Trauma diagnostic-related target proteins and their detection techniques.

Trauma is a significant health issue that not only leads to immediate death in many cases but also causes severe complications, such as sepsis, thrombosis, haemorrhage, acute respiratory distress syndrome and traumatic brain injury, among trauma patients. Target protein identification technology is a vital technique in the field of biomedical research, enabling the study of biomolecular interactions, drug discovery and disease treatment. It plays a crucial role in identifying key protein targets associated with specific diseases or biological processes, facilitating further research, drug design and the development of treatment strategies. The application of target protein technology in biomarker detection enables the timely identification of newly emerging infections and complications in trauma patients, facilitating expeditious medical interventions and leading to reduced post-trauma mortality rates and improved patient prognoses. This review provides an overview of the current applications of target protein identification technology in trauma-related complications and provides a brief overview of the current target protein identification technology, with the aim of reducing post-trauma mortality, improving diagnostic efficiency and prognostic outcomes for patients.

Predictors of mortality in patients with isolated gastrointestinal perforation.

Gastrointestinal (GI) perforation is common in the emergency department and has a high mortality rate. The present study aimed to identify risk factors for mortality in patients with GI perforation. The objective was to assess and prognosticate the surgical outcomes of patients, aiming to ascertain the efficacy of the procedure for individual patients. A retrospective cohort study of patients with GI perforation who underwent surgery in a public tertiary hospital in China from January 2012 to June 2022 was performed. Demographics, clinical characteristics, laboratory and imaging results, and outcomes were collected from electronic medical records. The primary outcome measure was in-hospital mortality, and patients were divided into survivor and non-survivor groups based on this measure. Univariate and multivariable logistic regression analyses were performed to obtain independent factors associated with mortality. A total of 529 patients with GI perforation were eligible for inclusion. The in-hospital mortality rate after emergency surgery was 10.59%. The median age of the patients was 60 years (interquartile range, 44-72 years). Multivariable logistic regression analysis indicated that age, shock on admission, elevated serum creatinine (sCr) and white blood cell (WBC) count <3.5x109 or >20x109 cells/l were predictors of in-hospital mortality. In conclusion, advanced age, shock on admission, elevated sCr levels and significantly abnormal WBC count are associated with higher in-hospital mortality following emergency laparotomy.

Deciphering the molecular mechanism of the THBS1 gene in the TNF signaling axis in glioma stem cells.

Glioma stem cells (GSCs) are thought to be responsible for the initiation and progression of glioblastoma (GBM). GBM presents highly invasive growth with a very high recurrence rate, so it has become a clinical problem to be solved urgently. RNAseq demonstrates that thrombospondin 1 (THBS1) acts not only in the angiogenic core of glioma but also with a high degree of invasiveness and infiltration. Nevertheless, defects in the signaling pathway research lead to a poor prognosis in glioma patients. To investigate the relevant molecular mechanism and signal pathway of glioma stem cell behavior mediated by THBS1, U251 astroglioma cells and GSCs were taken as model cells for in vitro experiments. The biological effects of THBS1 on glioma proliferation, migration, and adhesion were evaluated using Cell Counting Kit-8(CCK8) assays, EdU incorporation assays, migration assays, Transwell assays, Western blotting, and RNAseq. We found that the knockout of the THBS1 gene by CRISPR/Cas9 promoted proliferation and migration in U251 cells and GSCs, as well as influencing cell cycle progression by regulating the TNF/MAPK/NF-κB and TGF-ß/Smad signaling pathways. Moreover, U251 cells and GSCs showed different responses to THBS1 knockout, suggesting specific and potential targets for GSCs in signaling pathways mediated by THBS1.