Objective To explore the optimal methods to detect helicobacter pylori(Hp)antigen in children.Methods 13C labeled urea breath test(13C-UBT)was performed on 937 children of alimentary department from Sep.2000 to Feb.2006.Gastric mucosa biopsy of 96 children was detected.Hp stool antigen(HpSA)status of the 557 children were evaluated.Both 13C-UBT and HpSA were assayed in 105 children from Apr.2003 to Apr.2004.Method of 13C-UBT was taken as the golden standard on diagnosis of Hp infection.Results Forty-one point seven percent children was positive for 13C-UBT.Forty point six percent children was positive for gastric mucosa biopsy.Thirty-eight point two percent was positive for HpSA.The difference was not significant.2.Among the 105 children performed by both 13C-UBT and HpSA,41.9% was positive for 13C-UBT and 39.0% for HpSA.Taking 13C-UBT as the golden standard,sensitivity of HpSA to diagnose Hp infection was 91.8%,and its specificity was 81.8%.Consistency Kappa coefficient was 0.743(P=0),which denoted that there was no significant difference on the positive detection rate between 13C-UBT and HpSA(P=0.388).Conclusions 13C-UBT and HpSA as non-invasive technique is effective to detect the Hp antigen.Compared to 13C-UBT,as a convenient,noninvasive,economical method,HpSA detection is much more acceptable to children and their patients.

OBJECTIVETo study the effects of nimesulide, a selective COX-2 inhibitor, on cell viability, telomerase and PKB activities in human gastric cancer cell line SGC7901 and to explore its molecular mechanism of selective growth inhibition.

METHODSMTT assay was used to determine cell viability after incubation for 0, 12, 24, and 48 h in different concentrations (0, 25, 50, 100, 200 micro mol/L) of nimesulide and/or okadaic acid (300 nmol/L). Telomerase and protein kinase B (PKB) activities were detected using TRAP PCR-ELISA and nonradioactive IP-kinase assay.

RESULTSNimsulide caused a time and dose-dependent reduction of cell numbers of SGC7901. The telomerase and PKB activities were significantly inhibited, and the inhibition of telomerase activity was partly associated with decrease in PKB activity.

CONCLUSIONSelective COX-2 inhibitor nimesulide inhibits telomerase activity of gastric cancer cells by partly blocking the activation of protein kinase B. The results suggest an additional signaling pathway underlying the anti-cancer effect of COX-2 inhibitor.

Adenocarcinoma ; enzymology ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cyclooxygenase Inhibitors ; pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; drug effects ; Humans ; Protein-Serine-Threonine Kinases ; metabolism ; Proto-Oncogene Proteins ; metabolism ; Proto-Oncogene Proteins c-akt ; Stomach Neoplasms ; enzymology ; pathology ; Sulfonamides ; pharmacology ; Telomerase ; metabolism ; Time Factors

Animals ; Glutathione ; therapeutic use ; Liver ; metabolism ; physiopathology ; Male ; NF-kappa B ; biosynthesis ; Pancreatitis, Acute Necrotizing ; drug therapy ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley

PURPOSE: It is controversial whether folate status is a risk factor for the development of asthma or other allergic diseases. This study was conducted to investigate whether indirect or direct exposure to folate and impaired folate metabolism, reflected as methylene-tetrahydrofolate reductase (MTHFR) C677T polymorphism, would contribute to the development of asthma and other allergic diseases. METHODS: Electronic databases were searched to identify all studies assessing the association between folate status and asthma or other allergic diseases. Two reviewers independently assessed the eligibility of studies and extracted data. The relative risk (RR) or odds ratio (OR) with 95% confidence intervals (CI) was calculated and pooled. RESULTS: Twenty-six studies (16 cohort, 7 case-control, and 3 cross-sectional studies) were identified. Maternal folic acid supplementation was not associated with the development of asthma, atopic dermatitis (AD), eczema, and sensitization in the offspring, whereas exposure during early pregnancy was related to wheeze occurrence in the offspring (RR=1.06, 95% CI=[1.02-1.09]). The TT genotype of MTHFR C677T polymorphism was at high risk of asthma (OR=1.41, 95% CI=[1.07-1.86]). CONCLUSIONS: It is indicated that maternal folic acid supplementation during early pregnancy may increase the risk of wheeze in early childhood and that the TT genotype of MTHFR C677T polymorphism impairing folic acid metabolism would be at high risk of asthma development. These results might provide additional information for recommendations regarding forced folate consumption or folic acid supplements during pregnancy based on its well-established benefits for the prevention of congenital malformations. However, currently available evidence is of low quality which is needed to further elucidate.
Asthma* ; Case-Control Studies ; Cohort Studies ; Dermatitis, Atopic ; Eczema ; Folic Acid* ; Genotype ; Metabolism ; Odds Ratio ; Oxidoreductases ; Pregnancy ; Risk Factors*

OBJECTIVETo investigate the effects of host-derived p38 mitogen-activated protein kinase subunit 38 (p38MAPK) and the hepatitis B virus X antigen (HbxAg) on cell proliferation and apoptosis in human hepatocellular carcinoma (HCC), and to study the mechanism underlying hepatocarcinogenesis.

METHODSLiver tissues were biopsied from healthy individuals and patients with chronic hepatitis B (CHB), liver cirrhosis, paratumor cirrhosis, and HCC. Immunohistochemical staining was used to detect expressions of HBxAg, p38MAPK, cell cycle G2/M phase-related factors (cdc25B, p34cdc2, cyclin B1), and cell proliferation factor ki-67.The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method (known as TUNEL) was used to detect apoptosis.

RESULTSThe highest rates of HBxAg were detected in CHB (65.0%) and HCC (44.4%) liver samples, and the antigen was mainly expressed in nuclei. Increasingly higher rates of p38MAPK, cdc25B, cyclin B1, and p34cdc2 expression were detected with increases in disease severity: normal liver (40.0%, 20.0%, 20.0%, and 30.0%, respectively), chronic hepatitis B (60.0%, 65.0%, 40.0%, and 50.0%, respectively), liver cirrhosis (65.0%, 75.0%, 70.0%, and 55.0%, respectively), paratumor cirrhosis (66.7%, 75.0%, 75.0%, and 63.9%, respectively), and HCC (77.8%, 80.6%, 80.6%, and 72.2%, respectively). In addition, the intracellular location of p38MAPK expression was different under different disease conditions, showing nuclear expression in CHB and liver cirrhosis samples and cytoplasmic expression in paratumor cirrhosis and HCC samples (x2 = 1.11, P more than 0.05). The proliferation index (PI) and the apoptosis index (AI) were both increased along with disease severity (normal more than CHB more than paratumor cirrhosis more than HCC) (PI: 0.0000+/-0.000, 0.0502+/-0.011, 0.0411+/-0.009, 0.0762+/-0.017; AI: 0.0351+/-0.024, 0.0607+/-0.022, 0.0562+/-0.013, 0.0716+/-0.011), with the notable exception for liver cirrhosis (PI: 0.1810+/-0.036 and AI: 0.1200+/-0.018). PI in poorly-differentiated HCC (0.2285+/-0.062) was significantly higher than in well-differentiated HCC (0.1216+/-0.032, t = 2.082, P = 0.044). AI in well-differentiated HCC (0.152+/-0.026) was significantly higher than in poorly-differentiated HCC (0.081+/-0.022, t = 2.129, P = 0.041).

CONCLUSIONSIn the process of hepatocarcinogenesis, HBxAg may cause a series of abnormal changes in cell cycle, proliferation and apoptosis by affecting the expression of p38MAPK.

Apoptosis ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Cycle ; Cell Division ; Cell Proliferation ; Hepatitis B, Chronic ; pathology ; Humans ; Liver Cirrhosis ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Trans-Activators ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo assess lipid peroxidation and ultrastructural modifications in rat brains following perinatal exposure to lead (Pb) and/or cadmium (Cd).

METHODSFemale rats were divided into four groups: control group, Pb (300 mg/L) group, Cd group (10 mg/L) and Pb+Cd (300 mg/L, 10 mg/L) group. The compounds were delivered in the drinking water throughout pregnancy and lactation.

RESULTSThe levels of compounds in blood and brain of the Pb+Cd group were similar to those of other groups, but the effects of Pb+Cd on pups' body and brain weights were higher than on other compounds. Electron microscopy revealed that Pb and Cd had effects on mitochondrial swelling, disruption and cristae loss, Nissl body dissolution, degenerated organelles and vacuoles, cytomembrane disappearance, and nuclear chromoplasm concentration. The activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), acetylcholinesterase (AChE) was decreased, whereas the activity of maleic dialdehyde (MDA) was increased.

CONCLUSIONPerinatal exposure to low doses of Pb and Cd can produce alterations in lipid peroxidation and ultrastructural modifications in rat brains, and exposure to both metals can result in greater damages.

Animals ; Antioxidants ; metabolism ; Brain ; drug effects ; metabolism ; ultrastructure ; Cadmium ; toxicity ; Environmental Pollutants ; toxicity ; Female ; Lead ; toxicity ; Lipid Peroxidation ; drug effects ; Malondialdehyde ; metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Water

OBJECTIVETo gain insight into the mechanism by which sex-determining region of Y chromosome (SRY)-related high-mobility-group box 2 (SOX2) involved in carcinogenesis and cancer stem cells (CSCs).

DATA SOURCESThe data used in this review were mainly published in English from 2000 to present obtained from PubMed. The search terms were "SOX2," "cancer," "tumor" or "CSCs."

STUDY SELECTIONArticles studying the mitochondria-related pathologic mechanism and treatment of glaucoma were selected and reviewed.

RESULTSSOX2, a transcription factor that is the key in maintaining pluripotent properties of stem cells, is a member of SRY-related high-mobility group domain proteins. SOX2 participates in many biological processes, such as modulation of cell proliferation, regulation of cell death signaling, cell apoptosis, and most importantly, tumor formation and development. Although SOX2 has been implicated in the biology of various tumors and CSCs, the findings are highly controversial, and information regarding the underlying mechanism remains limited. Moreover, the mechanism by which SOX2 involved in carcinogenesis and tumor progression is rather unclear yet.

CONCLUSIONSHere, we review the important biological functions of SOX2 in different tumors and CSCs, and the function of SOX2 signaling in the pathobiology of neoplasia, such as Wnt/β-catenin signaling pathway, Hippo signaling pathway, Survivin signaling pathway, PI3K/Akt signaling pathway, and so on. Targeting towards SOX2 may be an effective therapeutic strategy for cancer therapy.

Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms ; metabolism ; Neoplastic Stem Cells ; metabolism ; SOXB1 Transcription Factors ; metabolism

To look for the toxicity fraction of Euphorbia pekinensis and discuss the vinegar processing mechanism. The level of intestinal edema, water content of intestine and stool, IC50 values of IEC-6 were applied to evaluate the toxicity of different fractions. RT-PCR was employed for detecting AQP1, AQP3 mRNA expression. The petroleum ether (PE) fraction and ethyl acetate (EtOAc) fraction could significant cause intestinal edema in mice, increase the water content of duodenum, colon and stool, inhibited the mRNA expression of AQP1 and increased the mRNA level of AQP3 in colon, and the petroleum ether (PE) fraction was more poisonous. After the petroleum ether (PE) fraction was processed with vinegar, the level of intestinal edema, water content of duodenum, colon, stool and inhibition ratio of cells line were reduced. And we compared the composition change after vinegar processing, finding that the conpekinensis.
Acetic Acid ; chemistry ; Animals ; Cell Line ; Chemistry, Pharmaceutical ; methods ; Drugs, Chinese Herbal ; chemistry ; toxicity ; Euphorbia ; chemistry ; toxicity ; Male ; Mice ; Mice, Inbred ICR ; Molecular Structure

OBJECTIVESTo investigate the prognostic significance of Omi/HtrA2 expression, and the correlation between Omi/HtrA2 and Hypoxia-inducible factor (HIF)-1α in primary hepatocellular carcinoma cells.

METHODSThe expression of HIF-1α and Omi/HtrA2 in 43 cases of hepatic carcinoma tissues were detected immunohistochemically. Follow-up data were obtained to perform the Kaplan-Meier survival analysis. The change of Omi/HtrA2 expression in HepG2 cell was measured after HIF-1α expression of HepG2 in vitro was regulated by Tet-on expression system.

RESULTSOmi/HtrA2 expression was correlated with lymph node metastasis and recurring within liver during 2 years. Statistical analysis estimation showed the cumulative survival rate of post-hepatectomy for the patients with the positive expression of Omi/HtrA2 was higher than that for other patients with the negative expression of Omi/HtrA2 (χ(2) = 6.13, P = 0.013). In the common paraffin-embedded specimen of hepatocellular carcinoma, most of the samples showing negative or weak positive HIF-1α immunopositivity showed moderate positive or strong positive Omi/HtrA2 immunopositivity, while most of the samples showing moderate positive or strong positive HIF-1α immunopositivity showed negative or weak positive Omi/HtrA2 immunopositivity. The mRNA expression intensity of Omi/HtrA2 was decreasing with the HIF-1α expression increasing, and the difference was statistically significant(F = 106.766, P < 0.01).

CONCLUSIONSOmi/HtrA2 may be an important prognostic marker for primary hepatocellular carcinoma. Omi/HtrA2 expression is reversely correlated with HIF-1α expression in hepatocellular carcinoma. During the apoptotic process Omi/HtrA2 participating in hepatocellular carcinoma cells, HIF-1α is involved in the controlling and regulating of Omi/HtrA2 expression.

Adolescent ; Adult ; Aged ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Follow-Up Studies ; Hep G2 Cells ; High-Temperature Requirement A Serine Peptidase 2 ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Liver Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Mitochondrial Proteins ; metabolism ; Neoplasm Recurrence, Local ; metabolism ; pathology ; Prognosis ; Serine Endopeptidases ; metabolism ; Transfection ; Tumor Cells, Cultured ; Young Adult

OBJECTIVESTo study the possible relationship between CYP1A1, NAT2 genetic polymorphisms and the susceptibility of prostate cancer.

METHODSForty-eight patients with prostate cancer and 112 healthy cases were selected as the control randomly. NAT2 and CYP1A1 gene polymorphisms were analysed with the methods of PCR-RFLP, ASA and real-time fluorescence Light-Cycler. The difference of frequency between the patients and the controls was compared.

RESULTSAmong prostate cancer patients and their matched controls, the frequencies of alleles and genotypes were significantly different with Ile-Val gene Polymorphisms (P < 0.05), in which the frequency of the allele G and GG genotypes were significantly higher than those in their matched controls with an odds ratio of 1.59 and 3.06(P < 0.05), respectively; No significant differences of the frequencies of the MspI alleles and genotypes were found between the patients with prostate cancer and the matched controls(P > 0.05). No significant differences of NAT2 slow acetylator genotype frequency were found between the controls and prostate cancer patients (P > 0.05).

CONCLUSIONSThe CYP1A1 Ile-Val gene polymorphisms might be associated with the occurrence of prostate cancer, while MspI gene polymorphisms and NAT2 slow acetylator genotype might not be associated with the occurrence of prostate cancer.

Adult ; Aged ; Arylamine N-Acetyltransferase ; genetics ; Cytochrome P-450 CYP1A1 ; genetics ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Prostatic Neoplasms ; genetics