The significance of admission blood lactate and fibrinogen in pediatric traumatic brain injury: a single-center clinical study.

BACKGROUND: Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in pediatric patients, leading to long-term physical, cognitive, and psychological impairments. Blood lactate and fibrinogen levels have emerged as potential biomarkers associated with tissue hypoperfusion and coagulation dysfunction, respectively. However, limited research has specifically focused on the significance of these biomarkers in pediatric TBI. This study aimed to investigate the clinical significance of blood lactate and fibrinogen levels upon admission in pediatric patients with traumatic brain injury. METHODS: The medical records of 80 children with a traumatic brain injury who were admitted from January 2017 to January 2021 were retrospectively analyzed. The two groups were compared according to whether the blood lactate in the admission arterial blood gas increased and the fibrinogen content in the coagulation function decreased. The clinical data of the children in the two groups were different, and then they were divided into a good prognosis group and a poor prognosis group according to the GOS prognostic score, and the differences in the clinical indicators of the two groups were compared. RESULTS: Among the 80 patients, 33 had elevated blood lactate levels, 34 had decreased fibrinogen levels, and 29 had an unfavorable outcome (GOS < 4). Compared to the normal blood lactate group, there were no statistically significant differences in age, sex ratio, or platelet count in the elevated blood lactate group (P > 0.05). However, the elevated blood lactate group had lower Glasgow Coma Scale (GCS) scores upon admission, higher blood lactate levels, lower fibrinogen levels, longer hospital stay, lower GOS scores, and a higher proportion of GOS < 4 (P < 0.05). Compared to the normal fibrinogen group, there were no statistically significant differences in age, sex ratio, or platelet count in the decreased fibrinogen group (P > 0.05). However, the decreased fibrinogen group had lower GCS scores upon admission, higher blood lactate levels, lower fibrinogen levels, longer hospital stays, lower GOS scores, and a higher proportion of GOS < 4 (P < 0.05). Compared to the favorable outcome group, there were no statistically significant differences in age, sex ratio, or platelet count in the unfavorable outcome group (P > 0.05). However, the unfavorable outcome group had lower GCS scores upon admission, higher blood lactate levels, lower fibrinogen levels, longer hospital stays, a higher incidence of pulmonary infection, a higher incidence of stress ulcers, and lower GOS scores (P < 0.05). CONCLUSION: The levels of blood lactate and fibrinogen may represent the severity of children with traumatic brain injury and may be risk factors for poor prognosis of children with traumatic brain injury.

[Small interfering RNA-mediated α-enolase knockdown suppresses glycolysis and proliferation of human glioma U251 cells in vitro].

OBJECTIVE: To investigate the role of α-enolase (ENO1) in regulating glucose metabolism and cell growth in human glioma cells. METHODS: Glucose uptake and lactate generation were assessed to evaluate the changes in glucose metabolism in human glioma U251 cells with small interfering RNA (siRNA)-mediated ENO1 knockdown. MTT assay and 5-ethynyl-2'-deoxyuridine (EdU) staining were used to examine the cell growth and cell cycle changes following siRNA transfection of the cells. RESULTS: Transfection of U251 cells with siRNA-ENO1 markedly reduced glucose uptake (P=0.023) and lactate generation (P=0.007) in the cells and resulted in significant suppression of cell proliferation (*P<0.05) since the second day following the transfection. Transfection with siRNA-ENO1 also obviously suppressed cell cycle G1/S transition in the cells (P=0.0425). The expressions of HK2 and LDHA, the marker genes for glucose metabolism, were significantly down-regulated in the cells with siRNA-mediated ENO1 knockdown. CONCLUSION: ENO1 as a potential oncogene promotes glioma cell growth by positively modulating glucose metabolism.