PURPOSE With constraints and a risk of complication, tissue expansion in child's burn sequelae need a controlled surgical procedure, and a therapeutic plan appropriate to the specific pediatric healing, growth, and development. MATERIAL AND METHODS Our principles of management and technical points are described. A retrospective study of tissue expansion in child's burn sequelae between 2005 and 2016 is submitted. RESULTS There are 185 expanders, 98 protocols in 41 children, over half of sequelae concerning scalp, neck and chest. Mean age at the first expansion was 10.3 years old (5.8 years after burn). There are in average 2,4 (1-8) protocols by patient, with 1.9 (1-4) expanders by procedure. Surgical repair was a flap (78.8%), a full-thickness skin graft (13.3%) or both. Fifteen patients (30 expanders (14.6%) and 22 protocols (22.4%)), had expansion's complications, mostly infections and expositions. Eight patients (14 expanders (7.6%) and 10 protocols (10.2%)) had reconstructive's complications. An increase of burn area was a risk factor of complication (significant). Complicated expanders rate by location was 7.9% (scalp), 12.5% (neck), 9.8% (supraclavicular), 10.5% (chest), 19.4% (abdomen), 30% (buttock), 29.4% (lower limb), 1/2 (face). CONCLUSION Tissue expansion in child's burn sequelae is ideal in scalp, good in neck, chest and proximal upper limb, and to do carefully in lower limb and face. BACKGROUND Heart failure is the leading cause of death in grown-up congenital heart disease patients (GUCH). Although heart transplantation (OHT) remains the gold standard in end-stage heart failure, the ratio of GUCH patients undergoing this procedure remains low. OBJECTIVE Describe the cohort of GUCH patients undergoing heart transplantation at a third-level hospital. METHODS A retrospective review of GUCH patients undergoing OHT between 1997 and 2019 was conducted at a single tertiary university hospital. We included different preoperative (demographic and clinical data, cardiac catheterization data from the last routine hemodynamic monitoring) and postoperative variables (complications, survival). RESULTS Fourteen patients were enrolled. The median age was 25.5 years (range, 20.7-32.2). Eight patients (57.1%) were male. The median preoperative left ventricular ejection fraction was 37% (range, 22.5%-55%). As for preoperative hemodynamic evaluation, the median for the mean arterial pulmonary pressure was 19 mm Hg (range, 12-22.5), for the capillary wedge pressure was 16 mm Hg (range, 13.5-19.5), and for pulmonary vascular resistance was 1.83 Wood units (range, 1-4). After OHT, 6 patients (42.9%) suffered an infection, the most common of which was respiratory (3 out of 6). Four patients (28.6%) needed renal replacement therapy, and 4 patients (28.6%) presented liver failure. Four patients (28.6%) developed graft failure, thus requiring mechanical support with extracorporeal membrane oxygenation during a median of 6 days (range, 1-17.5). Survival rate of patients under extracorporeal membrane oxygenation was 50%, and overall survival rate was 78.6%. CONCLUSION OHT represents a good option for GUCH patients, with good overall survival rates. Increasing evidences demonstrate that circular RNAs (circRNAs) are extensively implicated in various cancers including colorectal cancer (CRC). In the present study, we found that circRNA HIPK3 (circPIK3) was upregulated in CRC. We identified that circHIPK3 was closely related with unfavorable clinicopathological features in patients with CRC. Apalutamide supplier Functional transwell assay and proliferation assay indicated that circHIPK3 served as an oncogene and promoted CRC cells migration, invasion and proliferation. Meanwhile, we found that formin like 2 (FMNL2) was a key downstream molecule in circHIPK3-induced metastasis and proliferation in CRC cells. We further verified that circHIPK3 was mainly located at cytoplasm through an immunofluorescence assay. An online bioinformatics screening and a GEO datasets analysis showed that microRNA 1207-5p (miR-1207-5p) was downregulated in CRC. Also, we found that miR-1207-5p shared a similar miR-1207-5p response elements (MREs-1207-5p). Meanwhile, we showed that miR-1207-5p suppressed CRC cells migration, invasion and proliferation via directly targeting of FMNL2. Even further, via a constructed luciferase assay, we indicated that circHIPK3 was another target of miR-1207-5p. Functionally, we proved that circHIPK3 enhanced FMNL2 mediated promotion of migration, invasion and proliferation by sponging of miR-1207-5p in CRC cells. In summary, the outcomes of this study illustrated that circHIPK3 promoted CRC cells migration, invasion and proliferation modulating of FMNL2 by sponging of miR-1207-5p. Our findings indicated that circHIPK3/miR-1207-5p/FMNL2 axis might be a new strategy in molecular treatment of CRC. Homeostasis of metal micronutrients such as copper is tightly regulated to ensure deficiency does not occur while restricting damage resulting from excess accumulation. Using LC-MS the effect on the proteome of intestinal Caco-2 cells of exposure to the chelator triethylenetetramine (TETA) was investigated. Continuous exposure of TETA at 25 μM to Caco-2 cells caused decreased cell yields and morphological changes. These effects were reversed when cells were no longer exposed to TETA. Quantitative proteomic analysis identified 957 mostly low-fold differentially expressed proteins, 41 of these returned towards control Caco-2 expression following recovery. Proteins exhibiting this "reciprocal" behaviour included upregulated deoxyhypusine hydroxylase (DOHH, 15.69- fold), a protein essential for eIF-5A factor hypsuination, a post translational modification responsible for eIF-5A maturation, which in turn is responsible for translation elongation. Exposure to TETA also resulted in 87 proteins, the expression of which was stable and remained differentially expressed following recovery. This study helps to elucidate the stable and transient proteomic effects of TETA exposure in intestinal cells. Telmisartan, an angiotensin II type 1 receptor blocker (ARB), is widely used to treat hypertension. Dysfunction of vascular smooth muscle cells (VSMCs) is well-established to contribute to the pathogenesis of various vascular diseases. A growing body of evidence indicates that increased VSMC contractility plays a primary role in the development of pathological artery spasms. Nevertheless, effect of telmisartan on VSMC contractility, and its mechanism of action remain unknown. Here, we investigated the mechanism by which telmisartan inhibits VSMC contractility and vessel contraction in rat VSMCs and endothelium-deprived aortas. Telmisartan inhibited phenylephrine-induced vessel contraction in endothelium-deprived aortas, and decreased myosin light chain kinase (MLCK) levels (without altering corresponding mRNA levels) and myosin light chain (MLC) phosphorylation at Ser19 (p-MLC-Ser19) in VSMCs. MG-132 but not doxycycline significantly restored telmisartan-inhibited MLCK expression and p-MLC-Ser19. Telmisartan induced AMP-activated protein kinase (AMPK) phosphorylation at Thr172 (p-AMPK-Thr172), and compound C or ectopic expression of the dominant negative (dn)-AMPKα1 gene significantly reversed telmisartan-inhibited MLCK expression and p-MLC-Ser19.