BackgroundE-learning resources (e-resources) have been widely used to facilitate self-directed learning among medical students. The Department of Biochemistry at Christian Medical College (CMC), Vellore, India, has made available e-resources to first-year medical students to supplement conventional lecture-based teaching in the subject. This study was designed to assess students’ perceptions of the impact of these e-resources on various aspects of their learning in biochemistry.MethodsSixty first-year medical students were the subjects of this study. At the end of the one-year course in biochemistry, the students were administered a questionnaire that asked them to assess the impact of the e-resources on various aspects of their learning in biochemistry.ResultsNinety-eight percent of students had used the e-resources provided to varying extents. Most of them found the e-resources provided useful and of a high quality. The majority of them used these resources to prepare for periodic formative and final summative assessments in the course. The use of these resources increased steadily as the academic year progressed. Students said that the extent to which they understood the subject (83%) and their ability to answer questions in assessments (86%) had improved as a result of using these resources. They also said that they found biochemistry interesting (73%) and felt motivated to study the subject (59%).ConclusionsWe found that first-year medical students extensively used the e-resources in biochemistry that were provided. They perceived that these resources had made a positive impact on various aspects of their learning in biochemistry. We conclude that e-resources are a useful supplement to conventional lecture-based teaching in the medical curriculum.

SummaryATOH8 has previously been shown to be an iron-regulated transcription factor, however its role in iron metabolism is not known. ATOH8 expression in HEK293 cells resulted in increased endogenous HAMP mRNA levels as well as HAMP promoter activity. Mutation of the E-box or SMAD response elements within the HAMP promoter significantly reduced the effects of ATOH8, indicating that ATOH8 activates HAMP transcription directly as well as through bone morphogenic protein (BMP) signalling. In support of the former, Chromatin immunoprecipitation assays provided evidence that ATOH8 binds to E-box regions within the HAMP promoter while the latter was supported by the finding that ATOH8 expression in HEK293 cells led to increased phosphorylated SMAD1,5,8 levels. Liver Atoh8 levels were reduced in mice under conditions associated with increased erythropoietic activity such as hypoxia, haemolytic anaemia, hypotransferrinaemia and erythropoietin treatment and increased by inhibitors of erythropoiesis. Hepatic Atoh8mRNA levels increased in mice treated with holo transferrin, suggesting that Atoh8 responds to changes in plasma iron. ATOH8 is therefore a novel transcriptional regulator of HAMP, which is responsive to changes in plasma iron and erythroid activity and could explain how changes in erythroid activity lead to regulation of HAMP.

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Hepatic Fe overload has often been reported in patients with advanced alcoholic liver disease. However, it is not known clearly whether it is the effect of alcohol that is responsible for such overload. To address this lacuna, a time-course study was carried out in mice in order to determine the effect of alcohol on Fe homoeostasis. Male Swiss albino mice were pair-fed Lieber-DeCarli alcohol diet (20 % of total energy provided as alcohol) for 2, 4, 8 or 12 weeks. Expression levels of duodenal and hepatic Fe-related proteins were determined by quantitative PCR and Western blotting, as were Fe levels and parameters of oxidative stress in the liver. Alcohol induced cytochrome P4502E1 and oxidative stress in the liver. Hepatic Fe levels and ferritin protein expression dropped to significantly lower levels after 12 weeks of alcohol feeding, with no significant effects at earlier time points. This was associated, at 12 weeks, with significantly decreased liver hepcidin expression and serum hepcidin levels. Protein expressions of duodenal ferroportin (at 8 and 12 weeks) and divalent metal transporter 1 (at 8 weeks) were increased. Serum Fe levels rose progressively to significantly higher levels at 12 weeks. Histopathological examination of the liver showed mild steatosis, but no stainable Fe in mice fed alcohol for up to 12 weeks. In summary, alcohol ingestion by mice in this study affected several Fe-related parameters, but produced no hepatic Fe accumulation. On the contrary, alcohol-induced decreases in hepatic Fe levels were seen and may contribute to alcohol-induced suppression of hepcidin.