ABSTRACT
A total of 40 patients with COPD (excluding those with correlated/relevant diseases)were measured for inflammation parameters of erythrocyte sedimentation rate (ESR) and c-reactive protein (CRP) after hospital admission and some coagulation/fibrinolysis parameters including D-dimer,thrombinantithrombin (TAT),prothrombin fragment 1 + 2,(tissue plasminogen activator) tPA,plasminogen activator inhibitor 1 (PAI-1),von Willebrand factor (von WF),endothelin receptor A,thromboxane B2,P-selectin and pulmonary arterial pressure (PAP) by ultrasonic cardiography after the settling of the symptons of acute period.All patients were then divided into 2 groups according to PAP [＜ 40 mm Hg (1 mmHg=0.133 kPa) (n=24),＞40 mm Hg (n=16)].The values of CRP and ESRin the group with PAP ＞ 40 mm Hg were significantly higher than those in another group (P =0.044 and P =0.002respectively) while tPA was lower (P =0.04).A moderate positive correlation existed between tPA and TXB2 (r =0.547).Moreover,a highly positive correlation was found between TXB2 and PAl-1 (r =0.929).The results indicated that the COPD patients with pulmonary arterial hypertension (PAH) tend to have a higher level of inflammation,and their fibrinolysis becomes impaired leading to a prothrombotic state.
ABSTRACT
Objective To explore the effects of polymorphisms of Crohn's disease related NOD2 gene and human beta-defensin 2 (hBD-2) on transcription of hBD-2 gene and its mechanism. Methods HEK293T cells were transfected with hBD-2 gene and NOD2 eukaryotic expression plasmid, and were then stimulated with LPS, TNF-α, or BAY 11-7082 (antagonist of NF-κB), respectively. Transcriptional activity of hBD-2 was detected afterwards. Results LPS could suppress transcription of hBD-2 (P=0. 020), which was increased by TNF-α in a dose-dependent manner (P =0. 004). In the presence of LPS, there was sig-nificant difference in transcriptional activity of hBD-2 between wild-NOD2 transfected group and mutated NOD2 (P268S) transfected group (P=0. 008), but there was no significant difference between wild hBD-2 transfected group and mutated hBD-2 transfected group (P=0. 053). With the stimulation of TNF-α (5 ng/ml), there was a significant difference between mutated hBD-2 transfected group and wild hBD-2 transfected group (P=0. 006), but no significant difference between wild-NOD2 transfected and mutated NOD2 transfected group was defected (P = 0. 064). Pretreatment with BAY 11-7082 before TNF-α (5 ng/ml) significantly inhibited the transcriptional activity of hBD-2 (P < 0. 001). Conclusion The poly-morphism of NOD2 affects the innate expression of hBD-2, the polymorphism of site in hBD-2 promoter (-233) may lead to significant decline of the inducible expression of hBD-2, and NF-κB might be a key pathway that NOD2 protein mediates the expression of defensin.
ABSTRACT
Objective To investigate the association of two single nuclear peptides(SNPs)polymorphisms(rs11209026 and rs11805303)which lies in interleukin-23 receptor(IL23R)gene with susceptibility to inflammatory bowel disease(IBD).Methods The target SNPs were directly sequenced by polymerase chain reaction(PCR)and gene polymorphisms of 50 healthy and 81 patients with IBD (Crohn's disease in 41 patients and ulcerative colitis in 40 patients)were analyzed using chromassoftware.Results The geno-type frequency and allelic frequency of rs11209026 were 7.3%and 3.7%in patients with Crohn's disease respectively,15.0%and 7.5%in patients with ulcerative colitis respectively as well as 14.0%and 7.0%in normal population respectively(all P value＞0.05).The geno-type frequency and allelic frequency of rs11805303 were 22.0%and 52.4%in patients with Crohn's disease respectively,15.0% and 41.2% in patients with ulcerative colitis respectively as well as 34.0%and 59.0%in normal population respectively(all P value＞0.05).But in allelic frequency there was significant difference between ulcerative colitis patients and normal population(P=0.018).The polymorphisms of rs11805303 loci did not correlate with age,gender,disease duration.activity and site in patients with ulcerative colitis.Conclusions IL23R gene polymorphism is not associated with the susceptibility to Crohn's disease.rs11805303 allele may be related with susceptibility to ulcerative colitis.But no correlation was found between the SNP polymorphisms and the clinical characteristic of ulcerative colitis.
ABSTRACT
Telomerase activity in 43 biopsy of gastric mucosa was detected with the modified telomeric repeat amplification protocol(TRAP) assay to elucidate pathogenesis of gastric cancer.The detected positive rates were as follows:87%(20/23) in gastric cancer,28 6%(2/7) in moderate and non-typical gastritis ,0%(0/10 in atrophic and superficial gastritis,respectively.These results suggest that the detection of telomerase activity may play a significant role in the diagnosis of gastric cancer.