Excessive fat liver is an important manifestation of nonalcoholic fatty liver disease (NAFLD), associated with obesity, insulin resistance, and oxidative stress. In the present study, the effects of a high-fat, high-fructose diet (HFFD) on mRNA levels and activities of the antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), were determined in mouse livers and brains. The histomorphology of the livers was examined and the state of nonenzymatic reducing system was evaluated by measuring the glutathione system and the lipid peroxidation. Histopathology of the liver showed that fat accumulation and inflammation depended on the period of the HFFD-consumption. The levels of mRNA and enzymatic activities of SOD, CAT, and GPx were raised, followed by the increases in malondialdehyde levels in livers and brains of the HFFD mice. The oxidized GSSG content was increased while the total GSH and the reduced GSH were decreased, resulting in the increase in the GSH/GSSG ratio in both livers and brains of the HFFD mice. These observations suggested that liver damage and oxidative stress in the significant organs were generated by continuous HFFD-consumption. Imbalance of antioxidant condition induced by long-term HFFD-consumption might increase the risk and progression of NAFLD.
Background. Assessment of DNA methylation of specific genes is one approach to the diagnosis of cancer worldwide. Early stage detection is necessary to reduce the mortality rate of cancers, including those occurring in the stomach. For this purpose, tumor cells in circulating blood offer promising candidates for non-invasive diagnosis. Transcriptional inactivation of tumor suppressor genes, like PCDH10 and RASSF1A, by methylation is associated with progression of gastric cancer, and such methylation can therefore be utilized as a biomarker.Methods. The present research was conducted to evaluate DNA methylation in these two genes using blood samples of gastric cancer cases. Clinicopathological data were also analyzed and cumulative survival rates generated for comparison.Results. High frequencies of PCDH10 and RASSF1A methylations in the gastric cancer group were noted (94.1% and 83.2%, respectively, as compared to 2.97% and 5.45% in 202 matched controls). Most patients (53.4%) were in severe stage of the disease, with a median survival time of 8.4 months after diagnosis. Likewise, the patients with metastases, or RASSF1A and PCDH10 methylations, had median survival times of 7.3, 7.8, and 8.4 months, respectively. A Kaplan–Meier analysis showed that cumulative survival was significantly lower in those cases positive for methylation of RASSF1A than in their negative counterparts. Similarly, whereas almost 100% of patients positive for PCDH10 methylation had died after five years, none of the negative cases died over this period. Notably, the methylations of RASSF1A and PCDH10 were found to be higher in the late-stage patients and were also significantly correlated with metastasis and histology.Conclusions. PCDH10 and RASSF1A methylations in blood samples can serve as potential non-invasive diagnostic indicators in blood for gastric cancer. In addition to RASSF1A methylation, tumor stage proved to be a major prognostic factor in terms of survival rates.
BackgroundHuman papillomavirus (HPV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV) cause sexually transmitted diseases (STDs) that are frequently found in men who have sex with men (MSM) with human immunodeficiency viral (HIV) infection.MethodsThis study investigated the prevalence of infection and anatomical site distribution of these viruses in asymptomatic MSM. DNA, extracted from cells collected from the anorectum, oropharynx and urethra of 346 participants, was investigated for the presence of EBV, HPV and HSV using real-time PCR. Demographic data from the participants were analyzed.ResultsAll three viruses were found in all sampled sites. EBV was the commonest virus, being detected in the anorectum (47.7% of participants), oropharynx (50.6%) and urethra (45.6%). HPV and HSV were found in 43.9% and 2.9% of anorectum samples, 13.8% and 3.8% of oropharynx samples and 25.7% and 2% of urethra samples, respectively. HPV infection of the anorectum was significantly associated with age groups 21–30 (odds = 3.043, 95% CI = 1.643–5.638 and P = 0.001) and 46–60 years (odds = 2.679, 95% CI = 1.406–5.101 and P = 0.03). EBV infection of the urethra was significantly correlated with age group 21–30 years (odds = 1.790, 95% CI = 1.010–3.173 and P = 0.046). EBV/HPV co-infection of the anorectum (odds = 3.211, 95% CI = 1.271–8.110, P = 0.014) and urethra (odds = 2.816, 95% CI = 1.024–7.740, P = 0.045) was also associated with this age group. Among HIV-positive MSM, there was a significant association between age-group (odds = 21.000, 95% CI = 1.777–248.103, P = 0.016) in HPV infection of the anorectum. A failure to use condoms was significantly associated with HPV infection of the anorectum (odds = 4.095, 95% CI = 1.404–11.943, P = 0.010) and urethra (odds = 7.187, 95% CI = 1.385–37.306, P = 0.019). Similarly, lack of condom use was significantly associated with EBV infection of the urethra (odds = 7.368, 95% CI = 1.580–34.371, P = 0.011).ConclusionThese results indicate that asymptomatic MSM in Northeast Thailand form a potential reservoir for transmission of STDs, and in particular for these viruses.Electronic supplementary materialThe online version of this article (10.1186/s12879-018-3406-0) contains supplementary material, which is available to authorized users.
Human papillomavirus (HPV) infection is associated with several genetic alterations including oncogene amplification, leading to increased aggression of tumors. Recently, a relationship between HPV infection and oncogene amplification has been reported, but this finding remains controversial. This study therefore investigated relationships between HPV infection and amplification of genes in the epidermal growth factor receptor (EGFR) signaling cascade in oral squamous cell carcinoma (OSCC). Extracted DNA from 142 formalin-fixed paraffin-embedded (FFPE) OSCC tissues was performed to investigate the copy number of EGFR, KRAS, c-myc and cyclin D1 genes using real-time polymerase chain reaction (RT-PCR) and compared with calibrators. A tissue microarray of OSCC tissues was used for detection of c-Myc expression and HPV infection by immunohistochemistry and HPV E6/E7 RNA in situ hybridization, respectively. HPV infection was also investigated using PCR and RT-PCR. Of the 142 OSCC samples, 81 (57%) were HPV-infected cases. The most frequently amplified gene was c-myc (55.6%), followed by cyclin D1 (26.1%), EGFR (23.9%) and KRAS (19.7%). Amplification of c-myc was significantly associated with levels of its protein product. EGFR amplification was also significantly associated with amplification of genes in the signaling cascade: KRAS (50.0%), c-myc (34.2%) and cyclin D1 (46.0%). Interestingly, HPV infection was significantly associated with amplification of both EGFR (76.5%) and cyclin D1 (73.0%). Only cyclin D1 amplification was significantly associated with severity of OSCC histopathology. HPV infection may play an important synergistic role in amplification of genes in the EGFR signaling cascade, leading to increased aggression in oral malignancies.
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