Objective:To investigate the value of the size-specific dose estimate (SSDE) on dose estimations of children's head CT scans.Methods:A retrospective study was conducted on plain head CT scans of 252 patients with the 64-row detector CT device of Discovery 750HD in the Union Hospital, Tongji Medical College, Huazhong University of Science and Technology from January to September in 2019. The volume CT dose index (CTDI vol)values were recorded. The head circumference (HC), area, and CT value were measured using a self-developed computer program, and the water equivalent diameter (WED), size-specific conversion factors ( f293 and f220), and absorbed dose (SSDE 293 and SSDE 220) were calculated according to the AAPM reports 293 and 220.The patients were divided into three groups by the quartering meth odaccording to their HC(<47.8 cm, 47.8-52.7 cm, >52.7 cm)and four groups based on their ages(0-2, 3-6, 7-10 and 11-14 years old). The difference between parameters ( f220 and f293, SSDE 220 and SSDE 293、SSDE 293 and CTDI vol) were compared for different groups, and the correlation of HC with f293 and SSDE 293 was analyzed. Results:There was an overestimation of f220 by 11.11% ( t=252.61, P<0.05) compared with f293. SSDE 220 was overestimated by 10.31% ( t=228.21, P<0.05) compared with SSDE 293, and SSDE 293 was underestimated by 9.60% ( t=-31.34, P<0.05)compared with CTDI vol. For the three HC groups, SSDE 220 was overestimated by 8.54%, 10.37%, and 11.57% ( t=73.73, 438.58, 275.52, P<0.05)compared with SSDE 293, and SSDE 293 was underestimated by 1.30%, 9.79%, and 14.61% ( t=-1.91, -60.95, -47.64, P<0.05)compared with CTDI vol. For the four age groups SSDE 220 was overestimated by 8.45%, 10.00%, 10.57%, and 11.36% ( t=63.58, 232.29, 247.84, 302.95, P< 0.05)compared with SSDE 293, and SSDE 293 was underestimated by 1.49%, 8.27%, 10.63%, and 13.78% ( t=-1.83, -28.27, -37.30, -49.80, P< 0.05)compared with CTDI vol. Furthermore, HC was highly correlated with f293 and SSDE 293 ( r2=0.88 and 0.76, respectively, P< 0.05). Conclusions:The radiation dose in children′s head CT scanning can be more accurately estimated according to the AAPM Report 293, while it can be overestimated by CTDI vol. Meanwhile, the CT radiation dose can be patently overestimated with the AAPM Report 220 compared with Report 293.HC is closely correlated with f293 and SSDE 293 and it can be used to estimatee more accurately for SSDE and the radiation dose received by children during head CT scanning.

Previously, we proposed a new perspective of triptolide (TP)-associated hepatotoxicity: liver hypersensitivity upon lipopolysaccharide (LPS) stimulation. However, the mechanisms for TP/LPS-induced hepatotoxicity remained elusive. The present study aimed to clarify the role of LPS in TP/LPS-induced hepatotoxicity and the mechanism by which TP induces liver hypersensitivity upon LPS stimulation. TNF- inhibitor, etanercept, was injected intraperitoneally into mice to investigate whether induction of TNF- by LPS participated in the liver injury induced by TP/LPS co-treatment. Mice and hepatocytes pretreated with TP were stimulated with recombinant TNF- to assess the function of TNF- in TP/LPS co-treatment. Additionally, time-dependent NF-B activation and NF-B-mediated pro-survival signals were measured and . Finally, overexpression of cellular FLICE-inhibitory protein (FLIP), the most potent NF-B-mediated pro-survival protein, was measured and to assess its function in TP/LPS-induced hepatotoxicity. Etanercept counteracted the toxic reactions induced by TP/LPS. TP-treatment sensitized mice and hepatocytes to TNF-, revealing the role of TNF- in TP/LPS-induced hepatotoxicity. Mechanistic studies revealed that TP inhibited NF-B dependent pro-survival signals, especially FLIP, induced by LPS/TNF-. Moreover, overexpression of FLIP alleviated TP/LPS-induced hepatotoxicity and TP/TNF--induced apoptosis . Mice and hepatocytes treated with TP were sensitive to TNF-, which was released from LPS-stimulated immune cells. These and other results show that the TP-induced inhibition of NF-B-dependent transcriptional activity and FLIP production are responsible for liver hypersensitivity.