ients with acute TBI, but its value in selection of appropriate imaging modalities awaits further investigation. Serum S100B protein level, GCS score, and Rotterdam CT score can be used as indicators for evaluating the severity of acute TBI, and they are all closely related with early prognosis of the patients. The combination of serum S100B protein, GCS score and Rotterdam CT score has better performance than any of the 3 indexes alone for predicting early prognosis of the patients. Serum S100B protein level is correlated with head imaging findings of patients with acute TBI, but its value in selection of appropriate imaging modalities awaits further investigation. To explore the clinical phenotype and changes in joint structure and function in adolescent patients with severe hemophilia A under different doses of FVIII. Forty- three adolescents with severe hemophilia A aged 4-18 years were divided into on-demand group ( =7), low-dose group (FVIII dose of 10-15 U/kg, 2-3 times a week, and ≤30 U/kg a week; =17), and intermediate-dose group (FVIII dose of 15-20 U/kg, 2-3 times a week, and 45-60 U/kg a week ( =19). The 3 groups were compared for their clinical bleeding phenotype, annual bleeding rate (ABR), annual joint bleeding rate (AJBR), annual the most severe joint bleeding rate, joint imaging scores (ultrasound HEAD-US score and IPSG MRI score), Hemophilia Joint Health Score (HJHS) and Functional Independence Score in Hemophilia (FISH) within 24 months. Compared with that in on-demand group, the ABR was significantly reduced in the low- and intermediate-dose groups ( =0.004 and 0.000, respectively), and was reduced by 32.87% in the intermediate-dose group atermediate-dose groups ( =0.003 and 0.000, respectively), and the scores increased at a steady rate in the on-demand group but tended to decrease in the latter two groups. The FISH score was decreased by 0.29±3.09 in the on-demand group but was increased significantly in the low- and intermediate-dose groups compared with the on-demand group ( =0.000). In Chinese adolescents with severe hemophilia A, low- and intermediate-dose FVIII prophylaxis, especially at the intermediate dose, is better than on- demand treatment for protecting joint structure and function. In Chinese adolescents with severe hemophilia A, low- and intermediate-dose FVIII prophylaxis, especially at the intermediate dose, is better than on- demand treatment for protecting joint structure and function. To investigate the role of hepatocyte mitochondrial NDUFA13 loss in the liver fibrogenesis in mice and explore the possible mechanisms. We used liver-specific NDUFA13 heterozygous knockout mouse models (NDUFA13 ; Alb-Cre) established previously by intercrossing NDUFA13 and Alb-Cre mice, with their littermate control NDUFA13 mice as the control ( =8). The mice were euthanized at the age of 4 weeks and 2 years, and the liver tissues were collected for HE and Masson staining to observe the pathological changes and fibrosis phenotypes. Western blotting was performed to detect the expression of NDUFA13 protein in the liver tissues, and the infiltration of F4/80 macrophages and the expressions of TGF-β1, TNF-α and IL-1β were analyzed by immunofluorescence assay. The expression levels of α-SMA, matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteases 1 (TIMP-1), collagen-Ⅰ and collagen-Ⅲ were assayed by immunohistochemistry. HE and Masson staining showed obvious inflammatory ipecific NDUFA13 deficiency can trigger spontaneous and chronic liver fibrosis phenotypes in mice probably in association with abnormal activation of hepatic stellate cells induced by macrophages and inflammatory factors. To analyze spontaneous activities and energy metabolism in the medial prefrontal cortex (mPFC) of mice with chronic unpredictable mild stress (CUMS) and explore the correlation of these changes with the mTORC1 signaling pathway. Normal C57Bl/6 mice were randomly divided into control group ( =16) and depression model group ( = 16), and the mice in the latter group were subjected to 8 weeks of modeling with CUMS. Behavioral tests including open field test, sucrose consumption test, tail suspension test and forced swimming test were performed, and the changes in prefrontal gray matter volume and the amplitude of low frequency fluctuation (ALFF) in the mice were detected with functional magnetic resonance imaging. The CUMS mice were then randomized into two groups for treatment with ketamine ( =8) or saline ( =8). The mPFC tissues of the mice were collected for detecting the phosphorylation levels of mTORC1-related proteins with Western blotting and ATP level and NADP /NADPH ratio with ELISA in the 3 gration and can be alleviated by activating the mTORC1 pathway with ketamine. The mPFC of CUMS mice shows increased spontaneous activities but lowered productivity efficiency, indicating the presence of energy metabolism disorder in the mPFC, which is related with reduced mTORC1 phosphorylation and can be alleviated by activating the mTORC1 pathway with ketamine. To investigate the effect of protein C activator (PCA) from venom (AAV) in modulating early adaptive immune response of septic rats. Rat models of sepsis were established by intraperitoneal injection of lipopolysaccharide (LPS; 10 mg/kg) in 36 SD rats, which were divided into 6 groups ( =6) for sample collection at 4, 6, 8, 12, 16 and 24 h after LPS injection, with 6 rats injected with saline as the control group. Another 36 rats were divided into two groups, and 30 min after LPS injection, the rats were treated with SEW2871 (a sphingosine-1-phosphate receptor 1 agonist; 0.5 mg/kg) or PCA group (0.1 mg/kg), and each group was divided into 3 groups ( =6) for sample collection at 6, 12 and 24 h after LPS injection. https://www.selleckchem.com/ALK.html Plasma IL-4, S1P, IL-12 and IFN-γ levels of the rats were detected using ELISA, and the expressions of S1PR1 and CD103 in the mesenteric lymph nodes were detected with immunofluorescence assay. The plasma levels of S1P, IL-12, IL-4 and IFN-γ ( < 0.05) and the expressions of S1PR1 and CD103 in the mesenteric lymph nodes ( < 0.