Development and Initial Validation of an Admission Test for Bachelor Psychology Studies

Extensive evidence clearly endorses the use of standardized reasoning ability tests and subject-specific knowledge tests as valid and useful tools for admission-restricted study programs. Yet, tests are still rarely applied for university admission in Germany. Instead, current admission practices are predominantly based on grade point average (GPA) achieved in high school. In the present study, we report the development and validation of a test battery for admission into bachelor’s degree programs in psychology for German universities. Its compilation is driven by evidence from international validity generalization, consensual models of cognitive abilities, and a taxonomy of the B.Sc. psychology degree in Germany. It consists of three subtests for reasoning ability, two tests that tap relevant declarative knowledge, and two psychology-specific text comprehension tests. N = 371 freshmen from five German universities completed the tests and university GPA was retrieved 2.5 years later. We use confirmatory factor analyses and structural equation modeling to investigate the construct and criterion validity of the test battery. The results indicate that individual tests, as well as the test battery, meet psychometric requirements. As expected, the test battery predicts university GPA substantially and incrementally beyond high school GPA. The results illustrate the substantial added value that standardized achievement tests provide in university admissions

Protein expression is increased by a class III AU-rich element and tethered CUG-BP1.

International audienceIn mammalian somatic cells, the post-transcriptional control of cytokine or proto-oncogene expression is often achieved by factors binding to sequence elements in the 3' untranslated region (3'UTR). The most studied are the AU-rich elements (ARE) that have been divided into three classes. Here, we show that in mammalian cells, the presence of the class III c-jun ARE in the 3'UTR of a reporter mRNA enhanced reporter protein expression. In contrast, the presence of a class II ARE in the 3'UTR decreased reporter protein expression. CUG-BP1/CELF1 is able to bind c-jun ARE. Protein expression was enhanced similarly to what was observed for c-jun ARE when the reporter mRNA contained a synthetic CUG-BP1/CELF1-binding site, or when this protein was tethered to the 3'UTR of a reporter mRNA. These results reveal an unexpected complexity of ARE-mediated post-transcriptional regulations, and indicate a function for CUG-BP1/CELF1 in class III ARE directed regulations

Psychological models of development of idiopathic environmental intolerances: Evidence from longitudinal population-based data

The origin of idiopathic environmental intolerances (IEIs) is an open question. According to the psychological approaches, various top-down factors play a dominant role in the development of IEIs. The general psychopathology model assumes a propensity towards mental ill-health (negative affectivity) increases the probability of developing IEIs. The attribution model emphasizes the importance of mistaken attribution of experienced somatic symptoms; thus, more symptoms should lead to more IEIs. Finally, the nocebo model highlights the role of expectations in the development of IEIs. In this case, worries about the harmful effects of environmental factors are assumed to evoke IEIs. We estimated cross-lagged panel models with latent variables based on longitudinal data obtained at two time points (six years apart) from a large near-representative community sample to test the hypothesized associations. Indicators of chemical intolerance, electromagnetic hypersensitivity, and sound sensitivity fit well under a common latent factor of IEIs. This factor, in turn, showed considerable temporal stability. However, whereas a positive association was found between IEIs and increased somatic symptoms and modern health worries six years later, the changes therein could not be predicted as hypothesized by the three psychological models. We discuss the implications of these results, as well as methodological aspects in the measurement and prediction of change in IEIs

Integrated clinical and omics approach to rare diseases : Novel genes and oligogenic inheritance in holoprosencephaly

Holoprosencephaly is a pathology of forebrain development characterized by high phenotypic heterogeneity. The disease presents with various clinical manifestations at the cerebral or facial levels. Several genes have been implicated in holoprosencephaly but its genetic basis remains unclear: different transmission patterns have been described including autosomal dominant, recessive and digenic inheritance. Conventional molecular testing approaches result in a very low diagnostic yield and most cases remain unsolved. In our study, we address the possibility that genetically unsolved cases of holoprosencephaly present an oligogenic origin and result from combined inherited mutations in several genes. Twenty-six unrelated families, for whom no genetic cause of holoprosencephaly could be identified in clinical settings [whole exome sequencing and comparative genomic hybridization (CGH)-array analyses], were reanalysed under the hypothesis of oligogenic inheritance. Standard variant analysis was improved with a gene prioritization strategy based on clinical ontologies and gene co-expression networks. Clinical phenotyping and exploration of cross-species similarities were further performed on a family-by-family basis. Statistical validation was performed on 248 ancestrally similar control trios provided by the Genome of the Netherlands project and on 574 ancestrally matched controls provided by the French Exome Project. Variants of clinical interest were identified in 180 genes significantly associated with key pathways of forebrain development including sonic hedgehog (SHH) and primary cilia. Oligogenic events were observed in 10 families and involved both known and novel holoprosencephaly genes including recurrently mutated FAT1, NDST1, COL2A1 and SCUBE2. The incidence of oligogenic combinations was significantly higher in holoprosencephaly patients compared to two control populations (P < 10 -9). We also show that depending on the affected genes, patients present with particular clinical features. This study reports novel disease genes and supports oligogenicity as clinically relevant model in holoprosencephaly. It also highlights key roles of SHH signalling and primary cilia in forebrain development. We hypothesize that distinction between different clinical manifestations of holoprosencephaly lies in the degree of overall functional impact on SHH signalling. Finally, we underline that integrating clinical phenotyping in genetic studies is a powerful tool to specify the clinical relevance of certain mutations

High Risk of Anal and Rectal Cancer in Patients With Anal and/or Perianal Crohn’s Disease

International audienceBackground & AimsLittle is known about the magnitude of the risk of anal and rectal cancer in patients with anal and/or perineal Crohn’s disease. We aimed to assess the risk of anal and rectal cancer in patients with Crohn’s perianal disease followed up in the Cancers Et Surrisque Associé aux Maladies Inflammatoires Intestinales En France (CESAME) cohort.MethodsWe collected data from 19,486 patients with inflammatory bowel disease (IBD) enrolled in the observational CESAME study in France, from May 2004 through June 2005; 14.9% of participants had past or current anal and/or perianal Crohn’s disease. Subjects were followed up for a median time of 35 months (interquartile range, 29–40 mo). To identify risk factors for anal cancer in the total CESAME population, we performed a case-control study in which participants were matched for age and sex.ResultsAmong the total IBD population, 8 patients developed anal cancer and 14 patients developed rectal cancer. In the subgroup of 2911 patients with past or current anal and/or perianal Crohn’s lesions at cohort entry, 2 developed anal squamous-cell carcinoma, 3 developed perianal fistula–related adenocarcinoma, and 6 developed rectal cancer. The corresponding incidence rates were 0.26 per 1000 patient-years for anal squamous-cell carcinoma, 0.38 per 1000 patient-years for perianal fistula–related adenocarcinoma, and 0.77 per 1000 patient-years for rectal cancer. Among the 16,575 patients with ulcerative colitis or Crohn’s disease without anal or perianal lesions, the incidence rate of anal cancer was 0.08 per 1000 patient-years and of rectal cancer was 0.21 per 1000 patient-years. Among factors tested by univariate conditional regression (IBD subtype, disease duration, exposure to immune-suppressive therapy, presence of past or current anal and/or perianal lesions), the presence of past or current anal and/or perianal lesions at cohort entry was the only factor significantly associated with development of anal cancer (odds ratio, 11.2; 95% CI, 1.18-551.51; P = .03).ConclusionsIn an analysis of data from the CESAME cohort in France, patients with anal and/or perianal Crohn’s disease have a high risk of anal cancer, including perianal fistula–related cancer, and a high risk of rectal cancer