Angiogenesis plays a central role in wound healing. Among many known growth factors, vascular endothelial growth factor (VEGF) is believed to be the most prevalent, efficacious, and long-term signal that is known to stimulate angiogenesis in wounds. Whereas a direct role of copper to facilitate angiogenesis has been evident two decades ago, the specific targets of copper action remained unclear. This report presents first evidence showing that inducible VEGF expression is sensitive to copper and that the angiogenic potential of copper may be harnessed to accelerate dermal wound contraction and closure. At physiologically relevant concentrations, copper sulfate induced VEGF expression in primary as well as transformed human keratinocytes. Copper shared some of the pathways utilized by hypoxia to regulate VEGF expression. Topical copper sulfate accelerated closure of excisional murine dermal wound allowed to heal by secondary intention. Copper-sensitive pathways regulate key mediators of wound healing such as angiogenesis and extracellular matrix remodeling. Copper-based therapeutics represents a feasible approach to promote dermal wound healing.

In mammalian organs under normoxic conditions, O ₂ concentration ranges from 12% to <0.5%, with O ₂ ≈14% in arterial blood and <10% in the myocardium. During mild hypoxia, myocardial O ₂ drops to ≈1% to 3% or lower. In response to chronic moderate hypoxia, cells adjust their normoxia set point such that reoxygenation-dependent relative elevation of P o ₂ results in perceived hyperoxia. We hypothesized that O ₂ , even in marginal relative excess of the P o ₂ to which cardiac cells are adjusted, results in activation of specific signal transduction pathways that alter the phenotype and function of these cells. To test this hypothesis, cardiac fibroblasts (CFs) isolated from adult murine ventricle were cultured in 10% or 21% O ₂ (hyperoxia relative to the P o ₂ to which cells are adjusted in vivo) and were compared with those cultured in 3% O ₂ (mild hypoxia). Compared with cells cultured in 3% O ₂ , cells that were cultured in 10% or 21% O ₂ demonstrated remarkable reversible G ₂ /M arrest and a phenotype indicative of differentiation to myofibroblasts. These effects were independent of NADPH oxidase function. CFs exposed to high O ₂ exhibited higher levels of reactive oxygen species production. The molecular signature response to perceived hyperoxia included (1) induction of p21, cyclin D1, cyclin D2, cyclin G1, Fos-related antigen-2, and transforming growth factor-β1, (2) lowered telomerase activity, and (3) activation of transforming growth factor-β1 and p38 mitogen-activated protein kinase. CFs deficient in p21 were resistant to such O ₂ sensitivity. This study raises the vital broad-based issue of controlling ambient O ₂ during the culture of primary cells isolated from organs.

Adiponectin, secreted mainly by mature adipocytes, is a protein with insulin-sensitising and anti-atherogenic effects. Human adiponectin is encoded by the ADIPOQ gene on the chromosomal locus 3q27. Variations in ADIPOQ are associated with obesity, type 2 diabetes (T2DM) and related phenotypes in several populations. Our aim was to study the association of the ADIPOQ variations with body weight, serum adiponectin concentrations and conversion to T2DM in overweight subjects with impaired glucose tolerance. Moreover, we investigated whether ADIPOQ gene variants modify the effect of lifestyle changes on these traits.

Sleep disorders have become increasingly prevalent affecting health and working ability. Restorative sleep may be considered important for athletes’ successful recovery and performance. However, some athletes seem to experience major problems in sleeping. Thus far, there is limited scientific information about their sleep. This study aimed to evaluate the quality of sleep and the prevalence of sleep disorders as well as the impact of a structured sleep counselling protocol in professional athletes. A total of 107 professional ice hockey players participated in the study. The exploratory observational 1-year follow-up study consisted of questionnaire-based sleep assessment followed by general sleep counselling and, when needed, polysomnography and an individual treatment plan. One in every four players was found to have a significant problem in sleeping. All athletes considered sleep essential for their health and three in every four players considered that counselling would improve their performance. Counselling and individual treatment were found to improve significantly the quality of sleep with the mean alteration of 0.6 (95% CI 0.2–1.0, P = 0.004) in a scale from 0 to 10. Our results support that sleep problems are common in professional athletes. However, systematic examination, counselling and individual treatment planning can improve the quality of their sleep.