Objective To investigate human cardiac acidic isoferritin as a specific index of hepatic cancer.Methods Acidic isoferritin was isolated and purified from human heart muscle. A radioimmunoassay for the acidic isoferritin in human serum has been developed, on the equilibrium method. The antiserum was obtained from rabbits immunized with purified acidic isoferritin. The 125 I-acidic isoferritin was prepared by the chloramine-T method. The data were processed using the automated smoothed spline function data processing program.Results The intra- and inter-assay CV of acidic isoferritin RIA were 1.65% and 9.71%, respectively, and the recovery rate was 102%. The antiserum provided a linear response from 7.0 to 369.6 μg/L with ED50 of 27.50 μg/L. The cross reactivity with AFP, CEA, lactoferrin and transferrin was negligible, and that with ferritin was 1.74%. The serum acidic isoferritin concentration showed a considerable variation in different sex and age groups. The serum acidic isoferritin was measured in liver diseases including hepatic cancer, hepatic cirrhosis and acute and chronic hepatitis. Its sensitivity for diagnosis of hepatic cancer was 73.05%, independent from the severity of hepatic injury. In 8 malignant tumors studied, acidic isoferritin appeared the most valuable in the diagnosis of hepatic cancer, with its positive, negative, false positive and false negative rates all being ideal.Conclusions Acidic isoferritin may turn to be a rather specific index of hepatic cancer. Combination of monitoring both acidic isoferritin and AFP would raise the positive detection and specificity in the diagnosis of hepatic cancer.

Objective To observe the gastric changes in adult male Sprague-Dawly (SD) rats irradiated by the single large dose electron beam,providing animal experimental evidence for intraoperative radiotherapy for gastric cancer.Methods Thirty-eight SD rats were randomly divided into the control and experimental groups.The stomach of the rats in the experimental group were subject to single 6 MeV 20 Gy irridiation by using the patent technology of Accurate Irradiation Experiment Table for Small Animal Radiation.The general conditions,gastric injury and body weight change were observed at different days following irradiation.Results The most severe gastric damage of rats was observed on the 14th d after irradiation.The gastric injury was gradually repaired accompanied with glandular atrophy at 28 d postirradiation,and the gastric injury was manifested as cellulose fibrinous repair on the 56th d after irradiation.Within 1 week post-irradiation,weight loss was noted in the experimental group,which significantly differed from the rats in the control group (P＜0.05).During the 2nd week,the body weight was increased in the experimental group,significantly lower compared with the rats in the control group (P＜ 0.05).The body weight of rats did not significantly differ between two groups at 6 weeks after irradiation (P＞ 0.05).Conclusions The most severe gastric injury is observed at 2 weeks after the single-dose 6 MeV electron beam 20 Gy irradiation,whereas no gastric perforation occurs.The gastric injury can be restored to normal status within 8 weeks following irradiation.

Background Mitochondrial dynamin-related protein 1 (DRP1) regulates mitochondrial division and plays an important role in maintaining hepatocyte function. However, the role of DRP1 in cadmium exposure-induced maternal liver damage in pregnant mice remains unclear. Objective To investigate the role and mechanism of DRP1 in maternal liver damage induced by cadmium exposure during pregnancy. Methods This study consisted of animal experiments and cell experiments. (1) Animal experiments. Mice at 14 days of gestation were randomly divided into three groups: a control group, a low-dose cadmium group (LCd group: 2.5 mg·kg⁻¹), and a high-dose cadmium group (HCd group: 5 mg·kg⁻¹). The pregnant mice were intraperitoneally injected with cadmium chloride (CdCl₂) for 6 and 24 h in the next morning. The weights of pregnant mice, uterus, maternal liver, and fetal mice were recorded after sacrifice. Serum and liver of pregnant mice were collected, the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were detected, and liver tissues were stained with HE to observe changes in liver function and liver tissue structure. The expressions of oxidative phosphorylation-related proteins, hypoxia inducible factor-1α (HIF-1α) and DRP1 proteins in liver of pregnant mice were detected by Western blotting. (2) Cell experiments. AML12 cells were treated with CdCl₂ (10 μmol·L⁻¹) for 0, 2, 6, 12, and 24 h. The expressions of oxidative phosphorylation-related proteins, DRP1, and hypoxia inducible factor-1α (HIF-1α) proteins were detected. AML12 cells were pretreated with DRP1 inhibitor Mdivi-1 for 1 h and then CdCl₂ (10 μmol·L⁻¹) for 12 h to detect the expression of oxidative phosphorylation-related proteins and DRP1 protein. AML12 cells were treated with Hif-1α siRNA for 48 h and CdCl₂ (10 μmol·L⁻¹) for 6 h to detect the expression of HIF-1α and DRP1 proteins. Results The results of animal experiments showed that cadmium exposure in pregnant mice had no effects on maternal liver weight and liver coefficient. However, the histomorphological changes and necrosis in hepatocytes were observed. Compared with the control group, the serum ALT and AST levels of pregnant mice in the LCd group were significantly increased after 6 h (P＜0.05), and the levels in the HCd group were significantly increased after 6 and 24 h (P＜0.05). Cadmium exposure during pregnancy significantly up-regulated HIF-1α and DRP1 expressions and down-regulated the expressions of oxidative phosphorylation-related proteins in maternal livers. In vitro cell experiments showed that the expressions of oxidative phosphorylation-related proteins was significantly decreased and HIF-1α and DRP1 protein expressions were significantly increased in the AML12 cells treated with CdCl₂ for 6 h. Mdivi-1 pretreatment significantly antagonized the inhibitory effect of cadmium on the expressions of oxidative phosphorylation-related proteins in AML12 cells, while Hif-1α siRNA pretreatment significantly antagonized the up-regulative effect of cadmium on DRP1 expression in AML12 cells. Conclusion Cadmium exposure in pregnant mice may up-regulate DRP1 expression by activating HIF-1α signaling, then inhibit oxidative phosphorylation level of hepatic cells, and ultimately lead to maternal liver damage.