The present data proved the over-expression of Notch1/JAGD1 and its association with tumor progression in human cervical cancer, which might be a potential valuable biomarker for cervical cancer and further studies need.

Summary Purpose The objective of this study is to assess the effect of the candesartan on the progression of atherosclerosis through the downregulation of NF‐κβ and interference with oxidative pathway. Methods Twenty‐four rabbits were assigned to three groups: control group fed normal diet; induced untreated group fed 1% cholesterol diet; and treated candesartan group also fed 1% cholesterol diet. Plasma lipid profiles were measured, and ELISA for plasma cytokines and chemokine was performed. Analyses of NF‐κβ and VCAM‐1 were performed using Western blotting with RT‐PCR for NF‐κB activity at mRNA. Doppler ultrasound was used to evaluate aortic intima‐media thickness, and atheroma was detected by H&E staining. Immunofluorescent staining was performed to confirm accumulation of monocytes and PMNs. Results Candesartan markedly reduced the levels of the plasma lipid profile including total cholesterol [TC], triglycerides [TG], and LDL‐C, while significantly elevating levels in the plasma HDL‐C, in addition to reducing cytokine (TNF‐α, IL‐6, IL‐1β) and chemokine levels (MCP‐1). Also, it decreased the aortic malondialdehyde (MDA) concentration and elevated the aortic glutathione (GSH) level compared with untreated animals (P < 0.05). The triplex Doppler ultrasound study confirmed that the candesartan attenuated intima‐media thickness at 6 months of study. All candesartan‐treated rabbits showed significantly attenuated atherosclerosis lesions with reduced accumulation of monocytes and had significantly reduced VCAM‐1 expression and NF‐κβ activity. Conclusion Candesartan retards the progression of atherosclerosis via interference with NF‐κβ and oxidative pathways.

Background. Myocardial ischemial reperfusion represents a clinically relevant problem associated with thrombolysis, angioplasty, and coronary bypass surgery. Injury of myocardium due to ischemial reperfusion includes cardiac contractile dysfunction, arrhythmias, and irreversible myocytes damage. These changes are considered to be the consequence of imbalance between the formation of oxidants and the availability of endogenous antioxidants in the heart. Objective. This study was undertaken to investigate the potential role of Simvastatin in the amelioration of myocardial I/R injury induced by ligation of coronary artery in a rat model. Materials and Methods. Adult male Swiss Albino rats were randomized into 4 equal groups. Group (1): sham group: rats underwent the same anesthetic and surgical procedures as those in the control group except ligation of LAD coronary artery, group (2): control group: rats were subjected to regional ischemia for 25 min and reperfusion for 2 hours by ligation of LAD coronary artery, group (3): control vehicle group: rats received vehicle of Simvastatin (normal saline) via IP injection and were subjected to regional ischemia for 25 min and reperfusion for 2 hours by ligation of LAD coronary artery, group (4): Simvastatin treated group: rats were pretreated with Simvastatin 1 mg/kg i.p. 1 hr before ligation of LAD coronary artery. At the end of experiment (2 hr of reperfusion), blood samples were collected from the heart for the measurement of plasma level of cardiac troponin I (cTnI). After that the heart was harvested and divided into 3 parts; one part was used for measurement of apoptosis, another part was homogenized for the measurement of tissue tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6, monocyte chemoattractant protein-1, and macrophage inflammatory protein-1α, and the last part for histopathology study. Results. Compared with the sham group, levels of myocardial TNF-α and IL-1β, IL-6, MCP-1, and MIP-1α and plasma cTnI were increased (P < 0.05). Histologically, all rats in control group showed significant (P < 0.05) cardiac injury. Furthermore, all rats in control group showed significant (P < 0.05) apoptosis. Simvastatin significantly counteracted the increase in myocardium level of TNF-α, IL-1B, IL-6, MCP-1 and MIP-1α, plasma cTnI, and apoptosis (P < 0.05). Histological analysis revealed that Simvastatin markedly reduced (P < 0.05) the severity of heart injury in the rats that underwent LAD ligation procedure. Conclusions. The results of the present study reveal that Simvastatin may ameliorate myocardial I/R injury in rats via interfering with inflammatory reactions and apoptosis which were induced by I/R injury.

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Objective: The main goal of the current study was to isolate and detect the phylogenetic characterization of Listeria monocytogenes isolate from clinical and non-clinical specimens.Methods: L. monocytogenes was isolated from 353 samples including: (94) Vaginal swabs, (81) piece of placenta, (51) frozen chicken, (69) soft cheese, and (58) frozen red meat samples using the Association of Official Agricultural Chemists method. Polymerase chain reaction (PCR) was performed for the detection of virulence gene hlyA followed by DNA sequence analysis for this gene.Results: A total of 13 isolates of L. monocytogenes were isolated from 2 (2.1%) vaginal swabs, 4 (4.9%) piece placenta, 2 (3.9%) frozen chicken, 3 (4.3%) frozen soft cheese, and 2 (3.4%) frozen red meat samples, and hlyA gene was detected in 100% of L. monocytogenes isolates.Conclusion: All the isolates tested positive for hlyA gene, so this is important role in the study of the L. monocytogenes infection and its pathogenicity. The phylogenetic analysis showed a clear convergence in the L. monocytogenes isolates from chicken, red meat, and soft cheese 70%, while there is a marked difference in isolates of L. monocytogenes isolated from placenta and vaginal swabs.

It has been hypothesized that human cytomegalovirus (CMV) may be associated with many cancers in human. However, the role of CMV infection in breast cancer remains unclear. We aimed to assess whether CMV infection have a role in development of breast cancer. A 120 women presented to breast cancer clinic with breast mass. Full history from each woman was taken, full examination including breast examination and lymph-node. Blood was aspirated from each woman for detection of CMV IgG, IgM, tp53 and CA15-3 by ELISA. A 50 patients were documented to have breast cancer by histopathological examination. The study reveal that was heights level of CMV IgG and IgM among patients with malignant breast mass (12/50) and (8/50) respectively in other side the lowest level in benign tumor (6/50) and (2/50) respectively and high prevalence of CMV in breast cancer. In conclusion There is strong evidence suggest that CMV has an important role in the development of breast cancer.

Although reperfusion of an ischemic organ is essential to prevent irreversible tissue damage, it may amplify tissue injury. This study investigates the role of endogenous testosterone in myocardial ischemia reperfusion and apoptosis in male rats. Material and method. Twenty four male rats were randomized into 4 equal groups: Group (1), sham group, rats underwent the same anesthetic and surgical procedure as the control group except for LAD ligation; Group (2), Active control group, rats underwent LAD ligation; Group (3), castrated, rats underwent surgical castration, left 3wks for recovery, and then underwent LAD ligation; and Group (4), Goserelin acetate treated, rats received 3.6 mg of Goserelin 3 wks before surgery and then underwent LAD ligation. At the end of experiment, plasma cTn I, cardiac TNF-α, IL1-β, ICAM-1, and Apoptosis level were measured and histological examination was made. Results. Compared to sham group, the levels of myocardial TNF-α, IL-1β, ICAM-1, apoptosis, and plasma cTn I were significantly increased (P < 0.05) in control group and all rats showed significant myocardial injury (P < 0.05). Castration and Goserelin acetates significantly counteract the increase in myocardial levels of TNF-α, IL-1β, ICAM-1, plasma cTn I, and apoptosis (P < 0.05) and significantly reduce (P < 0.05) the severity of myocardial injury. We conclude that castration and Goserelin acetates ameliorate myocardial I/R injury and apoptosis in rats via interfering with inflammatory reactions.

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