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Breast cancer is the most common cancer in women around the world, and novel prognosis strategies is needed to control more accurate and effective of this malignant disease. Among the latest prognostic markers is E-cadherin, which mediates cell-cell adhesion by associating with catenins. Loss of E-cadherin gene (CDH1) function by genetic or epigenetic alteration leads to tumorigenesis. The aim of our study was to investigate E-cadherin gene promoter methylation in breast cancer, and its correlation with E-cadherin protein expression. Fifty primary breast cancers tissue with ductal type and 50 normal breast sample from the same patients that was located adjacent to tumor region as controls were provided by Imam Reza-based referral and teaching hospital affiliated to Tabriz University of Medical Sciences, Tabriz, Iran. CDH1 promoter region CpG sites methylation and E-cadherin protein expression were determined by bisulfite-specific polymerase chain reaction and Western blot analysis, and the resulting products were sequenced on an ABI automated sequencer for firm conclusion. CDH1 hypermethylation in breast tumor specimen (ductal type) was observed in 94 % (47 of 50) comparing with normal samples methylation, and the significant difference was (p = 0.000). Protein expression in tumor samples tends to diminish with the CDH1 promoter region methylation. In the group of 50 ductal carcinomas cases, most of the cases showing CDH1 hypermethylation correlated inversely with the reduced levels of expression of E-cadherin proteins (95 % of full-methylated tumor samples had no protein expression, and 4.5 % of them had weak expression levels). Possible association was observed between CDH1 methylation and its protein expression (p = 0.000). The results of methylation analysis in promoter region in ten CpG sites (863, 865, 873, 879, 887, 892, 901, 918, 920, and 940) suggested that abnormal CDH1 methylation occurs in high frequencies in ductal breast tumors probably sounds the process of carcinogenesis progression.

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Background: This study aimed to compare the effects of preoperative administration of midazolam and dexmedetomidine on cognitive dysfunction prevention after cataract surgery. Materials and Methods: This research was a double-blind controlled clinical trial. In this study, 150 candidates for cataract surgery under general anesthesia, over 65 years, and similar to American Society of Anesthesiologists I and II characteristics were selected as the sample and randomly assigned to three groups. Participants of these three groups were treated with 0.1 mg/kg of midazolam, 1 μg/kg of dexmedetomidine, and the same volume of normal saline (control), respectively. Hemodynamic parameters and cognitive dysfunction score of the participants were measured using the Mini-Mental State Examination (MMSE) before the surgery, 24 h and 1 week after the surgery. Results: An evaluation of hemodynamic parameters before anesthesia up to 24 h after the surgery showed no significant difference between the midazolam, dexmedetomidine, and control groups in terms of systolic and diastolic blood pressure, heart rate, and blood oxygen saturation ( P > 0.05). In addition, there was no statistically significant difference between the midazolam and dexmedetomidine groups in the MMSE score before the surgery and 24 h and 1 week after that ( P > 0.05). However, there was a significant difference between these two groups and control ( P < 0.05). Conclusion: There was no significant difference between midazolam and dexmedetomidine in reducing postoperative cognitive dysfunction (POCD). However, there is a significant difference between these two groups and control. Hence, either midazolam or dexmedetomidine can be prescribed to reduce POCD in cataract surgeries.

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