ObjectiveTo evaluate the correlation between ultrasound detected fetal heart abnormality and chromosomal abnormality.Methods The data of 3307 cases of prenatal fetal echocardiography and karyotype analysis results were retrospectively analyzed.The correlation between heart abnormality and chromsomal abnormality was analyzed.ResultsIn 3307 cases d pregnant women,194cases (5.87％) were found signs of fetal heart abnormality,and 3113 cases (94.13％) were not found any sign of fetal heart abnormality.And 124 cases(3.75％) were found chromosomal abnormality.The rate of chromosomal abnormality in fetus with heart abnormality was higher than that in fetus without heart abnormality[ 19.59％ (38/194) vs.2.76％ ( 86/3113 ),P ＜ 0.01 ],the relative risk ratio was 7.0903.One hundred and twenty-four cases of chromosomal abnormality in the 18-three-body(42 cases) and 21-three-body(36 cases) were the most common.ConclusionsFetal heart abnormality incidence of chromosomal abnormality is high relatively.When the signs of heart abnormality are found,it is suggested that the fetus should examine karyotype analysis.

Objective To investigate plasma levels of high-sensitivity C-reactive protein (hs-CRP) in patients with coronary heart disease (CHD) and relationship between hs-CRP levels and cardiac function. Methods The serum hs-CRP concentrations in 894 CHD patients diagnosed by coronary angiography and 141 healthy controls were measured by particle enhanced immunoturbidimetric assay. Results The median of hs-CRP levels was 1.70 (0.13-19.53 ) mg/L and abnormal ratio was 37.6% (336/894), that were significantly higher in CHD group than healthy controls [0. 99(0. 13-19. 53) rag/L, 7. 1% (10/141) ] (Z=-6. 476,X<'2> = 50. 882, P <0.01 ). The median of hs-CRP levels was 5.35 (0. 18-19. 10) mg/L and abnormal ratio was 63.9% (92/144), that were much higher in acute myocardial infarction (AMI) group than in old myocardial infarction (OMI) group [2.27 (0.13-19.19) mg/L, 43.7% (129/295) ] (Z = -3.353 ,X<'2> = 15. 732, P <0. 01 ). The median of hs-CRP levels was 1.45 (0.19-19.53) mg/L in unstable angina pectoris(UAP) group and abnormal ratio was 29.1% (73/251), that were was higher in stable angina pectoris (SAP) group [1.04 (0.13-16.31 ) mg/L, 20. 6% (42/204) ] (Z=-2.981, P = 0.003;X<'2> = 4.30, P=0.038 ) . Furthermore, Kruskal-Wallis test showed the concentrations of hs-CRP and NT-proBNP was increased along with increment of CHD severity (NYHA functional classification) (X<'2> = 120.185,424.945, P <0.001 ). Multivariate analysis showed that hs-CRP levels positively correlated with NYHA functional classification ( r = 0.328, P <0.01 ) as well as NT-proBNP levels (r=0.413, P <0.01 ). Conclusion Serum hs-CRP level increases along with CHD severity, indicating that hs-CRP may play a certain role in the occurrence and development of CHD.

AIM:To investigate the role of B cells in CD45RB antibody-induced transplantation immune toler-ance.METHODS:Single cell suspension was made from the spleen of BALB/c nude mice disposed by CD45RB antibod-y, then mixed cultured with T cells of BALB/c mice and spleen cells of C57BL/6 mice.The Th1, Th2, Treg and Tm cells were monitored by flow cytometry during the culture process .The skin graft model was set up with B 6.μMT-/-mice as re-ceptors and BALB/c mice as donors.CD45RB antibody was intraperitoneally injected into the receptors after transplantation and then CD3+CD45RBhi cells were detected by flow cytometry .In another mixed lymphocyte culture , CD45RB antibody was added, and then B cells were isolated and injected into B6.μMT-/-mice through the tail vein.The heart transplanta-tion model was established with B 6.μMT-/-mice as receptors and BALB/c mice as donors, and then the survival and the migration of B cells to the thymus were observed .RESULTS:When T lymphocytes were co-cultured with B lymphocytes treated with anti-CD45RB monoclonal antibody (mAb) in vivo, the percentages of Th2 and Treg cells were up-regulated and Th1 cells were down-regulated, but Tm cells were not altered as compared with the control .In vivo without B lympho-cytes, anti-CD45RB mAb also down-regulated the expression of CD45RB in T lymphocytes.The reduction was faster and the percentage of CD3 +CD45RBhi T cells was not altered as compared with the control .The B lymphocytes treated with an-ti-CD45RB mAb in vitro prolonged the lifetime of receptor in heart transplantation model but failed to induce complete toler -ance.After recieving B cells treated with anti-CD45RB mAb and allogeneic heart transplantation , B cells migrated to the thymus in B6.μMT-/-mice.CONCLUSION:B lymphocytes play a definite role in the transplantation immune tolerance induced by anti-CD45RB mAb through their affection on T-cell subgroups and also in the central tolerance .However, the induction of immune tolerance can not only rely on B cells .

Objective To analyze the causes of misdiagnosis and mistreatment of Dravet syndrome. Methods Patients with Dravet syndrome diagnosed according to clinical features and SCN1A gene mutation detection were recruited within recent 3 years. The patients were grouped into correct diagnosis-treatment group and misdiagnosis-mistreatment group according to whether the patients had ever been misdiagnosed and mistreated by sodium channel blockers. The clinical features were compared between two groups. Results Thirty-five cases with Dravet syndrome were collected and the rate of misdiagnosis reached 40%, Nine cases were misdiagnosed as symptomatic focal epilepsy, 4 as Lennox-Gastaut syndrome and 1 as Doose syndrome. The average age of onset in misdiagnosis-mistreatment group was (5.50 ± 3.56) months,and the age of confirmed diagnosis was (83.57 ± 105.62) months. The percentage of abnormal EEG, onset seizure with partial seizure, the seizure frequency within the first year from onset, onset with afebrile seizure, patients with status epilepticus or cluster seizures was higher in misdiagnosis-mistreatment group but it showed no significant statistical significance when compared with that of correct diagnosis-treatment group. The percentage of patients with mental retardation and focal neurological signs was significantly higher in misdiagnosis-mistreatment group (P=0.005 and 0.002, respectively). Conclusions Dravet syndrome is frequently misdiagnosed as symptomatic focal epilepsy. The appearance of focal neurological signs and mental retardation before confirmed diagnosis are important factors for misdiagnosis. Gene mutation screening will be helpful for differential diagnosis of Dravet syndrome.

Objective:To compare the therapeutic outcomes between use of antibiotic cement versus non-use of antibiotic cement in the treatment of tibial osteomyelitis after radical debridement.Methods:A retrospective analysis was made of the 68 patients with local tibial osteomyelitis of Cierny-Mader Type Ⅳ who had been treated at Department of Orthopaedic Trauma, The Second People’s Hospital of Shenzhen from January 2010 to June 2015. The dead space was filled with antibiotic-impregnated bone cement beans after radical debridement of the infected bone in 32 of them (cement group) but was not in 36 of them (no-cement group). The operations for both groups were performed by the same surgical team who filled the bone defects after excision of infected bone using Ilizarov bone transport. The 2 groups were compared in terms of Paley functional scores of bone and limb, external fixation index (EFI), infection recurrence rate, total hospital costs and other complications.Results:The 2 groups were comparable because there was no significant difference between them in the preoperative general data ( P>0.05). The cement group was followed up for (71.2±8.9) months and the no-cement group for (71.6±9.7) months, showing no significant difference ( P>0.05). By the Paley functional scores, the good to excellent rate for bone was 100% for both groups (32/32 versus 36/36) while the good to excellent rate for limb was 93.8% (30/32) for the cement group and 94.4% (34/36) for the no-cement group, showing no significant differences between them ( P>0.05). The EFI was (49.0±10.5) d/cm for the cement group and (49.5±11.4) d/cm for the no-cement group, showing no significant differences between them ( P>0.05). The infection recurrence rate at the final follow-up was 3.12% (1/32) for the cement group and 2.78% (1/36) for the no-cement group, showing no significant differences between them ( P>0.05). The total hospital cost was (70,944.1 ± 1,135.5) Yuan RMB for the cement group and (55,205.2 ± 897.3) Yuan RMB for the no-cement group, showing a significant difference ( P<0.05). No serious complications with sequelae were found in either of the 2 groups. Conclusion:In the treatment of local tibial osteomyelitis of Cierny-Mader Type Ⅳ, it is not necessary to fill the dead space with antibiotic cement when radical debridement is achieved.

Objective To investigate the dynamic changes of regulatory T cells (Treg ) and the surface expression of programmed death (PD)‐1 and the level of transforming growth factor (TGF )‐βduring antiviral treatment in patients with chronic hepatitis C (CHC) .Methods Eighty‐six CHC patients referred to the First Affiliated Hospital of Zhengzhou University from October 2012 to October 2013 were included ,and all of them were administered with pegylated interferon α‐2a and ribavirin .Thirty healthy controls were enrolled .The percentage of Treg cells ,PD‐1 expression and TGF‐β level were analyzed by flow cytometry at baseline and at time of achieving rapid virological response (RVR ) , early viral virological (EVR ) , end‐of‐treatment virological response (ETVR ) and sustained virological response (SVR) ,or not achieving SVR .Comparison between two groups was analyzed by t test .Results Among 86 CHC patients ,the proportions of RVR ,EVR ,ETVR ,and SVR at week 24 of follow‐up were 29 cases ,67 cases ,79 cases and 67 cases ,respectively .Percentage of Treg cells in CHC patients was much higher than that in healthy controls (10 .31 ± 5 .61 vs 2 .18 ± 0 .65 ,t = 2 .28 , P< 0 .05) .During antiviral therapy ,percentages of Treg cells declined ,not only in CHC patients with HCV genotype 1b (at baseline , RVR ,EVR ,and ETVR :14 .44 ± 3 .78 ,11 .01 ± 1 .79 ,8 .24 ± 2 .98 ,and 5 .36 ± 1 .47 ,respectively ) ,but also in those infected with HCV genotype 2a (at baseline ,RVR ,EVR ,and ETVR :12 .34 ± 2 .82 ,8 .99 ± 1 .68 ,7 .53 ± 2 .96 ,and 4 .79 ± 1 .23 ,respectively ) .Expressions of PD‐1 and TGF‐β also decreased .At baseline ,the expressions of PD‐1 in patients with SVR and without SVR were 29 .11 ± 14 .65 and 37 .73 ± 11 .65 ,respectively (t = 2 .15 , P = 0 .04) ,and the levels of TGF‐β were 41 .20 ± 18 .96 and 56 .75 ± 14 .42 ,respectively (t= 2 .66 ,P< 0 .01) .At week 24 ,the expressions of PD‐1 in patients with SVR and without SVR were 10 .36 ± 4 .81 and 36 .46 ± 10 .52 ,respectively (t= 13 .95 ,P< 0 .01) ,and the levels of TGF‐β were 10 .06 ± 4 .64 and 45 .23 ± 17 .85 , respectively ( t = 11 .85 , P < 0 .01 ) . Conclusions Percentages of Treg cells and expressions of PD‐1 and TGF‐β decrease during antiviral treatment in CHC patients .Thus ,it could be of assist to predict the treatment response by monitoring these parameters .

Objective We aimed to explore the mechanism by which Bushen Yangjing Soup improves elderly infertility based on oocyte mitochondrion.Methods C57BL/6J mice were used,including 15 young females(6-8 weeks old),45 elderly females(10 months old),and ten young males(6-8 weeks old).The female 6-8-week-old young mice were assigned to the young group,and the female 10-month-old elderly mice were randomly divided into the model group,the dehydroepiandrosterone(DHEA)group,and the Bushen Yangjing Soup group.Mice in the DHEA and Bushen Yangjing Soup groups were given DHEA[11.26 mg/(kg·d)]and Bushen Yangjing Soup[11.41 g/(kg·d)].Mice in the other groups were given normal saline.After 45 days,oocytes were collected,the number of oocytes and the proportion of mature oocytes were recorded,and in vitro fertilization(IVF)was carried out,followed by calculation of the successful fertilization rate.Real-time PCR was used to determine the copy number of mitochondrial DNA in oocytes,mito-tracker green was used to observe the distribution of mitochondria,and the mitochondrial membrane potential(MMP)of oocytes was determined using the JC-1 kit.The mRNA and protein levels of mitofusin 2(Mfn2)in oocytes were determined by real-time PCR and Western blotting,respectively.Results Compared with the young group,the number of oocytes,the proportion of mature oocytes,and the IVF rate were significantly reduced(P＜0.01),the copy number of mitochondrial DNA in oocytes was decreased,the rate of abnormal mitochondrial distribution was increased,the MMP was decreased(P＜0.01),and the mRNA and protein levels of Mfn2 were decreased(P＜0.01)in the elderly model mice.Compared with the elderly model group,the number of oocytes,the proportion of mature oocytes,and the IVF rate were significantly increased(P＜0.05),the copy number of mitochondrial DNA in oocytes was increased(P＜0.05),the rate of abnormal mitochondrial distribution was decreased,the MMP was increased(P＜0.05),and the mRNA and protein levels of Mfn2 were increased(P＜0.01)in the Bushen Yangjing Soup group.Compared with the DHEA group,the number of oocytes,the proportion of mature oocytes,and the IVF rate were increased,the copy number of mitochondrial DNA in oocytes was increased,the rate of abnormal mitochondrial distribution was decreased,the MMP was increased,the mRNA and protein levels of Mfn2 were increased in the Bushen Yangjing Soup group,and there was a significant difference in the number of oocytes and the expression of Mfn2 protein(P＜0.05).Conclusion Bushen Yangjing Soup may improve the quantity,distribution,and function of oocyte mitochondria by increasing the mRNA and protein levels of Mfn2,thereby improving oocyte quality.This is one of the possible mechanisms for clinical application of Bushen Yangjing Soup to improve ovarian function and treat elderly infertility.

Background::Hyperglycemia frequently induces apoptosis in endothelial cells and ultimately contributes to microvascular dysfunction in patients with diabetes mellitus (DM). Previous research reported that the expression of integrins as well as their ligands was elevated in the diseased vessels of DM patients. However, the association between integrins and hyperglycemia-induced cell death is still unclear. This research was designed to investigate the role played by integrin subunit β5 (ITGB5) in hyperglycemia-induced endothelial cell apoptosis.Methods::We used leptin receptor knockout (Lepr-KO) ( db/ db) mice as spontaneous diabetes animal model. Selective deletion of ITGB5 in endothelial cell was achieved by injecting vascular targeted adeno-associated virus via tail vein. Besides, we also applied small interfering RNA in vitro to study the mechanism of ITGB5 in regulating high glucose-induced cell apoptosis. Results::ITGB5 and its ligand, fibronectin, were both upregulated after exposure to high glucose in vivo and in vitro. ITGB5 knockdown alleviated hyperglycemia-induced vascular endothelial cell apoptosis and microvascular rarefaction in vivo. In vitro analysis revealed that knockdown of either ITGB5 or fibronectin ameliorated high glucose-induced apoptosis in human umbilical vascular endothelial cells (HUVECs). In addition, knockdown of ITGB5 inhibited fibronectin-induced HUVEC apoptosis, which indicated that the fibronectin-ITGB5 interaction participated in high glucose-induced endothelial cell apoptosis. By using RNA-sequencing technology and bioinformatic analysis, we identified Forkhead Box Protein O1 (FoxO1) as an important downstream target regulated by ITGB5. Moreover, we demonstrated that the excessive macroautophagy induced by high glucose can contribute to HUVEC apoptosis, which was regulated by the ITGB5-FoxO1 axis. Conclusion::The study revealed that high glucose-induced endothelial cell apoptosis was positively regulated by ITGB5, which suggested that ITGB5 could potentially be used to predict and treat DM-related vascular complications.

Objective To review the characteristics of animal models of sequelae of pelvic inflammatory disease(SPID)to provide a reference for standardizing the modeling process and improving the modeling rate.Methods Literature relevant to animal models of SPID from the past 40 years was searched,and animal species,modeling method,modeling cycles,modeling substances,positive control drugs,and evaluation indexes were summarized and analyzed.Results A total of 243 study manuscripts were included,most of which induced the SPID model in rats via the phenol paste or microbial infection method.The modeling cycles were typically between 14 and 16 days,and the success of the models was mostly determined by pelvic tissue morphology observation and pathological HE staining.Few research reports have focused on the traditional Chinese medicine(TCM)disease combination model.Conclusions No consistent criteria have been established for SPID animal model modeling,and thus it is recommended that researchers evaluate changes to animal behavior,pelvic histomorphology,and pathology.TCM syndrome modeling lacks effective method and evaluation standards,which need further research and development.Finally,the selection and use of positive-control drugs need to be further explored and perfected.