Expression of Myostatin (Mstn) and Myogenin (Myog) Genes in Zi And Rhine Goose and Their Correlation with Carcass Traits

The aim of this study was to investigate the effects of Myostatin (MSTN) and MyoGenin (MyoG) on goose skeletal muscle growth. In this study, MSTN and MyoG gene expression in breast and leg muscle of Zi and Rhine goose were detected by Real-time Polymerase Chain Reaction (PCR), and the correlations between genes expression levels and carcass traits were investigated. The results showed that the breast muscle weight and breast muscle percentage of Rhine goose were significantly higher than Zi goose (p 0.01). MSTN mRNA and MyoG mRNA expression in breast muscle of Zi goose were significantly higher than that of Rhine goose and the level of MSTN in leg muscle of Rhine was significantly higher than that of Zi goose (p 0.01). There was a significant difference between MSTN mRNA expression in breast muscle and in leg muscle of Zi goose (p 0.01). MSTN mRNA expression in leg muscle was significantly higher than that of breast muscle of Rhine goose (p 0.05). There was a significant difference between MyoG mRNA expression in breast muscle and in leg muscle of Zi goose and Rhine goose (p 0.01). There was a negative correlation between MSTN mRNA expression in breast muscle and body weight, breast muscle weight and breast muscle percentage.

Expression of Myostatin (Mstn) and Myogenin (Myog) Genes in Zi And Rhine Goose and Their Correlation with Carcass Traits

The aim of this study was to investigate the effects of Myostatin (MSTN) and MyoGenin (MyoG) on goose skeletal muscle growth. In this study, MSTN and MyoG gene expression in breast and leg muscle of Zi and Rhine goose were detected by Real-time Polymerase Chain Reaction (PCR), and the correlations between genes expression levels and carcass traits were investigated. The results showed that the breast muscle weight and breast muscle percentage of Rhine goose were significantly higher than Zi goose (p 0.01). MSTN mRNA and MyoG mRNA expression in breast muscle of Zi goose were significantly higher than that of Rhine goose and the level of MSTN in leg muscle of Rhine was significantly higher than that of Zi goose (p 0.01). There was a significant difference between MSTN mRNA expression in breast muscle and in leg muscle of Zi goose (p 0.01). MSTN mRNA expression in leg muscle was significantly higher than that of breast muscle of Rhine goose (p 0.05). There was a significant difference between MyoG mRNA expression in breast muscle and in leg muscle of Zi goose and Rhine goose (p 0.01). There was a negative correlation between MSTN mRNA expression in breast muscle and body weight, breast muscle weight and breast muscle percentage.(AU)

Association between the pre-miR-196a2 rs11614913 polymorphism and gastric cancer susceptibility in a Chinese population.

We did a case-control study to provide a more comprehensive evaluation of the association of the pre-miR-196a2 rs11614913 polymorphism with gastric cancer. Between January 2013 and December 2014, 182 patients newly diagnosed with primary gastric cancer and 182 control subjects were recruited at Zhengzhou People's Hospital. For SNP genotyping, we used the Assay Designer 3.1 to design the primers of polymerase chain reaction. Using the chi-square test, we found that patients with gastric cancer were more likely to be alcohol drinkers (χ(2) = 4.4, P = 0.04), to have a family history of cancer in the first relatives (χ(2) = 5.29, P = 0.02), and to be infected with Helicobacter pylori (χ(2) = 23.39, P < 0.001). A significant difference in the genotype distributions of rs11614913 was observed in our study (χ(2) = 6.66, P = 0.04). By logistic regression analysis, we found that the CC genotype of rs11614913 was associated with an increased risk of gastric cancer in a codominant model (OR = 2.68, 95%CI = 1.17-6.44). By stratification analysis, we found that the CC genotype was associated with a strongly increased risk of gastric cancer in drinkers when compared with the TT+TC genotype (OR = 5.63, 95%CI = 1.54-30.76). In conclusion, the results of our study suggest an association between the rs11614913 gene polymorphism and an elevated risk of gastric cancer, especially in drinkers.

Association between ERCC5 gene polymorphisms and gastric cancer risk in a Chinese population.

We conducted a hospital-based case-control study to investigate the association between 3 common SNPs in the ERCC5 gene (rs1047768, rs751402, and rs17655) and the risk of developing gastric cancer. Between January 2013 and December 2014, samples were collected from 216 gastric cancer patients and 216 control subjects. ERCC5 rs1047768, rs751402, and rs17655 polymorphisms were genotyped by polymerase chain reaction combined with restriction fragment length polymorphism analysis. By conditional logistic regression analysis, the GG genotype of rs17655 was found to be associated with an elevated risk of gastric cancer in a codominant model, and the adjusted OR (95%CI) was 1.96 (1.10-3.50). Moreover, in a dominant model, the CG + GG genotype of rs17655 was correlated with an increased risk of gastric cancer compared to the CC genotype (OR = 1.48; 95%CI = 1.00-2.22). rs1047768 and rs751402 were not significantly correlated with an increased or decreased gastric cancer risk.

Cloning and expression pattern analysis of BkGRAS2 from Betula kirghisorum.

GRAS proteins are plant-specific transcription factors that are involved in the regulation of root and shoot growth. Here, we cloned BkGRAS2 from Betula kirghisorum (abbreviated to Bk) and analyzed the physicochemical properties and expression pattern of the encoded protein. BkGRAS2 had an open reading frame of 1614 bp encoding 537 amino acid residues. The deduced BkGRAS2 protein was hydrophilic, and it contained highly conserved VHIID and SAW motifs. BkGRAS1 and BkGRAS2 showed considerable sequence similarities. An expression analysis indicated that BkGRAS2 was expressed in root, stem, and leaf, with the highest level in the leaf. Expression of BkGRAS2 was increased following stress treatment with 0.6% NaHCO3. Transient expression analysis of GFP-BkGRAS2 in onion epidermal cells revealed that the BkGRAS2 protein was localized in the cytoplasm, but could also be detected in the nucleus. Our study provides the basis for future research on the role of the GRAS gene family in B. kirghisorum.

Erlotinib enhances the CIK cell-killing sensitivity of lung adenocarcinoma A549 cells.

We examined the effects and molecular mechanism of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib on NKG2D ligand expression in human lung adenocarcinoma A549 cells and the cytotoxicity of cytokine-induced killer cells. Flow cytometry was used to detect NKG2D ligand expression in A549 cells under effects of erlotinib and EGFR downstream molecules, including LY294002 (phosphoinositide 3-kinase inhibitor), SB203580 (mitogen-activated protein kinase inhibitor), and STAT21 (signal transduction and transcription 3 inhibitor) after 24 h. A lactate dehydrogenase release assay was used to detect, at different effector-to-target ratios, the A549 cell killing activity of cytokine-induced killer cells before and after treatment with 10 mM erlotinib. Erlotinib suppressed MICA expression in A549 cells and upregulated MICB and UL16 binding protein 1 expression. EGFR downstream molecules mitogen-activated protein kinase and signal transduction and transcription 3 inhibitor did not affect the expression of NKG2D ligands in A549 cells. The phosphoinositide 3-kinase inhibitor reduced MICA expression in A549 cells, while erlotinib enhanced the killing sensitivity of cytokine-induced killer cells in A549 cells. The anti-lung carcinoma effects of EGFR tyrosine kinase inhibitor were associated with the sensitivity of lung cancer cells to enhanced immune cell killing.

Single Nucleotide Polymorphisms in IGFBP-2 Gene and Their Associations with Body Weight Traits on Jinghai Yellow Chicken

Insulin-like growth factor binding protein-2 (IGFBP-2) regulates a broad spectrum of biological activities involved in growth, development, and differentiation. This study aimed at comparing polymorphisms in intron2 of the IGFBP-2 gene among four chicken breeds and at analyzing the associations between its genotypes and body weight in Jinghai Yellow chicken by using PCR-SSCP technique. For primer P2, three genotypes (AA, AB and BB) were observed in the four chicken breeds. Gene sequencing revealed one insertion/deletion (the inserted/deleted TC after position 552bp) in the intron 2 of IGFBP-2 gene. For primer P5, three genotypes were identified in Jinghai Yellow chickens, and named CC, CD and DD. Gene sequencing revealed two SNPs (C1107G, C1130T) and one inserted/deleted GCCAGGT after 1115bp in the intron 2 of IGFBP-2 gene. The results of the linear model analysis showed that Jinghai Yellow chickens with AA genotype had significantly heavier body weight, at hatch and 12 weeks of age, than those of the AB genotype (p 0.05). The A allele had a positive effect on body weight. We speculate that mutations in intron 2 could be used as genetic markers for body weight in Jinghai Yellow chicken. This study provides valuable information for the protection of genetic resources and for breeding of Jinghai Yellow chicken.(AU)

Single Nucleotide Polymorphisms in IGFBP-2 Gene and Their Associations with Body Weight Traits on Jinghai Yellow Chicken

Insulin-like growth factor binding protein-2 (IGFBP-2) regulates a broad spectrum of biological activities involved in growth, development, and differentiation. This study aimed at comparing polymorphisms in intron2 of the IGFBP-2 gene among four chicken breeds and at analyzing the associations between its genotypes and body weight in Jinghai Yellow chicken by using PCR-SSCP technique. For primer P2, three genotypes (AA, AB and BB) were observed in the four chicken breeds. Gene sequencing revealed one insertion/deletion (the inserted/deleted TC after position 552bp) in the intron 2 of IGFBP-2 gene. For primer P5, three genotypes were identified in Jinghai Yellow chickens, and named CC, CD and DD. Gene sequencing revealed two SNPs (C1107G, C1130T) and one inserted/deleted GCCAGGT after 1115bp in the intron 2 of IGFBP-2 gene. The results of the linear model analysis showed that Jinghai Yellow chickens with AA genotype had significantly heavier body weight, at hatch and 12 weeks of age, than those of the AB genotype (p 0.05). The A allele had a positive effect on body weight. We speculate that mutations in intron 2 could be used as genetic markers for body weight in Jinghai Yellow chicken. This study provides valuable information for the protection of genetic resources and for breeding of Jinghai Yellow chicken.

Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway

The aim of this study was to investigate the effect of propofol pretreatment on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the role of the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway in this procedure. Survival was determined 48 h after LPS injection. At 1 h after LPS challenge, the lung wet- to dry-weight ratio was examined, and concentrations of protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) were determined using the bicinchoninic acid method or ELISA. Lung injury was assayed via lung histological examination. PI3K and p-Akt expression levels in the lung tissue were determined by Western blotting. Propofol pretreatment prolonged survival, decreased the concentrations of protein, TNF-α, and IL-6 in BALF, attenuated ALI, and increased PI3K and p-Akt expression in the lung tissue of LPS-challenged rats, whereas treatment with wortmannin, a PI3K/Akt pathway specific inhibitor, blunted this effect. Our study indicates that propofol pretreatment attenuated LPS-induced ALI, partly by activation of the PI3K/Akt pathway.

Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway.

The aim of this study was to investigate the effect of propofol pretreatment on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the role of the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway in this procedure. Survival was determined 48 h after LPS injection. At 1 h after LPS challenge, the lung wet- to dry-weight ratio was examined, and concentrations of protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) were determined using the bicinchoninic acid method or ELISA. Lung injury was assayed via lung histological examination. PI3K and p-Akt expression levels in the lung tissue were determined by Western blotting. Propofol pretreatment prolonged survival, decreased the concentrations of protein, TNF-α, and IL-6 in BALF, attenuated ALI, and increased PI3K and p-Akt expression in the lung tissue of LPS-challenged rats, whereas treatment with wortmannin, a PI3K/Akt pathway specific inhibitor, blunted this effect. Our study indicates that propofol pretreatment attenuated LPS-induced ALI, partly by activation of the PI3K/Akt pathway.

Expression analysis of miRNA and target mRNAs in esophageal cancer

We aimed to investigate miRNAs and related mRNAs through a network-based approach in order to learn the crucial role that they play in the biological processes of esophageal cancer. Esophageal squamous-cell carcinoma (ESCC) and adenocarcinoma (EAC)-related miRNA and gene expression data were downloaded from the Gene Expression Omnibus database, and differentially expressed miRNAs and genes were selected. Target genes of differentially expressed miRNAs were predicted and their regulatory networks were constructed. Differentially expressed miRNA analysis selected four miRNAs associated with EAC and ESCC, among which hsa-miR-21 and hsa-miR-202 were shared by both diseases. hsa-miR-202 was reported for the first time to be associated with esophageal cancer in the present study. Differentially expressed miRNA target genes were mainly involved in cancer-related and signal-transduction pathways. Functional categories of these target genes were related to transcriptional regulation. The results may indicate potential target miRNAs and genes for future investigations of esophageal cancer.

Expression analysis of miRNA and target mRNAs in esophageal cancer.

We aimed to investigate miRNAs and related mRNAs through a network-based approach in order to learn the crucial role that they play in the biological processes of esophageal cancer. Esophageal squamous-cell carcinoma (ESCC) and adenocarcinoma (EAC)-related miRNA and gene expression data were downloaded from the Gene Expression Omnibus database, and differentially expressed miRNAs and genes were selected. Target genes of differentially expressed miRNAs were predicted and their regulatory networks were constructed. Differentially expressed miRNA analysis selected four miRNAs associated with EAC and ESCC, among which hsa-miR-21 and hsa-miR-202 were shared by both diseases. hsa-miR-202 was reported for the first time to be associated with esophageal cancer in the present study. Differentially expressed miRNA target genes were mainly involved in cancer-related and signal-transduction pathways. Functional categories of these target genes were related to transcriptional regulation. The results may indicate potential target miRNAs and genes for future investigations of esophageal cancer.

In vitro proliferation and differentiation of hepatic oval cells and their potential capacity for intrahepatic transplantation.

Hepatic oval cells (HOCs) are recognized as facultative liver progenitor cells that play a role in liver regeneration after acute liver injury. Here, we investigated the in vitro proliferation and differentiation characteristics of HOCs in order to explore their potential capacity for intrahepatic transplantation. Clusters or scattered HOCs were detected in the portal area and interlobular bile duct in the liver of rats subjected to the modified 2-acetylaminofluorene and partial hepatectomy method. Isolated HOCs were positive for c-kit and CD90 staining (99.8% and 88.8%, respectively), and negative for CD34 staining (3.6%) as shown by immunostaining and flow cytometric analysis. In addition, HOCs could be differentiated into hepatocytes and bile duct epithelial cells after leukemia inhibitory factor deprivation. A two-cuff technique was used for orthotopic liver transplantation, and HOCs were subsequently transplanted into recipients. Biochemical indicators of liver function were assessed 4 weeks after transplantation. HOC transplantation significantly prolonged the median survival time and improved the liver function of rats receiving HOCs compared to controls (P = 0.003, Student t-test). Administration of HOCs to rats also receiving liver transplantation significantly reduced acute allograft rejection compared to control liver transplant rats 3 weeks following transplantation (rejection activity index score: control = 6.3 ± 0.9; HOC = 3.5 ± 1.5; P = 0.005). These results indicate that HOCs may be useful in therapeutic liver regeneration after orthotopic liver transplantation.

In vitro proliferation and differentiation of hepatic oval cells and their potential capacity for intrahepatic transplantation

Hepatic oval cells (HOCs) are recognized as facultative liver progenitor cells that play a role in liver regeneration after acute liver injury. Here, we investigated the in vitro proliferation and differentiation characteristics of HOCs in order to explore their potential capacity for intrahepatic transplantation. Clusters or scattered HOCs were detected in the portal area and interlobular bile duct in the liver of rats subjected to the modified 2-acetylaminofluorene and partial hepatectomy method. Isolated HOCs were positive for c-kit and CD90 staining (99.8% and 88.8%, respectively), and negative for CD34 staining (3.6%) as shown by immunostaining and flow cytometric analysis. In addition, HOCs could be differentiated into hepatocytes and bile duct epithelial cells after leukemia inhibitory factor deprivation. A two-cuff technique was used for orthotopic liver transplantation, and HOCs were subsequently transplanted into recipients. Biochemical indicators of liver function were assessed 4 weeks after transplantation. HOC transplantation significantly prolonged the median survival time and improved the liver function of rats receiving HOCs compared to controls (P=0.003, Student t-test). Administration of HOCs to rats also receiving liver transplantation significantly reduced acute allograft rejection compared to control liver transplant rats 3 weeks following transplantation (rejection activity index score: control=6.3±0.9; HOC=3.5±1.5; P=0.005). These results indicate that HOCs may be useful in therapeutic liver regeneration after orthotopic liver transplantation.