CEA, CA19-9, C72-4 and CA50 concentrations were determined by ABBOTT ARCHITECT I2000 SR. We found the CFD concentrations have significant differences between GC patients, benign gastric disease (BGD) patients and healthy controls (<i>P</i> < 0.05).
CEA, CA19-9, C72-4 and CA50 concentrations were determined by ABBOTT ARCHITECT I2000 SR. We found the CFD concentrations have significant differences between GC patients, benign gastric disease (BGD) patients and healthy controls (<i>P</i> < 0.05).
CEA, CA19-9, C72-4 and CA50 concentrations were determined by ABBOTT ARCHITECT I2000 SR. We found the CFD concentrations have significant differences between GC patients, benign gastric disease (BGD) patients and healthy controls (<i>P</i> < 0.05).
CEA, CA19-9, C72-4 and CA50 concentrations were determined by ABBOTT ARCHITECT I2000 SR. We found the CFD concentrations have significant differences between GC patients, benign gastric disease (BGD) patients and healthy controls (<i>P</i> < 0.05).
A frequent Toll-like receptor 1 gene polymorphism affects NK- and T-cell IFN-γ production and is associated with Helicobacter pylori-induced gastric disease.
Altogether, we suggest the role of mitochondrial GR-O<sub>2</sub><sup>•-</sup>-fission cohort in brain-mitochondria cross-talk during acute mental stress and advocate the utilization of this pathway as a potential target to prevent mitochondrial unrest and gastropathy bypassing central nervous system.
Besides, protein level analysis were performed to compare ERCC6 and ERCC8 expression in different stages of gastric diseases, and to correlate SNPs jointly with gene expression.
Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against <i>H. pylori</i>-related hypergastrinemia and consequently gastric disease development, including gastric cancers.
Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against <i>H. pylori</i>-related hypergastrinemia and consequently gastric disease development, including gastric cancers.
Elucidation of the mechanism of gastrin modulation by HB-EGF-mediated EGF receptor transactivation should facilitate the development of therapeutic strategies against <i>H. pylori</i>-related hypergastrinemia and consequently gastric disease development, including gastric cancers.
Expression of both MIB2 variants affected NOTCH signalling, proliferation and apoptosis in primary rat cardiomyocytes.In conclusion, we report the first example of left ventricular hypertrabeculation/LVNC with germline MIB2 variants resulting in altered NOTCH signalling that might be associated with a gastropathy clinically overlapping with Ménétrier disease.
H pylori isolates show high frequencies of cagA gene and CagA expression, but the infections by CagA(+) H pylori strains are not the most decisive factors to cause gastric diseases.
Helicobacter pylori isolated from a patient with Ménétrier's disease increases hepatocyte growth factor mRNA expression in gastric fibroblasts: comparison with Helicobacter pylori isolated from other gastric diseases.
Immunohistochemistry was performed to localize and quantify the expression of periostin in benign gastric diseases and gastric cancer, and immunostaining results were correlated with gastric cancer pathological stages.
In conclusion, our results suggest that the nonfunctional TLR1 602S/S genotype is associated with a reduced risk of H. pylori-induced gastric diseases, probably via diminished Th1 responses.
In the present study, real-time quantitative reverse transcription-polymerase chain reaction was used to analyze miR-421 levels in gastric juice from patients with gastric cancer or benign gastric disease, or normal.