ABSTRACT
BACKGROUND:Tissue factor (TF) is the initiation factor of the extrinsic coagulation pathway, and plays a critical role in the process of thrombosis. This study aimed to investigate the expression of TF and to explore their clinical effect on the pulmonary artery after acute pulmonary thromboembolism. METHODS:Thirty-four Japanese white rabbits (Level II animals) supplied by Tianjin Medical University were randomly assigned into:group A, specimens of the pulmonary artery taken 3 hours after pulmonary embolism (n=8); group B, specimens of the pulmonary artery taken 8 hours after pulmonary embolism (n=8); group C, specimens of the pulmonary artery taken 24 hours after pulmonary embolism (n=8); and control group, pseudo-operations performed without injection of autologous blood clots (n=10). The animal model of pulmonary thrombo-embolism was established by injection of autologous blood clots into the jugular vein through a 5F catheter, and was confirmed by digital subtraction angiography. The mRNA expression of TF in different parts of the pulmonary artery was accessed by RT-PCR. Theq test was used if there was a significant difference in a given continuous variable among the three groups assessed by ANOVA. The experiment equipment was supplied by the State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, the Chinese Academy of Medical Sciences and Peking Union Medical College. RESULTS:The TF expression in the specimen adjacent to emboli was stable at 3, 8 or 24 hours after embolism. The mRNA expression of TF at 3 and 8 hours after embolism was lower in the specimens taken from the distal end of the morbid pulmonary artery than those adjacent to emboli. While at 24 hours after embolism, there were similar mRNA levels in specimens either adjacent or distal to emboli. CONCLUSION:The high level of TF expression in pulmonary artery tissue adjacent to emboli could lead to locally increased coagulation activity, indicating the necessity of initiating anti-coagulation treatment as soon as possible after acute pulmonary embolism.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the association of serotonin transporter gene linked polymorphic region (5-HTTLPR) insertion/deletion polymorphism with early onset myocardial infarction(MI) and platelet membrane glycoprotein I b(GP I b) in Northern Han population of China.</p><p><b>METHODS</b>A total of 150 patients with early onset MI and 150 age- and sex-matched controls with negative coronary arteriography were genotyped for the 5-HTTLPR polymorphism by using a polymerase chain reaction-based technique. The percentage of positive platelet membrane GP I b and the average fluorescence intensity were quantified by flow cytometry.</p><p><b>RESULTS</b>The genotype frequencies of LL, LS and SS in the 5-HTTLPR were 32%, 47% and 21% in the MI patients, 17%, 43% and 39% in the controls respectively(P<0.01). The L allele frequency in the MI patients was significantly higher than that of the control group (56% vs 39%, P<0.01). The percentage of positive platelet membrane GP I b and the fluorescence intensity in subjects with LL homozygote were markedly lower than that of LS and SS genotypes in the MI and control groups (all P<0.01). Multivariate logistic regression analysis showed that the 5-HTTLPR LL genotype was independently related to the occurrence of early onset MI(OR was 1.961, P was 0.037).</p><p><b>CONCLUSION</b>The LL genotype of the 5-HTTLPR might be associated with the susceptibility to developing early MI in Northern Han population of China. The platelet activation is increased in individuals of LL genotype.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Age of Onset , Alleles , Asian People , Genetics , Case-Control Studies , Ethnicity , Genetics , Gene Frequency , Homozygote , INDEL Mutation , Logistic Models , Myocardial Infarction , Genetics , Metabolism , Pathology , Platelet Glycoprotein GPIb-IX Complex , Metabolism , Polymorphism, Genetic , Serotonin Plasma Membrane Transport Proteins , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between tryptophan hydroxylase (TPH) gene A218C in intron 7 and 5-hydroxytryptamine transporter (5-HTT) gene variable number tandem repeat (VNTR) in intron 2 and gene-linked polymorphic region (LPR) deletion/insertion polymorphism and essential hypertension (EH) in Chinese northern Han population.</p><p><b>METHODS</b>A total of 280 EH patients and 200 normotensive controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism technique.</p><p><b>RESULTS</b>There were no significant differences in the frequencies of the genotypes and alleles of TPH gene A218C and 5-HTTVNTR between EH patents and controls (all P > 0.05). The genotype frequencies of SS, LS and LL in the 5-HTTLPR polymorphism was 68%, 29% and 3% in EH patients, 53%, 37% and 10% in the controls respectively (P < 0.01). The frequencies of allele S and L of the 5-HTTLPR were 82% and 18% in EH patients, 72% and 28% in the controls respectively (P < 0.01). Compared with the carriers of L allele (LS + LL), the EH risk was significantly higher in the SS homozygote (OR = 1.90, 95%CI = 1.31 - 2.77, P = 0.001). After adjustment of age, gender, body mass index, blood lipids, fasting blood glucose and blood uric acid level, the binary logistic regression analysis demonstrated that SS genotype in the 5-HTTLPR polymorphism was significantly related to occurrence of EH (OR = 1.47, 95%CI = 1.06 - 2.04, P = 0.021).</p><p><b>CONCLUSIONS</b>The SS genotype of the 5-HTTLPR might be a susceptible gene to EH, while the TPH gene A218C and 5-HTTVNTR polymorphism is not associated with EH in Chinese northern Han population.</p>