ABSTRACT
AIM: To analyze the relationship between rs128912 single nucleotide polymorphism(SNP)in the promoter region of Toll-like receptor 3(TLR3)gene and cataract in Chinese Han population.METHODS: A total of 263 patients with cataract admitted to our hospital from June 2019 to June 2021 were selected as study group, and 150 patients with lens dislocation were included in control group. Western blotting was used to detect the expression of TLR3 protein in the anterior capsular tissues of lens in the two groups, and direct sequencing method was applied to analyze the polymorphism of rs128912 locus in the promoter region of TLR3 gene. The expression of peripheral blood TLR3 mRNA of patients with different genotypes was detected by real-time quantitative polymerase chain reaction(RT-qPCR).RESULTS: The expression level of TLR3 protein in the anterior capsular tissues in the study group was higher than that in the control group(P<0.05). The frequencies of genotypes(AA, AT, TT)at rs128912 locus in the TLR3 gene promoter region in the study group and the control group were in accordance with Hardy-Weinberg genetic equilibrium, and there were differences in the frequencies of genotypes(AA, AT, TT)and frequencies of alleles(A, T)at rs128912 locus in the TLR3 gene promoter region between both groups(P<0.05). The relative expression level of peripheral blood TLR3 mRNA in patients with TT genotype in the study group was higher than that in patients with AA or AT genotypes(P<0.05).CONCLUSION: The expression of TLR3 protein in anterior capsular tissues of lens of patients with cataract is significantly up-regulated, and rs128912 locus polymorphism in the TLR3 gene promoter region is related to the susceptibility of cataract in Chinese Han population, and people with TT genotype are more prone to cataract.
ABSTRACT
Objective: To compare the clinical features between very late stent thrombosis (VLST) and very late in-stent restenosis, to discuss the potential risk factors for VLST occurrence. Methods: Our research included in 2 groups: VLST group, 21 ACS patients with coronary angiography (CAG) confirmed VLST admitted in our hospital and Control group, 38 ACS patients with CAG confirmed very late in-stent restenosis at same period of time. Basic clinical data, laboratory tests and relevant examinations were compared between 2 groups; potential risk factors for VLST occurrence were studied by Logistic regression analysis. Results: ① There were 8 (38.1%) patients discontinued anti-platelet therapy in a month by themselves in VLST group and 5 (13.2%) in Control group, P=0.03. ② 13 (61.9%) patients presented as ST-segment elevation myocardial infarction (STEMI) in VLST group, while all (100%) patients presented as Non-ST-segment elevation ACS (NST-ACS) in Control group, P<0.001. ③ The age, gender, previous histories of hypertension, diabetes, MI, smoking and interventional therapy were similar between 2 groups, P>0.05. ④ Compared with Control group, VLST group had decreased LVEF, P=0.001, increased peak values of TnI and NT-pro BNP, elevated WBC and hs-CRP, all P<0.001. ⑤ The index of echocardiography, blood lipid profiles, glucose and creatinine were similar between 2 groups, P>0.05. ⑥ Logistic regression analysis showed that discontinued anti-platelet therapy, elevated NT-pro BNP and hs-CRP were the independent risk factors for VLST occurrence, P<0.05. Conclusion: VLST may have life-threatening clinical features, insisted anti-platelet therapy and improved cardiac function could reduce VLST occurrence.
ABSTRACT
The purpose of this study was to investigate the effects of Celecoxib on the proliferation of the FLT3-ITD positive and negative acute myeloid leukemia cells and its mechanism. The proliferation inhibition effect of Celecoxib with different doses on the FLT3-ITD positive cells MV4-11 and the FLT3-ITD negative K562 cells was detected by CCK-8 method, the cell apoptosis was determined by flow cytometry, and the MEK, Mcl-1, pAKT expression was tested by Western blot. The results showed that Celecoxib inhibited the proliferation of both MV4-11 and K562 cells, but the IC50 for MV4-11 was (29.14 ± 2.4) µmol/L, which was significantly lower than that of K562 cells (39.84 ± 1.0) µmol/L (P < 0.05); The induced apoptosis rate of Celecoxib at 20-80 µmol/L on MV4-11 was not observed, but there was apparent influence on K562 at the same concentration. Western blot showed that Celecoxib down-regulated the expression of MEK and Mcl-1 but did not change the expression of pAKT obviously on MV4-11 cells, while the expression of Mcl-1 was reduced a little, but no obvious change were found in the expression of MEK and pAKT on K562 cells. It is concluded that the Celecoxib can inhibit the proliferation of FLT3-ITD positive AML cells distinctly, and the potential mechanism may be related to the inhibition of the MEK/Mcl-1 signaling pathway.