Objective: To investigate the values of CECT (contrast-enhanced computed tomogramphy) and CEUS (contrast-enhanced ultrasonography) in the diagnosis of cancerous lesions in the liver before and after RFA (radiofrequency ablation) for liver cancer. Methods: The clinical records of 90 patients with liver cancer (65 primary liver cancer and 25 metastatic liver cancer) undergoing RFA between May 2008 and September 2010 were retrospectively analyzed. A total of 104 cancerous lesions in the liver were treated with CT- or ultrasound-guided RFA. Each patient underwent CEUS and CECT one week before RFA and one month after RFA. The diagnostic abilities of CEUS and CECT before RFA and the values of CEUS and CECT in the evaluation of therapeutic effect of RFA were assessed. Results: Before RFA, 93 and 96 cancerous lesions in the liver were detected by CECT and CEUS, respectively. However, CECT combined with CEUS found 104 lesions. One month after RFA, 90 lesions showed no enhancement on CECT, and 91 lesions showed no enhancement on CEUS. CECT combined with CEUS found that 86 lesions showed no enhancement. CECT, CEUS and the CECT combined with CEUS found 5, 8 and 11 recurrent lesions in the liver, respectively. Conclusion: CECT combined with CEUS can increase the detection rates of cancerous lesions in the liver before RFA and the residual lesions and recurrent lesions after RFA. © 2012 by Tumor.

OBJECTIVETo investigate the effects of survivin antisense oligonucleotide (ODN) on cell proliferation and apoptosis of HL-60 cells.

METHODSSynthetic ODN was completely phosphorothioate-modified. Cationic lipid-mediated antisense ODN was transferred into HL-60 cells. The expression of survivin mRNA and protein was detected by RT-PCR and Western Blot. The incorporation of MTT was used as the measurement of HL-60 proliferation. The cell-cycle and apoptosis were analyzed by flow cytometry.

RESULTSHL-60 cells spontaneously expressed survivin mRNA and protein. Both mRNA and protein expression of survivin decreased significantly in the antisense ODN transfected cells in comparison to that in the original cells and cells transfected with sense ODN. Survivin antisense ODN significantly inhibited cell proliferation and induced apoptosis in a dose-dependent manner. The cell-cycle in the antisense ODN-transfected cells stopped at the G2/M phase.

CONCLUSIONSAntisense ODN targeting at survivin mRNA can inhibit HL-60 cell proliferation and induce G2/M stop and apoptosis.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; HL-60 Cells ; drug effects ; Humans ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; antagonists & inhibitors ; genetics ; Neoplasm Proteins ; antagonists & inhibitors ; genetics ; Oligonucleotides, Antisense ; pharmacology ; RNA, Messenger ; analysis

OBJECTIVESTo test the effect of rapamycin (RAPA) on hepatic tumor growth and metastasis in Sprague-Dawley (SD) rat model and explore the possible mechanism.

METHODSSD rat hepatocellular carcinoma (HCC) model with metastatic potential was induced by diethylnitrosamine (DEN) and N-nitrosomorpholine (NMOR). 120 SD rats were randomized into four groups 16 weeks after DEN and NMOR treatment, and received 4-week intraperitoneal injection of RAPA (1.5 or 4.5 mg x kg(-1) x d(-1)), CsA (25 mg x kg(-1) x d(-1)) or equal volume of 0.9% saline, respectively. Tumor growth and metastasis were checked after the 4-week treatment. Serum vascular endothelial growth factor (VEGF) was determined by enzyme-linked immunosorbent assay (ELISA). Antiangiogenetic effects were assessed by CD34 immunostaining. The levels of hypoxia-inducible factor 1 alpha (HIF-1 alpha) and VEGF proteins and mRNAs were detected by immunohistochemistry, western blot and reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTSThe mean liver weight (5.58% +/- 0.42% and 5.69% +/- 0.74%), the metastatic liver nodules (5.12 +/- 0.68 and 5.67 +/-1.12), the metastasis lung nodules (0.43 +/- 0.11 and 0.45 +/- 0.83), and the lung metastasis rate (17.2% and 14.8%) were lower in rats treated with RAPA 1.5 mg x kg(-1) x d(-1) or 4.5 mg x kg(-1) x d(-1) than those in rats treated with saline, which were 10.42% +/- 1.86%, 12.36 +/- 3.45, 1.81 +/- 0.3 and 50.0% respectively (P < 0.01 or P < 0.05). The intratumoral microvessel density (MVD), serum VEGF, and the levels of HIF-1 alpha and VEGF were lower in RAPA-treated rats than those in control rats. However, CsA-treated rats showed an opposite trend compared with the RAPA-treated rats.

CONCLUSIONRAPA can repress the expression of angiogenesis-promoting factors HIF-1 alpha and VEGF, and significantly inhibits the growth and metastasis of HCC.

Animals ; Carcinoma, Hepatocellular ; blood supply ; metabolism ; pathology ; Cyclosporine ; pharmacology ; therapeutic use ; Disease Models, Animal ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Immunohistochemistry ; Immunosuppressive Agents ; pharmacology ; therapeutic use ; Liver Neoplasms, Experimental ; blood supply ; metabolism ; pathology ; Male ; Microvessels ; pathology ; Neoplasm Metastasis ; Neovascularization, Pathologic ; RNA, Messenger ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Sirolimus ; pharmacology ; therapeutic use ; Vascular Endothelial Growth Factors ; genetics ; metabolism

OBJECTIVETo evaluate effects of celecoxib (a selective cox-2 inhibitor)combined with fluvastatin (a HMG-CoA reductase inhibitor) on tumor growth and cell apoptosis in hepatocellular carcinoma xenograft in nude mice.

METHODSHepatocellular carcinoma BEL-7402 cells were inoculated subcutaneously into the left armpit of nude mice, the mice (n = 32) were then randomly divided into 4 groups: the control group, the celecoxib group,the fluvastatin group and the combination group. At the end of the study, Tumor Tissues were collected for analysis. Cell apoptosis was determined by flow cytometry analysis and TUNEL assay. Akt, p-Akt and survivin protein levels were measured by Western blot. Statistical comparisons were made using factorial analysis of variance (ANOVA) and multiple comparisons between each two groups were calculated using SNK-q test.

RESULTSThe combination of Celecoxib and fluvastatin resulted in a greater inhibition of tumor growth than either agent alone, the tumor inhibitory rate was 34.0% in the Celecoxib group, 25.0% in the fluvastatin group and 72.2% in the combination group. The percentages of TUNEL--positive cancer cells in the celecoxib and fluvastatin alone treatment groups were 8.5%+/-1.4% and 9.4%+/-1.7% respectively as compared to the control group which was 3.5%+/-0.8%. Combination therapy showed a significantly greater increase in tumor cell apoptosis in comparison with the control and single-therapy groups (apoptotic index: 19.4%+/-3.0%; P value is less than 0.01 versus celecoxib or fluvastatin groups). The results of flow cytometry analysis also showed the same tendency. a small number of apoptotic cells were detected in the control tumours (4.1%+/-1.6%), whereas a large number of apoptotic cells were detected in tumours treated with celecoxib (9.1%+/-2.1%) or fluvastatin (10.1%+/-2.3%) alone; and the combination therapy resulted in even more apoptotic cells (23.6%+/-5.8%; P value is less than 0.01 versus celecoxib or fluvastatin groups). Western blot analysis demonstrated that the combination of celecoxib and fluvastatin significantly down-regulated p-Akt (0.23+/-0.08 versus 1.12+/-0.07 and surviving (0.50+/-0.07 versus 1.47+/-0.19) in BEL-7402 tumours compared with the control (P value is less than 0.01 for all).

CONCLUSIONThe present study provided evidence that treatment with celecoxib in combination with fluvastatin resulted in the inhibition of HCC tumour growth in an in vivo mouse model.

Animals ; Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; drug therapy ; metabolism ; pathology ; Celecoxib ; Cell Line, Tumor ; Cyclooxygenase 2 Inhibitors ; administration & dosage ; pharmacology ; Fatty Acids, Monounsaturated ; administration & dosage ; pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; administration & dosage ; pharmacology ; Indoles ; administration & dosage ; pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Pyrazoles ; administration & dosage ; pharmacology ; Sulfonamides ; administration & dosage ; pharmacology ; Xenograft Model Antitumor Assays

OBJECTIVETo investigate the expression and its clinical significance of estrogen receptor (ERα) and phosphorylated estrogen receptor (p-ERα) in patients with hepatocellular carcinoma. The associations between ERα, p-ERα and IL-6 were also analyzed.

METHODSImmunohistochemistry was used to detect the expression of ERα, p-ERα and IL-6 in tumor tissues from 77 cases with hepatocellular carcinoma. The relations between ERα and the clinical pathological parameters and prognosis were also analyzed.

RESULTSThe positive rates of ERα, p-ERα and IL-6 in hepatocellular carcinoma were 39.0% (30/77), 45.4% (35/77) and 72.7% (56/77), respectively. The expression of ERα and p-ERα were negatively correlated with the expression of IL-6 (r=-0.468, P<0.01; r=-0.370, P<0.01, respectively). The positive rate of ERα in patients with tumor size≤5 cm, serum level of alpha-fetoprotein<400 µg/L, with complete encapsulation and non-microvascular invasion was significantly higher than those with tumor size>5 cm, serum level of alpha-fetoprotein&ge;400 µg/L, non-complete encapsulation and with microvascular invasion (all P<0.05). The overall survival rates of ERα-positive and ERα-negative patients were 66.7% and 23.4% (P<0.05). And the disease-free survival rates of ERα-positive and ERα-negative patients were 83.3% and 57.4% (P<0.05).

CONCLUSIONSThe tumor biological features of ERα-positive patients are better than that of ERα-negative patients. The role of ERα in hepatocellular carcinoma may be related to IL-6 level.

Adult ; Aged ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Estrogen Receptor alpha ; metabolism ; Female ; Hepatitis B ; metabolism ; pathology ; Humans ; Interleukin-6 ; metabolism ; Kaplan-Meier Estimate ; Liver Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Phosphorylation ; Prognosis ; Proportional Hazards Models ; Young Adult

OBJECTIVETo explore the immunogenetic features of human leukocyte antigen DRB1, DQB1 locus and children with Helicobacter pylori (H. pylori) infection in Han ethnic population in Kunming and its association with digestive diseases and H. pylori to better understand the immunogenetic features of the H. pylori infection.

METHODSPolymerase chain reaction-sequence specific primer (PCR-SSP) method was used to study the HLA-DRB1, DQB1 allelic frequency distribution on 35 children with H. pylori infection and 37 healthy controls in Han ethnic population in Kunming.

RESULTSAllelic frequencies of HLA-DRB1 * 0901, DQB1 * 03032 in the H. pylori infection group were lower than those of the healthy control group (7.14% vs. 31.08%, chi(2) = 13.16, Pc < 0.012; 5.71% vs. 25.68%, chi(2) = 10.68, Pc = 0.007) but the rest alleles' frequencies did not show significant differences.

CONCLUSIONThese result suggested that HLA-DRB1 * 0901, DQB1 * 03032 might protect the H. pylori infection in Han ethnic population in Kunming.

Adolescent ; Alleles ; Child ; China ; epidemiology ; ethnology ; Female ; HLA-DQ Antigens ; genetics ; immunology ; HLA-DQ beta-Chains ; HLA-DR Antigens ; genetics ; immunology ; HLA-DRB1 Chains ; Helicobacter Infections ; epidemiology ; genetics ; immunology ; Helicobacter pylori ; Humans ; Male ; Polymerase Chain Reaction

Schmallenberg virus (SBV), a novel orthobunyavirus, was first isolated in 2011. SBV preferentially infects the central nervous system of cattle and sheep and causes fever, diarrhea, a drop in milk yields, congenital malformations and stillbirths. Until June 2014, more than 200 scientific publications regarding SBV have been published. Although more than 20 articles on SVB were published in China, most of these articles provided only a brief introduction of the disease without fully discussing the associated disease characteristics. As a new disease, it has been made a focus of the National Research Center for Exotic Animal Diseases at the China Animal Health and Epidemiology Center. In this review, in order to provide a reference for research into SBV in China, we have reviewed the state of current research progress on the etiology, diagnosis and epidemiology of SBV, and vaccine development.
Animals ; Bunyaviridae Infections ; diagnosis ; epidemiology ; veterinary ; virology ; Cattle ; China ; epidemiology ; Goats ; Host Specificity ; Orthobunyavirus ; classification ; genetics ; isolation & purification ; physiology ; Sheep

This study aimed to establish a method for the detection and identification of H7N9 avian influenza viruses based on the NA gene by pyrosequencing. According to the published NA gene sequences of the avian influenza A (H7N9) virus, a 15-nt deletion was found in the NA gene of H7N9 avian influenza viruses. The 15-nt deletion of the NA gene was targeted as the molecular marker for the rapid detection and identification of H7N9 avian influenza viruses by pyrosequencing. Three H7N9 avian influenza virus isolates underwent pyrosequencing using the same assay, and were proven to have the same 15-nt deletion. Pyrosequencing technology based on the NA gene molecular marker can be used to identify H7N9 avian influenza viruses.
Animals ; Base Sequence ; Birds ; Chickens ; High-Throughput Nucleotide Sequencing ; methods ; Influenza A Virus, H7N9 Subtype ; classification ; enzymology ; isolation & purification ; Influenza in Birds ; virology ; Molecular Sequence Data ; Neuraminidase ; genetics ; Phylogeny ; Poultry Diseases ; virology ; Viral Proteins ; genetics

OBJECTIVETo explore the relationship between quinone oxidoreductase1 (NQO1) gene nonsynonymous cSNP and the genetic susceptibility of esophageal cancer.

METHODSPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Allele-Specific PCR (AS-PCR) were employed to assess the polymorphism of NQO1 genes both in 106 patients with esophageal cancer and control subjects matched by age, gender and origin.

RESULTSIt was shown that no C/C genotype was found at 406 of NQO1. The allelic frequency of NQO1 609T was significantly higher in patients with esophageal cancer than in the control subjects (P < 0.005) and the individuals with 609T allelic genotype of NQO1 gene were at greater risk to develop esophageal cancer (OR = 4.76, 95% CI = 1.064 - 3.397). But Individuals with mutant allele of NQO1 465 genotype did not show the rising risk of esophageal cancer.

CONCLUSIONSThe NQO1 C609T polymorphisms should likely be associated with the genetic susceptibility of esophageal cancer.

Alleles ; China ; Esophageal Neoplasms ; ethnology ; genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymorphism, Single Nucleotide

BACKGROUNDKeloid is an intricate lesion that is probably regulated by many genes. In this study, the authors used the technique of complementary DNA (cDNA) microarray to analyse abnormal gene expression in keloids and normal control skins.

METHODSThe polymerase chain reaction (PCR) products of 8400 genes were spotted in an array on chemical-material-coated-glass plates. The DNAs were fixed on the glass plates. The total RNAs were isolated from freshly excised human keloid and normal control skins, and the mRNAs were then purified. The mRNA from both keloid and normal control skins were reversely transcribed to cDNAs, with the incorporation of fluorescent dUTP, for preparing the hybridisation probes. The mixed probes were then hybridised to the cDNA microarray. After thorough washing, the cDNA microarray was scanned for differing fluorescent signals from two types of tissues. Gene expression of tissue growth factor-beta1 (TGF-beta1) and of c-myc was detected with both RT-PCR and Northern blot hybridisation to confirm the effectiveness of cDNA microarray.

RESULTSAmong the 8400 human genes, 402 were detected with different expression levels between keloid and normal control skins. Two hundred and fifty genes, including TGF-beta1 and c-myc, were up-regulated and 152 genes were down-regulated. Higher expressions of TGF-beta1 and c-myc in keloid were also revealed using RT-PCR and Northern blot methods.

CONCLUSIONcDNA microarray analysis provides a powerful tool for investigating differential gene expression in keloid and normal control skins. Keloid is a complicated lesion with many genes involved.

DNA, Complementary ; analysis ; Humans ; Keloid ; genetics ; Oligonucleotide Array Sequence Analysis ; methods ; Polymerase Chain Reaction ; RNA, Messenger ; analysis ; Skin