Objective:To evaluate the value of CT angiography (CTA) in the assessment of risk factors for rupture of intracranial aneurysm (IA).Methods:The clinical and CT imaging data of 46 patients with IA in the Second Affiliated Hospital of Bengbu Medical College from January 2018 to June 2020 were retrospectively analyzed. The morphological parameters of aneurysm were analyzed by CTA post-processing images: aneurysm number, site, morphology, maximum diameter, height/neck width, maximum diameter/parent artery proximal diameter, aneurysm incidence angle. The morphological risk factors of aneurysm rupture were evaluated by univariate analysis and multivariate logistic regression analysis. We used receiver operating characteristics curve (ROC) to evaluate the diagnostic efficacy in predicting aneurysm rupture.Results:A total of 58 aneurysms were detected by CTA, 30 ruptured aneurysms and 28 unruptured aneurysms. There was no statistically significant difference in gender and age between patients with ruptured and unruptured aneurysms ( P>0.05). In the morphological parameters of ruptured and unruptured aneurysms, there were no statistically significant differences in the number, site and height/neck width of aneurysms ( P>0.05), while there were statistically significant differences in aneurysm morphology, maximum diameter, maximum diameter/parent artery proximal diameter and aneurysm incidence angle ( P<0.05). Multivariate logistic regression analysis showed that maximum diameter/parent artery proximal diameter and aneurysm incidence angle were independent risk factors for aneurysm rupture ( P<0.05). ROC curve analysis showed that when the maximum diameter of the tumor / the diameter of the proximal carrying artery >1.985, the area under the curve was 0.748, and the sensitivity and specificity were 76.7% and 64.3%, respectively; When the incidence angle of blood flow was >117.5°, the area under the curve was 0.673, and the sensitivity and specificity were 53.3% and 75.0% respectively. Conclusions:The maximum diameter/parent artery proximal diameter >1.985 and the aneurysm incidence angle >117.5° are independent risk factors for aneurysm rupture.

Objective:To investigate the effect of high-dose vitamin B6 on stress-induced liver cell death in rats with severe trauma and its possible mechanism.Methods:Thirty-two male SD rats were selected and divided into sham surgery group, sham surgery+B6 group, trauma group, and trauma+B6 group by using a random number table, with 8 rats in each group. Rat models of severe trauma were established by inducing abdominal wall injury, bilateral femoral fractures, unilateral cranial injury, and withdrawal of 4 ml blood from the femoral artery. The sham surgery+B6 group and trauma+B6 group were treated with saline solution plus high-dose vitamin B6, while the sham surgery group and trauma group with infusion of saline solution only. At 36 hours after injury, rat liver tissues were collected for the following experiments: (1) the genes differentially expressed in the liver tissues of the rats of the trauma group and the trauma+B6 group were screened with next-generation sequencing, followed by an analysis of the possible involvement of cell death pathways; (2) validation was conducted to ascertain whether high-dose vitamin B6 could influence various cell death pathways in the liver cells in the sham surgery group, sham surgery+B6 group, trauma group, and trauma+B6 group: apoptosis was confirmed through terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining; necroptosis was verified by mixed lineage kinase domain-like protein (MLKL) immunohistochemical staining; autophagy was examined via transmission electron microscopy; ferroptosis was confirmed by detecting oxidative malondialdehyde (MDA) levels, oxidized glutathione levels, Prussian blue staining with diaminobenzidine (DAB) enhancement, transmission electron microscopy, and immunohistochemical staining for acyl-CoA synthetase long-chain family member 4 (ACSL4); (3) Biological information analyses [Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Enrichment analysis (GSEA)] were performed for biological processes and signaling pathways represented by liver tissue sequencing results of rats between the trauma group and the trauma+B6 group.Results:(1) In the liver tissues of rats, there were 344 significantly differentially expressed genes between the trauma group and trauma+B6 group, comprising 137 upregulated genes and 207 downregulated genes, of which 18 genes were associated with apoptosis, autophagy, necroptosis, ferroptosis, and pyroptosis. (2) No significant differences were found in TUNEL staining among the sham surgery group, sham surgery+B6 group, trauma group or trauma+B6 group; MLKL protein expression levels in the liver tissues after trauma were improved, of which the trauma+B6 group was lower than that of the trauma group; Electron microscopy showed that autophagic activity in the liver cells were significantly increased after trauma, which was significantly lower of the trauma+B6 group than that of the trauma group; MDA levels in the rat liver tissues were (0.20±0.05)nmol/mg, (0.17±0.07)nmol/mg, (0.69±0.11)nmol/mg and (0.52±0.07)nmol/mg in the sham surgery group, sham surgery+B6 group, trauma group, and trauma+B6 group respectively ( P<0.01), with the trauma group having the highest MDA levels and trauma+B6 group having lower MDA levels than the trauma group; Oxidized glutathione levels in the liver tissues of the four groups were (11.75±2.09)μmol/g, (11.69±1.66)μmol/g, (19.75±3.40)μmol/g, and (14.51±1.46)μmol/g respectively ( P<0.01), with the trauma group having the highest levels and trauma+B6 group having lower levels than the trauma group; Significantly increased iron deposition was observed in the liver tissues after trauma, with lower iron deposition in trauma+B6 group than the trauma group; Electron microscopy revealed significantly lower mitochondrial membrane density in the trauma+B6 group compared to the trauma group. ACSL4 protein expression level was lower in the trauma+B6 group compared to the trauma group; (3) GO, KEGG and GSEA enrichment analyses suggested that high-dose vitamin B6 may enhance cholesterol synthesis metabolism in the liver cells and alleviate oxidative stress to reduce liver cell damage and restore normal liver cell function after trauma. Conclusions:High-dose vitamin B6 attenuates stress-induced liver injury in rats with severe trauma by inhibiting the progression of necroptosis, autophagy and ferroptosis. Its molecular mechanism may be associated with enhanced hepatic cholesterol synthesis metabolism and alleviation of oxidative stress in the liver cells.