Molecular characterization of mitochondrial transferRNAGln and transferRNAMet A4401G mutations in a Chinese family with hypertension.

Mutations in mitochondrial (mt)transfer (t)RNA (mt­tRNA) have been reported to serve important roles in hypertension. To determine the underlying molecular mechanisms of mt­tRNA mutations in hypertension, the present study screened for mt­tRNA mutations in a Chinese family with a high incidence of essential hypertension. Sequence analysis of the mt­tRNA genes in this family revealed the presence of an A4401G mutation in the glycine­and methionine­tRNA genes, and a G5821A mutation in the cysteine­tRNA (tRNACys) gene. The G5821A mutation was located at a position conserved in various species, and disrupted G6­C67 base­pairing. It was hypothesized that the G5821A mutation may decrease the baseline expression levels of tRNACys, and consequently result in failure of tRNA metabolism. The A4401G mutation was reported to cause the mitochondrial dysfunction responsible for hypertension. Thus, the combination of G5821A and A4401G mutations may contribute to the high incidence of hypertension in this family. Mt­tRNA mutations may serve as potential biomarkers for hypertension.

Association Between IL-17, IL-8 and IL-18 Expression in Peripheral Blood and Helicobacter Pylori Infection in Mongolian Gerbils.

BACKGROUND: Persistent Helicobacter pylori infection confers an increased risk for serious illnesses such as peptic ulcers and gastric cancer. Various cytokines are involved in the regulation of inflammatory immune response in H. pylori-infected gastric mucosa. OBJECTIVES: The current study aimed to obtain evidence regarding the association between IL-17, IL-8 and IL-18 expression in peripheral blood and H. pylori infection in Mongolian gerbils. MATERIALS AND METHODS: Mongolian gerbils were inoculated with H. pylori by a metal stomach catheter. After sacrifice, their gastric mucosae were examined in macroscopic, histological and electron microscopy levels. In addition, enzyme linked immunosorbent assay (ELISA) assay was performed on the IL-17, IL-8 and IL-18 cytokines in the blood samples. RESULTS: Serum levels of IL-17, IL-8 and IL-18 were remarkably up-regulated compared to those of the control group. There was an obvious correlation between the increase of IL-17 and the serious extent of gastritis in the current study. However, the serum levels of IL-8 and IL-18 without getting increasingly more for repetitive intragastric administration. There were plenty of neutrophils infiltrating in the infected group mucosal. Intestinal metaplasia and gastric ulcers were also founded in H. pylori infected animals after enhanced inoculation. The edema, degeneration and necrosis changes could be found in organelles by transmission electron microscopy. More serious pathological changes were detected in the enhanced inoculation groups compared to the cycle group. CONCLUSIONS: The serum levels of IL-17, but not IL-8 and IL-18 may serve as a potential biomarker for diagnosis and predicting the prognosis of gastritis caused by H. pylori.

Relationship between CIP2A expression, and prognosis and MDR-related proteins in patients with advanced gastric cancer.

CIP2A is highly expressed in a variety of malignancies. We determined the expression and clinical significance of CIP2A in patients with advanced gastric cancer. CIP2A protein was expressed in 25 of 37 cancer tissue specimens. There was no correlation between CIP2A and PGP, GST-π, Topo-II, and LRP expression. Survival analysis showed significant differences between the survival rate of the CIP2A protein-positive and -negative groups (χ(2)=4.509, P=0.034), but the degree of positive expression was unrelated to survival time (χ(2)=4.639, P=0.098). CIP2A expression may have no prospective value for optimizing chemotherapy regimens, but it can be an indicator for patient prognosis.

[Investigation of etiology of massive infection with porcine pseudorabies virus in Henan and neighboring Provinces].

In early 2011, the serious outbreak of porcine pseudorabies virus (PRV) infection suddenly recurred in Henan and neighboring Provinces. To investigate the etiology of massive infection with PRV, 16 800 serum samples, 905 porcine epidemic diarrhea virus (PEDV) back-feeding tissues, and 56 PR gene deleted live vaccines were colleted from January 2011 to May 2013 to detect PRV field infection using a PRV gE antibody test kit. The gE and TK genes of 11 new epidemic PRV strains were sequenced by PCR, and their molecular characteristics were analyzed. Moreover, virus titer determination, protective test against PRV, and vaccine potency testing were performed. The results showed that the detection rate of PRV field infection-positive pig farms was 68.06%, and the overall positive rate of PRV field infection in serum was 38.47%; the positive rates in breeding sows, breeding boars, reserve pigs, and commercial pigs were 40.12%, 30.88%, 54.67%, and 26.52%, respectively. The new epidemic strains were in the same evolutionary branch and belonged to the virulent strain group. Compared with the classical PRV strain, the virulence of new epidemic strains changed a little. The length of gE gene was 1 787 bp, and the length of TK gene was 963 bp. The nucleotide homologies of gE and TK genes to Chinese reference strains were 98.2%-99.8% and 98.90%-99.6%, respectively, and the amino acid homologies were 97.1%-99.8% and 97.5%-99.4%, respectively. Commercial vaccine had a 100% protective effect against the new epidemic strains. The positive rate of PRV field infection was 0% in vaccine and 40.44% in back-feeding tissues. The results confirmed that PRV field infection rates were rising sharply among pigs in Henan and neighboring Provinces after 2011. The main virulence genes of new epidemic PRV strains did not change significantly over the years. PR gene deleted live vaccines had no PRV field infection and could completely resist the attack of new strains. The virus carriage of breeding boars and reserve pigs and the serious PRV field infection in PEDV back-feeding tissues were the main causative factors for massive infection with PRV and epidemic outbreak in Henan and neighboring Provinces from 2011 to 2013.

[Identification of differentially expressed genes in recurrent nasopharyngeal carcinoma and analysis of their chromosomal location].

OBJECTIVE: To identify differentially expressed genes in recurrent nasopharyngeal carcinoma (rNPC) by DNA microarrays, and analyze chromosomal localizations and molecular function by bioinformatics. METHODS: The primary nasopharyngeal carcinoma (pNPC) tissue samples and rNPC tissue samples were selected, and Affymetrix Gene1.0 ST gene chips were used to identify differential expressed genes in rNPC, and the bioinformatics was used to analyze their chromosomal localizations as well as molecular functions. RESULTS: A total of 44 genes were identified to be differential expressed in rNPC. Thirty-six genes were down regulated, 8 genes were up regulated. Functional classification of down-regulation genes showed that most genes (10 genes, 27.8%) belonged to the enzyme activity genes, followed by calcium ion binding genes (7 genes, 19.4%), protein binding genes (5 genes, 13.9%), receptor activity genes (4 genes, 11.1%), ATP binding genes (2 genes, 5.6%), transcription factor genes (2 genes, 5.6%), extracellular matrix binding and growth factor binding have 1 gene respectively (each accounted for 2.8%). In addition, the functions of 4 genes (11.1%) were unknown. Functional classification of up-regulation genes showed most genes (3 genes, 37.5%) were unknown, followed enzyme activity genes (2 genes, 25.0%), receptor activity, calcium ion binding and voltage-gated ion channel activity genes have 1 genes respectively (each accounted for 12.5%). These genes were localized randomly on the most the chromosomes, with a majority of them localized on chromosomes 1, 17. Chromosome 1 contained the most differentially expressed genes (10, 22.7%), followed by chromosomes 17 (5, 11.3%). CONCLUSIONS: The differential expressed genes in rNPC were supposed to be randomly distributed on most chromosomes, but the majorities were found on chromosomes 1, 17. Abnormality in three groups of genes, including in enzyme activity, calcium ion binding and protein binding associate genes, might play important roles in rNPC. Those genes need to be further studied.

Mutations in preS genes of genotype C hepatitis B virus in patients with chronic hepatitis B and hepatocellular carcinoma.

BACKGROUND: Hepatitis B virus (HBV) preS mutations are frequently isolated from patients with severe forms of liver disease. Meanwhile, genotype C has been shown to cause more serious liver disease than genotype B. This study assesses the frequency of preS mutation in Chinese patients with genotype C chronic HBV infection and its relation to liver damage. METHODS: Seventy-nine persistently infected patients (25 asymptomatic carriers, 28 with chronic hepatitis, and 26 with hepatocellular carcinoma) with genotype C HBV were analyzed. Levels of HBV DNA, hepatitis B e antigen (HBeAg), alanine aminotransferase, and aspartate transaminase and mutations in the preS region were determined. RESULTS: The correlations of preS deletion with disease progression were distinct: preS deletion mutations were more commonly found in the hepatocellular carcinoma (HCC) group than in the chronic hepatitis B (CHB) or asymptomatic carrier (ASC) groups, with the frequencies of 38.46% (10/26) in the HCC, 7.14% (2/28) in the CHB, and 4.00% (1/25) in the ASC (P = 0.001) groups. The HBeAg-positive rate and HBV DNA levels were comparable between patients with the preS mutation and those without. CONCLUSIONS: PreS deletion mutations of genotype C HBV might play a role in HBV-related hepatocarcinogenesis.