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1.
Chinese Journal of Radiation Oncology ; (6): 57-60, 2020.
Artigo em Chinês | WPRIM | ID: wpr-798808

RESUMO

Objective@#To investigate the effect of LncRNA OIP5-AS1 on radiosensitivity of non-small cell lung cancer (NSCLC) cells and its mechanism.@*Methods@#The radiation-resistant cell A549R was established by using A549 cells irradiated by X-ray 6Gy in 5 fractions. The expression levels of OIP5-AS1 and miR-34c-5p in A549 and A549R cells were detected by qRT-PCR. OIP5-AS1 inhibitor or miR-34c-5p mimetic was transfected into A549R cells, or OIP5-AS1 overexpression plasmid was transfected into A549 cells. Cell apoptosis was detected by flow cytometry. Cell radiosensitivity was analyzed by colony formation assay. The expression levels of p-Chk2 and p-ATM proteins were measured by Western blot. Dual luciferase assay was adopted to verify the relationship between OIP5-AS1 and miR-34c-5p.@*Results@#Compared with A549 cells, the expression of OIP5-AS1 was significantly up-regulated in A549R cells (1.97±0.11 vs.1.01±0.05, P<0.05), whereas the expression of miR-34c-5p was remarkably down-regulated (0.43±0.02 vs.1.02±0.06, P<0.05). The expression levels of p-Chk2 and p-ATM proteins in A549R cells in the silencing OIP5-AS1+ 6Gy group were significantly lower (0.43±0.03 vs.1.39±0.15, 0.51±0.0 5 vs.1.21± 0.11, both P<0.05), whereas the apoptotic rate was significantly higher than those in the silencing control+ 6Gy group [(13.29±1.25)% vs. (28.47±2.31)%, P<0.05)]. The expression levels of p-Chk2 and p-ATM proteins in A549 cells in overexpressing OIP5-AS1+ 6Gy group were significantly higher than those in overexpression control+ 6Gy group (1.23±0.13 vs.0.75±0.06, 1.08±0.11 vs.0.59±0.04, both P<0.05). Inhibiting miR-34c-5p expression reversed the effect of silencing OIP5-AS1 on survival fraction of A549R cells (SER=1.42). OIP5-AS1 negatively regulated the expression of miR-34c-5p.@*Conclusion@#Silencing OIP5-AS1 enhances the radiosensitivity of radiation-resistant A549 cells by up-regulating the expression of miR-34c-5p, providing a potential target for radiotherapy of NSCLC cells.

2.
Chinese Journal of Radiation Oncology ; (6): 57-60, 2020.
Artigo em Chinês | WPRIM | ID: wpr-868549

RESUMO

Objective To investigate the effect of LncRNA OIP5-AS1 on radiosensitivity of non-small cell lung cancer (NSCLC) cells and its mechanism.Methods The radiation-resistant cell A549R was established by using A549 cells irradiated by X-ray 6Gy in 5 fractions.The expression levels of OIP5-AS1 and miR-34c-5p in A549 and A549R cells were detected by qRT-PCR.OIP5-AS1 inhibitor or miR-34c-5p mimetic was transfected into A549R cells,or OIP5-AS1 overexpression plasmid was transfected into A549 cells.Cell apoptosis was detected by flow cytometry.Cell radiosensitivity was analyzed by colony formation assay.The expression levels of p-Chk2 and p-ATM proteins were measured by Western blot.Dual luciferase assay was adopted to verify the relationship between OIP5-AS1 and miR-34c-5p.Results Compared with A549 cells,the expression of OIP5-AS1 was significantly up-regulated in A549R cells (1.97±0.11 vs.1.01±0.05,P<0.05),whereas the expression of miR-34c-5p was remarkably down-regulated (0.43±0.02 vs.1.02±0.06,P<0.05).The expression levels of p-Chk2 and p-ATM proteins in A549R cells in the silencing OIP5-AS1 +6Gy group were significantly lower (0.43±0.03 vs.1.39±0.15,0.51 ±0.0 5 vs.1.21 ± 0.11,both P<0.05),whereas the apoptotic rate was significantly higher than those in the silencing control + 6Gy group [(13.29± 1.25)% vs.(28.47± 2.31)%,P<0.05)].The expression levels of p-Chk2 and p-ATM proteins in A549 cells in overexpressing OIP5-AS1+6 Gy group were significantly higher than those in overexpression control+6 Gy group (1.23±0.13 vs.0.75±0.06,1.08±0.11 vs.0.59± 0.04,both P<0.05).Inhibiting miR-34c-5p expression reversed the effect of silencing OIP5-AS1 on survival fraction of A549R cells (SER =1.42).OIP5-AS1 negatively regulated the expression of miR-34c-5p.Conclusion Silencing OIP5-AS1 enhances the radiosensitivity of radiation-resistant A549 cells by up-regulating the expression of miR-34c-5p,providing a potential target for radiotherapy of NSCLC cells.

3.
Chinese Journal of Practical Nursing ; (36): 273-278, 2018.
Artigo em Chinês | WPRIM | ID: wpr-696996

RESUMO

Objective To explore the effect of family integrated care (FIC) model on the growth and development in preterm infants. Methods A total of 128 cases of hospitalized preterm infants from January 2016 to June 2016 were selected and divided into intervention group(64 cases)and control group (64 cases) by random number table. Intervention group was received FIC after the condition was stable, control group was adopted current traditional preterm infants care. The weight, body length and head circumference of both group were recorded at 3rd month,Neonatal Behavioral Neurological Assessment (NBNA)was assessed at correction gestational aged 40 weeks,hospital stays were counted while outpatient visits and readmission case were collected within 3 month after discharge. Results The study included 118 cases,56 cases in intervention group and 62 cases in control group.The weight,body length and head circumference in intervention group was (4 315.77 ± 856.48) g,(54.22 ± 2.74)cm, (36.23 ± 1.25) cm at 3rd month,while in control group was(3 886.52±812.94)g,(53.84±2.61)cm,(35.99± 1.58)cm.It showed that the weight,body length and head circumference in intervention group were significantly higher than those in control group(t =2.785, 2.512, 1.785, P<0.01 or 0.05). The score of NBNA was (36.85 ± 2.01) points and hospital stays was(16.96±8.01)d in intervention group,while (35.97±1.86)points and(20.41±7.26)d in control group,there were significant differences(t=2.692,-2.534,all P<0.05).Incidence of outpatient visits and readmission were 14.29%(8/56),3.57%(2/56)in intervention group and 32.26%(20/62),14.51% (9/62) in control group, incidence of outpatient visits and readmission were significantly lower in intervention group as compared with control group (χ2=5.251, 4.170, all P<0.05). Conclusions FIC model is implemented in neonatal progressive care unit for preterm infants, it could promote growth and development in preterm infants,shorten the length of hospital stays,while decrease incidence of outpatient visits and readmission.

4.
West China Journal of Stomatology ; (6): 58-62, 2015.
Artigo em Chinês | WPRIM | ID: wpr-261138

RESUMO

<p><b>OBJECTIVE</b>We aims to evaluate the therapeutic effect of maxillary protraction on maxillary maldevelopment using Coben analysis to illustrate the advantages of Coben analysis in identifying pathogenic mechanisms and in designing treatment plans for Class III malocclusions.</p><p><b>METHODS</b>A total of 120 patients were diagnosed to have skeletal Class I maloc- clusions with maxillary maldevelopment. These patients were selected as the subjects of the present research. Maxillary protraction was exerted to promote maxilla growth. Cephalometric analysis was conducted by using Coben analysis and angle analyses of Beijing Medical University to collect data before and after maxillary protraction.</p><p><b>RESULTS</b>According to Coben analysis measurements, the height of facies cranii increased after maxillary protraction. The depth of lower face decreased, whereas that of mid-face increased and the Ptm-A value increased significantly in the mid-face (P < 0.001). In the angle ana- lysis of Beijing Medical University, SNA, ANB, U1/NA, U1/SN, MP/SN, and Y-axis angles increased significantly (P < 0.001), whereas SNB, U1/L1 (P < 0.001), and L1/MP (P < 0.05) decreased.</p><p><b>CONCLUSION</b>Maxillary protraction has a significant effect on growing skeletal Class III malocclusions withthe chief mechanism of Ptm-A value just diagnosed as minor by Coben analysis. Coben analysis is visual and clear in identifying pathogenic mechanisms of Class III malocclusions.</p>


Assuntos
Humanos , Cefalometria , Face , Má Oclusão Classe III de Angle , Maxila
5.
Chinese Journal of Microbiology and Immunology ; (12): 501-506, 2013.
Artigo em Chinês | WPRIM | ID: wpr-438337

RESUMO

Objective To explore the regulatory effects of HTLV-1 ( human T-cell leukemia virus type 1 ) Tax protein on the expression of HMGB 1 ( high mobility group box 1 ) gene in T cells .Methods Total RNA and protein were extracted from Tax +-T cells ( TaxP ) , Tax--T cells ( TaxN ) and Jurkat cells which were stably transfected with pCMV-Tax and pCMV-Neo, respectively.Then, the expression levels of HMGB1 mRNA and protein in different CD 4+T cells were analyzed by real-time PCR and Western blot (WB).By using liposome-mediated method, pGL3-HMGB1-luc reporter genes and pGL3-neo-luc were tran-siently transfected into TaxP and TaxN cells and the basal transcriptional activity was observed in different T cells.Additionally, pCMV-Tax and pGL3-HMGB1-luc reporter genes were also co-transfected into Jurkat cells and the regulatory effects of Tax protein on HMGB 1 gene was detected .The chromatin immunoprecipi-tation (ChIP) assay was used to identify HMGB1 genomic sites directly targeted by Tax .Results The ex-pression levels of HMGB1 mRNA and protein in Tax+-T cells ( TaxP) were higher than those in Tax--T cells (TaxN).The transcription regulation trends for HMGB1 gene in TaxN and TaxP cells were similar but not identical in diverse T cells.pHLuc3 (containing -504-+83 HMGB1) showed the highest transcriptional ac-tivity of HMGB1 gene in both TaxP and TaxN cells , but HMGB1 transcriptional activity of pHLuc 6 in TaxP cells was significantly stronger than that in TaxN cells .Luciferase assays also showed that Tax protein promo-ted the transcription of HMGB1 gene in a dose-dependent manner .The ChIP assay further confirmed that Tax protein enriched at the HMGB1 region of -1163--1043.Conclusion The region of nt -504--383 is essen-tial for the basal promoter activity of -1163-+83 HMGB1 gene originated from pHLuc 6 reporter plasmid , and Tax protein enriched probably at the HMGB 1 site of -1163--1043 enhances HMGB1 transcription.

6.
Chinese Journal of Microbiology and Immunology ; (12): 989-992, 2008.
Artigo em Chinês | WPRIM | ID: wpr-381512

RESUMO

Objective To study the mutation of papillomavirus type 16 (HPV16) E6 gene, and to compare with the result of other researchers. Methods DNA was extracted from cervical cancer tissue sam-pies, then HPV16 E6 genes were amplified and sequenced using the HPV16 E6 specific primers from cervi-cal cancer DNA samples. Results HPV16 E6 gene mutations at the position of nt178 were found in 18 case from 35 cervical cancer samples, the mutation rate was 51.43%, resulting in nucleotide change of Asp to Glu. E6 mutations are found at the position of nt442 in 4 cervical samples. E6 mutation was found in 1 to 2 case in other nucleotide. Conclusion High frequency mutations of E6 gene of HPV16 at the position of nt178, nt442 have been found in cervical cancer samples in Hubei, China. The role of E6 gene mutation in cervical cancer development should be studied further.

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