Objective:To investigate the effect of long non-coding RNA HOTAIR (LncRNA HOTAIR) on the proliferation, apoptosis and drug resistance of Wilms tumor cells and its molecular mechanism.Methods:Collected nephroblastoma tissues and normal tumor side tissues in 32 children with renal syblastoma surgical treatment at Zhengzhou University Children′s Hospital from 2015 to 2019. Real-time quantitative reverse transcription polymerase chain reaction, (qRT-PCR)was used to detect the expression of HOTAIR in Wilms tumor tissues and adjacent tissues. Small interfering RNA technology was used to delete the expression of HOTAIR in Wilms tumor cell SK-NEP-1. Cell counting kit-8 (CCK-8)was used to detect cell proliferation after transfection. Flow cytometry and terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) staining to detect the apoptosis. Western blot was used to detect the expression of Wnt/β-catenin signaling pathway related proteins.CCK-8 was used to detect the proliferation inhibition of cells treated with different concentrations of cisplatin after transfection.Results:Compared with adjacent tissues, HOTAIR was highly expressed in Wilms tumor tissues ( P<0.05). The expression levels of Wnt, β-catenin, Cyclin D1, c-myc in the control group were (0.89±0.08), (0.94±0.10), (0.72±0.06), (1.10±0.11), and (1.06±0.11), (0.92±0.08), (0.66±0.07), (1.25±0.11) of the si-RNA group, while (0.54±0.05), (0.41±0.05), (0.25±0.03), (0.56±0.06) of the si-HOTAIR group. The expression levels of these protein were significantly down-regulated in the si-HOTAIR group when compared with the control group and the si-RNA group ( P<0.05). The absorbance (A) values of SK-NEP-1 cells in the si-HOTAIR group at 24, 48 and 72 hours after transfection were (0.31±0.02), (0.37±0.04), (0.69±0.07), significantly lower than (0.49±0.05), (0.78±0.08), (1.22±0.14) in the control group and (0.57±0.06), (0.68±0.07), (0.94±0.09) in the si-RNA group ( P<0.05). The apoptosis rate in the si-HOTAIR group was (13.81±1.25)%, significantly higher than (6.54±0.72)% in the control group and (4.35±0.40)% in the si-RNA group ( P<0.05). The cell positive rate of TUNEL cells in the si-HOTAIR group was (35.14±3.50)%, significantly higher than (20.16±2.18)% in the control group and (21.09±2.35)% in the si-RNA group ( P<0.05). The median inhibitory concentration (IC 50) of the si-HOTAIR group was (62.48±5.97) μmol/L, significantly lower than (88.27±9.05) μmol/L of the control group and (92.50±9.11) μmol/L of the si-RNA group ( P<0.05). Conclusions:Suppression of LncRNA HOTAIR can inhibit the proliferation of Wilms tumor cells, promote cell apoptosis, decrease cell resistance to cisplatin. The mechanism may be related to the inhibition of Wnt/β-catenin signaling pathway activation.

Objective:To investigate the effect of long non-coding RNA HOTAIR (LncRNA HOTAIR) on the proliferation, apoptosis and drug resistance of Wilms tumor cells and its molecular mechanism.Methods:Collected nephroblastoma tissues and normal tumor side tissues in 32 children with renal syblastoma surgical treatment at Zhengzhou University Children′s Hospital from 2015 to 2019. Real-time quantitative reverse transcription polymerase chain reaction, (qRT-PCR)was used to detect the expression of HOTAIR in Wilms tumor tissues and adjacent tissues. Small interfering RNA technology was used to delete the expression of HOTAIR in Wilms tumor cell SK-NEP-1. Cell counting kit-8 (CCK-8)was used to detect cell proliferation after transfection. Flow cytometry and terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) staining to detect the apoptosis. Western blot was used to detect the expression of Wnt/β-catenin signaling pathway related proteins.CCK-8 was used to detect the proliferation inhibition of cells treated with different concentrations of cisplatin after transfection.Results:Compared with adjacent tissues, HOTAIR was highly expressed in Wilms tumor tissues ( P<0.05). The expression levels of Wnt, β-catenin, Cyclin D1, c-myc in the control group were (0.89±0.08), (0.94±0.10), (0.72±0.06), (1.10±0.11), and (1.06±0.11), (0.92±0.08), (0.66±0.07), (1.25±0.11) of the si-RNA group, while (0.54±0.05), (0.41±0.05), (0.25±0.03), (0.56±0.06) of the si-HOTAIR group. The expression levels of these protein were significantly down-regulated in the si-HOTAIR group when compared with the control group and the si-RNA group ( P<0.05). The absorbance (A) values of SK-NEP-1 cells in the si-HOTAIR group at 24, 48 and 72 hours after transfection were (0.31±0.02), (0.37±0.04), (0.69±0.07), significantly lower than (0.49±0.05), (0.78±0.08), (1.22±0.14) in the control group and (0.57±0.06), (0.68±0.07), (0.94±0.09) in the si-RNA group ( P<0.05). The apoptosis rate in the si-HOTAIR group was (13.81±1.25)%, significantly higher than (6.54±0.72)% in the control group and (4.35±0.40)% in the si-RNA group ( P<0.05). The cell positive rate of TUNEL cells in the si-HOTAIR group was (35.14±3.50)%, significantly higher than (20.16±2.18)% in the control group and (21.09±2.35)% in the si-RNA group ( P<0.05). The median inhibitory concentration (IC 50) of the si-HOTAIR group was (62.48±5.97) μmol/L, significantly lower than (88.27±9.05) μmol/L of the control group and (92.50±9.11) μmol/L of the si-RNA group ( P<0.05). Conclusions:Suppression of LncRNA HOTAIR can inhibit the proliferation of Wilms tumor cells, promote cell apoptosis, decrease cell resistance to cisplatin. The mechanism may be related to the inhibition of Wnt/β-catenin signaling pathway activation.

Objective To investigate the bacterial resistance profile of clinical isolates collected in the hospitals across Chuzhou in 2016. Methods Antimicrobial susceptibility testing was carried out by Kirby-Bauer method. The data were analyzed using WHONET 5.6 software according to CLSI 2015 breakpoints. Results A total of 5 465 clinical isolates were collected during 2016, of which gram positive organisms and gram negative organisms accounted for 25.9％ (1 416/5 465) and 74.1％ (4 049/5 465), respectively. Prevalence of MRSA was 37.6％ among S. aureus and the prevalence of MRCNS was 78.1％ in CNS. All Staphylococcus, E. faecalis and E. faecium isolates were sensitive to vancomycin and linezolid. The prevalence of extended spectrum-lactamases (ESBLs) positive strains was 51.2％ in E. coli, 23.4％ in Klebsiella spp. (K. pneumoniae and K. oxytoca), and 23.6％ in P. mirabilis isolates, respectively. The Enterobacteriaceae strains were highly sensitive to carbapenems. The percentage of the P. aeruginosa isolates resistant to the antimicrobials tested was lower than 30％. The percentage of the Acinetobacter strains resistant to meropenem and imipenem was 65.6％ and 67.4％, respectively. Conclusions The situation of antibiotic resistance is still very serious, especially multi-drug or pan-drug resistant strains, which is of great concern.