Diabetes-associated complications, such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis, the main consequences of long-term hyperglycemia, often lead to organ dysfunction, disability, and increased mortality. A common denominator of these complications is the myofibroblast-driven excessive deposition of extracellular matrix proteins. Although fibroblast appears to be the primary source of myofibroblasts, other cells, including endothelial cells, can generate myofibroblasts through a process known as endothelial to mesenchymal transition (EndMT). During EndMT, endothelial cells lose their typical phenotype to acquire mesenchymal features, characterized by the development of invasive and migratory abilities as well as the expression of typical mesenchymal products such as α-smooth muscle actin and type I collagen. EndMT is involved in many chronic and fibrotic diseases and appears to be regulated by complex molecular mechanisms and different signaling pathways. Recent evidence suggests that small RNAs, in particular microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are crucial mediators of EndMT. Furthermore, EndMT and miRNAs are both affected by oxidative stress, another key player in the pathophysiology of diabetic fibrotic complications. In this review, we provide an overview of the primary redox signals underpinning the diabetic-associated fibrotic process. Then, we discuss the current knowledge on the role of small RNAs in the regulation of EndMT in diabetic retinopathy, nephropathy, cardiomyopathy, and atherosclerosis and highlight potential links between oxidative stress and the dyad small RNAs-EndMT in driving these pathological states.

Vaginal candidiasis (VC) continues to be a health problem to women worldwide. Although the majority of VC cases are caused by Candida albicans (C. albicans), non-albicans Candida spp. like C. glabrata and C. tropicalis are emerging as important and potentially resistant opportunistic agents of VC. The objective of this study was to evaluate the prevalence and epidemiology of VC in the UAE through retrospective analysis of pertinent data compiled by the microbiology and infection control unit at Latifa Hospital, Dubai between 2005 and 2011. The incidence of VC significantly increased from 10.76% in 2005 to 17.61% in 2011; average prevalence was 13.88%. C. albicans occurred at a frequency of 83.02%, C. glabrata at 16.5% and C. tropicalis at 1.2%. A single C. dubliniensis isolate was identified in the sample population. The percentage of C. albicans significantly decreased from 83.02% in the sample population as a whole to 60.8% in subjects over 45 years of age (P < 0.01) and that of C. glabrata, C. tropicalis and C. krusei significantly increased from 13.88%, 0.9% and 0.03% to 29.7%, 6.7% and 1.4% (P < 0.05) respectively. The incidence of VC in the UAE is on the rise and the frequency of non-albicans Candida spp. is noticeably increasing especially in postmenopausal women.

Clinical and experimental observations have long suggested that elevated levels of estrogen associate with increased serum iron availability. Additionally, recent work has shown that estrogen can downregulate hepcidin synthesis in vitro. This study aims at assessing whether the ability of estrogen to downregulate hepcidin synthesis translates into changes in serum iron status. Hepcidin synthesis was evaluated in MCF-7, Hep-G2 and SKOV-3 cells treated with increasing concentrations of estrogen and cultured for up to 24 h post treatment. The correlation between levels of serum estrogen, hepcidin and iron was assessed using serum samples collected from 153 premenopausal women at random and samples collected from 6 women at days 1, 5, 10, 16, 21 and 28 of the monthly cycle. Estrogen-treated MCF-7 cells showed a significant reduction in hepcidin synthesis, especially at 20 nM/24 h E2 treatment. Hepcidin synthesis was also significantly reduced in Hep-G2 and SKOV-3 cells at 20 nM/24 h E2 treatment. In serum samples collected at random, estrogen (P=0.022; R=-0.213) and iron (P=0.028; R=-0.316) correlated negatively with hepcidin and positively with each other (P=0.033; R=0.319). An overall similar pattern was also observed in monthly cycle-timed samples. These findings suggest that elevated levels of estrogen reduce hepcidin synthesis as means of enhancing serum iron content in menstruating women.

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