Autoimmune hepatitis (AIH)-related hepatocellular carcinoma (HCC) is defined as HCC that develops on the basis of long-term AIH and has a relatively low incidence rate of 0-6%. The risk factors for HCC in AIH patients include old age, male sex, diabetes, alcohol use, AIH recurrence and persistent alanine aminotransferase abnormalities, failure in immunosuppressive therapy and related treatments, and long-term liver cirrhosis. Liver cirrhosis is an important stage for the development of HCC in AIH, and the incidence rate of HCC increases significantly after AIH progresses to liver cirrhosis. At present, there are few reports on the mechanism of HCC in AIH, which may be associated with the changes in specific molecular biological characteristics (including chromosomes, telomeres, and genes) induced by liver cirrhosis, the cell death-inflammation-cancer pathway, and intestinal microecological disorders. It is of great importance to identify the AIH population at a high risk of HCC in a timely manner and enhance intervention, follow-up, and monitoring.

OBJECTIVE To optimize the parameters of passive cutaneous anaphylaxis(PCA)in rats immunized by ovalbumin(OVA). METHODS 1-2 month-old Sprague-Dawley rats were immu?nized by ip injection of OVA(0.2,1.0 and 5.0 mg per rat)mixed with complete Freund′s adjuvant once every other day 3 times. Serum was collected on the 12th-16th days after final immunization. Then the rats were intracutaneously injected with sensitized serum and then stimulated by iv injection of the same dose of OVA mixed with Evans blue after a latent period of 0.5,1.5,3,6,12,24,36,48 and 60 h. Finally,the diameters of blue spots in the skin were measured at stimulation. RESULTS Serum total-IgE(T-IgE)and OVA-specific IgE(sIgE)levels increased significantly and reached the peak on the 3rd-7th days and 12th-16th days after final immunization,respectively. There was no correlation between the serum T-IgE level and OVA-sIgE level when the rats were immunized with OVA at OVA 0.2-5.0 mg per rat. The rats experienced PCA after injection of OVA 1.0 and 5.0 mg per rat. Diameters of blue spots in the skin reached the maximum value after rats were sensitized for 0.5-3 h. Moreover,the shape,color and size of blue spots were better 30-60 min after stimulation. CONCLUSION Optimized PCA is as follows:1-2 month-old rats are immunized on the 1st,3rd and 5th days by ip injection of OVA 1.0-5.0 mg. The immunizing serum is collected at 12-16 d after final immunization. The rats are stimulated by OVA and Evans blue after a latent period of 0.5-3 h. Diameters of blue spots in rats′ skin are then measured 30-60 min after stimulation.

To investigate the expressions of placental growth factor (PLGF) in placenta with hypertensive disorders of pregnancy (HDP), 45 women with HDP and 20 normally pregnant women were studied. Among 45 women with HDP, there were 23 cases of severe preeclampsia and one case of eclampsia. The location and level of PLGF proteins was determined by immunohistochemistry and Western blot. The expression of PLGF mRNA in placenta was assessed by reverse transcriptional-polymerase chain reaction (RT-PCR). The results showed that: (1) The distribution of PLGF in placenta with HDP was similar to normal one, which was mainly in the cytoplasm of villous syncytiotrophoblast and villous stroma; (2) The expression of PLGF protein was significantly decreased in placentas with mild and severe preeclampsia compared to the normal ones (0.3 +/- 0.4 vs 0.6 +/- 0.4, 0.2 +/- 0.5 vs 0.6 +/- 0.4, P < 0.01). There were no differences between the gestational hypertension placenta and normal one (0.5 +/- 0.6 vs 0.6 +/- 0.4, P > 0.05); (3) The transcription levels of the PLGF mRNA in placentas with preeclampsia were significantly lower than in normal groups (3.33 +/- 0.39 vs 4.87 +/- 0.60, 1.97 +/- 0.29 vs 4.87 +/- 0.60, P < 0.01), and no differences were found between the gestational hypertension placenta and normal groups. These findings suggest that the abnormal expression of PLGF in placentas is related to the pathogenesis of HDP.
Placenta/*metabolism ; Pre-Eclampsia/*metabolism ; Pregnancy/*metabolism ; Pregnancy Proteins/*biosynthesis ; Pregnancy Proteins/genetics

The expression of endothelial nitric oxide synthase traffic inducer (NOSTRIN) in the placenta of the patients with pregnancy induced hypertension (PIH) was detected and its role in the pathogenesis of PIH was studied. The pathological changes in placental vessels were observed by HE staining. NO2-/NO3-, the stable metabolic end products of NO, was measured with nitrate reductase. The eNOS activity in placental tissues was assayed by spectrophotometry. Western blot analysis was applied to detect NOSTRIN expression. The incidence of thickening and fibronoid necrosis of placental vessels was significantly higher in women with PIH than in the normal group (P < 0.01). The levels of placental NO2-/NO3- in PIH patients (27.53 +/- 7.48 micromol/mg) were significantly lower than in normal group (54.27 +/- 9.53 micromol/mg, P < 0.01). The activity of eNOS was significantly decreased in PIH group (12.826 +/- 3.61 U/mg) as compared with that in normal group (21.72 +/- 3.83 U/mg, P < 0.01). Western blot analysis revealed that both groups expressed 58 kD NOSTRIN, but the protein level was significantly higher in women with PIH than in the normal group (P < 0.01). A significant negative correlation existed between the expression of NOSTRIN protein and the activity of eNOS in placental tissue of women with PIH (r = -0.57, P < 0.01). It was concluded that the level of NOSTRIN expression in placenta of women with PIH was increased, which may play an important role in the pathogenesis of PIH.

To investigate the expressions of placental growth factor (PLGF) in placenta with hypertensive disorders of pregnancy (HDP), 45 women with HDP and 20 normally pregnant women were studied. Among 45 women with HDP, there were 23 cases of severe preeclampsia and one case of eclampsia. The location and level of PLGF proteins was determined by immunohistochemistry and Western blot. The expression of PLGF mRNA in placenta was assessed by reverse transcriptionalpolymerase chain reaction (RT-PCR). The results showed that: (1) The distribution of PLGF in placenta with HDP was similar to normal one, which was mainly in the cytoplasm of villous syncytiotrophoblast and villous stroma; (2) The expression of PLGF protein was significantly decreased in placentas with mild and severe preeclampsia compared to the normal ones (0.3±0.4 vs 0.6± 0.4, 0.2±0.5 vs 0.6±0. 4, P＜0.01). There were no differences between the gestational hypertension placenta and normal one (0.5±0.6 vs 0.6±0.4, P＞0. 05); (3) The transcription levels of the PLGF mRNA in placentas with preeclampsia were significantly lower than in normal groups (3.33±0.39 vs4.87±0.60, 1.97±0.29 vs 4.87±0. 60, P＜0.01), and no differences were found between the gestational hypertension placenta and normal groups. These findings suggest that the abnormal expression of PLGF in placentas is related to the pathogenesis of HDP.

The expression of endothelial nitric oxide synthase traffic inducer (NOSTRIN) in the placenta of the patients with pregnancy induced hypertension (PIH) was detected and its role in the pathogenesis of PIH was studied. The pathological changes in placental vessels were observed by HE staining. NO2-/NO3- , the stable metabolic end products of NO, was measured with nitrate reductase. The eNOS activity in placental tissues was assayed by spectrophotometry. Western blot analysis was applied to detect NOSTRIN expression. The incidence of thickening and fibronoid necrosis of placental vessels was significantly higher in women with PIH than in the normal group (P＜0.01). The levels of placental NO2-/NO3- in PIH patients (27.53±7.48 μmol/mg) were significantly lower than in normal group (54.27±9.53 μmol/mg, P＜0.01). The activity of eNOS was significantly decreased in PIH group (12. 826±3.61 U/mg) as compared with that in normal group (21. 72±3.83 U/mg, P＜0.01). Western blot analysis revealed that both groups expressed 58 kD NOSTRIN, but the protein level was significantly higher in women with PIH than in the normal group (P＜0.01). A significant negative correlation existed between the expression of NOSTRIN protein and the activity of eNOS in placental tissue of women with PIH (r=-0. 57, P＜0. 01). It was concluded that the level of NOSTRIN expression in placenta of women with PIH was increased, which may play an important role in the pathogenesis of PIH.