Findings from studies are congruent with obesity having a viral origin, but what about obesity-related nafld?

Infection has recently started receiving greater attention as an unusual causative/inducing factor of obesity. Indeed, the biological plausibility of infectobesity includes direct roles of some viruses to reprogram host metabolism toward a more lipogenic and adipogenic status. Furthermore, the probability that humans may exchange microbiota components (virome/virobiota) points out that the altered response of IFN and other cytokines, which surfaces as a central mechanism for adipogenesis and obesity-associated immune suppression, is due to the fact that gut microbiota uphold intrinsic IFN signaling. Last but not least, the adaptation of both host immune and metabolic system under persistent viral infections play a central role in these phenomena. We hereby discuss the possible link between adenovirus and obesity-related nonalcoholic fatty liver disease (NAFLD). The mechanisms of adenovirus-36 (Ad-36) involvement in hepatic steatosis/NAFLD consist in reducing leptin gene expression and insulin sensitivity, augmenting glucose uptake, activating the lipogenic and pro-inflammatory pathways in adipose tissue, and increasing the level of macrophage chemoattractant protein-1, all of these ultimately leading to chronic inflammation and altered lipid metabolism. Moreover, by reducing leptin expression and secretion Ad-36 may have in turn an obesogenic effect through increased food intake or decreased energy expenditure via altered fat metabolism. Finally, Ad-36 is involved in upregulation of cAMP, phosphatidylinositol 3-kinase, and p38 signaling pathways, downregulation of Wnt10b expression, increased expression of CCAAT/enhancer binding protein-beta, and peroxisome proliferator-activated receptor gamma 2 with consequential lipid accumulation

Atherosclerosis and Its Related Laboratory Biomarkers

Atherosclerosis constitutes a persistent inflammatory ailment, serving as the predominant underlying condition for coronary artery disease (CAD), peripheral artery disease (PAD), and cerebrovascular disease. The progressive buildup of plaques within the walls of medium- and large-caliber arteries characterizes the atherosclerotic process. This accumulation results in significant narrowing that impedes blood flow, leading to critical tissue oxygen deficiency. Spontaneous blockage of thrombotic vessels can precipitate stroke and myocardial infarction, which are complications representing the primary global causes of mortality. Present-day models for predicting cardiovascular risk incorporate conventional risk factors to gauge the likelihood of cardiovascular events over a ten-year span. In recent times, researchers have identified serum biomarkers associated with an elevated risk of atherosclerotic events. Many of these biomarkers, whether used individually or in combination, have been integrated into risk prediction models to assess whether their inclusion enhances predictive accuracy. In this review, we have conducted a comprehensive analysis of the most recently published literature concerning serum biomarkers associated with atherosclerosis. We have explored the potential utility of incorporating these markers in guiding clinical decisions

p53 and telomerase control rat myocardial tissue response to hypoxia and ageing

Cellular senescence implies loss of proliferative and tissue regenerative capability. Also hypoxia, producing Reactive Oxygen Species (ROS), can damage cellular components through the oxidation of DNA, proteins and lipids, thus influencing the shortening of telomeres

pPKCα mediated-HIF-1α activation related to the morphological modifications occurring in neonatal myocardial tissue in response to severe and mild hyperoxia

In premature babies birth an high oxygen level exposure can occur and newborn hyperoxia exposure can be associated with free radical oxygen release with impairment of myocardial function, while in adult animal models short exposure to hyperoxia seems to protect heart against ischemic injury. Thus, the mechanisms and consequences which take place after hyperoxia exposure are different and related to animals age. The aim of our work has been to analyze the role played by HIF-1α in the occurrence of the morphological modifications upon hyperoxia exposure in neonatal rat heart. Hyperoxia exposure induces connective compartment increase which seems to allow enhanced blood vessels growth. An increased hypoxia inducible factor-1α (HIF-1α) translocation and vascular endothelial growth factor (VEGF) expression has been found upon 95% oxygen exposure to induce morphological modifications. Upstream pPKC-α expression increase in newborn rats exposed to 95% oxygen can suggest PKC involvement in HIF-1α activation. Since nitric oxide synthase (NOS) are involved in heart vascular regulation, endothelial NOS (e-NOS) and inducible NOS (i-NOS) expression has been investigated: a lower eNOS and an higher iNOS expression has been found in newborn rats exposed to 95% oxygen related to the evidence that hyperoxia provokes a systemic vasoconstriction and to the iNOS pro-apoptotic action, respectively. The occurrence of apoptotic events, evaluated by TUNEL and Bax expression analyses, seems more evident in sample exposed to severe hyperoxia. All in all such results suggest that in newborn rats hyperoxia can trigger oxygen free radical mediated membrane injury through a pPKCα mediated HIF-1α signalling system, even though specificity of such response could be obtained by in vivo administration to the rats of specific inhibitors of PKCα. This intracellular signalling can switch molecular events leading to blood vessels development in parallel to pro-apoptotic events due to an immature anti-oxidant defensive system in newborn rat hearts

The Influence of Physical Education on Self-Efficacy in Overweight Schoolgirls: A 12-Week Training Program

The purpose of this randomized controlled study was to investigate the impact of a 12- week physical education (PE) program on the self-efficacy of overweight schoolgirls. We randomly assigned 60 overweight schoolgirls (15–17 years) to either an experimental moderate to vigorous aerobic exercise (∼90 min, three times a week) group (n = 30) or a control group (CG) (n = 30) that received non-specific regular PE lessons with activities chosen by the curricular teacher mainly focused on team games and sports skills that aimed to achieve general psycho-physical wellness (∼90 min, three times a week). To assess the starting level of students and significant changes reached, at baseline and after training, a battery of standardized assessment motor tests and a psychometric scale (generalized self-efficacy scale, GES) were administered. At the end of the intervention, the experimental group reported a considerable decrease in body mass index (BMI) and a large improvement in self-efficacy (p < 0.001). No significant changes were found in the CG. The results suggested that the 12-week moderate to a vigorous aerobic exercise program is an effective weight loss intervention and a vehicle to promote a range of outcomes important to the qualitative growth of adolescents. In fact, it could provide a positive and significant impact on the self-efficacy of overweight schoolgirls

Regulation of CREB activation by p38 mitogen activated protein kinase during human primary erythroblast differentiation.

Among the molecular events underlying erythroid differentiation, we analyzed the signalling pathway leading to cAMP response element binding (CREB) nuclear transcription factor activation. Normal donor blood light density cells differentiated to pro-erythroblasts during the proliferative phase (10 days) of the Human Erithroblast Massive Amplification (HEMA) culture, and to orthochromatic erythroblasts, during the differentiative phase (4 additional days) of the culture. Since erythropoietin was present all over the culture, also pro-erythroblasts left in proliferative medium for 14 days continued their maturation without reaching the final steps of differentiation. p38 Mitogen Activated Protein Kinase (p38 MAPK) and CREB maximal activation occurred upon 4 days of differentiation induction, whereas a lower activation was detectable in the cells maintained in parallel in proliferative medium (14 days). Interestingly, when SB203580, a specific p38 MAPK inhibitor, was added to the culture the percentage of differentiated cells decreased along with p38 MAPK and CREB phosphorylation. All in all, our results evidence a role for p38 MAPK in activating CREB metabolic pathway in the events leading to erythroid differentiation

Le Elezioni Politiche 2013

Le elezioni politiche del 24 e 25 febbraio 2013 hanno sancito un forte cambiamento della struttura del sistema partitico italiano. In un contesto di altissima volatilità elettorale e di accelerato declino della partecipazione al voto, il sistema è divenuto sostanzialmente tripolare, dopo vent’anni di strutturazione e tenuta del bipolarismo. A questo esito hanno concorso da un lato l’erosione dei principali schieramenti politici che a partire dal novembre 2011 avevano sostenuto l’esperienza del governo Monti (nonché la deludente prova elettorale dello stesso Presidente del Consiglio uscente), e dall’altro lo straordinario successo del Movimento 5 stelle. Quest’ultimo, al primo test elettorale di livello nazionale, ha raccolto un risultato sorprendente, giungendo ad oltre un quarto dei voti validi. Siamo di fronte ad una parentesi momentanea dovuta all’effetto combinato di crisi economica e crisi politica, oppure le contraddizioni interne alla Seconda Repubblica l’hanno condotta effettivamente al suo crepuscolo? Come uscirà il sistema partitico italiano da questa nuova fase di destabilizzazione? Questo quarto Dossier CISE, che raccoglie contributi apparsi sul sito web del Cise prima e dopo le elezioni, fornisce una prima analisi del voto, presentando elaborazioni su dati aggregati, stime dei flussi elettorali, alcune prime analisi su dati di sondaggio, nonché una panoramica dei nuovi eletti e un’appendice ricca di tabelle e mappe riassuntive del risultato elettorale. Come i precedenti Dossier, si tratta di uno strumento prodotto rapidamente all’indomani del voto, con l’intento di suggerire primi spunti di interpretazione da approfondire in seguito, cercando di contribuire alla lettura di un risultato elettorale cruciale, in una delicata fase di cambiamento del sistema partitico italiano

Chitlac-coated Thermosets Enhance Osteogenesis and Angiogenesis in a Co-culture of Dental Pulp Stem Cells and Endothelial Cells

Dental pulp stem cells (DPSCs) represent a population of stem cells which could be useful in oral and maxillofacial reconstruction. They are part of the periendothelial niche, where their crosstalk with endothelial cells is crucial in the cellular response to biomaterials used for dental restorations. DPSCs and the endothelial cell line EA.hy926 were co-cultured in the presence of Chitlac-coated thermosets in culture conditions inducing, in turn, osteogenic or angiogenic differentiation. Cell proliferation was evaluated by 3\u2013[4,5\u2013dimethyl\u2013thiazol\u20132\u2013yl\u2013]\u20132,5\u2013diphenyl tetrazolium bromide (MTT) assay. DPSC differentiation was assessed by measuring Alkaline Phosphtase (ALP) activity and Alizarin Red S staining, while the formation of new vessels was monitored by optical microscopy. The IL-6 and PGE2 production was evaluated as well. When cultured together, the proliferation is increased, as is the DPSC osteogenic differentiation and EA.hy926 vessel formation. The presence of thermosets appears either not to disturb the system balance or even to improve the osteogenic and angiogenic differentiation. Chitlac-coated thermosets confirm their biocompatibility in the present co-culture model, being capable of improving the differentiation of both cell types. Furthermore, the assessed co-culture appears to be a useful tool to investigate cell response toward newly synthesized or commercially available biomaterials, as well as to evaluate their engraftment potential in restorative dentistry