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Objective:To study the clinical significance of alveolar-arterial oxygen gradients (P A-aO 2) for late preterm and full-term infants with acute respiratory distress syndrome (ARDS). Methods:From January 2020 to June 2022, infants (gestational age ≥34 weeks) diagnosed with ARDS were admitted to the Neonatology Department of our hospital. The infants were assigned into the invasive group and the non-invasive group according to the ventilation mode. The infants with the same gestational age and diagnosed with neonatal wet lung were assigned into the control group. P A-aO 2 levels within 1 h after birth were compared among the three groups. The correlation of P A-aO 2 with ARDS, ventilation mode and duration were studied. Receiver operating characteristic (ROC) curve was used to determine the predictive value of P A-aO 2 within 1 h after birth for ARDS and the need of invasive ventilation. Results:A total of 36 cases were enrolled in the invasive group, 19 cases in the non-invasive group and 50 cases in the control group. Within 1 h after birth, P A-aO 2 in the invasive group was significantly higher than the non-invasive group and the control group ( P<0.05), and the non-invasive group higher than the control group ( P<0.05). Correlation analysis showed that P A-aO 2 within 1 h after birth in the invasive group was positively correlated with the duration of invasive ventilation and total mechanical ventilation ( r=0.601, P<0.001; r=0.504, P=0.002); P A-aO 2 before successful withdrawal of invasive ventilation was not correlated with subsequent non-invasive ventilation duration; and no correlation existed between P A-aO 2 within 1 h after birth and the duration of non-invasive ventilation in the non-invasive group. The area under the ROC curve for P A-aO 2 within 1 h after birth to predict ARDS was 0.875, with a sensitivity of 87.3% and a specificity of 72.0% at a cutoff value of 50.0 mmHg. The area under the ROC curve for predicting the need for invasive ventilation in infants with ARDS was 0.851, with a sensitivity of 80.0% at a cutoff value of 73.3 mmHg and a specificity of 75.0%. Conclusions:Late preterm and full-term infants have a higher risk of ARDS at P A-aO 2>50.0 mmHg within 1 h after birth. Infants with ARDS are more likely to require invasive ventilation if P A-aO 2>73.3 mmHg. The higher the level of P A-aO 2, the longer the duration of invasive ventilation and total duration of mechanical ventilation.
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Objective:To explore the expression of polypyrimidine tract-binding protein 1 (PTBP1) in gastric cancer (GC) tissues and GC cell lines, and the role of PTBP1 in the proliferation and metastasis of GC cells.Methods:From January to June in 2019 at The First Affiliated Hospital of Xi′an Jiaotong University, the cancer tissues and corresponding para-cancer tissues of GC patients underwent surgical resection were collected. The Kaplan-Meier Plotter database was used to analyze the survival of GC patients. The expression of PTBP1 was down-regulated by transfecting small interfering RNA (siRNA) in human GC cell lines SGC7901 and AGS with relatively high expression of PTBP1. The cells were divided into blank control group, negative control group, and PTBP1 knockdown group. The expression of PTBP1 at mRNA and protein level were detected by real-time fluorescence quantification polymerase chain reaction (RT-qPCR) and Western blotting. At 24, 48, 72 and 96-hour after transfection, the effect of PTBP1 on the proliferation of GC cells was observed by 3-(4, 5 dimethylthiazol)-2, 5 diphenyltetrazolium bromide (MTT) experiment. The changes of invasion and migration of GC cells after down-regulation of PTBP1 were detected by transwell assay. The expression changes of epithelial-mesenchymal transition (EMT) markers E-cadherin, N-cadherin and vimentin after down-regulation of PTBP1 in GC cells were determined by Western blotting. Indenpendent samples t test, analysis of variance and rank sum test were used for statistical analysis. Results:The Kaplan-Meier Plotter prognostic analysis showed that the overall survival of GC patients with high PTBP1 expression was shorter than that of GC patients with low PTBP1 expression (9.2 months, 6.2 months to 17.2 months vs. 19.0 months, 14.5 months to 28.4 months), and the difference was statistically significant ( Z=5.31, P<0.05). The results of RT-qPCR showed that in GC cell lines SGC7901 and AGS, the expression of PTBP1 at mRNA level of PTBP1 knockdown group was lower than that of blank control group and negative control group (SGC7901: 0.78±0.11 vs.3.10±0.19 and 2.99±0.23; AGS: 0.80±0.09 vs. 3.55±0.24 and 3.50±0.18), and the differences were statistically significant ( tSGC7901=10.57 and 8.08, tAGS=10.91 and 13.42; all P<0.01). The results of Western blotting indicated that in GC cell lines SGC7901 and AGS, the expression of PTBP1 at protein level of PTBP1 knockdown group was lower than those of blank control group and negative control group (SGC7901: 0.38±0.04 vs. 1.42±0.05 and 1.35±0.09; AGS: 0.17±0.02 vs. 1.52±0.08 and 1.38±0.45), and the differences were statistically significant ( tSGC7901=15.94 and 10.57, tAGS=16.60 and 20.80; all P<0.01). The results of MTT showed that at 48, 72 and 96-hour after transfection the absorbance values of PTBP1 knockdown group decreased by 0.25±0.01, 0.38±0.02, and 0.84±0.04 as compared with those of negative control group, and the decrease was the most significant at 96-hour after transfection, and the differences were statistically significant ( t=10.21、14.32, both P<0.01). The results of transwell experiment demonstrated that the number of invasion and migration cells of PTBP1 knockdown group were both less than that of the blank control group and the negative control group (SGC7901: 42.00±5.91 vs. 116.40±10.23 and 114.40±10.43; 39.60±6.77 vs. 125.80±11.51 and 122.40±5.90; AGS: 40.20±7.25 vs. 115.60±14.63 and 117.40±9.12; 36.00±5.20 vs. 122.40±12.10 and 125.40±12.74), and the differences were statistically significant ( tSGC7901=14.07, 13.50, 14.43 and 20.62; tAGS=10.27, 14.75, 14.68 and 16.76; all P<0.01). The results of Western blotting showed that the expression of E-cadherin of PTBP1 knockdown group was higher than that of the blank control group and the negative control group (SGC7901: 1.42±0.05 vs. 0.53±0.05 and 0.57±0.03; AGS: 1.34±0.04 vs. 0.54±0.03 and 0.61±0.01), however the expression levels of N-cadherin and vimentin were both lower than those of the blank control group and the negative control group (SGC7901: 0.50±0.03 vs. 1.64±0.05 and 1.46±0.07; 0.32±0.07 vs. 1.42±0.07 and 1.33±0.07; AGS: 0.37±0.06 vs. 1.47±0.04 and 1.36±0.04; 0.41±0.04 vs. 1.53±0.06 and 1.37±0.04), and the differences were statistically significant ( tSGC7901=11.63, 13.19, 18.83, 11.68, 11.43 and 10.43; tAGS= 15.02, 16.23, 14.67, 12.97, 14.45 and 17.18; all P<0.01). Conclusions:The expression levels of PTBP1 increase in GC tissues and cells, which may be involved in regulating the proliferation, metastasis and EMT of GC cells.
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Homocestkink is a mktabolitk of mkthionink,which has bkkn provkd to bk associatkd with multiplk sestkmic diskasks. In pkdiatric diskasks,homocestkinkmia has bkkn paid mork and mork attkntion in rkcknt ekars. Hepkr-homocestkinkmia is associatkd with somk diskasks of cardiovascular sestkm,rhkumatoid immunk sestkm,urinare sestkm, nkrvous sestkm,blood sestkm,digkstivk sestkm in childrkn. Lnd karle mkasurkmknt of homocestkinkmia plaes an impor-tant rolk in thk diagnosis,trkatmknt and prkvkntion of somk diskasks in childrkn. Through sunmmarizing thk mktacha-nism of homocestkink and its rklationship with multiplk sestkmic diskasks in childrkn,wk invkstigatk thk clinical valuk of homocestkink in childrkn.
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Objective To investigate the expression of DNA methyltransferase 3b (DNMT3B) in hepatocellular carcinoma (HCC) and its effect and mechanism on the proliferation,invasion and migration of HCC cells.Methods The expression of DNMT3B gene was detected by qRT-PCR in 46 cases of HCC tissues and corresponding adjacent tissues;the results and clinical pathological parameters were analyzed.SiRNA targeting DNMT3B was transfected into MHCC97-H cells by RNA interference (RNAi) technique.The mRNA and protein expression levels of related genes were detected by qRT-PCR and Western blot.The cell proliferation was measured by MTT assay,and the invasion and migration abilities were measured by Transwell assay.Results In 46 HCC patients,the expression of DNMT3B (73.91％) was significantly higher in HCC than in adjacent normal tissue.The high expression of DNMT3B gene was associated with histological type and tumor size of HCC (all P＜0.05).Inhibition of DNMT3B gene expression decreased proliferation,invasion and migration of MHCC97-H cells.Interference with DNMT3B gene increased the expressions of tumor suppressor genes RASSFA1,APC and MTSS1 at mRNA and protein levels.Conclusion DNMT3B is associated with the progression of HCC.It may inhibit the proliferation,invasion and migration of HCC cells by regulating the methylation of downstream tumor suppressor gene.
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Objective To investigate the changes and diagnostic significance in plasma undercarboxylated osteocalcin in children with Kawasaki disease (KD),especially with coronary artery lesions (CALs).Methods The data of 36 KD children were collected,who were inpatients at Department of Cardiovascular and Rheumatology,Shanxi Province Children's Hospital from January 2015 to December 2015,including 20 boys and 16 girls,aged (2.3 ± 1.1)years old.According to the course of the disease,KD children were divided into an acute stage group and a subacute stage group.Based on the echocardiography findings,KD children were subdivided into CALs group and no coronary artery lesions (NCALs) group.Twenty-five healthy children from the physical examination during the same period were selected as the healthy control group,13 boys and 12 girls,aged (2.6-± 1.0) years old.Plasma undercarboxylated osteocalcin level was measured by double antibody sandwich enzyme-linked immunosorbent method.Sigrnaplot 12.5software was used to analyze the data statistically,and the receiver-operating characteristic (ROC) curve was used to evaluate the diagnostic effect of plasma undercarboxylated osteocalcin in KD with CALs.Results The levels of plasma undercarboxylated osteocalcin in the healthy control group,the acute stage group and the subacute stage group were (16.4 ± 1.6) μg/L,(14.2 ± 1.6) μg/L,(14.3-± 1.7) μg/L,respectively.Compared with the healthy control group,the plasma undercarboxylated osteocalcin level in the acute stage and the subacute stage were significantly lower,the differences were statistically significant (q =6.088,5.687,all P ＜ 0.01).But there was no difference of plasma undercarboxylated osteocalcin level between the acute stage group and the subacute stage group (q =0.466,P ＞ 0.05).The levels of plasma undercarboxylated osteocalcin in acute stage group with CALs and acute stage group with NCALs were (12.9 ± 1.2) μg/L,(15.0 ± 1.4) μg/L.Compared with healthy control group,the plasma undercarboxylated osteocalcin levels of children with CALs and with NCALs were obviously decreased,the differences were statistically significant (q =8.711,3.891,all P ＜ 0.01).There was a statistical difference in plasma undercarboxylated osteocalcin level between the acute stage with CALs and the acute stage with NCALs (q =5.171,P ＜ 0.01).The plasma undercarboxylated osteocalcin levels of KD children with CALs in the subacute stage was (13.0-± 1.3) μg/L.Compared with acute stage,there was no statistical difference (t =0.257,P ＞ 0.05).There was a sensitivity of 79％,specificity of 82％,positive predictive value of 88％ and negative predictive value of 70％ for the 15.7 μg/L undercarboxylated osteocalcin for diagnosing KD.There was a sensitivity of 83％,specificity of 88％,positive predictive value of 83％ and negative predictive value of 88％ for the 13.7 μg/L undercarboxylated osteocalcin for diagnosing KD with CALs.Conclusions Osteocalcin is related to the pathogenesis and development of KD.Plasma undercarboxylated osteocalcin contributes to the diagnosis of KD with CALs.
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Objective To further study the pathogenesis for congenital heart disease (CHD) and connective tissue growth factor(CTGF) for the early diagnosis of CHD and pulmonary hypertension (PH).Methods Sixty-six cases of children with CHD were selected from the thoracic surgery who were performed in the Children's Hospital of Shanxi Province during the period between Sep.2012 and Jan.2013.Based on the cardiac color Doppler estimation of the pulmonary artery systolic pressure,they were classified into several groups:unincorporated PH group with 16 cases,mild PH group with 18 cases,moderate PH group with 17 cases,and severe PH group with 15 cases.Based on types,the 66 cases could be classified as ventricular septal defect (VSD) group with 23 cases,atrial septal defect (ASD) group with 17 cases,patent ductus arteriosus(PDA) group with 14 cases,and composite(including 2 or more of the congenital cardiovascular anomalies) group with 12 cases.Twenty healthy children who had medical examination over the same period in the Children's Hospital of Shanxi Province were randomly chosen as the healthy control group.The serum concentration of CTGF in the research objects were determined with the aid of double antibody sandwich enzyme-linked immunosorbent assay method.According to the different pulmonary artery systolic pressure and different types of CHD,the serum concentration of CTGF were compared among groups.The correlation of between the CTGF concentration in the serum and pulmonary artery systolic pressure were also analyzed among the groups of children with CHD.Results Quantitative measurement revealed that the serum CTGF concentration measured in the groups of children with CHD were significantly higher than that in the healthy control group(P ＜ 0.05) ; the serum CTGF concentration of the children with CHD and PH was higher than that in the group of children with CHD alone(P ＜ 0.05).With the increase in pulmonary artery pressure,CHD patients serum levels of CTGF also increased(P ＜ 0.05).By the correlation analysis,the results showed that the serum level of CTGF in the CHD groups were positively correlated with the pulmonary artery pressure (r =0.670,P =0.005 ; r =0.514.P =0.029 ; r =0.517,P =0.034 ; r =0.707,P =0.003).The difference in terms of serum CTGF concentration in different types of CHD patients was not significant (F =0.270,P =0.847).Conclusions There exists certain damage in CHD early myocardial fibrosis(unincorporated PH),when combined with PH,myocardial fibrosis increases with the gradual increase of pulmonary artery pressure.However,the degree of myocardial fibrosis shows no correlation with the type of CHD.
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Objective: To investigate the significance of doctor -patient communication courses to medical staff.Methods:Using self-made questionnaire and self -evaluation of anxiety scale (SAS), selection in our u-niversity study of 200 cases of medical personnel , in accordance with the doctor -patient communication before and after the course is divided into classes before and after teaching group , respectively on two groups before and after learning the medical staff on the SAS scores and questionnaire survey .Results:Compared with group before teach-ing, teaching group after medical staff thought through the study of doctor -patient communication course , is con-ducive to cultivating communication consciousness , improve doctor -patient communication skills as well as pre-venting the doctor-patient contradiction (P<0.05).After teaching group SAS score (34.50 ±6.88), signifi-cantly lower than the teaching group SAS score (45.51 ±6.97), difference was statistically significant (t =15 .622 ,P<0 .01 ) .Conclusion:Doctor-patient communication courses are effective way to improve the ability to communicate , to alleviate the anxiety of the medical staff at the same time also has a certain value .
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Objective To assess the effect of PRISMA statement on intervention-related systematic reviews and meta-analyses published in Evidence-based medicine .Methods Intervention-related systematic reviews and meta-analyses published in Evidence-based medicine from 2001 to 2011 were assessed according to the PRISMA scale and analyzed by Meta Analysist software.Results Seventy intervention-related systematic reviews and meta-analyses involving 14-disease spectra were included in this study.PRISMA statement and systematic reviews and meta-analysespublished by au-thors in colleges and universities could improve their academic level (P<0.05), fund support and the number of authors showed no significant effect on their academic level.Conclusion Literature retrieval methods,literature screening methods,bias assessment methods, and other analyzing methods used systematic reviews and meta-analyses published in Evidence-based medicine and their academic level can be improved by PRISMA statement.
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Objective To assess the serum level of stromal-cell-derived factor 1 (SDF-1) in patients with congenital heart disease (CHD) and pulmonary arterial hypertension. Methods The heart color Doppler ultrasound was conducted to measure the tricuspid regurgitation velocity, in order to estimate pulmonary artery systolic pressure. According to the existing standards, a total of 86 patients were divided into CHD without pulmonary hypertension group (n=16), mild pulmonary hypertension group (n=18), moderate pulmonary hypertension group (n=17), severe pulmonary hypertension group (n=15). Another 20 healthy chil-dren were recruited as control group (n=20), The serum level of SDF-1 was detected by the ELISA method. Results The serum SDF-1 levels were signiifcantly lower in CHD groups than in control group (F=27.793, P<0.001). In CHD groups, CHD with se-vere pulmonary hypertension group had the lowest SDF-1 level, and CHD without pulmonary hypertension group had the highest SDF-1 level. There were signiifcant differences between CHD groups (P<0.05). The pulmonary artery systolic pressure was cor-related with serum SDF-1 levels (r=-0.737, P<0.001). Conclusions The serum level of SDF-1 is decreased in patients with CHD, and is negatively correlated with the severity of pulmonary arterial hypertension.
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Objective To assess the academic level of papers on systematic reviews and meta-analysis published in Chinese Journal of Pediatricsand methodology they used.Methods Basic data were extracted from 13 papers on sys-tematic reviews and meta-analysis published in Chinese Journal of Pediatrics .The methodology they used was assessed according to the preferred reporting items for systematic reviews and meta-analysis (PRISMA) and ANSTAR Scale and analyzed using the RevMan5.0.Results The PRISMA score was 14-23.5 (mean 20.0±3.11) and the AMSTAR score was 3-7.5 (mean 6.04±1.38) for the methodology used in papers on systematic reviews and meta-analysis published in Chinese Journal of Pediatrics .Conclusion The methodology used in papers on systematic reviews and meta-analy-sis published in Chinese Journal of Pediatrics is not quite valid and should thus be improved .
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10.3969/j.issn.1000-3606.2013.06.006
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Objective To explore the mechanisms of coronary artery lesions in patients with Kawasaki disease by detecting thrombomodulin level in both acute and convalescence stages. Methods Fifty-eight patients were recruited in which 34 were male and 24 were female. This group was further divided into coronary artery lesion group(25 cases) and non-coronary artery lesion group(33 cases). Normal control group was consisted of 30 healthy children in which 17 were male and 13 were female. Thrombomodulin was measured by enzyme linked immunosorbent assay. Results Compared with the control group, TM level was increased in the Kawasaki disease group. TM level in the acute stage group and convalescence group was higher than that of the control group, TM level in acute stage group was higher than that of the convalescence group (P<0.05). Compared with non-coronary artery lesion group, TM level of the coronary artery lesion group was increased and the difference was significant (P<0.01). Correlation analysis showed that the TM level was positively related with coronary complications of the Kawasaki disease (r=0.855, P<0.01 ). Conclusion TM increases significantly in Kawasaki disease. It is correlated with the development of coronary artery lesions. In addition, it is also associated with apparent hypereoagulation and thrombocytophilia. TM can predict the development of coronary artery lesions.
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Objective By exploring the alteration of tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor-1 (PAI-l) in plasma in Kawasaki disease (KD) patients to identify the pathophysiological mechanism of vascular damage and to detect the relationship between fibrinolytic system function and coronary artery lesion complications in Kawasaki disease patients. Method Plasma levels of t-PA, PAI-1 antigen were measured by enzyme-linked immunosorbent assay. Patients with KD were grouped into acute phase group, recovery phase group patients with coronary artery lesion group and non-coronary artery lesion group. Results Plasma t-PA and PAI-1 in acute phase and recovery phase groups were significantly higher than those in the healthy group (P