Objectives To investigate the effect of suppressor of fused (Sufu) on epidermal and dermal cellular properties and in wound healing. Approach Transgenic (TG) mice overexpressing human Sufu (hSufu) in the epidermis were applied to investigate the effects of Sufu on epidermal and dermal cellular properties and in wound healing. Results Histological staining revealed a reduction of epidermal and dermal thickness and an increase of hypodermal adipose tissue in homozygous K14-hSufu TG mice when compared with wild-type (WT) controls. TG mice exhibited significantly delayed skin wound healing. Moreover, the migratory and proliferative capabilities of cultured keratinocytes were decreased in K14-hSufuTG mice. Transforming growth factor-β treatment increased the expression of α-smooth muscle actin more in WT than in TG fibroblasts. Sufu overexpression significantly decreased the expression of β-catenin, glioma transcription factor 1 (Gli1), and matrix metalloproteinase-3 in wounds of K14-hSufu TG mice when compared with controls, probably indicating a delaying effect of Sufu on wound healing via blocking the hedgehog (Hh)/Gli and Wnt/β-catenin pathway. Innovation Our results indicate a new property of Sufu in the process of skin wound healing. It provides an important basis for Sufu as a potential target for skin wound healing. Conclusion Our findings suggest that Sufu overexpression in the epidermis impairs wound healing via dampening the Hh/Gli and Wnt/β-catenin signaling pathway. These data provide an important basis for further analyses of Sufu in skin wound healing. Copyright 2020, Mary Ann Liebert, Inc., publishers.Objective Acute gastric lesions are commonly seen in critically ill patients in the intensive care unit and can result in significant upper gastrointestinal bleeding. However, the signaling mechanisms that regulate this severe disease are still unclear. In this study, we explored the involvement of gastrokine 2 (GKN2) in the development of acute gastric lesions in mice. Approach We measured the degree of injury using the water immersion restraint stress mouse model. Inflammatory cells and factors were analyzed after gastric lesion induction. The luciferase reporter assay was used to detect the transcription activity of nuclear receptor subfamily 3 group C member 1 (NR3C1) in regulation of GKN2. We also detected the downstream pathway of GKN2 in gastric lesions. Results The results showed that GKN2 could aggravate stress-induced gastric lesions and gastric mucosal cell death. Moreover, the gastric lesion promoted by GKN2 was gastric acid independent. GKN2 could recruit neutrophils and promote the release of inflammatory factors to contribute to inflammation.  https://www.selleckchem.com/products/gf109203x.html  NR3C1, activated by cortisol under stress, could act as a transcription factor to upregulate the expression of GKN2. Innovation This study elucidates the process of gastric lesion at a molecular level and explores the possible contender biomarkers for diagnosis and drug targets in wound healing of gastric lesions. Conclusion In conclusion, GKN2, which was upregulated by cortisol, aggravated the gastric lesion through activation of the inflammasome and inflammatory reaction. Copyright 2020, Mary Ann Liebert, Inc., publishers.Objective Gastrostomy tubes (GTs) are one of the most common procedures in neonatal surgery, and their malfunction represents one of the most common complaints in the emergency room and clinic. Complications can occur in up to one-third of patients and include pain, peristomal leak, and infection, but can range in severity. We hypothesize that a preventative strategy employing a GT fixation dressing at the time of operation minimizes these postoperative complications in neonates. Approach All patients less than 1 year of age who underwent laparoscopic GT placement by a single surgeon in the study period were reviewed. All tubes were secured in place on the external abdominal wall for 2 weeks postoperatively. Demographics and outcomes were evaluated. Results Fifty-three percent of our cohort were male, and 47% were premature. The most common indication for placement was failure to thrive (59%), and common comorbid conditions were characterized as neurologic (71%), and cardiac (59%). The dressing did not prevent hypertrophic granulation tissue formation, but no patient experienced surgical site infection or device-related pressure injury at 30 and 120 days postoperatively. No patient required reoperation or readmission. Innovation This simple, one-time, cost-effective fixation dressing has the potential to reduce some of the most common postoperative surgical issues in neonatal patients and can be applied in almost any health care setting. Conclusions A dressing aimed at tube fixation and immobilization for the first two postoperative weeks averts some of the major complications of GT placement over a standard follow-up period as compared with the literature. Copyright 2020, Mary Ann Liebert, Inc., publishers.BACKGROUND Recently, as a possible therapy resolving solution, pentadecapeptide BPC 157 therapy, has been used in alleviating various vascular occlusion disturbances. BPC 157 was previously reviewed as novel mediator of Robert cytoprotection and endothelium protection in the stomach, and gut-brain axis, beneficial therapy in gastrointestinal tract, with particular reference to vascular recruitment, ulcerative colitis and tumor cachexia, and other tissues healing. Here we raised new hypothesis about BPC 157 therapy in the Budd-Chiari syndrome in rats, rapid bypassing of the suprahepatic inferior caval vein occlusion, and rats recovery with the active and effective pharmacotherapy treatment. AIM To investigate Budd-Chiari syndrome model (inferior caval vein suprahepatic occlusion) resolution, since BPC 157 resolves various rat vascular occlusion. METHODS We assessed the activated bypassing pathways between the inferior and superior caval veins and portocaval shunt, counteracted caval/portal hypertension, aortalior vena cava and portocaval shunt occurred rapidly. Even with severe caval ˃ portal hypertension, BPC 157 antagonized portal and caval hypertension and aortal hypotension, and also reduced refractory ascites. Thrombosis of portal vein tributaries, inferior vena cava, and hepatic and coronary arteries was attenuated. In addition, there was reduced pathology of the lungs (severe capillary congestion) and liver (dilated central veins and terminal portal venules), decreased intestine hemorrhagic lesions (substantial capillary congestion, submucosal edema and architecture loss), and increased liver and spleen weight. During the period of ligation, nitric oxide- and malondialdehyde-levels in the liver remained within normal healthy values, and increases in serum enzymes were markedly reduced. CONCLUSION BPC 157 counteracts Budd Chiari syndrome in rats. ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.