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Collated observations from several epidemiological studies have demonstrated that dietary intake of (poly)phenols from nuts, coffee, cocoa, grapes, and berries may protect against the development of atherosclerosis. Whereas this beneficial activity has previously been linked mainly to antioxidant or anti-inflammatory properties, recently emerging data suggest mechanisms by which (poly)phenolic substances can modulate cellular lipid metabolism, thereby mitigating atherosclerotic plaque formation. In this review, both experimental studies and clinical trials investigating the atheroprotective effects of the most relevant dietary (poly)phenols are critically discussed.

The incidence of overweight and obesity has reached epidemic proportions, making the control of body weight and its complications a primary health problem. Diet has long played a first-line role in preventing and managing obesity. However, beyond the obvious strategy of restricting caloric intake, growing evidence supports the specific antiobesity effects of some food-derived components, particularly (poly)phenolic compounds. The relatively new rediscovery of active brown adipose tissue in adult humans has generated interest in this tissue as a novel and viable target for stimulating energy expenditure and controlling body weight by promoting energy dissipation. This review critically discusses the evidence supporting the concept that the antiobesity effects ascribed to (poly)phenols might be dependent on their capacity to promote energy dissipation by activating brown adipose tissue. Although discrepancies exist in the literature, most in vivo studies with rodents strongly support the role of some (poly)phenol classes, particularly flavan-3-ols and resveratrol, in promoting energy expenditure. Some human data currently are available and most are consistent with studies in rodents. Further investigation of effects in humans is warranted.

Background Neonatal adrenal hemorrhage is a relatively uncommon condition (0.2–0.55%). Various risk factors have been reported in addition to birth asphyxia, such as sepsis, coagulation disorders, traumatic delivery, and perinatal injuries. Adrenal hemorrhage usually affects the right adrenal gland (about 70% of cases) while it involves the bilateral adrenal gland only in 10% of cases. In most cases, the event is asymptomatic but, in others, it may be so devastating to determine death by bleeding or adrenal insufficiency. Case presentation A case of bilateral neonatal adrenal hemorrhage, with adrenal insufficiency, but with no important risk factors and favorable evolution in a male infant. Conclusions This case emphasizes the importance of keeping a non-interventional attitude, avoiding early surgery but carrying out a serial sonographic follow-up. Serial ultrasound monitoring is the most reliable approach during conservative management. Electronic supplementary material The online version of this article (10.1186/s13052-019-0651-9) contains supplementary material, which is available to authorized users.

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Bolus milk feeding increases splanchnic oxygenation in both AGA and SGA infants, whereas continuous feeding does not. Splanchnic oxygenation is higher in AGA than in SGA infants both during bolus and continuous feeding. Continuous enteral feeding could help to limit the risk of hypoxic-ischemic gut damage in preterm infants in critical condition, especially in AGA infants.

Both a decrease in Rint > or =0.26 kPa L(-1) sec and a decrease in Z-score of > or =1.25 are appropriate for assessing BDR in preschool children with a history of recurrent wheezing. As Z-score is a more general solution, we recommend using a change in Z-score to determine BDR in preschool children. Further longitudinal studies will be required to determine the clinical utility of measuring BDR in managing lung disease in such children.

Adult hearts respond to increased workload such as prolonged stress or injury, by undergoing hypertrophic growth. During this process, the early adaptive responses are important for maintaining cardiac output whereas at later stages, pathological responses such as cardiomyocyte apoptosis and fibrosis cause adverse remodelling, that can progress to heart failure. Yet the factors that control transition from adaptive responses to pathological remodelling in the heart are not well understood. Here we describe the POU4F2/Brn-3b transcription factor (TF) as a novel regulator of adaptive hypertrophic responses in adult hearts since Brn-3b mRNA and protein are increased in angiotensin-II (AngII) treated mouse hearts with concomitant hypertrophic changes [increased heart weight:body weight (HW:BW) ratio]. These effects occur specifically in cardiomyocytes because Brn-3b expression is increased in AngII-treated primary cultures of neonatal rat ventricular myocytes (NRVM) or foetal heart-derived H9c2 cells, which undergo characteristic sarcomeric re-organisation seen in hypertrophic myocytes and express hypertrophic markers, ANP/βMHC. The Brn-3b promoter is activated by known hypertrophic signalling pathways e.g. p42/p44 mitogen-activated protein kinase (MAPK/ERK1/2) or calcineurin (via NFAT). Brn-3b target genes, e.g. cyclin D1, GLUT4 and Bax, are increased at different stages following AngII treatment, supporting distinct roles in cardiac responses to stress. Furthermore, hearts from male Brn-3b KO mutant mice display contractile dysfunction at baseline but also attenuated hypertrophic responses to AngII treatment. Hearts from AngII-treated male Brn-3b KO mice develop further contractile dysfunction linked to extensive fibrosis/remodelling. Moreover, known Brn-3b target genes, e.g. GLUT4, are reduced in AngII-treated Brn-3b KO hearts, suggesting that Brn-3b and its target genes are important in driving adaptive hypertrophic responses in stressed heart.