Experimental dermatology
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Experimental dermatology · Dec 2011
Letter Case ReportsA novel mutation of the glomulin gene in an Italian family with autosomal dominant cutaneous glomuvenous malformations.
Glomuvenous malformations (GVM) are hamartomas characterized histologically by glomus cells, which should be distinguished from glomus tumors. Familial GVM are rare, often present as multiple lesions, and exhibit familial aggregation, with autosomal dominant transmission. GVM are caused by mutations of the glomulin (GLMN) gene on chromosome 1p21-p22. ⋯ A second somatic 'hit' mutation in GLMN was not discovered in our family. We further provide histological, immunohistochemical and electron microscopic data exhibiting the classic features of GVM. The diagnosis of GVM is critical because of distinction from venous malformations and blue rubber bleb nevus syndrome, which may demonstrate clinical similarities but require different treatment.
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In psychophysical experiments, humans use different verbal responses to pruritic and algesic chemical stimuli to indicate the different qualities of sensation they feel. A major challenge for behavioural models in the mouse of chemical itch and pain in humans is to devise experimental protocols that provide the opportunity for the animal to exhibit a multiplicity of responses as well. ⋯ Meeting this criterion is complicated by the fact that the type of behavioural responses exhibited by the mouse depends in part on the site of chemical application such as the nape of the neck that evokes only scratching with the hind paw versus the hind limb that elicits licking and biting. Here, we review to what extent mice behaviourally differentiate chemicals that elicit itch versus pain in humans.
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Experimental dermatology · Jul 2011
Persistent CMV infection correlates with disease activity and dominates the phenotype of peripheral CD8+ T cells in psoriasis.
Previously, we have reported a frequent association of active plaque psoriasis with inflammation-mediated cytomegalovirus (CMV) reactivation. ⋯ Taken together with our previous results of inflammation-mediated CMV reactivation in psoriasis, our data support the concept of an interactive relationship between psoriasis and CMV infection which may be mediated by peripheral CD8+ T cells.
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Experimental dermatology · May 2011
Stress-induced epinephrine levels compromise murine dermal fibroblast activity through β-adrenoceptors.
Stress-induced catecholamine impairs the formation of granulation tissue acting directly in fibroblast activity; however, the mechanism by which high levels of catecholamines alter the granulation tissue formation is still unclear. Thus, the aim of this study was to investigate how high levels of epinephrine compromise the activity of murine dermal fibroblasts. Dermal fibroblasts isolated from the skin of neonatal Swiss mice were preincubated with α- or β-adrenoceptor antagonists. ⋯ In addition, the blockade of β3-adrenoceptors reversed the increase in fibroblast proliferation and nitric oxide synthesis as well as the reduction of fibroblast migration, AKT phosphorylation and active matrix metalloproteinase-2 expression induced by epinephrine. However, the blockade of α1- and α2-adrenoceptors did not alter the effects of epinephrine on the activity of murine dermal fibroblasts. In conclusion, high levels of epinephrine directly compromise the activity of neonatal mouse skin fibroblasts through the activation of β1-, β2- and β3-adrenoceptors, but not through α1- and α2-adrenoceptors.
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Burn injury is a complex traumatic event with various local and systemic effects, affecting several organ systems beyond the skin. The pathophysiology of the burn patient shows the full spectrum of the complexity of inflammatory response reactions. In the acute phase, inflammation mechanism may have negative effects because of capillary leak, the propagation of inhalation injury and the development of multiple organ failure. ⋯ Conversely, inflammation is a necessary prologue and component in the later-stage processes of wound healing. In this review, we are attempting to present the current science of burn wound pathophysiology and wound healing. We also describe the evolution of innovative strategies for burn management.