Moving from long case to scenario-based clinical examination: Proposals for making it feasible.

INTRODUCTION: Our faculty used one long case (LC) and three short cases for the clinical component of the final professional examinations. During the COVID-19 pandemic, the LC had to be replaced with scenario-based clinical examination (SBCE) due to the impracticability of using recently hospitalised patients. While keeping the short case component as usual, the LC had to be replaced with SBCE in 2020 for the first time at a short notice. To evaluate the positive and negative aspects of SBCE and LC to determine the feasibility of replacing LC with SBCE in future examinations. MATERIALS AND METHODS: We compared the LC scores of three previous years with those of the SBCE and studied the feedback of the three stakeholders: students, examiners, and simulated patients (SPs), regarding their experience with SBCE and the suitability of SBCE as an alternative for LC in future examinations. RESULTS: The SBCE scores were higher than those of the LC. Most of the examiners and students were not in favour of SBCE replacing LC, as such. The SPs were more positive about the proposition. The comments of the three stakeholders brought out the plus and minus points of LC and SBCE, which prompted our proposals to make SBCE more practical for future examinations. CONCLUSION: Having analysed the feedback of the stakeholders, and the positive and negative aspects of LC and SBCE, it was evident that SBCE needed improvements. We have proposed eight modifications to SBCE to make it a viable alternative for LC.

Relationship between apoptotic markers (Bax and Bcl-2) and biochemical markers in type 2 diabetes mellitus.

INTRODUCTION: Bax is essential for apoptosis in normal cells. However, overexpression of Bcl-2 enhances cell survival by suppressing apoptosis in cells subjected to apoptosis-inducing stimuli. The aim of this study was to examine the expression of apoptotic (Bax and Bcl-2) and biochemical markers in type 2 diabetics mellitus. METHODS: A test group comprising 41 type 2 diabetes mellitus patients and a control group comprising 36 non-diabetic patients were enrolled in this study. Skin biopsy tissue samples were stained immunohistochemically for Bcl-2 and Bax expressions. Fasting plasma glucose (FPG), triglycerides, total cholesterol (TC), high-density lipoprotein cholesterol (HDLC) and glycosylated haemoglobin A1c (A1C) were analysed. Low-density lipoprotein cholesterol (LDLC) was calculated. RESULTS: Bcl-2 expression was significantly higher (p-value is less than 0.001) in the control group. Bax expression was significantly higher (p-value is 0.018) in the diabetic group. Positive Bcl-2 expression was observed in 18 of 36 (50 percent) controls. Positive Bcl-2 expression was found in 5 of 41 (12.2 percent) diabetics. There was a significant difference (p-value is less than 0.001) between the two groups for mean FPG, HDLC and A1C. There was no significant difference for TC, LDLC and triglycerides between the two groups. Positive Bax expression was found in 11 of 35 (31.4 percent) controls. The odds of developing Bcl-2 among non-diabetics were 12.67 times compared to diabetics (p-value is less than 0.001). CONCLUSION: Prolonged hyperglycaemia induces apoptosis in the endothelial cells of diabetic ulcers, which aggravates microvasculopathy and delays tissue healing and regeneration.

Dominant action of mutated erythropoietin receptors on differentiation in vitro and erythroleukemia development in vivo.

J2E cells produce rapid, fatal erythroleukemias in vivo but still respond to erythropoietin (epo) in vitro by differentiating, proliferating and remaining viable in the absence of serum. Mutant epo receptors were introduced into these cells to determine whether they could influence the different biological responses to epo in vitro and the development of erythroleukemias. Three mutant receptors were used as cytoplasmic truncation mutants Delta257 and Delta321 (above box 1 and below box 2 respectively), and the cytoplasmic point mutant W282R (defective for JAK2 activation). Strikingly, the Delta321 mutation produced a hyper-sensitive response in vitro to epo-induced differentiation and viability, but not to proliferation. In contrast with the Delta321 receptor, the Delta257 and W282R mutants inhibited all biological responses to epo due to impaired JAK2 phosphorylation. Significantly, erythroleukemias took almost twice as long to develop with cells containing the W282R mutation, indicating that JAK2 plays an important role in the emergence of these leukemias. These data demonstrate that mutant epo receptors dominantly altered responses of J2E cells to epo in culture and the development of erythroleukemias. Oncogene (2000) 19, 953 - 960.