Selenium preserves keratinocyte stemness and delays senescence by maintaining epidermal adhesion.

Skin is constantly exposed to environmental factors such as pollutants, chemicals and ultra violet radiation (UV), which can induce premature skin aging and increase the risk of skin cancer. One strategy to reduce the effect of oxidative stress produced by environmental exposure is the application of antioxidant molecules. Among the endogenous antioxidants, selenoproteins play a key role in antioxidant defense and in maintaining a reduced cellular environment.

Clinical zinc deficiency as early presentation of Wilson disease.

Wilson disease is a rare autosomal recessive disorder of the copper metabolism caused by homozygous or compound heterozygous mutations in the ATP-ase Cu(2+) transporting polypeptide (ATP7B) gene. The copper accumulation in different organs leads to the suspicion of Wilson disease. We describe a child with clinical zinc deficiency as presenting symptom of Wilson disease, which was confirmed by 2 mutations within the ATP7B gene and an increased copper excretion.

Chemokine Expression in Inflamed Adipose Tissue Is Mainly Mediated by NF-κB.

Immune cell infiltration of expanding adipose tissue during obesity and its role in insulin resistance has been described and involves chemokines. However, studies so far have focused on a single chemokine or its receptor (especially CCL2 and CCL5) whereas redundant functions of chemokines have been described. The objective of this work was to explore the expression of chemokines in inflamed adipose tissue in obesity.

Bioeffects of a combination of trace elements on adipocyte biology.

The white adipose tissue plays a major role in the development of obesity and associated metabolic complications by producing a variety of pro and anti-inflammatory adipokines. Recently, studies in humans or in animals have shown a beneficial effect of certain trace elements such as zinc on insulin resistance and adipokine secretion. The aim of our study was to test the effect of a zinc-nickel-cobalt solution (ZnNiCo) on adipocyte function and to identify potential health effects of this solution in the context of obesity and associated disorders.

Hidradenitis suppurativa: the role of deficient cutaneous innate immunity.

Objective: To evaluate the expression of innate immunity markers at the site of nodules caused by hidradenitis suppurativa (HS).

Design: Prospective analysis of 12 patients with HS.

Setting: Unité de Cancéro-Dermatologie, Nantes Hospital, Nantes; Service de Dermatologie, Poitiers Hospital, Poitiers; and Service de Dermatologie, Clinique de Courlancy, Reims, France

Patients: Twelve patients (Hurley stage I or II) in whom the disease had progressed for at least 6 months and who had a minimum of 2 closed nodules in typical sites.

Symptomatic acquired zinc deficiency in at-risk premature infants: high dose preventive supplementation is necessary.

Zinc is a cofactor for several enzymes involved in many metabolisms. Zinc deficiency induces various disorders such as acrodermatitis enteropathica, either inherited or acquired. We report three cases of premature infants (24-31 wks gestational age) with low birthweight (650 to 940 g) and enteropathy, two of whom presented with necrotizing enterocolitis.

TNF-induced beta2 integrin activation involves Src kinases and a redox-regulated activation of p38 MAPK.

We previously demonstrated that the TNF-alpha-induced inside-out signaling leading to beta(2) integrin activation is redox regulated. To identify kinases involved in this pathway, the effects of kinase inhibitors on the expression of beta(2) integrin activation neoepitope (clone 24) were investigated. We show that both p38 MAPK (inhibited by SB203580) and Src kinases (inhibited by PP2) are involved in beta(2) integrin activation by TNF and oxidants in human neutrophils.