Aim: Enhanced oxidative stress contributes to the pathogenesis of diabetic retinopathy. The aim of this study is to detect oxidative stress parameters in type 2 diabetes mellitus with or without retinopathy and to investigate the relationship between oxidative stress and patients with type 2 diabetic retinopathy. Methods: Oxidative stress parameters included malondialdehyde (MDA), conjugated diene (CD), advanced oxidation protein products (AOPP), protein carbonyl and 8-hydroxydeoxyguanosin (8-OHdG) in serum measured in 33 patients with diabetes mellitus without complications, 27 diabetes mellitus retinopathy and 32 normal control subjects, respectively. Results: The concentrations of MDA and CD in type 2 diabetes mellitus (DM) were significantly higher than those of the control subjects (p<0.01). The concentration of MDA and CD in patients with retinopathy was significantly elevated in comparison with patients with diabetes without retinopathy (p<0.05). There was a significant increase in serum 8-OHdG in patients with diabetes compared with normal subjects (p<0.01), and serum 8-OHdG was much higher in diabetes mellitus retinopathy than that in patients with diabetes without retinopathy (p<0.05). This was significantly higher in serum AOPP and protein carbonyl in type 2 DM compared with normal subjects (p<0.01). Moreover, diabetes mellitus retinopathy patients had significantly higher AOPP and protein carbonyl compared with patients with diabetes without retinopathy (p<0.05). Conclusions: These results indicate that there were severe lipid peroxidation, protein oxidation, and oxidative DNA damage in diabetes. The augmented oxidative stress in diabetes may be speculated to contribute to the pathogenesis of diabetes mellitus. Oxidative stress is an important risk factor in the development of diabetic retinopathy. The levels and the types of serum oxidative stress by-products will be in favour of predicting the amount of retinopathy.

With widespread abuse of antibiotics, bacterial resistance has increasingly become a serious threat. Acinetobacter baumannii has emerged as one of the most important hospital-acquired pathogens worldwide. Bacteriophages (also called “phages”) could be used as a potential alternative therapy to meet the challenges posed by such pathogens. Endolysins from phages have also been attracting increasing interest as potential antimicrobial agents. Here, we isolated 14 phages against A. baumannii, determined the lytic spectrum of each phage, and selected one with a relatively broad host range, named vB_AbaP_PD-6A3 (PD-6A3 for short), for its biological characteristics. We over-expressed and purified the endolysin (Ply6A3) from this phage and tested its biological characteristics. The PD-6A3 is a novel phage, which can kill 32.4% (179/552) of clinical multidrug resistant A. baumannii (MDRAB) isolates. Interestingly, in vitro, this endolysin could not only inhibit A. baumannii, but also that of other strains, such as Escherichia coli and methicillin-resistant Staphylococcus aureus (MRSA). We found that lethal A. baumannii sepsis mice could be effectively rescued in vivo by phage PD-6A3 and endolysin Ply6A3 intraperitoneal injection. These characteristics reveal the promising potential of phage PD-6A3 and endolysin Ply6A3 as attractive candidates for the control of A. baumannii-associated nosocomial infections.

Gout is a metabolic disease and is the most common form of inflammatory arthritis affecting men. However, the pathogenesis of gout is still uncertain, and novel biomarkers are needed for early prediction and diagnosis of gout. The aim of this study was to develop a systemic metabolic profile of patients with asymptomatic hyperuricemia (HUA) and gout by using a metabolomics approach, and find potential pathophysiological mechanisms of and markers of predisposition to gout. Serum samples were collected from 149 subjects, including 50 patients with HUA, 49 patients with gout and 50 healthy controls. 1H nuclear magnetic resonance (NMR) spectroscopy combined with principal components analysis and orthogonal partial least squares-discriminant analysis were used to distinguish between samples from patients and healthy controls. Clinical measurements and pathway analysis were also performed to contribute to understanding of the metabolic change. By serum metabolic profiling, 21 metabolites including lipids and amino acids were significantly altered in patients with HUA or gout. The levels of identified biomarkers together with clinical data showed apparent alteration trends in patients with HUA or gout compared to healthy individuals. According to pathway analysis, three and five metabolic pathways were remarkably perturbed in patients with HUA or gout, respectively. These enriched pathways involve in lipid metabolism, carbohydrate metabolism, amino acids metabolism and energy metabolism. Taken together, we identified the biomarker signature for HUA and gout, which provides biochemical insights into the metabolic alteration, and identified a continuous progressive axis of development from HUA to gout.