Prolonged cord separation in a newborn: a rare case of an unusual epithelialised umbilical cord.

A female full-term neonate, accompanied by her parents, was referred to the paediatric surgery department on the day of after birth. She presented with a 9 cm length pathological umbilical cord, of which the first 7 cm was red and wet, with ulceration, necrosis and healing areas. The patient never had a fever. Abdominal palpation showed no umbilical hernia and abdominal Doppler ultrasound was normal. After several days of disinfection, by biseptine antiseptic solution, and a monthly follow-up, most of the umbilical cord fell out. It only remained a 4 cm length navel consisting of 2 cm of excessive skin and 2 cm of mucous tissue. The lesion was surgically excised at 6 months old. The patient was discharged on postoperative day 1. The results of the histology confirmed the diagnosis of an epithelialised umbilical cord. The 1-month follow-up was uneventful.

Modulation of Gene Expression in a Sterile Atopic Dermatitis Model and Inhibition of Staphylococcus aureus Adhesion by Fucoidan.

Atopic dermatitis is a multifactorial pathology that includes perturbations of gene expression and increased adhesion of Staphylococcus aureus. Fucoidans are seaweed-derived sulfated fucose-rich polysaccharides that are known to be anti-inflammatory and may inhibit adhesion of pathogens. Fucoidan was assessed for effects on gene expression of an in vitro 3D model of atopic dermatitis. It was also assessed for inhibitory effects on the adhesion of bacteria onto 3D reconstructed skin. Fucoidan significantly altered gene expression in the atopic dermatitis model, and there was a trend to reduce periostin levels. Fucoidan significantly inhibited the adhesion of Staphylococcus aureus and Cutibacterium acnes but did not affect the adhesion of Staphylococcus epidermidis. Fucoidan may be a useful topical agent to assist in the management of atopic dermatitis.

Thoracic skeletal anomalies following surgical treatment of esophageal atresia. Lessons from a national cohort.

INTRODUCTION: Thoracotomy as surgical approach for esophageal atresia treatment entails the risk of deformation of the rib cage and consequently secondary thoracogenic scoliosis. The aim of our study was to assess these thoracic wall anomalies on a large national cohort and search for factors influencing this morbidity. MATERIALS AND METHODS: Pediatric surgery departments from our national network were asked to send recent thoracic X-ray and operative reports for patients born between 2008 and 2010 with esophageal atresia. The X-rays were read in a double-blind manner to detect costal and vertebral anomalies. RESULTS: Among 322 inclusions from 32 centers, 110 (34.2%) X-rays were normal and 25 (7.7%) displayed thoracic malformations, including 14 hemivertebrae. We found 187 (58.1%) sequelae of surgery, including 85 costal hypoplasia, 47 other types of costal anomalies, 46 intercostal space anomalies, 21 costal fusions and 12 scoliosis, with some patients suffering from several lesions. The rate of patients with these sequelae was not influenced by age at intervention, weight at birth, type of atresia, number of thoracotomy or size of the center. The rate of sequelae was higher following a classical thoracotomy (59.1%), whatever the way that thoracotomy was performed, compared to nonconverted thoracoscopy (22.2%; p=0.04). CONCLUSION: About 60 % of the patients suffered from a thoracic wall morbidity caused by the thoracotomy performed as part of surgical treatment of esophageal atresia. Minimally invasive techniques reduced thoracic wall morbidity. Further studies should be carried out to assess the potential benefit of minimally invasive approaches to patient pulmonary functions and on the occurrence of thoracogenic scoliosis in adulthood. LEVELS OF EVIDENCE: Level III retrospective comparative treatment study.

The activation of cultured keratinocytes by cholesterol depletion during reconstruction of a human epidermis is reminiscent of monolayer cultures.

Transient cholesterol depletion from plasma membranes of human keratinocytes has been shown to reversibly activate signalling pathways in monolayer cultures. Consecutive changes in gene expression have been characterized in such conditions and were interestingly found to be similar to transcriptional changes observed in keratinocytes of atopic dermatitis (AD) patients. As an inflammatory skin disease, AD notably results in altered histology of the epidermis associated with a defective epidermal barrier. To further investigate whether the activation of keratinocytes obtained by cholesterol depletion could be responsible for some epidermal alterations reported in AD, this study was undertaken to analyse cholesterol depletion in stratified cultures of keratinocytes, i.e. a reconstructed human epidermis (RHE). RHE contains heterogeneous populations of keratinocytes, either proliferating or progressively differentiating and stratifying towards the creation of a cornified barrier. Cholesterol depletion induced in this model was found reversible and resulted in activation of signalling pathways similar to those previously identified in monolayers. In addition, selected changes in the expression of several genes suggested that keratinocytes in RHE respond to cholesterol depletion as monolayers. However, preserved histology and barrier function indicate that some additional activation, likely from the immune system, is required to obtain epidermal alterations such as the ones found in AD.

Increased abundance of cytoplasmic and nuclear caveolin 1 in human diploid fibroblasts in H(2)O(2)-induced premature senescence and interplay with p38alpha(MAPK).

Treatment of IMR-90 human diploid fibroblasts with a sublethal concentration of H(2)O(2) induces premature senescence. We investigated the protein abundance, subcellular localization and involvement of caveolin 1 in premature senescence. Caveolin 1 is a scaffolding protein able to concentrate and organize signaling molecules within the caveolae membrane domains. We report the first evidence of increased nuclear and cytoplasmic localization of caveolin 1 during establishment of H(2)O(2)-induced premature senescence. Moreover, we demonstrate that phosphorylation of caveolin 1 during treatment with H(2)O(2) is dependent on p38alpha mitogen-activated protein kinase.

Role of TGF-beta1-independent changes in protein neosynthesis, p38alphaMAPK, and cdc42 in hydrogen peroxide-induced senescence-like morphogenesis.

The role of TGF-beta1 in hydrogen peroxide-induced senescence-like morphogenesis has been described. The aim of this work was to investigate whether TGF-beta1-independent changes in protein synthesis are involved in this morphogenesis and to study possible mechanisms occurring earlier than TGF-beta1 overexpression. Among the multiple TGF-beta1-independent changes in protein neosynthesis, followed or not by posttranslational modifications, identified by proteomic analysis herein, those of ezrin, L-caldesmon, and HSP27 were particularly studied. Rho-GTPase cdc42 was shown to be responsible for p38(MAPK) activation, in turn triggering phosphorylation of L-caldesmon and HSP27. Cdc42 was also shown to be mainly responsible for the increase in TGF-beta1 mRNA level observed at 24 h after treatment with H(2)O(2) and onward. This study further clarified the mechanisms of senescence-like morphogenesis in addition to the previously demonstrated role of TGF-beta1 signaling pathways.

Upregulation of annexin A2 in H(2)O(2)-induced premature senescence as evidenced by 2D-DIGE proteome analysis.

Human diploid fibroblasts undergo premature senescence after treatment with sublethal concentration of H(2)O(2). We report the first proteomic study of microsomal proteins in the context of H(2)O(2)-induced premature senescence by using 2D-DIGE approach. Twelve different proteins with altered abundance at day 3 after treatment with H(2)O(2) were identified. Among them, we demonstrated a re-localization of annexin A2 in plasma membrane.

Transient increased extracellular release of H2O2 during establishment of UVB-induced premature senescence.

In this work, we found that extracellular release of H(2)O(2) is 1.5- to 6-fold higher in skin human diploid fibroblasts exposed to UVB in conditions inducing premature senescence when compared to control cells without exposure to UVB. The apparent decrease in H(2)O(2) production from 0 to 72 h after the last exposure to UVB was not due to increased enzymatic activity of catalase or glutathione peroxidase.

Comparison of replicative senescence and stress-induced premature senescence combining differential display and low-density DNA arrays.

Human diploid fibroblasts (HDFs) exposed to subcytotoxic stress display many features of senescence. Using differential display RT-PCR, gene expression of HDFs in premature senescence induced by tert-butylhydroperoxide or ethanol and in replicative senescence was compared to gene expression of HDFs at early cumulative population doublings. Thirty genes of known function were identified from the 265 differentially displayed cDNA fragments. A customized low-density array allowed to confirm the relative level of the corresponding 30 transcripts. We found differential expression of genes coding for proteins implicated namely in growth arrest (PTEN, IGFBP-3, LRP-1 and CAV1), senescent morphogenesis (TGF-beta1 and LOXL2) and iron metabolism (TFR and FTL).