The Ebola virus epidemic burst in West Africa in late 2013, started in Guinea, reached in a few months an alarming diffusion, actually involving several countries (Liberia, Sierra Leone, Nigeria, Senegal, and Mali). Guinea and Liberia, the first nations affected by the outbreak, have put in place measures to contain the spread, supported by international organizations; then they were followed by the other nations affected. In the present EVD outbreak, the geographical spread of the virus has followed a new route: the achievement of large urban areas at an early stage of the epidemic has led to an unprecedented diffusion, featuring the largest outbreak of EVD of all time. This has caused significant concerns all over the world: the potential reaching of far countries from endemic areas, mainly through fast transports, induced several countries to issue information documents and health supervision for individuals going to or coming from the areas at risk. In this paper the geographical spread of the epidemic was analyzed, assessing the sequential appearance of cases by geographic area, considering the increase in cases and mortality according to affected nations. The measures implemented by each government and international organizations to contain the outbreak, and their effectiveness, were also evaluated.
With the increase in average life expectancy, several individuals are affected by age-associated non-communicable chronic diseases (NCDs). The presence of NCDs, such as type 2 diabetes mellitus (T2DM), leads to the reduction in skeletal muscle mass, a pathological condition defined as sarcopenia. A key factor linking sarcopenia with cellular senescence and diabetes mellitus (DM) is oxidative stress. We previously reported as the absence of Peroxiredoxin 6 (Prdx6), an antioxidant enzyme implicated in maintaining intracellular redox homeostasis, induces an early-stage of T2DM. In the present study we sought to understand the role of Prdx6 in the crosstalk between aging and diabetic sarcopenia, by using Prdx6 knockout (Prdx6-/-) mice. Absence of Prdx6 reduced telomeres length and Sirtuin1 (SIRT1) nuclear localization. An increase in Sa-β-Gal activity and p53-p21 pro-aging pathway were also evident. An impairment in IGF-1 (Insulin-like Groth Factor-1)/Akt-1/mTOR pathway leading to a relative increase in Forkhead Box O1 (FOXO1) nuclear localization and in a decrease of muscle differentiation as per lower levels of myoblast determination protein 1 (MyoD) was observed. Muscle atrophy was also present in Prdx6-/- mice by the increase in Muscle RING finger 1 (MuRF1) levels and proteins ubiquitination associated to a reduction in muscle strength. The present study, innovatively, highlights a fundamental role of Prdx6, in the crosstalk between aging, sarcopenia, and DM.
Tyrosol (TR), a major polyphenol found in extra virgin olive oil (EVOO), exerts several antioxidant effects. However, only scarce evidences are present regarding its activity on adipocytes and obesity. This study evaluated the role of TR in adipogenesis. Murine 3T3-L1 preadipocytes were incubated with TR (300 and 500 μM), and TR administration inhibited adipogenesis by downregulation of several adipogenic factors (leptin and aP2) and transcription factors (C/EBPα, PPARγ, SREBP1c, and Glut4) and by modulation of the histone deacetylase sirtuin 1. After complete differentiation, adipocytes treated with 300 and 500 μM TR showed a reduction of 20% and 30% in lipid droplets, respectively. Intracellular triglycerides were significantly reduced after TR treatment ( p < 0.05 ). Mature adipocytes treated with TR at 300 and 500 μM showed a marked decrease in the inflammatory state and oxidative stress as shown by the modulation of specific biomarkers (TNF, IL6, ROS, and SOD2). TR treatment also acted on the early stage of differentiation by reducing cell proliferation (~40%) and inducing cell cycle arrest during Mitotic Expansion Clonal (first 48 h of differentiation), as shown by the increase in both S1 phase and p21 protein expression. We also showed that TR induced lipolysis by activating the AMPK-ATGL-HSL pathway. In conclusion, we provided evidence that TR reduces 3T3-L1 differentiation through downregulation of adipogenic proteins, inflammation, and oxidative stress. Moreover, TR may trigger adipose tissue browning throughout the induction of the AMPK-ATGL-UCP1 pathway and, subsequently, may have promise as a potential therapeutic agent for the treatment and prevention of obesity.
Diabetes mellitus is characterized by a state of hyperglycemia resulting from altered insulin secretion by pancreatic beta cell, insulin action or both. This pathological condition is frequently associated with muscle mass loss, a condition defined as sarcopenia, and diabetic myopathy, represented by an impairment of the regenerative power of muscle fiber and by an altered differentiation of progenitor cells. Oxidative stress has been identified as the main cause of muscular alterations typical of diabetic patients. We showed that Peroxiredoxin 6 (Prdx6), a relatively new antioxidant enzyme belonging from the Peroxiredoxin family, has a central role in glucose homeostasis by exerting a potent antioxidant role. Based on these results, in the present study we aimed to verify whether Prdx6 modulates the association between diabetes and the progression of myopathy and sarcopenia. Firstly, we evaluated the gene expression of the main factors involved in the differentiation of myogenic muscle cells such as MyoD and Myogenin in murine knockout models for Prdx6 (Prdx6-/-). We observed significant decreased levels of both genes in Prdx6-/- mice compared to controls, suggesting an impairment of the regenerative potential of muscle fibers. These data were, also, confirmed by using in vitro cell model of murine myoblasts (C2C7) knockdown for Prdx6. Moreover, in the murine models, the process of muscle atrophy was studied by evaluating the gene expression of MuRF1 and Atrogin-1 that finely regulate protein degradation at skeletal muscle level. According to our hypothesis, the expression levels of both enzymes were significantly increased confirming the presence of muscle atrophy. Our study, for the first time, highlights a fundamental role of Prdx6 in the preservation of muscle mass, suggesting how Prdx6 can be considered a potential therapeutic target for diabetic myopathy and sarcopenia. However, further studies are needed in order to understand the molecular mechanism underlying this phenomenon. Disclosure F. Pacifici: None. B. Capuani: None. F. Piermarini: None. D. Pastore: None. R. Arriga: None. A. Coppola: None. S. Rea: None. G. Donadel: None. A. Bellia: None. D. Della-Morte: None. D. Lauro: None.
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