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Background and Objective: Considering the role of the hippocampus in memory, this study was done to evaluate the effect of 3-4,methylenedioxymethamphetamine on CA1 hippocampal neurons in male rats. Materials and Methods: In this experimental study 18 sprague dawley male rats (200-250g) were randomly allocated into three groups as follow: control (intact), control sham and experimental groups. Sham and experimental groups were received normal salin (1 cc) and MDMA10mg/kg IP for 7 days, respectively. Following transcardial perfusion by paraformaldehid 4%, structure and ultrastructure of right CA1 hippocampus were assessed by crysel violet staining and electronic microscope. Data were analyzed using SPSS-16, ANOVA and Tukey tests. Results: There was no significant difference between control (mean=210±40.38) and sham groups (mean=199±38.7) in neuron density. Neuron number decreased significantly in experimental group (mean=98±25.4) in compare to control and sham groups (P<0.001). There was no ultrastructural abnormality in control and sham groups. Finally, ultrastructural changes with apoptosis characterized by mitochondrial cristae reduction, distribution of nuclear chromatin and loss of cytoplasmic organelles in MDMA groups. Conclusion: This study shows that MDMA administration can stimulate the cell death with apoptotic pattern in hippocampus.

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Background and Objective: Breast cancer is one of the most common diseases worldwide and the second leading cause of death among women. Immune responses play a critical role in inhibiting the onset and progression of this disease. Given the important role of T lymphocytes in identifying and preventing the spread of breast cancer tumor cells, this study was conducted to simultaneously evaluate the regulatory molecules CXC chemokine receptor 3 (CXCR3), programmed cell death protein 1 (PD-1), natural killer group 2 member D (NKG2D), and transforming growth factor beta 1 receptor II (TGF-βRII) on T lymphocytes of newly diagnosed breast cancer patients.
Methods: This case-control study was performed on 26 newly diagnosed breast cancer patients (mean age = 46.2±9.5 years) admitted to the Fifth Azar Educational-Therapeutic Center in Gorgan, Iran, and 12 non-breast cancer individuals (mean age = 42.9±9.9 years) selected from the staff and students of Golestan University of Medical Sciences during 2018-2019. First, blood sampling was performed and peripheral blood mononuclear cells (PBMCs) were isolated. Then, using flow cytometry, different cell populations were evaluated for the expression of CXCR3, PD-1, NKG2D, and TGF-βRII. Plasma levels of interferon gamma (IFN-γ) and major histocompatibility complex class I chain related gene-A (MIC-A) were measured by enzyme-linked immunosorbent assay (ELISA).
Results: The mean percentage of T lymphocyte population in newly diagnosed breast cancer patients was significantly lower compared to healthy individuals (P<0.05). Also, the mean percentage of T lymphocytes expressing PD-1 and TGF-βRII was higher in the case group compared to the control group, while the expression of NKG2D and CXCR3 showed lower levels (P<0.05). The results of comparing plasma concentrations of IFN-γ and MIC-A indicated that the case group had higher levels of MIC-A than the control group (P<0.05); however, no statistically significant difference was found regarding IFN-γ.
Conclusion: It seems that the increased expression of TGF-βRII and PD-1 along with the decreased expression of NKG2D and CXCR3 and the reduced level of MIC-A in newly diagnosed breast cancer patients may be related to upregulation and potent suppression of T lymphocyte immunity and their dysfunction in breast cancer disease.