Background:Coronary artery disease is mainly caused by atherosclerosis and its complications. Platelets and their activity have an important role in initiation of atherosclerotic lesions and coronary thrombus formation. Larger platelets are enzymatically and metabolically more active and have a higher potential thrombotic ability as compared with smaller platelets.Aims:To study the changes in platelet volume indices and platelet count in acute myocardial infarction, stable coronary artery disease and compare them with controls to assess their usefulness in predicting coronary events.Materials and Methods:This was a comparative study of 128 subjects; 39 patients with acute myocardial infarction (AMI), 24 patients with stable coronary artery disease (SCAD) and 65 controls. Venous sample were drawn from AMI subjects on admission (within 4 hours of chest pain) and collected in standardized EDTA sample tubes. Platelet count and volume indices were assayed within 30 minutes of blood collection, using Sysmex KX21-N autoanalyzer. Venous samples were also drawn from SCAD on who were admitted for angiography and subject attending routine checkups.Results:The mean platelet volume was significantly higher in patients with AMI (9.65 ± 0.96) as compared to SCAD (9.37 ± 0.88) and controls (9.21 ± 0.58). The best cut-off values for MPV when predicting AMI and SCAD in patients were 9.25 fl (sensitivity 56.4%; specificity 45.9%) and 9.15 fl (sensitivity 54.2%; specificity 42.23%), respectively.Conclusions:Measurements of MPV may be of some benefit in detecting those patients at higher risk for an AMI and CAD.

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Background: Triple Negative Breast Cancer (TNBC) commonly displays Epidermal growth factor receptor (EGFR). Effective EGFR degradation results in suppression of tumor in various models. Studies have addressed the relevance of this strategy in the treatment of TNBC. In the present study, we examined the effect of 17 β-estradiol on EGFR expression in MDA-MB-231 (TNBC) cell line and assessed whether 17 β-estradiol degrades EGFR by ubiquitination pathway. Objectives: To treat MDA-MB-231 cell lines with Cycloheximide with or without 17β-estrdiol to observe whether 17β-estradiol leads to EGFR degradation. To treat with MG-132 to assess whether degradation occurs through ubiquitination pathway. Methods: MDA-MB-231 cells were treated with 17β-estradiol (E2) and EGFR expression was studied by western blotting at different intervals by using Cycloheximide chase. To assess the ubiquitination pathway of degradation of EGFR in MDA-MB-231 cell line, MG-132 was used. Results: EGFR expression was reduced with β-estradiol treatment in MDA-MB-231 cell line with Cycloheximide chase. Upon Treatment with MG-132 and E2, EGFR expression did not reduce, suggesting that Estrogen degrades EGFR by ubiquitination pathway. Conclusion: Estrogen degrades EGFR in MDA-MB-231 cells and this degradation occurs by ubiquitination.

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