The integrated anatomy practical paper: a robust assessment method for anatomy education today

Assessing anatomy in a way that tests higher cognitive domains and clinical application is not always straightforward. The old "spotter" examination has been criticized for only testing low level "identify" knowledge, whereas other assessment modalities such as multiple choice questions do not reflect the three dimensional and application nature of clinical anatomy. Medical curricula are frequently integrated and subject specific examinations do not reflect the case based, spiral, integrative nature of the curricula. The integrated anatomy practical paper (IAPP) is a hybrid of the old "spotter" and an objective structured clinical examination but it demonstrates how higher levels of taxonomy can be assessed, together with clinical features and integrates well with other disciplines. Importantly, the IAPP has shown to be reliable and practical to administer. Data gathered from the Bachelor of Medicine five-year program over two academic years for four IAPP examinations, each being 40 minutes with (K?=?60 items) based on 440 students revealed consistently strong reliability coefficients (Cronbach alpha) of up to 0.923. Applying Blooms taxonomy to questions has shown a marked shift resulting in an increase in the complexity level being tested; between 2009 and 2013 a reduction of 26% in the number of low level "remember knowledge" domain questions was noted with up to an increase of 15% in "understanding" domain and 12% increase in the "applying" knowledge domain. Our findings highlight that it is possible to test, based in a laboratory, anatomy knowledge and application that is integrated and fit for practice. Anat Sci Educ. © 2014 American Association of Anatomists

Vitamin D reduces TGFβ₁-mediated phosphorylation of SMAD2.

<p>Representative Western blot images of HCF-av treated for 24 hours (A) and 48 hours (B) with TGFβ₁ in the presence and absence of 1,25(OH)₂D₃, which demonstrate a reduction in pSMAD2 with active vitamin D treatment. Densitometry of Western blot data shows significantly increased phosphorylation of SMAD2 at both 24 hours (C) and 48 hours (D) following treatment with TGFβ₁, which is significantly reduced with co-treatment with 1,25(OH)₂D₃. All data represent mean ± SEM. p-values were calculated using one way analysis of variance with a Bonferroni multiple comparison test. ***p<0.001, ****p<0.0001.</p

Study Cohort Demographic Information.

<p>Data expressed as mean (± SD) or n (%), p-values calculated using one-way analysis of variance for continuous variables and chi-square test for categorical variables.</p><p>Study Cohort Demographic Information.</p

Circulating levels of vitamin D are positively associated with myocardial fibrosis in heart failure patients.

<p>Collagen area as a fraction of total myocardial tissue area was significantly higher in patients with vitamin D deficiency as compared with vitamin D insufficient or sufficient patients. There was no difference in collagen area in patients without vitamin D deficiency. All data represent mean ± SEM. p-values were calculated using one way analysis of variance with a Bonferroni multiple comparison test. *p<0.05.</p

Vitamin D inhibits TGFβ₁-mediated myofibroblast contraction.

<p>Representative images of 48 hour timepoint from collagen gel contraction assay are shown in A-D. A) Untreated HCF-av; B) HCF-av treated with TGFβ₁; C) HCF-av treated with 1,25(OH)₂D₃; D) HCF-av treated with TGFβ₁ + 1,25(OH)₂D₃. A time course of gel contraction over 96 hours is shown in (E). Active vitamin D treatment significantly inhibited TGFβ₁-induced gel contraction at all time points post-treatment. All data points represent mean ± SEM. p-values calculated using two way repeated measures analysis of variance with Bonferroni multiple comparison test. *p<0.05, ***p<0.001. F and G) Confocal images of HCF-av at 48 hours following treatment. Stress fibers were stained with phalloidin. HCF-av treated with TGFβ₁(F) demonstrate increased presence of clearly defined stress fibers (white) as compared with cells treated with TGFβ₁ + 1,25(OH)₂D₃ (G). Scale bar: 70μm.</p

Vitamin D does not inhibit TGFβ₁-mediated cellular proliferation.

<p>Evaluation of proliferation rates in our treatment groups revealed no significant change in cellular proliferation between cells treated with active vitamin D and TGFβ₁ or TGFβ₁ alone. Proliferation was increased in the presence of TGFβ₁. All data represent mean ± SEM. p-values were calculated using one way analysis of variance with a Bonferroni multiple comparison test.</p

Vitamin D treatment inhibits expression of TGFβ₁-mediated α-smooth muscle actin.

<p>A) Representative Western blot of cells 48 hours after treatment. Expression of the discoidin domain receptor 2 (DDR2) is present in human primary adult ventricular cardiac fibroblasts (HCF-av). CYP24 expression was upregulated 48 hours after treatment with 1,25(OH)₂D₃±TGFβ₁. Expression of α-smooth muscle actin (αSMA) was upregulated 48 hours after treatment with TGFβ₁, and significantly reduced with 1,25(OH)₂D₃ co-treatment. B) Densitometry data generated from Western blots of HCF-av cells 48 hours after treatment with TGFβ₁±1,25(OH)₂D₃, and normalized to GAPDH. All data represent mean±SEM. p-values were calculated using one way analysis of variance with a Bonferroni multiple comparison test. *p<0.05, ***</p

Additional file 4: of Effect of short-term oral prednisone therapy on blood gene expression: a randomised controlled clinical trial

Figure S1 KEGG pathway map of NK cell mediated cytotoxicity. Rectangle and circle represent gene product including RNA and a compound, respectively. The blue boxes are hyperlinked to KEGG orthology entries and the red boxes represent genes which were significantly enriched in this pathway. Among genes which were responsive to short-term prednisone at a FDR < 0.05, KLRD1, PRF1, GZMB and NCR1 were significantly enriched in the pathway of NK cell mediated cytotoxicity at a FDR < 0.05. (PPTX 92 kb

Additional file 3: of Effect of short-term oral prednisone therapy on blood gene expression: a randomised controlled clinical trial

Table S3. Fifty-one genes differentially expressed by prednisone at a FDR < 0.05 in study 1. (DOCX 18 kb

Additional file 5: of Effect of short-term oral prednisone therapy on blood gene expression: a randomised controlled clinical trial

Table S4. Genes replicated in the Rapid Transition Program (RTP) Cohort at a FDR < 0.05. (DOCX 16 kb