Sepsis commonly occurs in severe post-burn patients, often resulting in death. We aimed to evaluate the influence of early enteral feeding on outcomes in patients with extensive burns, including infection incidence, healing and mortality. We retrospectively reviewed 60 patients with extensive burns, 35 who had received early enteral nutrition and 25 who had received parenteral nutrition. Average healing time, infection incidence and mortality were clinically observed. Hemoglobin and serum albumin were monitored weekly in both groups during treatment. Causative organisms were identified in patients with sepsis. Infection incidence was significantly less in the enteral nutrition group than the parenteral nutrition group (17.1% vs 44.0%; p = 0.023); and latency duration was longer in the enteral nutrition group than in the parenteral nutrition group (30.5 ± 4.7 days vs 14.5 ± 2.3 days; p<0.001). Duration of antibiotic therapy of the enteral nutrition group was significantly shorter than that of the parenteral nutrition group (12.5 ± 3.0 days vs 19.8 ± 3.6 days; p<0.001). Mean hemoglobin results (10.1 ± 1.3 g/L vs 8.3 ± 1.5 g/L; p<0.001) and serum albumin results (44.7 ± 5.7 g/L vs 36.2 ± 6.9 g/L; p<0.001) of enteral nutrition and parenteral nutrition groups, respectively, provided an overview of systemic nutrition and protein metabolism, suggesting higher systemic nutrition and protein synthesis in enteral nutrition group than in parenteral nutrition group. Risk of post-burn infection is reduced in burn patients who are supported by earliest possible enteral nutrition.

Intrauterine adhesions (IUAs) severely hamper women's reproductive functions. Human amniotic mesenchymal stromal cell (hAMSC) transplantation is effective in treating IUAs. Here, we examined the function of Notch signalling in IUA treatment with hAMSC transplantation. Forty‐five Sprague‐Dawley female rats were randomly divided into the sham operation, IUA, IUA + E2, IUA + hAMSCs and IUA + hAMSCs + E2 groups. After IUA induction in the rats, hAMSCs promoted endometrial regeneration and repair via differentiation into endometrial epithelial cells. In all groups, the expression of key proteins in Notch signalling was detected in the uterus by immunohistochemistry. The results indicated Notch signalling activation in the hAMSCs and hAMSCs + E2 groups. We could also induce hAMSC differentiation to generate endometrial epithelial cells in vitro. Furthermore, the inhibition of Notch signalling using the AdR‐dnNotch1 vector suppressed hAMSC differentiation (assessed by epithelial and mesenchymal marker levels), whereas its activation using the AdR‐Jagged1 vector increased differentiation. The above findings indicate Notch signalling mediates the differentiation of hAMSCs into endometrial epithelial cells, thus promoting endometrial regeneration and repair; Notch signalling could have an important function in IUA treatment.