Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add filters








Language
Year range
1.
Chinese Journal of Endocrine Surgery ; (6): 584-588, 2022.
Article in Chinese | WPRIM | ID: wpr-954644

ABSTRACT

Objective:To explore and analyze the relationship between serum KLK11 and MK levels and the effect of first iodine 131 ( 131I) ablation after operation for differentiated thyroid cancer. Method:108 patients with differentiated thyroid cancer who underwent total thyroidectomy in our hospital from Jun. 2020 to Jun. 2021 were consecutively selected, and received radioactive ablation after surgery. There were 37 males and 71 females. The age was (48.32±4.25) years, ranging from 28 to 79 years. The patients were divided into successful ablation according to whether the ablation was successful after treatment. There were 64 cases in the group and 44 cases in the unsuccessful group, and 60 healthy people with no abnormality in physical examination during the same period were selected as the control group. The patients were divided into a metastasis-positive group of 20 cases and a metastasis-negative group of 88 cases according to whether lymph nodes occurred. After surgery, serum samples of all subjects were taken, and enzyme-linked immunosorbent assay was used to detect the levels of serum kallikrein-related peptidases 11 (KLK11) and midkine (MK) , and the levels of serum KLK11 and MK were analyzed. Gender, age, BMI, TNM stage, TSH, maximum diameter of lesion, and duration of nail removal were collected. Univariate analysis and logistic regression analysis were used to analyze the independent risk factors of postoperative efficacy.Result:The levels of serum KLK11 and MK in the successful and unsuccessful groups were higher than those in the control group, while the levels of KLK11 and MK in the unsuccessful group were higher than those in the successful group (KLK11: t= 2.642, P<0.05; MK: t=11.906, P<0.05) . The serum levels of KLK11 and MK in the metastasis-positive group were higher than those in the metastasis-negative group (KLK11: t= 2.908, P<0.05; MK: t=14.907, P<0.05) . Univariate analysis showed that BMI ( χ2=6.780, P=0.009) , maximum diameter of lesions ( χ2=14.819, P=0.001) , TSH ( χ2=13.627, P=0.001) , serum KLK11 ( t=2.642, P=0.01) , and serum MK ( t=11.906, P<0.001) were associated with the effect of first 131I ablation after surgery for differentiated thyroid cancer ( P<0.05) . Taking the success of ablation as the dependent variable, a multivariate logistic regression analysis was performed. The results showed that the maximum diameter of the lesions greater than 2 cm ( OR=10.740, 95%CI: 7.033-16.401) , increased level of TSH ( OR=8.559, 95%CI: 2.812-26.057) , increased serum KLK11 level ( OR=16.710, 95%CI: .548-32.666) and increased serum MK level ( OR=10.580, 95%CI: 6.294-17.786) were the factors affecting the first 131I ablation effect after DTC surgery ( P<0.05) . Conclusion:The elevated levels of serum KLK11 and MK are independent risk factors affecting the efficacy of the first 131I ablation after surgery for differentiated thyroid cancer.

2.
Chinese Journal of Microbiology and Immunology ; (12): 891-896, 2018.
Article in Chinese | WPRIM | ID: wpr-734968

ABSTRACT

Objective To investigate the molecular mechanism of colistin resistance mediated by mcr-1and pmrAB genes in clinical Escherichia coli ( E. coli) isolates. Methods A total of 1988 clinical E. coli isolates were collected from the First People′s Hospital of Shangqiu from 2010 to 2017 and screened for colistin-resistant isolates using agar dilution method. The minimum inhibitory concentrations ( MICs) of nine common clinical antibiotics were determined using broth microdilution method. PCR and sequencing analysis were performed to detect the colistin resistance genes of mcr-1 and pmrAB. Conjugation experiments were used to test the transferability of the plasmid carrying mcr-1 gene. S1-PFGE and Southern blot were used to locate the plasmid carrying mcr-1. All colistin-resistant E. coli isolates were typed by multilocus se-quence typing ( MLST) . Results Six colistin-resistant E. coli isolates were obtained by agar dilution meth-od. The results of susceptibility testing showed that all of the six isolates were multidrug resistant. PCR and sequencing analysis revealed that four out of the six strains carried mcr-1 gene, and the other two isolates both had an amino acid substitution (L167P) caused by pmrB gene mutation. The results of conjugation ex-periments, S1-PFGE and Southern hybridization analysis showed that the plasmids of four mcr-1 gene-posi-tive E. coli strains were located on a conjugative plasmid about 60 kb in length. MLST analysis classified the six isolates into six distinct sequence types ( STs) . Conclusion This study suggested that mcr-1 gene and mutations in pmrAB gene were the main mechanisms mediating the resistance of E. coli to colistin. In clinical practice, the occurrence and spread of colistin-resistant E. coli should be further monitored, and the rational use of antibiotics should be promoted to prevent the spread of colistin-resistant strains.

3.
Chinese Journal of Organ Transplantation ; (12): 201-202, 2009.
Article in Chinese | WPRIM | ID: wpr-394800

ABSTRACT

Objective To investigate the effeet of eyclosporine A (CsA) on CD4+ Foxp3+ T cells in C57BL/6 mice and the underlying mechanism.Methods C57BL/6 mice, aging 8~ 10 weeks, were administered intraperitoneally with CsA at a dose of 20 mg· kg-1·d-1 for 2 weeks, while the control mice given sterile PBS.After 2 weeks, peripheral blood was collected, and splenoeytes and thymoeytes were prepared for the detection of CD4 + Foxp3 + T cells by using flow cytometry.Results The proportion of CD4+ Foxp3+ T cells in peripheral blood, spleen and thymus of CsA-treated mice was (0.581 ± 0.089) %, (2.189 ± 0.046) % and (0.472 ± 0.049) %, while that in PBS-treated mice was (1.751 ± 0.227) %, (3.684 ± 0.169) % and (1.412 ± 0.188) %, respectively (P < 0.001).Conclusion The reduction of CD4 + Foxp3+ T cells in CsA-treated mice suggests that CsA can inhibit the development of regulatory T cells.

SELECTION OF CITATIONS
SEARCH DETAIL