Objective To investigate the change of umbilical cord blood gas from early-stage neonates with pregnancy-induced hypertension syndrome (PHIS) affected mothers and its influence upon internal environment of body,and to evaluate the significance of postpartum umbilical cord blood gas analysis.Methods Retrospective study of 101 neonates(born of 97 PHIS-affected mothers),41 cases of mild group,34 cases of moderate group,26 cases of severe group,and enrolled 52 neonates born of non-PHIS mothers as the control group.Prior to neonate's first breath,umbilical cord artery blood gas analysis was performedimmediately to determine the values of pH,arterial carbon dioxide partial pressure (PaCO2),arterial oxygen tension (PaO2),HCO3-,base excess (BE),and Apgar score was completed within 1 min after birth.Results The pH,PaO2,HCO3-,BE in severe group was significantly lower than those in mild group,moderate group,and control group [7.16 ± 0.18 vs.7.25 ± 0.09,7.22 ± 0.11,7.29 ± 0.08 ; (12.01 ± 2.75) mmHg (1 mmHg =0.133 kPa) vs.(18.35 ± 1.75),(14.21 ± 2.01),(22.23 ± 1.45) mmHg; (17.11 ± 2.42) mmoFL vs.(19.82 ±3.85),(17.32 ± 3.21),(22.56 ± 3.38) mmol/L; (-9.15 ± 0.32) mmol/L vs.(-7.95 ± 0.60),(-7.21 ± 0.08),(-6.76 ± 0.03) mmol/L] (P ＜ 0.05),the PaCO2 in severe group was significantly higher than that in mild group,moderate group,and control group [(61.84 ± 32.93) mmHg vs.(54.48 ± 12.82),(58.38 ± 15.32),(51.66 ± 10.52) mmHg] (P ＜ 0.05),Apgar score 1 min after birth was positively correlated with umbilical arterial pH (P ＜ 0.05),the lower Apgar score,the lower pH.Among 65 cases of Apgar score ≤ 7 scores,37 cases of acidosis (pH ＜ 7.20),the incidence rate was 56.92％ (37/65) ; among 88 cases of Apgar score ≥ 8 scores,11 cases of acidosis,the incidence rate was 12.50％ (11/88),the difference was statistically significant (P ＜ 0.01).Conclusions Umbilical cord blood gas analysis is more objective than Apgar score,which could reflect neonate's hypoxia-ischemia degree bore of PIHS mothers,as well as contributed to the assessment of neonate' s prognosis.Conventional umbilical cord blood gas analysis is necessary for neonates bore of PIHS-affected mothers.Enhanced monitoring should be performed in a timely manner on those neonates born after intrauterine distress signs or with low Apgar score,the prevention and therapy as early as possible can improve the quality of birth.

Objective To investigate the molecular mechanism of bone marrow mesenchymal stem cells (BM-MSCs) in repairing cisplatin-induced acute renal injury.Methods The rats were injected 6 mg/kg of cisplatin intraperitoneally,and bone marrow mesenchymal stem cells (BM-MSCs group) or PBS (PBS group) were injected respectively via tail vein after 24 hours.The rats without injecting cisplatin were selected as a normal control group.The repair effect of BM-MSCs on renal injury was observed by HE staining and immunohistochemistry.In addition,NRK-52E cells were cultured in vitro and treated with cisplatin for 6 hours.Then,NRK-52E cells were continued to culture for 48 hours or co-cultured with BM-MSCs for 48 hours,and NRK-52E cells untreated with cisplatin were used as a control.The expression levels of miR-92b and its target gene PTEN were detected by qRT-PCR,and the expression level of p-Akt by western blot.Results HE staining showed that the tubular protein casts in BM-MSCs group were significantly less than that in PBS group,and that the renal tubular structure was significantly improved in BM-MSCs group.Immunohistochemical staining indicated that the number of cells expressing proliferating cell nuclear antigen (PCNA) in BM-MSCs group (131.0 ± 14.4) was significantly higher than that in PBS group (42.2 ±6.1,t =11.28,P ＜0.01).qRT-PCR results showed that in the vivo experiment,compared with the expression level of miR-92b and PTEN in the normal control group (1.11 ± 0.78,1.01 ± 0.21),PBS group were (4.64 ± 1.06) and (0.61 ± 0.2),respectively (all P ＜ 0.05);BM-MSCs group were (2.27 ± 0.81) and (1.1 ± 0.1),respectively (all P ＜ 0.05).In vitro experiment,compared with the expression level of miR-92b and PTEN in the negative control group (1.12 ± 0.77,1.02 ± 0.13),cisplatin group were (7.64 ± 0.72) and (0.58 ± 0.2),respectively (all P ＜ 0.05),cell group were (4.38 ± 0.50) and (1.15 ± 0.23),respectively (all P ＜ 0.05).Western blot results showed that compared with the expression level of p-Akt in cisplatin group (0.96 ± 0.18),p-Akt expression in cell group was (2.11 ± 0.11,P ＜ 0.01).Conclusion BM-MSCs may repair the cisplatin-induced acute renal injury via down-regulating the expression level of miR-92b.

Objective To investigate the diagnostic value of non-invasive cardiac output parameters:cardiac index (CI) and minute distance (MD), in premature infants with patent ductus arteriosus (PDA) and determine the cut-off value. Methods Clinical data of 98 premature infants admitted to the neonatal intensive care unit from January 2015 to June 2015 were collected. These premature infants were divided into the treated PDA group (n=30),the untreated PDA group (n=28) and the normal premature group (n=40) based on the results of echocardiogram in the first three days after birth and the use of drugs. Non-invasive cardiac output parameters were measured in the first three days after birth. The data were analyzed by t test, analysis of variance and SNK-q test. The diagnostic value of CI and MD for PDA was analyzed by the receiver operating characteristic curve. Results By preliminary analysis of the ROC curve,CI and MD were the most representative parameters for the diagnosis of PDA which need to be treated clinically, we thus chose CI and MD in this study. The aortic and pulmonary arterial CI and MD in the treated PDA group were significantly higher than in the untreated PDA group and the normal premature group (all P<0.05). There were no significant differences between the untreated PDA group and the normal premature group in the aortic and pulmonary arterial CI and MD (all P>0.05). The cut-off value of the aortic CI and MD was 2.95 L/(min·m2) and 21.50 m/min, respectively, while that of the pulmonary arterial CI and MD was 4.55 L/(min·m2) and 26.50 m/min, respectively. The sensitivity and specificity of the combined aortic CI and MD for the treated PDA group were 0.90 and 0.82, and those of combined pulmonary arterial CI and MD were 0.87 and 0.82;and those of combined aortic and pulmonary arterial CI and MD were 0.80 and 0.88, respectively. Conclusions The non-invasive cardiac output parameters CI and MD have good diagnostic value for the PDA needing clinical treatment, and the combined use of the two parameters can improve specificity, and help formulate the early treatment strategy for premature infants with PDA. When aortic CI was ≥ 2.95 L/(min·m2) and MD was ≥ 21.50 m/min, a preliminary diagnosis of the PDA needing clinical treatment, can be made, and simultaneously when the pulmonary arterial CI was ≥4.55 L/(min·m2) and MD was≥26.50 m/min, the arterial duct should be closed timely.

Objective To observe the expression of survivin and Aurora B in human pancreatic cancer BXPC3 cells after the treatment of sulindac and to explore the potential mechanism. Methods MTr assay was used to determine the effect of sulindac on the proliferation of the BXPC3 cells. RT-PCR was used to detect the expression of mRNA level of survivin and Aurora B, western blot was used to detect protein expression of survivin and Aurora B Thr-232. Cell cycle and apoptosis were detected by flow eytometry (FCM). Results The BXPC3 cells were inhibited by sulindac in a dose and time-dependent manner; the expression of mRNA of survivin and Aurora B were both significantly decreased from 1.5644 and 0.6554 to 0. 4372 and 0.1132 (P< 0.01), the expression of survivin protein and the phosphorylation of Aurora B Thr-232 were also decreased from 1.2735 and 0.4680 to 0.2126 and 0.2546 (P<0.01); the proportion of cells in the G0/G1 phase was increased from (56.65±1.93)% to (70.58±3.21)% (P<0.01). Conclusions Sulindac had inhibitory effects on the growth of BXPC3 cells, the possible mechanism was via decreasing the expression of survivin which depressed the activity of Aurora B, then the CPC was influenced. The most of the cells were blocked in the G0/G1 phase, and the cells' mitosis was inhibited.

Objective To evaluate the effects of early rehabilitation on development of infants with cerebral injury in pefinatal period.Methods 84 high risk infants with cerebral injury in pefinatal period were divided into two groups.Infants in the control group were treated with conventional medicament and those in intervention group received physical,visual,aural and haptic stimuli combined with Vojta and Bobath approach in addition.Clinical data and Gesell Development Schedules of 1 year old were used to evaluate the effect.Results The incidence of improvement was 92.86% in the intervention group and 73.81% in the control group(P<0.05).The development quotient of Gesell Development Schedules were obviously higher in the intervention group than in the control group in all the functional areas(P<0.05).Conclusion The early rehabilitation can improve the cerebral development in high risk infants with cerebral injury in pefinatal period.

Objective To explore the expression and significance of neutrophil gelatinase-associated lipocalin (NGAL) in lupus nephritis (LN) in mice. Methods Female MRL/lpr lupus mice (n=36) were randomly divided into the experimental group and intervention group, and female Kunming mice (n =18) served as controls. Each mice in the intervention group received intraperitoneal injection of 20 μg anti-mice interleukin (IL)-17 antibody. The serum concentrations of NGAL, IL-17,matrix metalloproteinase(MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 were measured by enzyme-linked immunosorbent assay (ELISA). And the protein expressions of NGAL, IL-17, MMP-9 and TIMP-1 in renal tissue were detected by immunohistochemisty. One-factor analysis of variance (ANOVA) or nonparametric rank sum test was used for the comparisons between the three groups. Associations between these factors were analyzed by Pearson′s test. Results The levels of serum NGAL, IL-17, MMP-9 and TIMP-1 in the experimental group were obviously increased as compared to those in the control group and intervention group [NGAL: (30.31±1.22) ng/ml vs (11.36±0.14) ng/ml, (20.09±0.35) ng/ml, F=986.524, P<0.001]. The protein expression of NGAL, IL-17, MMP-9 and TIMP-1 in the renal tubular epithelial cells in the experimental group was increased as compared to the control group and intervention group[NGAL:(11.27±0.58) vs(0.45±0.19),(9.22±0.67), H=15.158, P =0.001]. In the experimental group, a positive correlation was found between the level of serum NGAL
and the serum levels of IL-17, MMP-9 and MMP-9/TIMP-1(r=0.899, 0.789, 0.925, P<0.01). The protein expression of NGAL in renal tissue was positively correlated with IL-17, MMP-9 and MMP-9/TIMP-1 levels (r=0.929, 0.899, 0.723, P<0.01). Conclusion The level of NGAL in the serum and renal tissue is signifi-cantly increased in the MRL/lpr lupus mice. And it is closely correlated with the levels of IL-17 and MMP-9. Our results suggest the potential role of NGAL in the inflammation of lupus nephritis.

[ ABSTRACT] AIM:To investigate the role of the Notch pathway in Toll-like receptor 4 ( TLR4 )-mediated in-flammatory response in renal ischemia reperfusion injury ( IRI) in rats.METHODS: A total of 75 male sprague-Dawley rats were randomly divided into sham operation group , IRI group and DAPT treatment group .Blood samples and the kid-neys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion .The concentrations of blood urea nitrogen ( BUN) and serum creatinine (Scr) were measured.The serum levels of tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were detected by ELISA, and the expression of Notch1, TLR4 and NF-κB p65 in the renal tissues was assessed by im-munohistochemistry and Western blot .RESULTS: The serum levels of BUN, Scr, TNF-αand IL-6 in IRI group were markedly increased as compared with sham group (P<0.05).The protein levels of Notch1, TLR4 and NF-κB p65 in re-nal tubular epithelial cells in IRI group was significantly enhanced as compared with sham group ( P<0.05 ) .In DAPT group, the serum levels of BUN, Scr, TNF-αand IL-6 were significantly reduced compared with IRI group (P<0.05), and the protein levels of Notch1, TLR4 and NF-κB p65 were apparently less than those in IRI group (P<0.05).CON-CLUSION:Significant changes of renal function , a rise of serum inflammatory factor including TNF-αand IL-6 and en-hanced expression of Notch 1, TLR4 and NF-κB p65 in the renal tissue occurred in the rats with IRI .γ-Secretase inhibitor DAPT attenuates TLR4-mediated inflammatory response in the renal IRI through the inhibition of Notch 1 and down-regula-tion of NF-κB.

[ ABSTRACT] AIM:To investigate the expression of calprotectin ( CALP) in the rats with renal ischemia-reperfu-sion injury ( IRI) .METHODS:Male Sprague-Dawley rats were randomly divided into sham operation and IRI group ( n=25 in each group) .Blood samples and the kidneys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion.The pathological changes of the kidneys were observed.The serum concentrations of blood urea nitrogen ( BUN) and serum cre-atinine (SCr) were measured.The serum levels of CALP, tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) were detected by ELISA, and the expression of CALP, Toll-like receptor 4 ( TLR4) and NF-κB p65 in the renal tissues were de-termined by the methods of immunohistochemistry and Western blot.RESULTS: Different serial ischemia changes were observed in the renal tissues, mainly in the renal tubular epithelial cells and the mesenchyma, with the infiltration of in-flammatory cells.The serum levels of BUN, SCr, CALP, TNF-αand IL-6 in IRI group were markedly increased as com-pared with sham group (P<0.05).The protein expression of CALP, TLR4 and NF-κB p65 in the renal tubular epithelial cells in IRI group was greatly enhanced in comparison with that in sham group ( P<0.05) .CONCLUSION:The serum concentrations of CALP, TNF-αand IL-6, and the protein expression levels of CALP, TLR4 and NF-κB p65 in the renal tissue are significantly increased in the rats with IRI, suggesting that calprotectin plays an important role in the inflamma-tion in rats with IRI.

Objective To explore the effects and mechanism of implantation of umbilical blood mesenchymal stem cells(MSCs)on rats with cerebral infarction. Methods Umbilical blood MSCs were cultured in vivo,flow cytometry was ap-plied to test cytometric immunophenotype, and model of rat cerebral infarction was made by suture method; 120 rats were randomly assigned to MSCs implantation group and control group; rats' neurological function was evaluated;western-blot was applied to test the expression of GFAP protein. Fluorescence microscope was applied to observe changes of hippocampal formation in rats as well as the distribution of MSCs in rats' brain. Results According to the test of neurological function, the score of neurological function in the experiment group was reduced, and the score in the control group was improved. The difference was statistically significant(P<0.05). Expression of GFAP in MSCs im-plantation group was increased with a peak in the 7th day,while no significant changes in the control group(P<0.05). According to the observation of immunofluorescence microscopy, the distribution of MSCs in rats' brain was good in MSCs implantation group, and the hippocampal formation showed clear layers in the experiment group. Hippocampal structures in the control group were chaotic, and synapses and organelles were dissolved and compromised. Conclu-sion MSCs are able to promote the repair of hippocampal structures after cerebral infarction in rats, strengthen neuro-plasticity and promote the recovery of neurological functions.

Objective: To describe the molecular epidemiological characteristics of norovirus gastroenteritis outbreaks in Zhuhai from 2011 to 2016. Methods: Anal swab specimens were collected from 576 cases with 56 outbreaks of acute norovirus gastroenteritis from 2011 to 2016. Specimens were tested by real-time RT-PCR. Three to four of norovirus positive specimens were selected from every outbreak to amplify the VP1 gene by RT-PCR and one strain was chosen randomly from every outbreaks to determine the genotype by phylogenetic tree analysis. Results: Eight genotypes were identified from 56 outbreaks and all of them belonged to GⅡ genogroup. The genotype of norovirus strain changed with prevalence time. The GⅡ.4/2006b was dominant from 2011 to 2012, and replaced by GⅡ.4/Sydney _2012 during the 2012—2013 norovirus season, and both of them never appeared after Feb. 2013. GⅡ.17 was the only genotype during the 2014—2015 norovirus season. All the 7 outbreaks occurred from 2015 to 2016 were caused by GⅡ.3 norovirus. The GⅡ.17and GⅡ.3 were identified from Apr. to Sep. 2016; GⅡ.p16-GⅡ.2 were the only genotype in 12 outbreaks from Nov. to Dec. 2016. The GⅠ genogrope was never identified from 2011 to 2016 in Zhuhai. Conclusions The Norovirus GⅡ was the only pathogeny which caused the outbreaks of norovirus gastroenteritis. The recombinant norovirus strain GⅡ.p16-GⅡ.2 emerged and caused large outbreaks in the last two months of 2016 in Zhuhai; several recombinant strains of the GⅡ.p16 RdRp gene were found now, which suggests that attention should be focused on the prevalence and evolution of the recombinant norovirus.