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The pathophysiology of diabetic retinopathy (DR) was complex. Under hyperglycemic conditions, the release of proinflammatory cytokines and the adhesion of leukocytes to retinal capillaries contribute to endothelial damage and the subsequent increase in vascular permeability resulting in macular edema. Melatonin, produced in the retina to regulate redox reactions and dopamine metabolism, plays protective roles against inflammation and oxidative stress. Considering its anti-inflammatory and antioxidative properties, melatonin was speculated to exert beneficial effects in DR. In this study, we characterized the protective effects of melatonin on the inner blood-retinal barrier (iBRB), as well as the possible mechanisms in experimental DR. Results showed that in diabetic rat retinas, the leakage of iBRB and the expression of inflammatory factors (VEGF, TNF-α, IL-1β, ICAM-1, and MMP9) increased dramatically, while the expression of tight junction proteins (ZO-1, occludin, JAM-A, and claudin-5) decreased significantly. The above changes were largely ameliorated by melatonin. The in vivo data were confirmed in vitro. In addition, the protein expressions of p38 MAPK, NF-κB, and TXNIP were upregulated significantly in diabetes and were downregulated following melatonin treatment. Melatonin could maintain the iBRB integrity by upregulating the expression of tight junction proteins via inhibiting p38/TXNIP/NF-κB pathway, thus decreasing the production of inflammatory factors. This study may shed light on the development of melatonin-based DR therapy.Warsaw breakage syndrome (WABS), is caused by biallelic mutations of DDX11, a gene coding a DNA helicase. We have recently reported two affected sisters, compound heterozygous for a missense (p.Leu836Pro) and a frameshift (p.Lys303Glufs*22) variant. By investigating the pathogenic mechanism, we demonstrate the inability of the DDX11 p.Leu836Pro mutant to unwind forked DNA substrates, while retaining DNA binding activity. We observed the accumulation of patient-derived cells at the G2/M phase and increased chromosomal fragmentation after mitomycin C treatment. The phenotype partially overlaps with features of the Fanconi anemia cells, which shows not only genomic instability but also defective mitochondria. This prompted us to examine mitochondrial functionality in WABS cells and revealed an altered aerobic metabolism. This opens the door to the further elucidation of the molecular and cellular basis of an impaired mitochondrial phenotype and sheds light on this fundamental process in cell physiology and the pathogenesis of these diseases.
Owing to recent changes in consumer eating behaviours as well as potential cost savings for processors, pulse ingredients are finding more application in the meat processing industry. In this study, pea ingredients (pea fibre, FB; pea starch, ST; pea flour, PF) and chickpea flour (CF) were used, at 4% addition level, as fat replacers in low-fat breakfast sausages. The impact of these substitutions on processing and sensory characteristics of breakfast sausage was evaluated.

While reduction in fat content in breakfast sausage resulted in some detrimental changes in cooking as well as textural characteristics of the product, addition of binders significantly improved these attributes in low-fat breakfast sausages. Overall, treatment formulation did not significantly affect the pH and the instrumental colour attributes of cooked breakfast sausage. Addition of all binders resulted in reduced cooking loss and increased moisture retention in low-fat breakfast sausage (P < 0.05), whereas, FB and ST were significantly more effective in improving water holding capacity of low-fat breakfast sausage. Furthermore, while both FB and ST increased the hardness, cohesiveness and chewiness parameters of low-fat breakfast sausage (P < 0.05), PF and CF had no impact. Generally, the consumer overall liking and flavour acceptability of FB and ST in low-fat breakfast sausage were significantly higher than those of PF and CF.

The use of ST or FB as a fat replacer in breakfast sausages offers processors improved cook yield without negatively impacting the important sensory attributes of breakfast sausages. © 2021 Society of Chemical Industry.
The use of ST or FB as a fat replacer in breakfast sausages offers processors improved cook yield without negatively impacting the important sensory attributes of breakfast sausages. © 2021 Society of Chemical Industry.Hyaluronic acid (HA) exerts a critical role in the lubricating and buffering properties of synovial fluid in joints. The production of HA is regulated by growth factors, hormones, inflammatory cytokines and mechanical load. The reduction of HA contributes to the progression of osteoarthritis. Herein, we found that d-galactose (d-gal) induced the senescence of rabbit synovial membrane cells, accompanied by decreased HA production. The mRNA level of HA synthase 2 (HAS2) was downregulated by d-gal, as analysed by real-time polymerase chain reaction. Melatonin, an endocrine hormone, can regulate the homeostasis of bone and cartilage. this website We found that melatonin treatment attenuated d-gal-induced cell senescence and decreased the expression of p21, p16 and pp65 proteins. Melatonin could reverse HA production and maintain HAS2 expression. Furthermore, we revealed that Sirt1 signalling was required for melatonin effects. Sirt1 inhibitor could counteract melatonin-mediated HA production and HAS2 expression. Additionally, Sirt1 overexpression directly antagonized d-gal-induced cell aging and HA downregulation. Taken together, our results suggest that melatonin-Sirt1 signal has a protective effect on synovial membrane cells, enhancing HA synthesis and interrupting cell senescence.Cardiovascular disease has been the leading cause of death globally for the past 15 years. Following a major cardiac disease episode, the ideal treatment would be the replacement of the damaged tissue, due to the limited regenerative capacity of cardiac tissues. However, we suffer from a chronic organ donor shortage which causes approximately 20 people to die each day waiting to receive an organ. Bioprinting of tissues and organs can potentially alleviate this burden by fabricating low cost tissue and organ replacements for cardiac patients. Clinical adoption of bioprinting in cardiovascular medicine is currently limited by the lack of systematic demonstration of its effectiveness, high costs, and the complexity of the workflow. Here, we give a concise review of progress in cardiovascular bioprinting and its components. We further discuss the challenges and future prospects of cardiovascular bioprinting in clinical applications.
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