Placenta Accreta Spectrum (PAS) is an abnormal condition characterized by the placenta penetrating the myometrial wall and uterine serosa, accompanied by hyper-vascularization. Major risk factors for PAS include a history of cesarean sections, curettage, and in vitro fertilization. These procedures can lead to endometrial abnormalities that contribute to excessive trophoblast invasion, marking the early stages of PAS. Trophoblast invasion plays a crucial role in initiating growth, vasculogenesis, and angiogenesis. Disruptions in placentation during early pregnancy can arise from imbalanced angiogenesis and vasculogenesis. Reactive Oxygen Species (ROS), highly reactive molecules produced through the reduction of oxygen, are involved in cellular signaling pathways. During early pregnancy, low oxygen concentrations, influenced by ROS, and angiogenic factors such as Vascular Endothelial Growth Factor (VEGF) and Placental Growth Factor (PlGF) are essential for trophoblast invasion. Furthermore, ROS can affect bleeding due to their role in hemostasis; excess ROS may disrupt normal hemostatic function and contribute to abnormal bleeding.

Background: Breast cancer is a multifactorial potentially lethal disease that is triggered by genetic factors as well as numerous environmental factors. The present research aimed to examine the expression of Vascular endothelial growth factor messenger RNA (VEGF mRNA), cytokeratin-19 mRNA (CK19 mRNA), and vascular endothelial growth factor (VEGF) protein biomarker in the peripheral blood of patients with breast cancer.Methods: 40 patients with breast cancer were compared to 40 healthy individuals. The real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR) method was used to determine the expressions of the CK19 mRNA and VEGF mRNA biomarkers in the peripheral blood samples of the healthy participants and the patients. The VEGF protein was also compared using the (ELISA) method.Findings: The positive VEGF mRNA biomarker was observed in 30 of the 40 patients with breast cancer; thus the sensitivity of this marker was 75%. In the healthy participants group, 6 of the 40 participants showed a positive VEGF mRNA biomarker expression. The CK19 mRNA marker was positive in 25 of the 40 patients, which indicated a sensitivity of 62.5%. In the healthy participants group, the positive expression of the CK19 mRNA biomarker was observed in 7 of the 40 participants. VEGF was positive in 27 of the 40 patients. In the control group, 5 of the 40 participants showed the positive expression of this biomarker.Conclusion: In sum, based on the results of this research, the assessed breast cancer tumor markers can be used as screening tests for the early diagnosis of patients. To further prove the findings of this study, more extensive studies with larger sample sizes are recommended.

Background: The increasing incidence of infertility is alarming. About %30-10 of infertilities are classified as unexplained infertility (UI), which is not an absolute clinical condition. TGF-b1 is multifunctional cytokine and produced mainly by T regulatory (Treg) lymphocytes. This cytokine plays an important role in physiology of normal pregnancy. The association of single nucleotide Polymorphisms (SNPs) of TGF-b1 gene with many immunologic diseases has been reported. In this study, the association of TGF-b1 C29T (Pro10Leu) gene polymorphism with unexplained infertility was investigated in Iranian UI patients.Materials and Methods: In this case-control study blood samples were collected from 177 UI patients (142 male and 35 female) and 336 controls (232 male and 104 female) with no history of infertility. DNA was extracted by salting out method. Analysis of the TGF-b1 gene polymorphism C29T (Pro10Leu) was performed by PCR and automated sequencing method.Results: The genotype distributions and allele frequencies of TGF-b1 gene C29T (Pro10Leu) polymorphism were not statistically significant between different categories of UI patients and control group (p>0.05).Conclusion: The results of this study showed, C29T (Pro10Leu) polymorphism of TGF-b1 gene may not be associated with unexplained infertility and further studies are necessary to clarify the association of TGF-b1 polymorphisms and susceptibility to unexplained infertility.

Background: Impairment of the gene expression and nerve growth factors due to exposure to persistent pollutants in nature can lead to functional disorders in the nervous system. In the present study, the effects of exposure to perfluorooctanoic acid (PFOA) on the expression of nerve growth factors in the rat brain were investigated during pregnancy.Methods: The brains of 35 pregnant rats were used. the rats were divided into five groups include: control, sham, 1 mg/kg PFOA group, 5 mg/kg PFOA group, and 10 mg/kg PFOA group. In the group that received PFOA, this compound was gavaged daily. The brains of the newborn mice were removed 20 days after delivery, and the expression of nerve growth factors was analyzed using ELISA and Real-Time PCR methods.Findings: The results showed that NGF gene expression was significantly higher in the PFOA-treated groups, especially in the PFOA/5mg group (P ≤ 0.001). Also, there was a significant increase in NGF protein expression in the 5 mg PFOA dose group (P ≤ 0.01) and the 10 mg PFOA group (P ≤ 0.05) compared to the control and sham groups.Conclusion: The results of this study showed that exposure to PFOA during pregnancy can lead to increased expression of nerve growth factor. This can prevent the occurrence of neurological disorders caused by exposure to toxic agents.

Introduction: Squamous cell carcinoma (SCC) emerges from a dysplastic epithelial surface and comprises about 90% of head and neck cancers. VEGF (vascular endothelial growth factor) is one of the growth factors which directly affects vascular endothelial cells and evokes proliferation, migration and chemo taxis of endothelial cells. The aim of the present study was to assess and compare VEGF expression in the normal and dysplastic oral mucosa and in SCC.Materials and Methods: In this analytical-descriptive study, 20 normal mucosa, 20 dysplastic mucosa, and 20 SCC samples, which had been fixed with formalin and embedded in paraffin, were evaluated for expression of VEGF, using immunohistochemical technique and standard biotin streptavidin method. Data were analyzed by Kruskal-Wallis and Mann-Whitney tests at 95% confidence interval (a=0.05).Results: Means of VEFG expression were significantly higher in SCC samples compared to dysplastic samples (p value=0.024). In addition, VEGF expression in SCC samples was higher than that in the normal samples (p value=0.001). However, there was no significant relationship between the expression of VEFG in the dysplastic and normal mucosa samples (p value=0.108).Conclusion: Based on the results of the present study, there is an increase in the expression of VEGF during transition from normal mucosa to dysplastic mucosa to SCC.

Background: Hepatic fibrosis is often attributed to activation of hepatic stellate cells (HSCs) and excessive scar formation in the liver. Because these cells overproduce extracellular matrix, the advanced stages of the disease often lead to liver cirrhosis and hepatocellular carcinoma. In this study, the role of cholesterol in the activation of hepatic stellate cells was investigated. Methods: Cells were cultured in Dulbecco's modification of Eagle’ s medium (DMEM) with 10% Fetal Bovine Serum (FBS), and treated with 25, 50, 75, and 100 μ M cholesterol concentrations for 24 hours. Then, gene expression transforming growth factor beta (TGF-β ) and collagen1α , as well as Smad3C protein level were measured to assess liver fibrosis. Findings: The expression of TGF-β and collagen1α genes increased significantly compared to the control group at 75 and 100 μ M cholesterol concentrations. In addition, Smad3C protein level increased significantly compared to the control group after 4 hours of cell treatment with a concentration of 100 μ M cholesterol. Conclusion: Cholesterol increases the major proteins involved in the production of extracellular matrix, including collagen1α , by increasing the level of the Smad3C protein and activating the TGF-β signaling pathway. As a result, cholesterol can lead to the development of liver fibrosis.