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Misalignments in teaching pedagogies between secondary schools and tertiary institutions have exacerbated educational disparities among students from different backgrounds. Given the variation in students' educational background and competencies, there was a need to develop an Anatomy and Physiology (AP) Foundational Knowledge Assessment to establish the levels of preparedness of first-year medical students. Previous work that focused on the development of the assessment showed it to be effective in measuring students' foundational knowledge in human anatomy and physiology. The aim of this study was to assess the validity of the AP Foundational Knowledge Assessment in determining students' prior knowledge and predicting academic performance of first-year students in their anatomy and physiology studies. Three hundred seventy first-year students, across two cohort years, 2017 and 2018, completed the AP Foundational Knowledge Assessment. Data were analyzed through descriptive statistics, analysis of variance, and Pearson's correlation. Results show that for both cohorts ∼30% of students scored ≤55% and were potentially at risk of performing poorly in their anatomy and physiology studies. Pearson's correlation showed a significant relationship between students' performance on the foundational knowledge assessment and their anatomy and physiology assessments. For both cohorts,10% of students identified by the AP Foundational Knowledge Assessment were at risk of either failing the course, entering an extended degree program, or being excluded from the program. Results indicate that the assessment is a good predictor for differentiating medical students' performance in first-year anatomy and physiology.

International audience; The stress-activated p38α MAP Kinase is an integral and critical component of the UV-induced inflammatory response. Despite the advances in recent years in the development of p38 kinase inhibitors, validation of these compounds in the diseased models remains limited. Based on the pharmacological profile of p38α inhibitor lead compound, SB203580, we synthesized a series of pyrrole-derivatives. Using UV-irradiated human skin punch-biopsies and cell cultures, we identified and validated the inhibitory activity of the derivatives by quantitatively measuring their effect on the expression of p38α target genes using real-time PCR. This approach not only identified pyrrole-2 as a unique derivative of this series that specifically inhibited the UV-activated p38α kinase, but also documented the skin permeation, bioavailability and reversible properties of this derivative in a 3D structure. The successful skin permeation of pyrrole-2 and its impact on AREG, COX-2 and MMP-9 gene expression demonstrates its potential use in modulating inflammatory processes in the skin. This study underscored the importance of using adapted biological models to identify accurate bioactive compounds.

Decay accelerating factor (DAF) expression at the muscle endplate is an important defence against complement-mediated damage in myasthenia gravis. Previously we implicated the c.-198C > G DAF polymorphism with the development of treatment-resistant myasthenia-associated ophthalmoplegia by showing that the C > G DAF polymorphism prevented lipopolysaccharide-induced upregulation of lymphoblast DAF. We postulated that drugs used in myasthenia gravis may increase the susceptibility of extraocular muscles to complement-mediated damage and studied their effects on endogenous DAF using patient-derived lymphoblasts as well as mouse myotubes. We show that prednisone repressed C > G DAF expression in lymphoblasts and increased their susceptibility to cytotoxicity. Methotrexate, but not azathioprine or cyclosporine, increased DAF in C > G lymphoblasts. In mouse myotubes expressing wild-type Daf, prednisone also repressed Daf expression. Although cyclosporine, azathioprine, and methotrexate increased muscle Daf levels when used alone, upon co-treatment with prednisone only azathioprine maintained myotube Daf levels close to basal. Therefore, prednisone negatively influences DAF expression in C > G lymphoblasts and in myotubes expressing wild-type Daf. We speculate that myasthenic individuals at risk of developing the ophthalmoplegic complication, such as those with C > G DAF, may have inadequate endogenous levels of complement regulatory protein protection in their extraocular muscle in response to prednisone, increasing their susceptibility to complement-mediated damage. 2014 Elsevier B.V. All rights reserved.

The T-box gene family encodes highly conserved transcription factors that play important roles in embryonic development and have been implicated in carcinogenesis. One member of the family, Tbx2, is generally regarded as a transcriptional repressor but appears to be capable of functioning as an activator depending on the cellular context. This study shows that Tbx2 is expressed in normal human fibroblasts but is drastically reduced in several transformed fibroblast cell lines. This pattern of Tbx2 expression correlated with that observed for the human alpha2(1) collagen gene (COL1A2). Interestingly, stable expression of transfected Tbx2 in transformed fibroblast cell lines further reduces expression of the human endogenous COL1A2 gene. This ability of Tbx2 to repress the human COL1A2 gene was confirmed in luciferase reporter assays and shown to be independent of the consensus T-box binding element.

Tbx2 is a member of the T-box family of transcription factors that are crucial in embryonic development. Recent studies suggest that T-box factors may also play a role in controlling cell cycle progression and in the genesis of cancer. Tbx2 has been implicated in several developmental processes such as coordinating cell fate, patterning and morphogenesis of a wide range of tissues and organs including limbs, kidneys, lungs, mammary glands, heart, and craniofacial structures. Importantly, Tbx2 is overexpressed in several cancers including melanoma, small cell lung carcinoma, breast, pancreatic, liver, and bladder cancers and can suppress senescence, a cellular process, which serves as a barrier to cancer development. This review presents a state of the art overview of the role and regulation of Tbx2 in early embryonic development and in cancer. © 2009 IUBMB IUBMB Life, 62(2): 92–102, 2010