reactions, and carbohydrate metabolism and transport will be discussed. With regard to nutrients, we have focused on the most common nutrition-related stresses in plants, the deficiencies of macro- (nitrogen, phosphorous, and potassium) and micronutrients (iron, manganese, copper, and zinc). Other nutrient deficiencies (or toxicities, both in the cases of essential nutrient excess or heavy metals) are not reviewed here. For other nutrient deficiencies and toxicities, and the role of the above-mentioned, and other nutrients (such as calcium and magnesium) in gas exchange, and as intracellular signal transducers, enzyme activators, and structure and function stabilizers of biological membranes, readers are referred to papers published elsewhere (Marschner H, Mineral nutrition of higher plants. Academic, London, 1995; Cakmak I, Kirkby EA, Physiol Plant 133:692–704, 2008; Morales F, Warren CR, Photosynthetic responses to nutrient deprivation and toxicities. In: Flexas J, Loreto F, Medrano H (eds) Terrestrial photosynthesis in a changing environment: a molecular, physiological and ecological approach. Cambridge University Press, Cambridge, pp 312–330, 2012; Hochmal AK, Schulze S, Trompelt K, Hippler M, Biochim Biophys Acta 1847:993–1003, 2015).This study was supported by the Spanish Ministry of Economy and Competitiveness (MINECO; projects AGL2012-31988, AGL2013-42175-R, AGL2016-75226-R, and AGL2016-79868-R, co-financed with FEDER), the Aragón Government (Group A03), grant LO1204 (Sustainable development of research in the Centre of the Region Haná) from the National Program of Sustainability I, and by the Czech Science Foundation Agency (project 16-07366Y). FM wishes to thank JC Martínez for his help with some periodic bibliographic searches.Peer reviewe