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1.
Chinese Journal of Endocrinology and Metabolism ; (12): 567-573, 2021.
Article in Chinese | WPRIM | ID: wpr-911362

ABSTRACT

Objective:To explore the role of transgelin(TAGLN) in the occurrence and development of papillary thyroid carcinoma (PTC) and its possible signal pathway.Methods:One hundred cases of PTC tissues and corresponding paracancerous normal thyroid tissues were collected. Realtime quantitative PCR (RT-qPCR), Western blotting, and immunohistochemistry were used to analyze the expression of TAGLN in PTC tissues and corresponding paracancerous normal thyroid tissues. PTC cells were transfected with plasmid and shRNA lentivirus vector respectively to up-regulate or down-regulate the expression of TAGLN in order to detect the effects of them on the proliferation, invasion, and migration by cell proliferation assay(cell counting kit-8, CCK-8)and cell invasion and migration assays (Transwell). The effects of TAGLN on mitogen-activated protein kinase (MAPK)/extracellular-signal regulating kinase (ERK) signal pathway was detected with Western blotting.Results:RT-qPCR showed that there was no difference in the expression of TAGLN mRNA between PTC and corresponding paracancerous normal thyroid tissues ( P>0.05); Western blotting demonstrated that the expression of TAGLN protein in PTC tissues was significantly lower than that in corresponding paracancerous normal thyroid tissues ( P<0.01). Immunohistochemical results revealed that the expression of TAGLN in PTC tissues was significantly lower than that in corresponding paracancerous normal thyroid tissues. Overexpression of TAGLN inhibited the proliferation, invasion, and migration of PTC cells ( P<0.01), but knockdown of TAGLN promoted the proliferation, invasion, and migration of PTC cells ( P<0.01). Overexpression of TAGLN decreased the expression of phosphorylated ERK ( P<0.05), whereas silencing TAGLN increased phosphorylated ERK level in PTC cells( P<0.01). Conclusion:The expression of TAGLN in PTC is significantly decreased. It is related to the occurrence and development of PTC, and its mechanism may be related to MAPK/ERK signal pathway.

2.
Journal of Southern Medical University ; (12): 657-664, 2019.
Article in Chinese | WPRIM | ID: wpr-773552

ABSTRACT

OBJECTIVE@#To explore the impact of dietary sodium-intake on residual renal function in patients undergoing peritoneal dialysis (PD).@*METHODS@#Thirty-three patients on PD with stable dialysis were regularly followed up for 12 months. The daily sodium intake of the patients was calculated based on the 3-day dietary record. Based on the mean daily sodium intake, the patients enrolled were divided into low-salt group (sodium intake≤3.0 g/day, 19 patients) and high-salt group (sodium intake>3.0 g/day, 14 patients). The baseline data of the patients were recorded, and the indicators of residual renal function and peritoneal function were regularly tested. The patients were followed-up at 3-month intervals, and their urine volume, peritoneal ultrafiltration volume and other clinical indicators were recorded and the biochemical indexes were detected to evaluate the changes in the residual renal function and peritoneal function.@*RESULTS@#There was a positive correlation between the total sodium excretion and dietary sodium intake in these patients (=0.536, =0.0013), and sodium excretion by dialysis was positively correlated with their sodium intake (=0.901, =0.000). Regression analysis suggested that the total sodium excretion was correlated with dietary sodium intake (β=0.416, 95% : 0.170-0.666; < 0.0018); sodium excretion by dialysis was associated with dietary sodium intake (β=0.489, 95% : 0.395-0.582; < 0.001). The residual renal function was reduced by 17.48±11.22 L /(w·1.73 m) in the low-salt group, as compared to 30.20±18.30 L /(w·1.73 m) in the high-salt group (=0.032). The reduction in the residual renal function was correlated with sodium intake in the PD patients (=0.409, =0.018). Multivariate regression analysis showed that sodium intake was an independent factor contributing to the reduction of residual renal function (β=14.646, 95% CI 7.426-21.866, < 0.001).@*CONCLUSIONS@#Sodium excretion by PD in patients with continuous ambulatory PD is positively correlated with their dietary sodium intake, which contribute to the decrease of residual renal function. A high dietary sodium intake may accelerate the reduction of residual renal function in these patients.


Subject(s)
Humans , Kidney , Peritoneal Dialysis , Prospective Studies , Sodium, Dietary
3.
Chinese Journal of Endocrinology and Metabolism ; (12): 950-954, 2017.
Article in Chinese | WPRIM | ID: wpr-663842

ABSTRACT

Objective To explore the relationship between the polymorphisms of the primary gout predisposing gene (BCAS3) rs11653176 locus and the incidence of gout in Han Chinese men in coastal areas of Shandong Province. Methods One hundred and fifty-two cases of patients with gout remission,68 cases of acute stage,252 patients with hyperuricemia, and 280 healthy subjects, total males, were enrolled. Genotyping the rs11653176 locus of BCAS3 gene by TaqMan probe technique. The expression level of BCAS3 gene mRNA in each PBMC was measured by RT-qPCR. The levels of tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and interleukin-18(IL-18)in serum were measured by ELISA. Results The change of allele frequency of rs11653176 locus in BCAS3 gene was associated with gout(P<0.01). BCAS3 mRNA in patients with gout was significantly higher than that of healthy people and patients with hyperuricemia(P<0.01). In gout patients, the expression level of BCAS3 gene containing C allele was higher than that of T allele(mRNA,P<0.05). The inflammatory factors in the acute phase of gout were significantly higher than those in phases of remission and hyperuricemia(P<0. 01). Conclusion Changes in the allele frequency of BCAS3 alleles rs11653176(high C, low T)may contribute to the expression of this gene,and lead to gout. And the onset of gout is closely related to the production of inflammatory factors.

4.
Chinese Journal of Neurology ; (12)1999.
Article in Chinese | WPRIM | ID: wpr-543332

ABSTRACT

Objective To explore the relationship between calcium channel ?1 subunit (Cav1.1) gene intron 26 -67 A/G polymorphism and thyrotoxic periodic paralysis(TPP). Methods Cav1.1 gene polymorphism at position -67 was determined by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) in 46 male patients with TPP, 68 male Graves’ disease (GD) patients without TPP and 72 healthy male controls. The difference of genotype and the variation of allele frequencies were analyzed by Chi-square test. Results (1) Frequencies distribution of AG+GG genotype in TPP, GD and control groups were 47.83%, 14.71% and 29.17% respectively, and those of allele G were 44.57%, 13.24% and 27.78% for the three groups respectively. (2) Frequencies of -67 AG+GG genotype in TPP group were significantly higher than those in GD and CON group(OR=5.32, P

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