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ABSTRACT: Retinoic acid (RA) is a potent signaling molecule that plays pleiotropic roles in patterning, morphogenesis, and organogenesis during embryonic development. The synthesis from retinol (vitamin A) to retinoic acid requires two sequential oxidative steps. The first step involves the oxidation of retinol to retinal through the action of retinol dehydrogenases. Retinol dehydrogenases1l (RDH1l) is a novel zebrafish retinol dehydrogenase. Herein we investigated the role of zebrafish RDH1l in heart development and cardiac performance in detail.
RDH1l specific morpholino was used to reduce the function of RDH1l in zebrafish. The gene expressions were observed by using whole mount in situ hybridization. Heart rates were observed and recorded under the microscope from 24 to 72 hours post fertilization (hpf). The cardiac performance was analyzed by measuring ventricular shortening fraction (VSF).
The knock-down of RDH1l led to abnormal neural crest cells migration and reduced numbers of neural crest cells in RDH1l morphant embryos. The reduced numbers of cardiac neural crest cells also can be seen in RDH1l morphant embryos. Furthermore, the morpholino-mediated knock-down of RDH1l resulted in the abnormal heart loop. The left-right determining genes expression pattern was altered in RDH1l morphant embryos. The impaired cardiac performance was observed in RDH1l morphant embryos. Taken together, these data demonstrate that RDH1l is essential for the heart development and cardiac performance in zebrafish.
RDH1l plays a important role in the neural crest cells development, and then ultimately affects the heart loop and cardiac performance. These results show for the first time that an enzyme involved in the retinol to retinaldehyde conversion participate in the heart development and cardiac performance in zebrafish.
Chinese medical journal 02/2013; 126(4):722-8. · 0.86 Impact Factor
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ABSTRACT: To evaluate the fetal cardiac function in gestational diabetes mellitus (GDM) pregnancies under different maternal glycemic controls.
Forty four GDM mothers received 78 fetal echocardiographic evaluations at three gestational periods (<28, 28-34 and >34 weeks) and were divided into poorly-(DM1) and well-(DM2) controlled groups according to their glycemic control at examination. Seventy uncomplicated mothers were selected as controls. Parameters of fetal cardiac anatomy and function were measured and analyzed.
GDM fetuses' cardiac ventricular walls were thicker than controls', and the differences between DM1 and DM2 were not significant except for end-diastolic left ventricular walls. In both GDM groups, the aortic flow velocities increased earlier than pulmonary artery and DM1 fetuses changed earlier than DM2 ones. GDM fetuses' left atrial shortening fraction was smaller than the controls' in the period of ⩾34 weeks and negatively correlated with thicknesses of left ventricular walls and interventricular septum in DM1 fetuses (r=-0.438 and -0.506). The right ventricular diastolic function in DM1 and DM2 fetuses decreased after the period of 28-34 weeks and in the period of >34 weeks respectively. Tei index of both left and right ventricles increased in DM1 group after the period of <28 weeks and in DM2 group only in the period of ⩾34 weeks, with no significant differences between DM1 and DM2 groups in this period.
Fetuses of GDM mothers showed cardiac function impairments. Good maternal glycemic control may delay the impairments, but cannot reduce the degree. Some cardiac changes in GDM fetuses were similar to those in pregestational diabetic pregnancies except for several parameters and their changing time.
Biomedical and Environmental Sciences 02/2012; 25(1):15-22. · 1.35 Impact Factor
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ABSTRACT: To construct the folic acid deficient model in zebrafish and observe the abnormal cardiac phenotypes, to find the optimal period for supplementing folic acid that can most effectively prevent the heart malformation induced by folic acid deficiency, and to investigate the possible mechanisms by which folic acid deficiency induces malformations of heart.
The folic acid deficient zebrafish model was constructed by using both the folic acid antagonist methotrexate (MTX) and knocking-down dhfr (dihydrofolate reductase gene). Exogenous tetrahydrofolic acid rescue experiment was performed. Folic acid was given to folic acid deficient groups in different periods. The percent of cardiac malformation, the cardiac phenotypes, the heart rate and the ventricular shortening fraction (VSF) were recorded. The out flow tract (OFT) was observed by using fluorescein micro-angiography. Whole-mount in situ hybridization and real-time PCR were performed to detect vmhc, amhc, tbx5 and nppa expressions.
About (78.00 ± 3.74)% embryos in MTX treated group and (68.00 ± 6.32)% embryos in dhfr knocking-down group had heart malformations, including the abnormal cardiac shapes, the hypogenesis of OFT and the reduced heart rate and VSF. Giving exogenous tetrahydrofolic acid rescued the above abnormalities. Given the folic acid on 8 - 12 hours post-fertilization (hpf), both the MTX treated group (20.20% ± 3.77%) and dhfr knocking-down group (43.40% ± 4.51%) showed the most significantly reduced percent of cardiac malformation and the most obviously improved cardiac development. In folic acid deficient group, the expressions of tbx5 and nppa were reduced while the expressions of vmhc and amhc appeared normal. After being given folic acid to MTX treated group and dhfr knocking-down group, the expressions of tbx5 and nppa were increased.
The synthesis of tetrahydrofolic acid was decreased in our folic acid deficient model. Giving folic acid in the middle period, which is the early developmental stage, can best prevent the abnormal developments of hearts induced by folic acid deficiency. Folic acid deficiency did not disrupt the differentiations of myosins in ventricle and atrium. The cardiac malformations caused by folic acid deficiency were related with the reduced expressions of tbx5 and nppa.
Zhonghua er ke za zhi. Chinese journal of pediatrics 12/2010; 48(12):905-12.
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ABSTRACT: Tbx1 is the major candidate gene for DiGeorge syndrome (DGS). Similar to defects observed in DGS patients, the structures disrupted in Tbx1(-/-) animal models are derived from the neural crest cells during development. Although the morphological phenotypes of some Tbx1 knock-down animal models have been well described, analysis of the cardiac performance is limited. Therefore, myocardial performance was explored in Tbx1 morpholino injected zebrafish embryos.
To elucidate these issues, Tbx1 specific morpholino was used to reduce the function of Tbx1 in zebrafish. The differentiation of the myocardial cells was observed using whole mount in situ hybridization. Heart rates were observed and recorded under the microscope from 24 to 72 hours post fertilization (hpf). The cardiac performance was analyzed by measuring ventricular shortening fraction and atrial shortening fraction.
Tbx1 morpholino injected embryos were characterized by defects in the pharyngeal arches, otic vesicle, aortic arches and thymus. In addition, Tbx1 knock down reduced the amount of pharyngeal neural crest cells in zebrafish. Abnormal cardiac morphology was visible in nearly 20% of the Tbx1 morpholino injected embryos. The hearts in these embryos did not loop or loop incompletely. Importantly, cardiac performance and heart rate were reduced in Tbx1 morpholino injected embryos.
Tbx1 might play an essential role in the development of pharyngeal neural crest cells in zebrafish. Cardiac performance is impaired by Tbx1 knock down in zebrafish.
Chinese medical journal 05/2010; 123(9):1182-9. · 0.86 Impact Factor
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ABSTRACT: To study the feasibility of umbilical cord brain natriuretic peptide (BNP) level measurement for the evaluation of perinatal cardiac function in fetuses from pregnant women with abnormal blood glucose levels and the influence of abnormal blood glucose on fetal cardiac function.
Twenty-four mothers with gestational diabetes mellitus (n=18) or gestational impaired glucose tolerance (n=6) (diabetic group) were classified into two subgroups according to blood glucose level before delivery: good (n=17) and poor (n=7) glucose control. They underwent fetal echocardiography in their late pregnant periods and fetal cardiac sizes and function were measured. Twenty-five normal pregnant mothers served as the control group. Umbilical cord blood BNP concentrations were measured at delivery.
The umbilical cord blood BNP concentrations in the diabetic group were significantly higher than in the control group(114.0+/-39.0 pg/mL vs 80.6+/-13.7 pg/mL; p<0.01). The poor glucose control subgroup demonstrated higher umbilical cord blood BNP concentrations than the good glucose control subgroup (142.1+/-44.1 pg/mL vs 102.4+/-31.2 pg/mL; p<0.01). No difference was found between the gestational diabetes mellitus and the impaired glucose tolerance groups. The BNP concentration was positively correlated to the thicknesses of fetal left ventricular walls and the peak velocities of mitral A wave (r=0.715, 0.491 respectively, p<0.05), and negatively correlated to the mitral E/A ratio (r=-0.507, p<0.05).
The fetuses of pregnant women with abnormal blood glucose levels have an increased BNP level in umbilical cord blood. Umbilical cord BNP level is related to maternal blood glucose control and the changes in fetal cardiac function. It may reflex the latent impairments of fetal cardiac function. A good glucose control may decrease the impact of abnormal maternal blood glucose on fetal hearts.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 10/2009; 11(10):805-8.
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ABSTRACT: To assess prenatal heart disease screening program by ultrasound.
A total of 11,544 second-trimester screening scans were performed before 24 weeks' gestation on 11,410 women between February 2004 and May 2007 in Obstetrics and Gynecology Hospital of Fudan University. Fetal heart screening was based on four-chamber and outflow tract views (left ventricular outflow + three vessel view). The sensitivity and specificity of different views were evaluated. Follow-up data of newborns was obtained.
(1) Among 11,544 cases,48 cases of congenital heart disease (CHD) were diagnosed in utero. Six cases were false negative, and 2 cases were false positive. The incidence of CHD was 0.47% (54/11 544). (2) Thirty-three CHDs were detected based on the four-chamber view, including 18 ventricular septal defect (9 with conotruncal anomalies), 6 anomalous atrioventricle valve, 9 disproportion of left/right ventricle. The sensitivity of the four-chamber view alone was 61.11% (33/54), and the specificity was 99.98% (11 488/11 490). Fifteen CHDs were detected based on the left ventricular outflow and three vessel views, including 1 pulmonary atresia, 3 pulmonary valve stenosis, 2 transposition of the great arteries (TGA), 1 pulmonary stenosis with TGA, 6 tetralogy of Fallot, and 2 pulmonary stenosis. The sensitivity of the combination of the four-chamber and outflow tract views was 88.89% (48/54), and the specificity was 99.98% (11 488/11 490). (3) Of 48 CHDs, 11 cases were accompanied by other malformations. Eleven cases were performed amniocentesis, among whom 5 cases were trisomy 21.
The screening program based on four-chamber and outflow tract views shows good sensitivity and excellent specificity. Our prenatal heart screening program is clinically feasible.
Zhonghua fu chan ke za zhi 09/2008; 43(8):589-92.
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ABSTRACT: To investigate the roles of nitric oxide (NO) and eNOS in the pathogenesis of vasovagal syncope (VVS).
Fourteen children with VVS (group A), 10 children with syncope other than vasovagal (group B) and 20 healthy volunteers (group C) were enrolled. Plasma NO levels in groups A and B were determined before and at the termination of the head-up tilt table test (HUT). The G894T polymorphism within the eNOS gene was determined in the three groups.
Plasma NO levels in group A increased significantly when syncope attacked from 76.7+/-9.6 micromol/L (before HUT) to 90.0+/-11.4 micromol/L (P<0.05). After the syncope attack was improved, plasma NO level in group A was significantly reduced. There were no statistical differences in plasma NO levels before and after the HUT in group B. Determining the G894T polymorphism within the eNOS gene showed that group A was associated with a higher incidence of the GT gene type as compared to groups B and C (42.9% vs 10%; P<0.05).
Plasma NO may be involved in the pathogenesis of VVS. The increased plasma NO level may be associated with the G894T polymorphism of the eNOS gene.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 08/2008; 10(4):478-80.
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ABSTRACT: Kawasaki disease (KD) is a febrile illness of childhood. The etiology of KD remains unknown. Multiple theories exist, including an infectious etiology and an immunological abnormality. Cardiac involvement ranges from myocarditis and pericarditis in the acute stage to the development of coronary artery aneurysms later in the course. The present study aimed to explore the effect of monocyte chemotactic protein-1 (MCP-1) in Kawasaki disease and its relationship with damage to the coronary arteries during the development of KD.
Plasma MCP-1 concentrations were measured by enzyme-linked immunosorbent assay (ELISA), and MCP-1 mRNA expression in peripheral blood mononuclear cells (PBMC) was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in comparison of three groups: 56 patients with KD, 60 age-matched patients with non-infectious diseases, and 66 age-matched febrile patients with various diseases.
Plasma MCP-1 concentration and MCP-1 mRNA expression in PBMC of patients with active KD [(409.55 +/- 97.42) pg/ml] and (1.97 +/- 0.77) were higher than those of control group. Plasma MCP-1 levels and MCP-1 mRNA expression of inactive KD group [(301.64 +/- 71.55) pg/ml] and (1.31 +/- 0.39) were significantly higher than those of non-infectious diseases patients. There was a marked increase in patients with inactive KD than those of non-infective patients, but there were no significant differences between inactive KD and febrile patients. Plasma MCP-1 levels and MCP-1 mRNA expression were markedly increased in KD patients with coronary artery lesions than those in patients without coronary artery lesions.
Plasma MCP-1 concentration and MCP-1 mRNA expression in PBMC were significantly increased in patients with KD, and they were higher in KD with coronary artery lesions. It indicates that MCP-1 may be a useful parameter for monitoring disease activity in patients with KD.
Zhonghua er ke za zhi. Chinese journal of pediatrics 03/2008; 46(2):132-5.
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ABSTRACT: Folic acid is very important for embryonic development and dihydrofolate reductase is one of the key enzymes in the process of folic acid performing its biological function. Therefore, the dysfunction of dihydrofolate reductase can inhibit the function of folic acid and finally cause the developmental malformations. In this study, we observed the abnormal cardiac phenotypes in dihydrofolate reductase (DHFR) gene knock-down zebrafish embryos, investigated the effect of DHFR on the expression of heart and neural crest derivatives expressed transcript 2 (HAND2) and explored the possible mechanism of DHFR knock-down inducing zebrafish cardiac malformations.
Morpholino oligonucleotides were microinjected into fertilized eggs to knock down the functions of DHFR or HAND2. Full length of HAND2 mRNA which was transcribed in vitro was microinjected into fertilized eggs to overexpress HAND2. The cardiac morphologies, the heart rates and the ventricular shortening fraction were observed and recorded under the microscope at 48 hours post fertilization. Whole-mount in situ hybridization and real-time PCR were performed to detect HAND2 expression.
DHFR or HAND2 knock-down caused the cardiac malformation in zebrafish. The expression of HAND2 was obviously reduced in DHFR knock-down embryos (P < 0.05). Microinjecting HAND2 mRNA into fertilized eggs can induce HAND2 overexpression. HAND2 overexpression rescued the cardiac malformation phenotypes of DHFR knock-down embryos.
DHFR plays a crucial role in cardiac development. The down-regulation of HAND2 caused by DHFR knock-down is the possible mechanism of DHFR knock-down inducing the cardiac malformation.
Chinese medical journal 08/2007; 120(13):1166-71. · 0.86 Impact Factor
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ABSTRACT: Cardiac contractility is regulated tightly as an extrinsic and intrinsic homeostatic mechanism to the heart. The molecular basis of the intrinsic system is largely unknown. Here, we test the hypothesis that bone morphogenetic protein-2 (BMP-2) mediates embryonic cardiac contractility upstream of myocyte-specific enhancer factor 2A (MEF2A).
The BMP-2 and MEF2A expression pattern was analyzed by RT-PCR, Western blotting, whole-mount in situ hybridization, and an in vivo transgenic approach. The cardiac phenotype of BMP-2 and MEF2A knock-down zebrafish embryos was analysed. Cardiac contractions were recorded with a video camera. Myofibrillar organization was observed with transmission electron microscopy. Gene expression profiles were performed by quantitative real-time PCR analysis.
We demonstrate that BMP-2 and MEF2A are co-expressed in embryonic and neonatal cardiac myocytes. Furthermore, we provide evidence that BMP-2 is required for cardiac contractility in vitro and in vivo and that MEF2A expression can be activated by BMP-2 signaling in neonatal cardiomyocytes. BMP-2 is involved in the assembly of the cardiac contractile apparatus. Finally, we find that exogenous MEF2A is sufficient to rescue ventricular contractility defects in the absence of BMP-2 function.
In all, these observations indicate that BMP-2 and MEF2A are key components of a pathway that controls the cardiac ventricular contractility and suggest that the BMP2-MEF2A pathway can offer new opportunities for the treatment of heart failure.
Cardiovascular Research 06/2007; 74(2):290-303. · 6.06 Impact Factor
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ABSTRACT: DiGeorge/del22q11 syndrome is one of the most common genetic causes of outflow tract and aortic arch defects in human. DiGeorge/del22q11 is thought to involve an embryonic defect restricted to the pharyngeal arches and the corresponding pharyngeal pouches. Previous studies have evidenced that retinoic acid (RA) signaling is definitely indispensable for the development of the pharyngeal arches. Tbx1, one of the T-box containing genes, is proved to be the most attractive candidate gene for DiGeorge/del22q11 syndrome. However, the interaction between RA and Tbx1 has not been fully investigated. Exploring the interaction will contribute to discover the molecular pathways disrupted in DiGeorge/del22q11 syndrome, and will also be essential for understanding genetic basis for congenital heart disease. It now seems possible that genes and molecular pathways disrupted in DiGeorge syndrome will also account for some isolated cases of congenital heart disease. Accordingly, the present study aimed to extensively study the effects of external RA on the cardiac development and Tbx1 expression during zebrafish embryogenesis.
The chemical genetics approach was applied by treating zebrafish embryos with 5 x 10(-8) mol/L RA and 10(-7) mol/L RA at 12.5 hour post fertilization (hpf). The expression patterns of Tbx1 were monitored by whole-mount in situ hybridization and quantitative real-time RT-PCR, respectively.
The zebrafish embryos treated with 5 x 10(-8) mol/L RA and 10(-7) mol/L RA for 1.5 h at 12.5 hpf exhibited selective defects of abnormal heart tube. The results of whole-mount in situ hybridization with Tbx1 RNA probe showed that Tbx1 was expressed in cardiac region, pharyngeal arches and otic vesicle during zebrafish embryogenesis. RA treatment led to a distinct spatio-temporal expression pattern for Tbx1 from that in wild type embryo. The real-time PCR analysis showed that Tbx1 expression levels were markedly reduced by RA treatment. Tbx1 expression in the pharyngeal arches and heart were obviously down regulated compared to the wild type embryos. In contrast to 5 x 10(-8) mol/L RA-treated groups, 10(-7) mol/L RA caused a more severe effect on the Tbx1 expression level.
These results suggested that there was a genetic link between RA and Tbx1 during development of zebrafish embryo. RA could produce an altered Tbx1 expression pattern in zebrafish. RA may regulate the Tbx1 expression in a dose-dependant manner. RA could represent a major epigenetic factor to cause abnormal expression of Tbx1, secondarily, disrupt the pharyngeal arch and heart development.
Zhonghua er ke za zhi. Chinese journal of pediatrics 05/2007; 45(4):267-71.
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ABSTRACT: To establish a model of congenital heart disease with Tbx2 gene knockdown.
1200 fertilized eggs of zebrafish (Danio rerio) were divided into 3 groups: wild type group (n = 100), Tbx2-morpholino (MO) group (n = 600, to be injected with Tbx2-MO so as to knock down the Tbx2 gene), and control MO group (n = 500, to be injected with control MO). 12, 24, 36, 48, 72, and 96 hours after fertilization the heart structure, heart rate, rhythm, contractibility, and blood flow of the embryos were observed under anatomic microscope and digital camera was used to record the findings. Whole-mount in situ hybridization was conducted to observe the expression of versican in the heart.
Eight hours after fertilization 27.2% of the fertilized eggs of the Tbx2-MO group died, and 21.3%, 32.8%, and 18.7% of them showed mild, moderate, or severe developmental abnormality of heart, including hypogenetic ventricle, dilatation of atria, abnormal atrioventricular canal, slow heartbeat, arrhythmia, and blood regurgitation. Whole-mount in situ hybridization showed that versican did not decrease with the passage of time but was expressed abnormally in the atria and ventricles, and did not disappear 72 hours after fertilization; however, it was expressed normally in the statolith.
MO antisense oligonucleotide knockdown is a good method for the study of heart development. Tbx2 gene plays an important role in the differentiation of atria and ventricles and formation of atrioventricular canal.
Zhonghua yi xue za zhi 05/2007; 87(14):991-4.
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ABSTRACT: To study the effect of methotrexate (MTX), a folic acid antagonist which can lead to folic acid deficient, on the cardiac development and on the expressions of BMP2b and HAS2 in zebrafish.
The zebrafish embryos at 6-48 hrs post fertilization (hpf) were treated with various concentrations of MTX (0.5 x 10(-3), 1.0 x 10(-3) and 2.0 x 10(-3) M). At 48 hpf, the percentage of cardiac malformation and heart rate were recorded. The zebrafish embryos at 6-10 hpf treated with 1.5 x 10(-3) M MTX were used as the MTX treatment group. At 24 and 48 hpf the cardiac morphology was observed under a microscope. The expressions of BMP2b and HAS2 in zebrafish were detected by in situ antisense RNA hybridization and real-time PCR.
6-12 hpf, the early embryonic developmental stage, was a sensitive period that MTX affected cardiac formation of zebrafish. The retardant cardiac development and the evidently abnormal cardiac morphology was found in the MTX treatment group. The results of in situ antisense RNA hybridization showed that the expressions of BMP2b and HAS2 in the zebrafish heart were reduced in the MTX treatment group at 36 and 48 hpf. The real-time PCR results demonstrated that the BMP2b expression decreased at 12, 24, 36 and 48 hpf, and that the HAS2 expression decreased at 24, 36 and 48 hpf in the treatment group compared with the control group without MTX treatment.
The inhibition of folic acid function may affect cardiac development of early embryos, resulting in a retardant development and a morphological abnormality of the heart in zebrafish, possibly by down-regulating the expressions of BMP2b and HAS2.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 05/2007; 9(2):159-63.
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ABSTRACT: To evaluate the detection and accuracy of fetal echocardiography for congenital heart defects among high-risk populations.
A prospective observational study of prenatal diagnosis of congenital heart disease was conducted in two tertiary obstetrics and gynecology hospitals between January 2003 and December 2004. Consecutive fetuses at risk of congenital heart disease underwent detailed fetal echocardiography during the study period. B-mode and colour/pulsed Doppler flow imaging were used in all cases. Follow-up was sought for all pregnancies. Indications for referral, maternal and gestational age at diagnosis, as well as prenatal and postnatal diagnosis were recorded prospectively. By comparing prenatal and postnatal diagnoses, sensitivity, specificity, and predictive values were estimated.
A series of 2063 high-risk fetuses underwent detailed fetal echocardiography during the study period. The mean gestational age at examination was 26.5 weeks, ranging from 16 to 42 weeks. The most common indications for fetal echocardiography were advanced maternal age (31.7%), fetal arrhythmias (13.5%) and maternal infections (10.4%). Forty-three cases of fetal congenital heart disease were detected. The mean gestational age at prenatal diagnosis was 27.3 weeks ranging from 16 to 40 weeks. There were 3 false-negatives and 1 false-positive. The sensitivity, specificity, positive and negative predictive values were 92.1%, 99.9%, 97.2%, and 99.8%, respectively. Diagnostic accuracy was 86.1%. A cardiac defect suspected on routine prenatal sonography accounted for the highest proportion of abnormal cases (67.4%). As for pregnancy outcome, there were 24 (52.1%) terminations; 2.2% died in utero, 13% postnatally, and 28.3% survived.
(1) Fetal congenital heart disease can be identified reliably by prenatal echocardiography. (2) Possible congenital heart disease or suspected heart defect noted on a screening obstetric sonogram is an important indication for fetal echocardiography. (3) A sequential segmental approach is critical for correct evaluation of the cardiac malformation. (4) The outcome of the patients with congenital heart disease is poor and a multidisciplinary approach is needed to the parental counseling and perinatal management planning.
Zhonghua er ke za zhi. Chinese journal of pediatrics 11/2006; 44(10):764-9.
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ABSTRACT: This study examined the expressions of plasma stromal cell derived factor-1 (SDF-1) and CXCR4 mRNA in peripheral blood mononuclear cells (PBMC) of children with Kawasaki disease (KD) and aimed to explore the significance of SDF-1 and CXCR4 mRNA in KD.
Fifty-six children with KD (12 cases complicated by coronary artery lesions) and 60 age and gender-matched healthy children (normal controls) were enrolled in this study. Plasma SDF-1 levels and CXCR4 mRNA expression in PBMC were measured using ELISA and real-time quantitative PCR at the acute and convalescence stages of KD.
Plasma SDF-1 levels (1833 +/- 395 ng/L vs 1126 +/- 408 ng/L; P < 0.05) and the CXCR4 mRNA expression in PBMC (6.57 +/- 2.81 vs 2.58 +/- 1.01; P < 0.01) in KD patients were significantly higher than those in normal controls at the acute stage. Both plasma SDF-1 levels and CXCR4 mRNA expression in KD patients decreased significantly at the convalescence stage, but nevertheless remained higher than those in the normal controls. The patients with concomitant coronary artery lesions showed higher CXCR4 mRNA levels than without at the acute stage (8.19 +/- 2.39 vs 6.13 +/- 2.77; P < 0.05).
Plasma SDF-1 concentration and CXCR4 mRNA expression in PBMC increased in KD patients. CXCR4 mRNA might be involved in the development of coronary artery lesions in KD.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 08/2006; 8(4):283-6.
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ABSTRACT: Delta-sarcoglycan, one member of the sarcoglycan complex, is a very conservative muscle-specific protein exclusively expressed in the skeletal and cardiac muscles of vertebrates. Mutations in sarcoglycans are known to be involved in limb-girdle muscular dystrophy (LGMD) and dilated cardiomyopathy (DCM) in humans. To address the role of delta-sarcoglycan gene in zebrafish development, we have studied expression pattern of delta-sarcoglycan in zebrafish embryos and examined the role of delta-sarcoglycan in zebrafish embryonic development by morpholino. Strong expression of delta-sarcoglycan was observed in various muscles including those of the segment, heart, eye, jaw, pectoral fin, branchial arches, and swim bladder in zebrafish embryo. Delta-sarcoglycan was also expressed in midbrain and retina. Knockdown of delta-sarcoglycan resulted in severe abnormality in both the cardiac and skeletal muscles. Some severe ones displayed serious morphological abnormality such as hypoplastic head, linear heart, very weak heartbeats, and runtish trunk, all dead within 5 dpf. Whole-mount in situ hybridization analysis showed that adaxial cells and muscle pioneers were affected in delta-sarcoglycan knockdown embryos. In addition, absence of delta-sarcoglycan protein severely delayed the cardiac development and influenced the differentiation of cardiac muscle, and the cardiac left-right asymmetry was dramatically changed in morpholino-treated embryos. These data together suggest that delta-sarcoglycan plays an important role in early heart and muscle development.
Biochemical and Biophysical Research Communications 07/2006; 344(4):1290-9. · 2.48 Impact Factor
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Guo-Ying Huang,
Xiao-Jing Ma,
Min Huang,
Shu-Bao Chen,
Mei-Rong Huang, Yong-Hao Gui,
Shou-Bao Ning,
Tuo-Hong Zhang,
Zhong-Dong Du,
Hiroshi Yanagawa,
Tomisaku Kawasaki
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ABSTRACT: Epidemiologic features of Kawasaki disease in China is still not clear.
A questionnaire form and diagnostic guidelines for Kawasaki disease were sent to hospitals in Shanghai, which provided with pediatric medical care. All patients with Kawasaki disease diagnosed during January 1998 through December 2002 were recruited in this study.
A total of 768 patients with Kawasaki disease were reported. The incidence rates of Kawasaki disease for each year were 16.79 (1998), 25.65 (1999), 28.16 (2000), 28.05 (2001), and 36.76 (2002) per 100,000 children under 5 years of age. The male/female ratio was 1.83:1. The age at onset ranged from 1 month to 18.8 years (median: 1.8 years). The disease occurred more frequently in spring and summer. Fever was the most common clinical symptom, followed by oral changes, extremities desquamate, rash, conjunctive congestion, lymphadenopathy, extremities swelling, and crissum desquamate. Cardiac abnormalities were found in 24.3% of patients. The most common cardiac abnormality was coronary artery lesions including dilatation (68%) and aneurysm (10%). The case-fatality rate at acute stage of the disease was 0.26%. A second onset of the disease occurred in 1.82% of patients.
The incidence rate of Kawasaki disease in Shanghai is lower than that reported in Japan, but higher than those in western countries. The increasing trend in incidence, sex distribution and cardiac abnormalities are similar to those in previous reports. The seasonal distribution is similar to the report from Beijing and different from other reports.
Journal of Epidemiology 02/2006; 16(1):9-14. · 1.86 Impact Factor
