Patient-reported outcomes and their predictors 2 years after burn injury: A cross-sectional study.

This study aimed to describe patient-reported outcomes 2 years after burn injury and to comprehensively elucidate predictors that may influence these outcomes. This cross-sectional, prospective study included 352 patients who were admitted to the Department of Burn Surgery at a tertiary teaching hospital between January 2017 and December 2020. We collected demographic and disease-related data and instructed participants to complete the Readiness for Hospital Discharge Scale (RHDS) and the Burn Specific Health Scale-Brief (BSHS-B) questionnaire. The overall score of patient-reported outcomes 2 years after burn injury was 126.55 ± 33.32 points, and the dimensions with the lowest scores were "hand function" (13.96 ± 5.75), "heat sensitivity" (14.84 ± 4.90), "treatment regimens" (13.41 ± 6.77) and "work" (11.30 ± 4.97). Multiple linear regression analysis revealed that less postburn pruritus, better readiness for hospital discharge, less total body surface area (TBSA), better social participation, white-collar jobs, older age, better sleep quality and burns not caused by electricity were associated with better outcomes. Patients experienced poor patient-reported outcomes 2 years after burn injury. Integrated rehabilitative care is necessary to address patients' unique needs and improve long-term patient-reported outcomes.

Protective effects of Baicalin injection on severe acute pancreatitis through regulating follistatin-like-1 signaling pathway by down-regulating miR-429 expression in mice

Abstract In China, Scutellaria is used for treating inflammatory-related diseases. Baicalin is the main active component of Scutellaria and has protective effects on acute pancreatitis. However, the mechanism of Baicalin is still unclear. In this study, the protective effects of baicalin on acute pancreatitis induced by taurocholate and its mechanism are investigated. In this study, mice were randomly divided into three groups: sham operation, model, and treatment groups. Acute pancreatitis in mice was induced by intraperitoneal injection of taurocholate (35 mg/kg). The treatment group was given baicalin (100 mg/kg) 2 h before acute pancreatitis induction. The mRNA expression levels of miR-429, nuclear factor kappa B65(NF-kB65), toll-like receptor 4(TLR4), TNF receptor associated factor6 (TRAF6), NF-kappa-B inhibitor(IkB), Follistatin-like 1 (FSTL1), and interleukin-1 receptor-associated kinase (IRAK) in the liver tissues 24 h after intraperitoneal injection were detected by RT-PCR. Then, the expression levels of NF-kB65, p-NF-κB65, TLR4, TRAF6, IkB, FSTL1, IRAK, p- IRAK, and p- IkB-а proteins were detected by Western blot. IL-6, TNF-α and IL-1 ß in plasma were measured by ELISA, and histopathological changes in the pancreases of the mice were observed. The results showed that after baicalin treatment, miR-429 expression in the pancreatic tissues and the expression levels of NF-kB65, TLR4, TRAF6, p-IkB-а, FSTL1, and p-IRAK decreased. Similarly, pancreatic myeloperoxidase (MPO) activity and the plasma levels of IL-6, TNF-а, IL-12, IL-1ß1, endotoxin, serum amylase, and lipase were reduced. Thus, the pancreatic injury induced by taurocholate was alleviated. The present study indicates that pretreatment with Baicalin can alleviate acute pancreatic injury induced by taurocholate in mice. The mechanism may be associated with the decreased miR-429 expression, reduced FSTL1 signaling pathway activity, TLR4 and TLR4/MyD88 signaling pathway inhibition, and reduced pancreatic inflammation. FSTL1 is the regulatory target for miR-429

High level of calpain1 promotes cancer cell invasion and migration in oral squamous cell carcinoma.

Calpain1, termed conventional calpain and a member of the Ca2+-dependent neutral cysteine proteases, is considered to be involved in cancer formation and development. However, the effect of calpain1 on oral squamous cell carcinoma (OSCC) remains poorly understood. The aim of the present study was to evaluate the possibility of calpain1 as a potential molecular target for OSCC diagnosis and therapy. The present study demonstrates that calpain1 was overexpressed in OSCC cell lines and 4/7 of the tumor tissues in paired samples of tumor and noncancerous matched tissues (NCMT). In a cohort of 125 patients with primary OSCC, the high expression of calpain1 was an independent predictor for overall survival in a multivariate analysis (P=0.022). Furthermore, RNA interference-mediated suppression of calpain1 expression reduced the proliferation, migration and invasion potential of the HSC3 and CAL27 OSCC cell lines, but did not increase their apoptosis. These findings indicate that calpain1 may be a useful biomarker for novel prognostic and therapeutic strategies in oral squamous cell carcinoma.

Protective effect of Xuebijing injection on paraquat-induced pulmonary injury via down-regulating the expression of p38 MAPK in rats.

BACKGROUND: Exposure to paraquat results in acute lung injury. A systemic inflammatory response has been widely established as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of Xuebijing prevents inflammatory response-induced diseases. This study investigated whether consumption of Xuebijing protected rats against paraquat-induced acute lung injury. METHODS: Adult male Sprague Dawley rats were randomly divided into four groups: control group; paraquat group; paraquat + Xuebijing group; and paraquat + dexamethasone group. Rats in the paraquat, paraquat + Xuebijing and paraquat + dexamethasone groups were intraperitoneally injected with paraquat (30 mg/kg) or administered paraquat and Xuebijing at 8 mL/kg or dexamethasone at 5 mg/kg, respectively, via an injection into the tail vein. Lung p38 MAPK, NF-κB65, IkB, p-IκB-α, HIF-1α, Nrf2 and TGF-ß1 expression were essayed using western blotting. IL-6, TNF-α, IL-1ß, IL-10, TGF-ß1 and PIIIP were measured using ELISA. ROS, oxidised glutathione and glutathione activity were measured. RESULTS: After inducing acute lung injury with paraquat for 24 h, Xuebijing was observed to block lung p-p38 MAPK, NF-κB65, HIF-1α, p-IκB-α and TGF-ß1 expression, and increased Nrf2 and IkB expression. The numbers of neutrophils and lymphocytes and total number of cells were significantly lower in the Xuebijing group compared with the control group. IL-6, TNF-α, IL-1ß, TGF-ß1 and PIIIP levels were significantly decreased in the Xuebijing group. ROS and oxidised glutathione activity were markedly inhibited by Xuebijing. Histological evaluation showed attenuation of the effects of Xuebijing on paraquat-induced lung injury. Compared with the paraquat + dexamethasone group, the Xuebijing + paraquat group showed no significant differences. CONCLUSIONS: Inhibiting the expression of p38 MAPK and NF-κB65 was crucial for the protective effects of Xuebijing on paraquat-induced acute lung injury. The findings suggest that Xuebijing could effectively ameliorate paraquat-induced acute lung injury in rats. Xuebijing was as effective as dexamethasone at improving paraquat-induced lung injury by regulating lung inflammation, lung function and oxidative stress responses.

[Clinical phenotype and gene diagnostic analysis of Omenn syndrome].

OBJECTIVE: Omenn syndrome is a rare autosomal recessive hereditary severe combined immunodeficiency. The purpose of this study was to understand clinical characteristics and genetic mutation type of Omenn syndrome and to improve the recognition of Omenn syndrome among pediatric clinicians. METHOD: One suspected case of severe combined immunodeficiency was found to have pneumonia repeatedly, intractable diarrhea, poor antibiotic treatment effect, lymphadenopathy, hepatosplenomegaly and erythroderma. The patient was diagnosed as having Omenn syndrome by RT-PCR, and the expression of RAG1/RAG2 and gene analysis of RAG1/RAG2 were performed. RESULT: The classification of lymphocyte was CD3(+) cells (35.3%), CD19(+) cells (0.4%), CD16(+) cells (57.6%). After stimulation with phytohemagglutinin (PHA), lymphocyte proliferation of the child was extremely low. Genetic studies showed RAG1 homozygous deletion mutation (2302 del T). He had detectable activated T-lymphocytes with low circulating B-lymphocytes and no evidence of maternal T-cell engrafment as indicated by the short tandem repeat (STR) analysis. CONCLUSION: Omenn syndrome is a severe combined immunodeficiency disease caused by mutations in the RAG1/RAG2 gene. The disease has been reported rarely in China. The clinical manifestations of the disease is early postnatal repeated infections and erythroderma. Mutation analysis of RAG1/RAG2 gene may help to confirm the diagnosis and may be useful in early immune reconstitution and genetic counseling.