Atherosclerosis is a cardiovascular disease (CVD) known widely world wide. Several hypothesizes are suggested to be involved in the narrowing of arteries during process of atherogenesis. The oxidative modification hypothesis is related to oxidative and anti-oxidative imbalance and is the most investigated. The aim of this study was to review the role of oxidative stress in atherosclerosis. Furthermore, it describes the roles of oxidative/anti-oxidative enzymes and compounds in the macromolecular and lipoprotein modifications and in triggering inflammatory events. The reactive oxygen (ROS) and reactive nitrogen species (RNS) are the most important endogenous sources produced by non-enzymatic and enzymatic [myeloperoxidase (MPO), nicotinamide adenine dinucleotide phosphate (NADH) oxidase and lipoxygenase (LO)] reactions that may be balanced with anti-oxidative compounds [glutathione (GSH), polyphenols and vitamins] and enzymes [glutathione peroxidase (Gpx), peroxiredoxins (Prdx), superoxide dismutase (SOD) and paraoxonase (PON)]. However, the oxidative and anti-oxidative imbalance causes the involvement of cellular proliferation and migration signaling pathways and macrophage polarization leads to the formation of atherogenic plaques. On the other hand, the immune occurrences and the changes in extra cellular matrix remodeling can develop atherosclerosis process.

Background: Due to the enhanced oxygen requirement of the mitochondria-rich placenta primarily during the third trimester, pregnancy is associated with elevated levels of oxidative stress. This study was designed to determine the effects of daily consumption of probiotic yogurt on oxidative stress among Iranian pregnant women. Methods: This randomized single-blind controlled clinical trial was performed among 70 pregnant women, singleton primigravida, aged 18-30 in their third trimester. Subjects were randomly assigned to two groups to consume 200 g/day of either conventional yogurt (n = 33) or probiotic yogurt (n = 37) for 9 weeks. Fasting blood samples were taken at baseline and after a 9-week intervention to measure oxidative stress parameters. Results: Consumption of probiotic yogurt resulted in increased erythrocyte glutathione reductase (GR) levels as compared to the conventional yogurt (p = 0.01). Despite the significant effect of probiotic yogurt consumption on plasma glutathione (67.9 µmol/l, p = 0.01), erythrocyte glutathione peroxidase (163 mmol/min/ml, p = 0.04) and serum 8-oxo-7,8-dihydroguanine levels (-74.3 ng/ml, p = 0.04), no significant differences were found between the two yogurts in terms of their effects on the mentioned parameters. Conclusion: Consumption of probiotic yogurt among pregnant women resulted in increased levels of erythrocyte GR as compared to the conventional yogurt, but could not affect other indices of oxidative stress.

Previous studies have shown that inflammatory factors increases in pregnancy and is associated with several complications of pregnancy. The aim of this study was to assess effects of daily consumption of probiotic yoghurt on inflammatory factors in pregnant women. In a randomized clinical trial, seventy primigravid (the first pregnancy) and singleton pregnant women aged 18-30 years were assigned to two groups. Subjects consumed daily 200 g probiotic yoghurt containing Lactobacillus acidophilus La5 and Bifidobacterium animalis BB12 (10(7) CFU g(-1) for each) or 200 g conventional yoghurt for 9 weeks. Fasting blood samples were collected at baseline (28 weeks of gestation) and after intervention (37 weeks of gestation). Inflammatory factors, hs-CRP and TNF-alpha, were measured by Enzyme-linked Immunosorbent Assay (ELISA). Independent t-test was used to compare the two groups after intervention and paired-sample t-test compared variables before and after treatment. The results showed that the probiotic yogurt brought about a decrease in the serum hs-CRP level, from 10.44 +/- 1.56 to 7.44 +/- 1.03 microg mL(-1) (p = 0.041). There was no significant change in the conventional yogurt group in the serum hs-CRP level (12.55 +/- 1.57 to 14.51 +/- 1.62 microg mL(-1), p = 0.202). The probiotic yogurt had no effect on TNF-alpha (from 73.75 +/- 6.59 to 77.91 +/- 5.61 pg mL(-1), p = 0.633). Serum TNF-alpha did not change in the conventional yogurt group (p = 0.134). In conclusion probiotic yogurt significantly decreased hs-CRP in pregnant women but had no effect on TNF-alpha.

Hepatitis B virus (HBV), along with Hepatitis C virus chronic infection, represents a major risk factor for hepatocellular carcinoma (HCC) development. However, molecular mechanisms involved in the development of HCC are not yet completely understood. Recent studies have indicated that mutations in CTNNB1 gene encoding for β-catenin protein lead to aberrant activation of the Wnt/ β-catenin pathway. The mutations in turn activate several downstream genes, including c-Myc, promoting the neoplastic process. The present study evaluated the mutational profile of the CTNNB1 gene and expression levels of CTNNB1 and c-Myc genes in HBV-related HCC, as well as in cirrhotic and control tissues. Mutational analysis of the β-catenin gene and HBV genotyping were conducted by direct sequencing. Expression of β-catenin and c-Myc genes was assessed using real-time PCR. Among the HCC cases, 18.1% showed missense point mutation in exon 3 of CTNNB1, more frequently in codons 32, 33, 38 and 45. The frequency of mutation in the hotspots of exon 3 was significantly higher in non-viral HCCs (29.4%) rather than HBV-related cases (12.7%, P = 0.021). The expression of β-catenin and c-Myc genes was found upregulated in cirrhotic tissues in association with HBV infection. Mutations at both phosphorylation and neighboring sites were associated with increased activity of the Wnt pathway. The results demonstrated that mutated β-catenin caused activation of the Wnt pathway, but the rate of CTNNB1 gene mutations was not related to HBV infection. HBV factors may deregulate the Wnt pathway by causing epigenetic alterations in the HBV-related HCC.

Atherosclerosis is an underlying pathology of many vascular diseases as a result of cellular, structural and molecular dysfunctions within the sub-endothelial space. This review deals with the events involved in the formation, growth and remodeling of plaque, including the cell recruitment, cell polarization, and cell fat droplets. It also describes cross talking between endothelial cells, macrophages, and vascular smooth muscle cells, as well as the cellular pathways involved in plaque development in the plaque microenvironment. Finally, it describes the plaque structural components and the role of factors involved in the rupture and erosion of plaques in the vessel.