Objective:To investigate the effect of microRNA-144-3p (miRNA-144-3p) on drug resistance sensitivity of thyroid cancer cells by targeting and regulating paired box gene 8 (PAX8).Methods:Human thyroid cancer cell line FTC-133 was cultured in vitro and selected to construct the cisplatin-resistant cell stains. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the relative expression of miRNA-144-3p in FTC-133 cells and cisplatin-resistant FTC-133 cells. The cisplatin-resistant FTC-133 cells were divided into group A, group B, and group C. Group A received no treatment, group B was transfected with empty plasmids, and group C was transfected with pCDNA3.1+ miRNA-144-3p plasmids. RT-PCR was used to detect the relative expression levels of miRNA-144-3p and PAX8 in each group, and methyl thiazolyl tetrazolium (MTT) method was used to detect the half inhibitory concentration (IC 50) value of cisplatin on cells in each group, proliferation rate in each group was detected by cell counting kit-8 (CCK-8) method, and apoptosis rate in each group was detected by flow cytometry. Results:The relative expression level of miRNA-144-3p in cisplatin-resistant FTC-133 cells was significantly higher than that of FTC-133 cells [(0.93±0.24) vs (0.26±0.04), P<0.05]; The IC 50 value, proliferation rate, apoptosis rate and relative expression levels of miRNA-144-3p and PAX8 in cisplatin-resistant FTC-133 cells in group B were not significantly different from those in group A ( P>0.05). The IC 50 value, proliferation rate and relative expression of miRNA-144-3p of cisplatin resistant FTC-133 cells in group C were significantly higher than those in group B ( P<0.05), and apoptosis rate and relative expression of PAX8 were significantly lower than those in group B ( P<0.05). Conclusions:Overexpression of miRNA-144-3p may increase cisplatin resistance of thyroid cancer cells by up-regulating PAX8 gene expression, thus promoting the proliferation of thyroid cancer cells and inhibiting their apoptosis.

Objective:To investigate the effects of radix actinidiae chinensis extracts on the proliferation and apoptosis of breast cancer cells by regulating the vascular endothelial growth factor (VEGF)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway.Methods:Human breast cancer cell line MCF7 was cultured in vitro and divided into control group, low-dose group, medium dose group and high-dose group. The low-dose, medium dose and high-dose groups were added with DMEM culture medium diluted with 1, 10 and 100 μg/ml radix actinidiae chinensis extracts respectively. The control group was added with equal dose DMEM culture medium for 48 hours. The proliferation rate (detected by methyl thiazolyl tetrazolium method), apoptosis rate (detected by flow cytometry) and the protein expression of PI3K, VEGF and phosphorylation-AKT(p-AKT) in each group were compared (detected by Western blot). Results:Compared with the control group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in low dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in low dose group was significantly increased ( P<0.05); compared with low dose group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in medium dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in medium dose group was significantly increased ( P<0.05). Compared with the middle dose group, the proliferation rate of MCF7 cells and the expression of PI3K, VEGF and p-AKT protein in the high dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in the high dose group was significantly increased ( P<0.05). Conclusions:Radix actinidiae chinensis extracts may inhibit the proliferation and promote the apoptosis of breast cancer cells by inhibiting the VEGF/PI3K/AKT signaling pathway.

Objective To evaluate the right ventricular(RV)systolic function in patients with primary pulmonary hypertension(PPH)using real -time three -dimensional echocardiography(RT -3DE)and ultrasonic two-dimensional speckle tracking imaging(STI).Methods Patients with PPH were divided into three groups according to pulmonary arterial systolic pressure(PASP),consisted of mild group,moderate group and severe group,with 20 cases in each group.20 healthy cases were included as the control group.The global RV dysfunction,including RV end -diastolic volume(EDV),end -systolic volume(ESV),stroke volume(SV),ejection fraction(EF),tricuspid annular plane systolic excursion(TAPSE),longitudinal peak systolic strain(SL),longitudinal peak systolic strain rate(SRL), longitudinal peak systolic velocity(VL)in RV free wall and interventricular septum for basal,mid and apical segment were detected by using RT -3DE and STI.Results Global RV ESV increased in all groups(t =3.10,7.53,7.72,all P <0.01),but The RV EDV in the moderate and severe group was higher than that of normal and mild groups(t =4.02,5.82,3.04,5.15,all P <0.01),the RT SV and EF in all case groups was fewer than that of normal(t =-9.33 ~-2.71,all P <0.05).Linear correlation analysis showed negative correlation between EF and ESV,EDV (r =-0.776,-0.638,all P <0.01).The level of RV free wall peak systolic displacement of tricuspid annulus, ventricular septal annulus peak systolic displacement,tricuspid annulus peak systolic displacement midpoint and the right longitudinal ventricular shortening fraction were significantly lower than those of the control group(all P <0.01). Linear correlation analysis showed positive correlation between EF and TAPSE(r =0.761,0.593,0.745,0.773,all P <0.01).The VL and SL in RV free wall and interventricular septum for basal,mid and apical segment were fewer than the control group(P <0.05 or P <0.01),but SRL of RV for all segments showed no significantly different in all groups(P >0.05).Conclusion RT -3DE and STI technology can be useful in assessing RV function every period.

Objective:To construct and screen the high efficiency interference plasmid of TFAIP8-shRNA-pSIREN-RetroQ.Methods:Selected and synthesized three Target Sequence of TNFAIP8 shRNA1,TNFAIP8 shRNA2,TNFAIP8 shRNA3,and construct the TNFAIP8 interference plasmid.Transfection TNFAIP8-shRNA-pSIREN-RetroQ interference plasmid to A549 cells.Filter out the highest interference efficiency plasmid by detecting the mRNA and protein levels using RT-PCR and Western blot methods.Results:We successfully design and built three TNFAIP8-shRNA-pSIREN-RetroQ interference plasmids,and screen out the highest efficiency interference plasmid.Conclusion: Three interference plasmids targeting the TNFAIP8 gene have been constructed successfully and provide a useful tool for studying the function of TNFAIP8.

Objective To investigate the turnover intention and reasons of nurses in a class Ⅲ grade A hospital in Wenzhou so as to explore the countermeasures to reduce the turnover rate.Methods A survey was carried out on the turnover intentions of 132 practicing nurses in the hospital. The data of the 210 turnover nurses from 2013 to 2015 were collected. The differences between the high-turnover intention nurses and the actual turnover nurses were analyzed to explore the reasons and directions after turnover.Results A total of 132 nurses were enrolled in this study. Among them, 23 (17.42%) of the nurses had high intention to turnover. There were no significant differences in age, place of birth, education, title, marriage, working years, authorized or not and distribution of departments between the high and low turnover intention groups. A total of 210 nurses left from 2013 to 2015 in the hospital, with a turnover rate of 5.24%. Nurses with foreign account, low academic qualifications and the low title had higher turnover risks. More than half of the turnover nurses were still in the nursing profession,while the remaining 18.6% turnover nurses chose to work cross-border, and 22.9% turnover nurses chose to be full-time housewife. The main reasons for leaving were personal factors and work environment factors.Conclusions The nurses who have high intention to quit might not leave. Turnover is related to the account location, educational levels and professional titles. Therefore, the above factors should be taken into account in assessing the possibility of nurse leaving the hospital.

Objective To study the clinical effect of evidence-based prevention strategies of ventilator-associated pneumonia (VAP) in newborns with endotracheal intubation in neonatal intensive care unit (NICU).Method A retrospective analysis was carried out in neonates undergoing mechanical ventilation,who were admitted to the NICU of the hospital from 2016 to 2017.Intubated newborns from January 2016 to December 2016 were conducted with traditional method of preventing VAP and included as control group.While intubated newborns admitted from January 2017 to December 2017 with newly developed evidence-based prevention strategy for VAP were included as observation group.The positive rates of culture from swab or sputum or endotracheal intubation tube ends obtained within 48 hours after intubation and 48 hours after extubation were compared between groups.The neonates whose swab or sputum culture was negative before intubation were included.The positive rate was presented as the number of positive cases/1 000 intubation days.Result A total of 1 221 intubated infants were included,with 632 cases in the control group which were intubated 798 times,and 589 cases in the observation group which were intubated 720 times.The gestational age and birth weight of the observation group was lower than the control group.The rate of extremely low birth weight infant of the observation group was higher than that of the control group.The mechanical ventilation days were also longer in the observation group.The differences were statistically significant (P ＜ 0.05).In the control group,the number of positive cases was 112 and the total intubation days were 3 079 days,the positive rate was 36.4 cases/1 000 intubation days.In the observation group,the number of positive cases was 72 and the total intuhation days were 3 475 days,the positive rate was 20.7 cases/1 000 intubation days.The positive rate of observation group was lower than the control group,the differences was statistically significant (x2 =4.060,P =0.044).Conclusion Evidence-based neonatal VAP bundle can reduce the invasion of respiratory pathogenic bacteria in NICU.In the future work of NICU nursing,we should use bundle strategy to care for babies more and more,and the bundle should be supported by evidence.

Objective:To investigate the relationship between inherited dysplasminogenemia and cerebral infarction (CI) by phenotype and gene mutation analysis of 2 inherited dysplasminogenemia pedigrees.Methods:Retrospective analysis was carried out on clinical data of 2 patients diagnosed with CI who were treated in the Department of Neurology, the First Affiliated Hospital of Wenzhou Medical University in January and March 2021, and peripheral venous blood samples were collected from proband 1 and his family members (8 subjects, 4 generations in total) and proband 2 and her family members (5 subjects of 3 generations in total), and their plasminogen (PLG) activity (PLG:A), protein C activity, protein S activity, antithrombin activity and the content of PLG antigen (PLG: Ag), fibrinogen, D-dimer and fibrinogen degradation products were measured for definite diagnosis. All 19 exons,5′ and 3′ untranslated regions of PLG were amplified with polymerase chain reaction, and the amplification products were analyzed by direct DNA sequencing. The results were compared with human PLG reference sequences published in the National Center for Biotechnology Information database using Chromas software to find the mutation sites, and confirmed by reverse sequencing.Results:Both of the 2 patients with confirmed CI had a young onset, and PLG: A was reduced to 21% in the proband 1 and to about 50% in 4 family members; PLG: A was reduced to about 50% in the proband 2 and 2 family members; PLG:Ag and the above tests were essentially normal in both probands and family members. Gene analysis showed that the proband 1 had the homozygous mutation of c.1858G>A in exon 15, the 4 family members of the proband 1, proband 2 and her 2 family members had the heterozygous mutation of c.1858G>A in exon 15, which resulted in a mutation of alanine at position 620 in PLG to threonine (p.Ala620Thr).Conclusions:The decrease of PLG:A was caused by the p.Ala620Thr missense mutation of PLG gene. Proband having CI may be related to the inhibition of fibrinolytic function in the organism due to the p.Ala620Thr missense mutation.

Objective To explore the expression of FAT1 in esophageal squamous cell carcinoma ( ESCC) tissues, and its effect on cell proliferation. Methods The expression levels of FAT1 protein in human ESCC tissues and matched adjacent normal tissues were determined by immunohistochemistry ( IHC) . Lentivirus based knockdown of FAT1 was carried out in YSE2 and Colo680N cell lines and 3?( 4,5?dimethyl?2?thiazolyl)?2,5?diphenyl?2H tetrazolium bromide ( MTT) assays was performed to examine the effect of FAT1 on the proliferation of these ESCC cells. Colony formation assay was used to detect the colony formation ability. Flow cytometry was performed to analyze the cell cycle and apoptosis. The expression levels of cell cycle markers in FAT1 knock out ESCC cell lines were detected by real?time quantitative reverse transcription polymerase chain reaction( qRT?PCR) and Western blot. Results The relative expression of FAT1 in ESCC tissues was 66. 97 ± 21. 53, significantly lower than 78. 13 ± 16. 76 of adjacent normal tissues ( P<0.05) . Knockdown of FAT1 promoted cell proliferation and colony formation. In YSE2 cell, the division time in negative control (NC) group was (1570±51) min, significantly longer than (1356±31) min in shFAT1 group. In Colo680N cell, division time in NC group was (1532±53) min, significantly longer than (1290±30) min in shFAT1 group (P<0.05). Knockdown of FAT1 promoted G1?to S?phase transition and resulted in the upregulation of CDK4/CDK6/CCND1. Conclusion FAT1 inhibits the proliferation and G1?to S?phase transition of ESCC cells through regulating the protein expression of CDK4/CDK6/CCND1 complex.

Objective To explore the expression of FAT1 in esophageal squamous cell carcinoma ( ESCC) tissues, and its effect on cell proliferation. Methods The expression levels of FAT1 protein in human ESCC tissues and matched adjacent normal tissues were determined by immunohistochemistry ( IHC) . Lentivirus based knockdown of FAT1 was carried out in YSE2 and Colo680N cell lines and 3?( 4,5?dimethyl?2?thiazolyl)?2,5?diphenyl?2H tetrazolium bromide ( MTT) assays was performed to examine the effect of FAT1 on the proliferation of these ESCC cells. Colony formation assay was used to detect the colony formation ability. Flow cytometry was performed to analyze the cell cycle and apoptosis. The expression levels of cell cycle markers in FAT1 knock out ESCC cell lines were detected by real?time quantitative reverse transcription polymerase chain reaction( qRT?PCR) and Western blot. Results The relative expression of FAT1 in ESCC tissues was 66. 97 ± 21. 53, significantly lower than 78. 13 ± 16. 76 of adjacent normal tissues ( P<0.05) . Knockdown of FAT1 promoted cell proliferation and colony formation. In YSE2 cell, the division time in negative control (NC) group was (1570±51) min, significantly longer than (1356±31) min in shFAT1 group. In Colo680N cell, division time in NC group was (1532±53) min, significantly longer than (1290±30) min in shFAT1 group (P<0.05). Knockdown of FAT1 promoted G1?to S?phase transition and resulted in the upregulation of CDK4/CDK6/CCND1. Conclusion FAT1 inhibits the proliferation and G1?to S?phase transition of ESCC cells through regulating the protein expression of CDK4/CDK6/CCND1 complex.

Objective: To explore the expression of FAT1 in esophageal squamous cell carcinoma (ESCC) tissues, and its effect on cell proliferation. Methods: The expression levels of FAT1 protein in human ESCC tissues and matched adjacent normal tissues were determined by immunohistochemistry (IHC). Lentivirus based knockdown of FAT1 was carried out in YSE2 and Colo680N cell lines and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assays was performed to examine the effect of FAT1 on the proliferation of these ESCC cells. Colony formation assay was used to detect the colony formation ability. Flow cytometry was performed to analyze the cell cycle and apoptosis. The expression levels of cell cycle markers in FAT1 knock out ESCC cell lines were detected by real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR) and Western blot. Results: The relative expression of FAT1 in ESCC tissues was 66.97±21.53, significantly lower than 78.13±16.76 of adjacent normal tissues(P<0.05). Knockdown of FAT1 promoted cell proliferation and colony formation. In YSE2 cell, the division time in negative control (NC) group was (1 570±51) min, significantly longer than (1 356±31) min in shFAT1 group. In Colo680N cell, division time in NC group was (1 532±53) min, significantly longer than (1 290±30) min in shFAT1 group (P<0.05). Knockdown of FAT1 promoted G1-to S-phase transition and resulted in the upregulation of CDK4/CDK6/CCND1. Conclusion FAT1 inhibits the proliferation and G1-to S-phase transition of ESCC cells through regulating the protein expression of CDK4/CDK6/CCND1 complex.