Dermoscopie du dermatofibrosarcome protubérant (une étude de 15 cas)

Le dermatofibrosarcome protubérant est une tumeur cutanée maligne rare dont le diagnostic est souvent retardé du fait de l'absence de signe clinique spécifique précoce. Méthodes : Nous avons réalisé un examen dermoscopique de 15 cas consécutifs non sélectionnés de dermatofibrosarcome protubérant prouvés histologiquement. Dans un premier temps, 6 critères dermoscopiques ont été identifiés collégialement, puis tous les cas ont été réexaminés séparément par 6 dermoscopistes expérimentés. Pour une lésion donnée, seuls les critères retrouvés par l'ensemble des dermoscopistes ont été retenus. La médiane du nombre de critères dermoscopiques notés était de 4 par lésion. Les critères dermoscopiques retrouvés étaient les suivants : un fin réseau pigmenté (87% ), des vaisseaux (80%), des aires brunes sans structure (73%), des stries blanches brillantes (67%), un fond rosé (67%) et des aires hypo ou dépigmentées sans structure. Quand ils étaient retrouvés, les vaisseaux étaient arborescents dans 11 cas sur 12 et étaient flous, nets ou l'association des deux. La première étude réalisée sur la dermoscopie du dermatofibrosarcome protubérant identifie 6 critères dermoscopiques (souvent associés dans un patron multicomposé) et un patron vasculaire particulier. La performance de la dermoscopie pour le diagnostic d'une lésion suspecte de dermatofibrosarcome protubérant reste à évaluer par de futures étudesLYON1-BU Santé (693882101) / SudocSudocFranceF

Utilisation de la dermoscopie en pratique quotidienne (enquête chez les dermatologues libéraux français)

LYON1-BU Santé (693882101) / SudocSudocFranceF

Vemurafenib in melanoma with BRAF V600E mutation.

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Planar graphs, via well-orderly maps and trees

International audienceThe family of well-orderly maps is a family of planar maps with the property that every connected planar graph has at least one plane embedding which is a well-orderly map. We show that the number of well-orderly maps with $n$ nodes is at most $2^{\alpha n + O(\log n)}$, where $\alpha \approx 4.91$. A direct consequence of this is a new upper bound on the number $p(n)$ of unlabeled planar graphs with $n$ nodes, $\log_2 p(n) \leq 4.91n$. The result is then used to show that asymptotically almost all (labeled or unlabeled), (connected or not) planar graphs with $n$ nodes have between $1.85n$ and $2.44n$ edges. Finally we obtain as an outcome of our combinatorial analysis an explicit linear-time encoding algorithm for unlabeled planar graphs using, in the worst-case, a rate of $4.91$ bits per node and of $2.82$ bits per edge

Planar graphs, via well-orderly maps and trees

The family of well-orderly maps is a family of planar maps with the property that every connected planar graph has at least one plane embedding which is a well-orderly map. We show that the number of well-orderly maps with n nodes is at most 2 αn+O(log n) , where α ≈ 4.91. A direct consequence of this is a new upper bound on the number p(n) of unlabeled planar graphs with n nodes, log 2 p(n) � 4.91n. The result is then used to show that asymptotically almost all (labeled or unlabeled), (connected or not) planar graphs with n nodes have between 1.85n and 2.44n edges. Finally we obtain as an outcome of our combinatorial analysis an explicit linear time encoding algorithm for unlabeled planar graphs using, in the worst-case, a rate of 4.91 bits per node and of 2.82 bits per edge

In vitro evidence for a direct antifibrotic role of the immunosuppressive drug mycophenolate mofetil.

International audienceThe immunosuppressive drug mycophenolate mofetil (MMF) is used to prevent organ rejection after transplantation and has shown some efficacy to prevent the fibrotic complications that occur during autoimmune diseases such as systemic sclerosis or during graft-versus-host disease (GVHD). We tested the hypothesis that MMF may exert direct effects on fibroblast extracellular matrix remodeling. Incubation of human lung fibroblast cultures with MMF led to dose- and time-dependent reduction in the synthesis and expression of type I collagen. Inhibition of COL1A1 and COL1A2 mRNA steady-state levels occurred at the level of transcription via repression of their promoters. In contrast, MMF significantly enhanced the expression and the synthesis of interstitial collagenase (matrix metalloproteinase-1). MMF was also found to diminish the capacity of fibroblast to contract mechanically unloaded collagen lattices and to reduce the synthesis of alpha-smooth muscle actin, a marker of the contractile myofibroblast phenotype. In addition, MMF diminished the fibroblasts motility. In conclusion, we provide novel mechanism by which MMF alters fibroblast functions important for wound healing and implicated in the development of tissue fibrosis, e.g., collagen production, extracellular matrix contraction, and cell migration. Such properties may contribute to the beneficial therapeutic effects of MMF against fibrotic lesions developing in systemic sclerosis or during GVHD

Blisters and Loss of Epidermis in Patients With Lupus Erythematosus

International audienceThe nosology of bullous lesions or equivalents (vesicles, erosions, and crusts) in patients with lupus erythematosus (LE) is rarely addressed.The primary aim of this study was to draw up a precise phenotypic inventory of such skin lesions; the secondary objective was to assess a potential relationship between the different types of loss of epidermis and extracutaneous lupus manifestations.We conducted a retrospective multicenter study including 22 patients with definite LE and bullous lesions or equivalents. All biopsies were reviewed. Patients were recruited in the dermatology departments of 6 centers. Patients were included if they met the diagnosis of systemic LE according to American College of Rheumatology and/or Systemic Lupus International Collaborating Clinics criteria or diagnosis of cutaneous LE based on classic clinical criteria and/or histological ascertainment of LE. Patients were recruited through clinician's memory and photographic collections.Three clinico-pathological patterns could be individualized. First, toxic epidermal necrolysis (TEN)-like, sheet-like, skin detachment; sun-exposure, mild mucosal involvement, and dermal mucin deposition allow differential diagnosis with classical Lyell syndrome. Second, vesiculo-bullae and/or crusting occurring on typical lesions of subacute cutaneous lupus erythematosus or chronic cutaneous lupus erythematosus. Third, tense vesicles and/or blisters with an underlying neutrophilic dermatosis and a usual response to dapsone.A careful analysis of 22 LE patients with epidermal detachment reveals 2 main pathomechanisms: a classic LE interface dermatitis, which can be hyperacute and lead to TEN-like skin detachment; and a neutrophilic dermatosis, with tense vesicles and/or blisters, including classic bullous LE

Modulation of collagen and MMP-1 gene expression in fibroblasts by the immunosuppressive drug rapamycin. A direct role as an antifibrotic agent?

International audienceWe have examined whether rapamycin, an immunosuppressive drug, may exert part of its antifibrotic activity by directly targeting fibroblast extracellular matrix deposition. Incubation of human lung fibroblast (WI-26) cultures with rapamycin led to dose- and time-dependent reduction in the expression of types I and III collagens, both at the protein and mRNA levels. Rapamycin had no effect on collagen promoter activity but accelerated mRNA decay, indicating post-transcriptional control of collagen gene expression. In contrast, rapamycin significantly enhanced the expression of interstitial collagenase (MMP-1) at the protein and mRNA levels and transcriptionally. We determined that rapamycin efficiently activates AP-1-driven transcription by rapidly inducing c-jun/AP-1 phosphorylation with activation of the c-Jun N-terminal kinase (JNK) cascade, resulting in enhanced binding of AP-1.DNA complex formation and AP-1-dependent gene transactivation. Conversely, the JNK inhibitor SP600125 inhibited rapamycin-induced MMP-1 gene transactivation and AP-1/DNA interactions. A c-jun antisense expression vector efficiently prevented rapamycin-induced MMP-1 gene transcription. Pharmacological inhibition of either ERK or p38 MAPK pathways was without effect on rapamycin-induced MMP-1 gene expression. It thus appears that rapamycin may exert direct antifibrotic activities independent from its immunosuppressive action