Perfluorooctanoic acid (PFOA) is an emerging contaminant of concern due to its toxicity for human health and ecosystems. However, successful degradation of PFOA in aqueous solutions with a cost-effective method remains a challenge, especially for groundwater. In this study, the degradation of PFOA using activated persulfate under mild conditions was investigated. The impact of different factors on persulfate activity, including pH, temperature (25 °C–50 °C), persulfate dosage and reaction time, was evaluated under different experimental conditions. Contrary to the traditional alkaline-activated persulfate oxidation, it was found that PFOA can be effectively degraded using activated persulfate under acidic conditions, with the degradation kinetics following the pseudo-first-order decay model. Higher temperature, higher persulfate dosage and increased reaction time generally result in higher PFOA degradation efficiency. Experimental results show that a PFOA degradation efficiency of 89.9% can be achieved by activated persulfate at pH of 2.0, with the reaction temperature of 50 °C, molar ratio of PFOA to persulfate as 1:100, and a reaction time of 100 h. The corresponding defluorination ratio under these conditions was 23.9%, indicating that not all PFOA decomposed via fluorine removal. The electron paramagnetic resonance spectrometer analysis results indicate that both SO₄⁻• and •OH contribute to the decomposition of PFOA. It is proposed that PFOA degradation occurs via a decarboxylation reaction triggered by SO₄⁻•, followed by a HF elimination process aided by •OH, which produces one-CF₂-unit-shortened perfluoroalkyl carboxylic acids (PFCAs, C_n−1F_2n−1COOH). The decarboxylation and HF elimination processes would repeat and eventually lead to the complete mineralization all PFCAs. Full article

Human cytomegalovirus (HCMV) is a major risk factor in transplantation and AIDS patients, which induces high morbidity and mortality. These patients infected with HCMV experience an imbalance of redox homeostasis that cause accumulation of reactive oxygen species (ROS) at the cellular level. H2O2, the most common reactive oxygen species, is the main byproduct of oxidative metabolism. However, the function of H2O2 on HCMV infection is not yet fully understood and the effect and mechanism of N-acetylcysteine (NAC) on H2O2-stimulated HCMV replication is unclear. We, therefore, examined the effect of NAC on H2O2-induced HCMV production in human foreskin fibroblast cells. In the present study, we found that H2O2 enhanced HCMV lytic replication through promoting major immediate early (MIE) promoter activity and immediate early (IE) gene transcription. Conversely, NAC inhibited H2O2-upregulated viral IE gene expression and viral replication. The suppressive effect of NAC on CMV in an acute CMV-infected mouse model also showed a relationship between antioxidants and viral lytic replication. Intriguingly, the enhancement of HCMV replication via supplementation with H2O2 was accompanied with the activation of the p38 mitogen-activated protein kinase pathway. Similar to NAC, the p38 inhibitor SB203580 inhibited H2O2-induced p38 phosphorylation and HCMV upregulation, while upregulation of inducible ROS was unaffected. These results directly relate HCMV replication to H2O2, suggesting that treatment with antioxidants may be an attractive preventive and therapeutic strategy for HCMV. Full article

The role of dynamic processes on self-assembled structures of 4'-([2,2':6', 2''-terpyridin]-4'-yl)-[1,1'-biphenyl]-4-carboxylic acid (l) molecules on Au(III) has been studied by scanning tunneling microscopy. The as-deposited monolayer is closed-packed and periodic in a short-range due to dipole forces. A thermal annealing process at 110 degrees drives such disordered monolayer into ordered chain-like structures, determined by the combination of the dipole forces and hydrogen bonding. Further annealing at 130 degrees turns the whole monolayer into a bowknot-like structure in which hydrogen bonding plays the dominant role in the formation of assembled structures. Such dependence of an assembled structure on the process demonstrates that an assembled structure can be regulated and controlled not only by the molecular structure but also by the thermal process to form the assembled structure. Full article

To analyze the association between non-alcoholic fatty liver disease (NAFLD) and the incidence of diabetic nephropathy in patients with type 2 diabetes, the incidence of diabetic nephropathy was assessed in 413 type 2 diabetic patients, by testing the 24 h urinary albumin excretion rate (UAER). The NAFLD was diagnosed based on patient’s medical history and liver ultrasound. The difference in diabetic nephropathy incidence between patients with and without NAFLD was tested by χ². Multivariate logistic regression analysis was used to assess the factors associated with diabetic nephropathy among type 2 diabetic patients. Total 363 out of 413 type 2 diabetic patients were enrolled in this study. The incidences of NAFLD and diabetic nephropathy in participants were approximately 56% (202/363) and 38% (137/363) respectively, and there was no significant difference in the prevalence of diabetic nephropathy between patients with and without NAFLD (37.1% vs. 38.5%, p = 0.787). The duration of diabetes (odds ratio [OR] 1.065, 95% confidence interval [CI] 1.014–1.120, p = 0.012), waist circumference (OR 1.077, 95% CI 1.040–1.116, p = 0.000), and fasting blood glucose (FBG; OR 1.136, 95% CI 1.023–1.1262, p = 0.017) were significantly associated with diabetic nephropathy, whereas sex, high blood pressure, total cholesterol (TC), triglyceride (TG), and ankle brachial pressure index (ABI) were not significantly associated with the disorder. The present results suggest that NAFLD is not related to the incidence of diabetic nephropathy in type 2 diabetes, but the duration of diabetes, waist circumference, and FBG are important factors for diabetic nephropathy in type 2 diabetes. Full article

Fluctuations in serum autofluorescence (AF) intensity have recently been widely used as markers of certain diseases such as cancer. To determine the diagnostic value of serum AF intensity for liver fibrosis in rats, we induced liver fibrosis by subcutaneous injection of carbon tetrachloride into rats. The rat serum AF intensities were detected at the excitation wavelength of 337 nm and the emission wavelength of 512 nm. The degree of liver fibrosis was evaluated by Van Gieson’s staining. The relationship between serum AF intensity and the degree of liver fibrosis was analyzed by Spearman and Pearson Correlation. The diagnostic sensitivity and specificity of the serum AF was determined by analyzing the receiver operating characteristic (ROC) curves. Our results show that the serum AF intensity in the rat liver fibrosis model increased when compared with control rats eight weeks and twelve weeks post induction of liver fibrosis. However, there was no significant difference in serum AF intensity between fibrotic and control rats at four week post induction. Furthermore, serum AF intensity correlated positively with the severity of the degree of hepatic fibrosis. ROC analysis further suggested that serum AF intensity is a valid marker for staging fibrosis. Therefore, it may potentially be developed as a novel diagnostic tool for hepatic fibrosis. Full article

Treatment trends of retinoblastoma (RB) have gradually evolved from eye enucleation and external radiation to local treatment. Combined treatment with an oncolytic virus and chemotherapy is currently a new method in RB treatment. To investigate the therapeutic effect of oncolytic adenovirus SG600 in combination with vincristine (VCR) on retinoblastoma in vitro, the cell viability, cell cycle effects and apoptotic activity of HXO-RB₄₄ cells treated with SG600, VCR or SG600 plus VCR were measured using a cell counting kit-8-based procedure and flow cytometry. Western blot analysis for Akt, p-Akt, p-p53 and p-Rb protein was performed to investigate the underlying mechanisms of combined therapy. The combination therapy exerted a synergistic antitumor effect via a type of G₂/M and S phase arrest rather than the induction of apoptosis. The combination of VCR and SG600 further reduced Akt phosphorylation compared with cells treated with VCR alone, suggesting that SG600 could overcome chemoresistance, perhaps by down-regulating Akt in RB cells. An increase in the expression of p-p53 and decrease in p-Rb expression in HXO-RB₄₄ after co-treatment might be associated with cell cycle block. Western blot examination revealed that VCR might enhance SG600 replication. These results suggest that viro-chemo combination therapy is a feasible and potentially promising approach for the treatment of retinoblastoma. Full article