Species composition and diversity of parasitoids and hyper-parasitoids in different wheat agro-farming systems.

Insect communities depend on both their local environment and features of the surrounding habitats. Diverse plant communities may enhance the abundance and species diversity of local natural enemies, which is possible due to a higher abundance and species diversity in complex landscapes. This hypothesis was tested using cereal aphid parasitoids and hyper-parasitoids by comparing 18 spring wheat fields, Triticum aestivum L. (Poales: Poaceae), in structurally-complex landscapes (dominated by semi-natural habitat, > 50%, n = 9) and structurally-simple landscapes dominated by arable landscape (dominated by crop land, > 80%, n = 9). The agricultural landscape structure had significant effects on the number of parasitoid and hyper-parasitoid species, as 26 species (17 parasitoids and 9 hyper-parasitoids) were found in the complex landscapes and 21 were found in the simple landscapes (14 parasitoids and 7 hyper-parasitoids). Twenty-one species occurred in both landscape types, including 14 parasitoids and 7 hyper-parasitoids species. The species diversity of parasitoids and hyper-parasitoids were significantly different between the complex and simple landscapes. In addition, arable fields in structurally-simple agricultural landscapes with little semi-natural habitats could support a lower diversity of cereal aphid parasitoids and hyper-parasitoids than structurally-complex landscapes. These findings suggest that cereal aphid parasitoids and hyper-parasitoids need to find necessary resources in structurally-complex landscapes, and generalizations are made concerning the relationship between landscape composition and biodiversity in agricultural landscapes. Overall, abundance, species richness, and species diversity increased with increasing plant diversity and landscape complexity in spring wheat fields and increasing amounts of semi-natural habitats in the surrounding landscape.

[The effect of resistin on nuclear factor-kB and tumor necrosis factor-a expression in hepatic steatosis].

OBJECTIVE: To investigate the potential regulatory role played by the hormone resistin in lipid metabolism and expression of nuclear factor (NF)-kB and tumor necrosis factor (TNF)-a during hepatic steatosis. METHODS: A non-alcoholic fatty liver disease (NAFLD) cell model was established by treating the normal human hepatic cell line, L02, with palmitic acid. Four research groups of L02 cells were generated: C group (control, no palmitic acid treatment), P group (NAFLD model, treated with 20 microg/ml palmitic acid), CR group (C group treated with 50 microg/L recombinant human resistin), and PR group (P group treated with 50 microg/L recombinant human resistin). All treatments were carried out for 72 hours. Oil red O staining was used to detect the intracellular changes in lipid drops. Biochemical assays were used to measure triglycerides (TGs), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transpeptidase (GGT) levels in culture medium. The mRNA and protein expression levels of insulin receptor substrate (IRS)-2, NF-kB, and TNF-a were determined by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS: The TG, ALT, AST, and GGT levels were higher in the P, CR, and PR groups than in the C group. The NF-kB mRNA level was also higher in the P, CR, and PR groups (Student's t = 17.64, 22.03, 26.06 respectively) than in the C group, as was the TNFa mRNA level ( t = 5.67, 5.38, 11.64), but the IRS-2 mRNA level was lower ( t = 8.19, 9.23, 20.93) (all, P less than 0.05). In addition, no significant difference in these mRNA levels were found between the P group and the CR group (NF-kB: t = 1.75, TNFa: t = 0.58, IRS-2: t = 2.14; all, P more than 0.05). The detected protein levels of NF-kB, TNFa, and IRS-2 were consistent with the mRNA levels. CONCLUSION: Resistin can promote steatosis in LO2 cells through the NF-kB signaling pathway, thereby contributing to the NAFLD pathogenic process.

[Clinical significance of histopathologic and ultrastructural pathologic examination in etiological diagnosis of infantile cholestatic diseases].

OBJECTIVE: To study the features of histopathologic and ultrastructural pathologic changes of liver biopsy in patients with infantile cholestatic disease, and to investigate its diagnostic significance combining with the clinical data. METHODS: Thirty-six children diagnosed as infantile cholestatic disease and received liver biopsy in Chongqing Medical University Children's Hospital from Jun 2007 to Oct 2008 were enrolled and the pathologic and ultrastructural pathologic changes of liver were analyzed. RESULTS: Morphologic changes under light microscope in liver tissues included hepatocyte swelling, hepatocyte denaturation, hepatocyte necrosis, multinucleated giant cell formation, bile duct proliferation, fiber tissues proliferation and inflammatory cells infiltration in liver lobules and portal regions. The characteristics of cholestasis including intralobular cholestasis, acinus formation, feather-like cytoplasmic filaments and bile stasis in bile canaliculi were observed. The morphologic changes of biliary atresia were observed in 7 cases whose image investigations showed no obstruction of biliary tract. Nuclear changes, resolution of cytoplasm, inflammatory cell infiltration, collagen fiber proliferation and increased number of lysosomes were observed under electromicroscope. Two cases of glycogen storage disease, 1 case of Niemann-Pick disease and 1 case of lipid storage disease with unknown cause were confirmed by the combination of histological changes and clinical manifestations. CONCLUSION: Common pathologic changes of liver tissues existed under light microscope or electroscope. The diagnosis of hereditary metabolic disorders could be made increasingly by application of these two technologies in clinical practice. It is difficult to diagnose biliary atresia in early childhood by image investigations and the pathological changes of liver tissues are helpful.

[The clinicopathological study of infantile cytomegalovirus hepatitis].

OBJECTIVE: To investigate the clinicopathological features of infantile cytomegalovirus hepatitis. METHOD: Liver biopsies from 30 cases of infantile cytomegalovirus hepatitis were observed under optical microscope and electronic microscope. RESULT: The main clinical manifestations were jaundice, splenohepatomegaly and hypohepatia. Laboratory test showed dysfunction of liver, high level of CMV DNA, and high titer of anti-CMV antibody. Imaging examination demonstrated hepatomegaly. The histological changes were hepatocellular degeneration, necrosis, apoptosis, and fibrosis. The histological characteristics of cytomegalovirus hepatitis, including intranuclear inclusions in multinucleated giant cells and pseudo-lumens, were also observed under optical microscope. In addition, virion was observed in the nuclei and cytoplasm of hepatocytes under electronic microscope. CONCLUSION: The viral DNA and serological tests have limited utility for the diagnosis of infantile cytomegalovirus hepatitis, and the final diagnosis depends on histopathology.

[Effect of tea polyphenols on expression of nuclear factor kappa B].

OBJECTIVE: To investigate the effect of tea polyphenols (TP) on expression of nuclear factor kappa B (NF-kB) in rats with alcoholic liver diseases and in cells treated with alcohol. METHODS: 22 female Wistar rats were randomly divided into three groups: a control group, an alcohol model group and a TP plus alcohol group. All treatments were injected into stomach through intragastric tube. L02 cells were divided into five groups: a control group, an alcohol treated group, a prevention group (cells were treated with TP for 3 days, and then treated with alcohol), an intervention group (cells treated with TP and alcohol), and a therapeutic group (cells were treated with alcohol for 3 days, and then treated with TP). Histopathology was observed under light microscope (LM); serum MDA, ROS in cells were quantified by optical density measurement; the expression of NF-kB and IkB was determined by RT-PCR; and the activity of NF-kB was checked with Electrophoretic Mobility Shift Assay (EMSA). RESULTS: LM indicated hepatocytes were injured obviously in the model group. Serum MDA and cells ROS in TP treated groups were significantly lower than the alcohol treated group. The level of NF-kB mRNA expression in TP treated groups(rats: 0.58+/-0.16, cells: 0.60+/-0.03, 0.59+/-0.01, 0.59+/-0.01) were significantly lower than the alcohol treated group (rats: 1.15+/-0.03, cells: 0.76+/-0.03) (P<0.01), the level of IkB mRNA expression in the prevention group, intervention group, and therapeutic group (0.51+/-0.01, 0.50+/-0.01, 0.50+/-0.12) were significantly higher than the alcohol treated group (0.61+/-0.03) (P<0.05), the difference among the three groups was not significant (P>0.05). The activity of NF-kB in TP treated rats(DNA stain: 669.85+/-41.34, Protein stain: 675.35+/-18.27) was significantly lower than the alcohol treated rats(DNA stain: 1410.78+/-22.19, Protein stain:1426.08+/-33.15) (P<0.01); NF-kB activity in cells of the prevention, intervention, therapeutic groups (DNA stain: 713.07+/-11.91, 710.79+/-14.99, 693.45+/-71.69; Protein stain: 758.88+/-34.65, 753.07+/-76.78, 725.77+/-36.09) was significantly lower than the alcohol treated cells (DNA stain: 849.94+/-12.45, Protein stain: 925.96+/-5.78) (P<0.01), the difference among the three TP treated groups was not significant (P>0.01). CONCLUSION: TP can alleviate and prevent alcohol-induced liver injury via inhibiting NF-kB activation.

[Expression of augmenter of liver regeneration in hepatic tumor cells and its clinical significance].

OBJECTIVE: To investigate the effects of augmenter of liver regeneration (ALR) on the proliferation of hepatocytes and hepatic tumor cells and the expression of ALR in herpatocellular carcinoma (HCC). METHODS: Primary rat hepatocytes, QGY and HepG2 cells were cultured separately with ALR from different species. Cell proliferation was detected by their 3H-TdR uptake. The expression of ALR was examined in 9 normal hepatic tissues and 21 HCC cases using immunohistochemistry method. RESULTS: Different ALRs could stimulate the proliferation of HepG2 and QGY cells in a dose-dependent way in vitro, but all ALR had no influence in the proliferation of primary rat hepatocytes. The expression of ALR was absent in normal hepatic tissues, but present in all HCC hepatic tissues. However, the expression of ALR had no relationship with the differentiation and size of the carcinomas. CONCLUSION: ALR might play an important role in the occurrence and development of HCC.

[A study on the clinical and pathological efficacy of lamivudine in the treatment of chronic hepatitis B].

OBJECTIVE: To investigate clinical effect, liver pathohistological changes (including pathology, HBV markers in liver tissue) in patients with chronic hepatitis B. METHODS: 70 patients of chronic hepatitis B were administered 100 mg Lamivudine orally daily for 1 year. The serum HBV-DNA, HBeAg/anti-HBe, hepatic chemistry and the hepatic fibrosis markers were studied. The needle biopsy of liver were performed in 35 patients before and after treatment and Knodell pathological score were done, HBsAg, HBcAg, alpha-SMA in liver tissue were examined by immunohistochemistry method. RESULTS: After 1 year treatment the full response rate, partial response rate and no response rate were 23.72%, 69.49% and 6.78%, the patients in whom HBeAg seroconversion had higher base-line Alanine aminotransferase levels than the patients without seroconversion. Activity index of hepatic histology in 41.18% patients had a significant decrease. Histological assessment revealed that necrosis in portal area, pylenphlebitis and fibrosis were obviously alleviated. The liver immunohistochemistry examination showed HBcAg and alpha-SMA in liver decreased significantly in the patients with HBeAg seroconversion, no obvious alteration was observed in HBsAg expression. Lamivudine seems an effective compound with high safety and low side effect. CONCLUSION: These results suggested that lamivudine (100mg/d) could suppress HBV-DNA replication, promote ALT normalization, accelerate HBeAg/anti-HBe seroconversion, improve the liver pathological changes, slow down the development of liver fibrosis

[Effect of Rhein on the development of hepatic fibrosis in rats].

OBJECTIVE: To investigate the effect of rhein on the development of hepatic fibrosis. METHODS: The animal models were made with carbon tetrachloride (CCl(4)) mixed with vegetable oil (3/2, v/v), which was injected subcutaneously twice a week for 6 weeks, and with 5% ethanol for free drinking water. At the same time, Rhein was administrated at the dose of 25 mg/kg or 100 mg/kg once a day for 6 weeks. The changes of both biochemical markers, such as the levels of alanine aminotransferase (ALT), hyaluronic acid (HA), procollagen type III (PCIII) in serum and SOD, malondialdehyde (MDA) in liver, and related histopathological parametres were determined. RESULTS: Compared with the model group, there were three kinds of changes in the larger quantity of rhein treated group. (1) The levels of ALT, HA, PCIII in serum and MDA in liver homogenate were decreased significantly (from 150 U/L +/- 16 U/L to 78 U/L +/- 18 U/L, 321 microg/L +/- 97 microg/L to 217 microg/L +/- 75 microg/L, 31 microg/L +/- 14 microg/L to 16 microg/L +/- 6 microg/L and 3.67 nmol/mg +/- 0.68 nmol/mg to 1.88 nmol/mg +/- 0.34 nmol/mg, respectively, t > or 2.977, P<0.01). However the level of SOD in liver was increased (from 62.45 NU/mg +/- 8.74 NU/mg to 91.26 NU/mg +/- 14.04 NU/mg, t=4.453, P<0.01). (2) The expressions of transforming growth factor beta 1 (TGF-beta 1) and alpha-smooth muscle actin (alpha-SMA) in liver were markedly reduced (P<0.05 and P<0.01). (3) The collagen staining positive area was decreased and the grade of fibrosis was reduced significantly in liver (P<0.05 and P<0.01). CONCLUSION: Rhein can protect hepatocyte from injury and prevent the progress of hepatic fibrosis in rats, which may associate with that rhein plays a role in antioxidation, anti-inflammation, inhibiting the expression of TGF-beta1 and suppressing the activation of hepatic stellate cells (HSCs).

The effects of MIBG on the invasive properties of HepG2 hepatocellular carcinoma cells.

The aim of the present study was to investigate the effects of meta-iodobenzylguanidine (MIBG) on the invasive properties of hepatocellular carcinoma (HCC) cells and examine whether these effects are due to the ability of MIBG to inhibit arginine-specific mono-ADP-ribosylation. Samples from patients with HCC were divided into 2 groups, a metastatic group and a non-metastatic group. Immunohistochemistry and RT-PCR were used to detect the protein and mRNA expression of arginine-specific adenosine diphosphate-ribosyltransferase 1 (ART1) and integrin α7 in the HCC tissues. In addition, the expression of ART1 was measured in HepG2 HCC cells by immunofluorescence. The inhibition of the metastasis of HepG2 cells by MIBG at various concentrations was measured by MTT assay. In addition, the effects of MIBG on HepG2 cell metastasis were measured using a scratch wound assay and a transwell invasion assay. Western blot analysis was used to detect the protein expression of ART1, integrin α7, focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K) and urokinase-type plasminogen activator (uPA) in the HepG2 cells. The mRNA and protein levels of ART1 and integrin α7 were higher in the metastatic HCC samples than in the non-metastatic HCC samples. ART1 expression was detected in the HepG2 cells. The half maximal inhibition concentration (IC50) of MIBG in the HepG2 cells was 200 µmol/l (P<0.05). Within a certain dose range, MIBG exerted inhibitory effects on HepG2 cell migration in a dose-dependent manner. Treatment with MIBG significantly inhibited the migration and invasion of the HepG2 cells relative to the control cells (P<0.05) and reduced the protein expression of ART1, integrin α7, FAK, PI3K and uPA (P<0.05). Our data demonstrate that ART1 and integrin α7 may be involved in the invasive and metastatic properties of HCC cells. MIBG inhibited the migration and invasion of HepG2 cells, possibly through the inhibition of arginine-specific single-adenosine diphosphate ribosylation and the suppression of the protein expression of integrin α7ß1, FAK and PI3K and the secretion of uPA, leading to reduced invasion by HepG2 cells.

[Effects of resistin on hepatic fibrosis: possible mechanisms in non-alcoholic fatty liver disease in in vitro and in vivo].

To investigate the effects and possible mechanisms of resistin on hepatic fibrosis in non-alcoholic fatty liver disease, this review used an in vivo model utilizing Wistar rats with a high fat diet. Recombinant resistin was selected to play role in hepatic stellate cells in the HSC-T6 cell line. We observed the degrees of hepatic fibrosis, measured the levels of Liver fibrosis spectrum and detected expression levels of resistin mRNA and protein in liver tissue as well as the expression levels of TGFß-1 and TNF-α mRNA in HSC-T6. The results showed that expression of resistin in rat liver tissue and the degree of hepatic fibrosis increased over time with a high fat diet. Along with the increased concentration of resistin and levels of fibrosis index, TGFß-1and TNF-α also increased in HSC-T6 cells. Compared with the control group, significant differences were found between each group, suggesting resistin by proinflammatory cytokine TNF-α and TGF-ß1 induced the occurrence and development of NAFLD in hepatic fibrosis.

[Effects of Ezrin on differentiation and adhesion of hepatocellular carcinoma].

BACKGROUND & OBJECTIVE: Ezrin is a member of the ERM family, which acts as links between the plasma membrane and the actin cytoskeleton. It affects differentiation, invasion, and metastasis of cancers by modulating adhesion molecules on the surface of the cell membrane. The purpose of the experiment is to examine the expressions of Ezrin and two cellular membrane adhesion molecules, namely Cadherin and CD44, on hepatocellular carcinomas, in order to investigate the effects of Ezrin on the regulation of adhesion molecules in tumor cells and the invasive growth of hepatic carcinoma cells. METHOD: Sixty-seven specimens of hepatic carcinoma were obtained from surgical excisions (52 cases with both cancerous and non-carcerous liver tissue), and examined the role of Ezrin as a potential regulator of the adhesion by the inhibition of Ezrin in HepG6 cells. Immunohistochemical stainings of Ezrin, E-Cadherin, and CD44v6 were performed, RESULTS: Twenty-seven cases were Ezrin positive in the tumor tissue (27/67, 40.30%); E-Cadherin, 37 cases (37/67, 55.22%). Both stainings directly correlated with cell differentiation; the poorer the differentiation, the weaker the expression. The specimens lost expression in highly undifferentiated tissue. Compared with the non-carcerous liver tissue, there was a significant difference. CD44v6 was positive in 18 cases (18/67, 26.87%). There was a drastic loss of expression in the non-cancerous tissue. Decrease in E-Cadherin and increase in CD44V6 OF HepG6 cells using anti-ezrin. CONCLUSION: A decrease in Ezrin expression affects cell differentiation and adhesion of hepatocellular carcinoma by modulating adhesion molecules E-Cadherin and CD44v6.