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Objective To compare the clinical effect of the zirconia inlay and gold alloy inlay in the restoration of the second class defect of molar with vital pulp.Methods 60 teeth were randomly divided into zirconia inlay group and gold alloy inlay group, with 30 teeth in each group. Evaluate the restoration effect in 2 group at 1-year follow-.Results At 1-year follow-up, according to US Public Health Service Criteria, the success rate in anatomy zirconia group was93.53%, which was statistically higher than that of the gold alloy group (P

Aim: To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells., Methods: Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates., Results: In portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased., Conclusion: H₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.

Objective: To investigate the regulatory effects of RhoGTPase on the transition of liver sinusoidal endothelial cells and the potential mechanism thereof on the sinusoidal capillarization in schistosomal hepatic fibrosis., Methods: Eight-eight mice underwent abdominal infection of schistosomal cercaria so as to establish liver fibrosis models. 13 weeks later the mice were divided into 5 groups: Group A (normal control group, n = 10), Group B (group of schistosomiasis, n = 24), Group C (anti-schistosoma control group, treated with biltricide), Group D (group of schistosomiasis + hydroxyfasudil, treated with hydroxyfasudil since the week 14, n = 18), and Group E (biltricide + hydroxyfasudil, treated with biltricide since week 13 and added with hydroxyfasudil since week 14, n = 18). The mice in Group A and 6 mice of Group B were killed in week 13, and 6 mice of Groups B, C, D, and E were killed in weeks 16, 19, and 21 each. The livers were taken out to undergo electron microcopy. Immunohistochemistry was used to detect the expression of p-moesin, connective tissue growth factor (CTGF), RhoA, collagen IV (Col IV), and laminin (LN) protein expressions were assessed by Western blotting, and RT-PCR was used to detect the mRNA expression of CTGF, RhoA, and ROCK II., Results: Compared with Group A, the mRNA levels of RhoA, ROCK II, and CTGF were significantly increased (all P < 0.05) and the protein expression levels of p-moesin, CTGF, RhoA, Col IV, and LN were significantly increased (all P < 0.05) in Group B. After intervention with biltricide and/or hydroxyfasudil, the CTGF mRNA expression was significantly decreased (P < 0.05) in Group E in week 16 and the protein expression levels of CTGF, Col IV, and LN were decreased (all P < 0.05) compared with other groups, and the expression of p-moesin of Group E was significantly lower than that of Group D (P < 0.05). Electron microcopy showed that the liver sinusoids of the mice in Group E was significantly better compared with the other groups, and there was no significant difference between Groups B and D., Conclusion: An upregulation of RhoGTPase that contributes to increased CTGF expression and phosphorylation of moesin may induce a transition of liver sinusoidal endothelial cells in schistosomiasis.

Background: Liver fibrosis is the result of an imbalance between synthesis and degradation of extracellular matrix proteins of the liver. At the cellular and molecular levels, this progressive process is mainly characterized by activation of hepatic stellate cells (HSCs). Schistosoma japonica is one of the most prevalent causes of liver fibrosis in China. It is characterized by hepatocyte damage, inflammation, and chronic parasite egg-induced granuloma formation leading to fibrosis. This study aimed to investigate the inhibitory effects of prostaglandin E1 (PGE1) on activation of HSCs and the alteration of type I and III collagen in rabbits with schistosomiasis. The study may promote the clinical application of praziquantel and PGE1 as a combined therapy to reverse hepatic fibrosis caused by schistosomiasis., Methods: Rabbits were percutaneously infected with cercaria of S. japonicum. Seven rabbits were subjected to intravenous injections of PGE1 (2.5 mug/kg daily) from days 60 to 120 after infection. The ultrastructural changes in activated HSCs were observed under transmission electron microscopy. The expression of alpha-smooth muscle actin (alpha-SMA) was detected by immunohistochemistry. Fibril-forming collagens were detected by picrosirius staining., Results: Activation of HSCs was a characteristic alteration in schistosome-induced hepatic fibrosis. The expression of contraction-related alpha-SMA and the content of collagens were increased. Exogenous PGE1 markedly inhibited the activation of HSCs and reduced the expression of alpha-SMA around the hepatic sinusoids (P<0.01). The contents of type I and III collagens were significantly attenuated. The ratio of staining area to the whole field (10X3.3) under a polarized light microscope in the untreated and treated groups was 37.25+/-9.71 vs. 13.38+/-4.24 (P<0.01) and 9.66+/-3.52 vs. 6.23+/-1.81 (P<0.05), respectively., Conclusions: Activation of HSCs may play a key role in the progress of schistosome-induced hepatic fibrosis. PGE1 effectively protects rabbit liver from fibrosis, at least in part by inhibiting the activation of HSCs.

Objective: To investigate the pathologic features of the pulmonary tissue in portal hypertensive rabbits with schistosomal cirrhosis, and to study the role of endothelin-1 (ET-1) and nitric oxide (NO) in pathogenesis of portal hypertensive pulmonary vasculopathy., Methods: The experimental group included 10 rabbits infected percutaneously with cercariae of Schistosomiasis Japonica. The control group included 10 normal rabbits. HE stain, Masson trichrome stain and transmission electron microscopy were applied to detect the pathologic features of the pulmonary tissue. The expression and distribution of endothelin-1 (ET-1) and nitric oxide synthase (NOS) in the lung tissues were analyzed by immunohistochemistry., Results: After 120 d, the pathological morphology alteration of the pulmonary tissue was observed in the rabbits in experimental group. Both of ET-1 and NOS-containing cells were more abundant in distribution and expression in the lung tissue of experimental group than those of the control group. There was significant difference between the two groups in the parameter of area, lightness and gray level of ET-1 and NOS (P < 0.01)., Conclusions: Pulmonary pathologic changes occur in the portal hypertensive rabbits with schistosomal cirrhosis. ET-1 and NOS-containing cells are more abundant in pulmonary vessel of portal hypertension, then followed by dilation of intrapulmonary vessel. It is deduced that ET-1 and NO might play an important role in the pathogenesis of portal hypertensive pulmonary vasculopathy.