Affiliated Bayi Childrens Hospital

Beijing, China

Affiliated Bayi Childrens Hospital

Beijing, China
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Wang S.,Affiliated Bayi Childrens Hospital | Sun J.,Affiliated Bayi Childrens Hospital | Tu Y.,Affiliated Bayi Childrens Hospital | Zhu L.,Affiliated Bayi Childrens Hospital | Feng Z.,Affiliated Bayi Childrens Hospital
Experimental and Therapeutic Medicine | Year: 2017

Pyridoxine-dependent epilepsy (PDE) is a rare disorder caused by aldehyde dehydrogenase 7 family member A1 (ALDH7A1) deficiency. The present study reported on three Chinese cases of PDE with phenotypic variability for providing further insight into this disease. All three patients presented with recurrent seizures and readily responded to treatment with pyridoxine, in line with the typical symptomology of PDE. The three cases varied in their clinical manifestations with regard to the time of onset, seizure type, EEG findings and mental development. Four ALDH7A1 mutations were identified in Case 1 (c.1008+1G>A and c.871+5G>A) and Case 2 (c.977A>G and c.1463A>G). To the best of our knowledge, the present study was the first to report on the mutations c.871+5G>A and c.1463A>G. Early definitive diagnosis and timely treatment with pyridoxine was the cornerstone of management of PDE. Timely treatment was associated with excellent prognosis. A high index of suspicion in cases and early genetic testing may facilitate early diagnosis of this rare disease. © 2017, Spandidos Publications. All rights reserved.


Zhang P.,Harbin University of Commerce | Zhou W.-Q.,Affiliated Bayi Childrens Hospital | Dong X.-Z.,Harbin University of Commerce | Yang M.-H.,Beijing Institute of Pharmacology and Toxicology | Bi M.-G.,Harbin University of Commerce
Chinese Journal of Pharmacology and Toxicology | Year: 2010

OBJECTIVE: To screen 6′-hydroxy justicidin A(JR6)-sensitive tumor cells and explore the cell redox function. METHODS: The human bladder cancer cells EJ, human liver cancer cells Bel, human lung cancer cells A549, human colon cancer cells HCT-8 and HT-29, human gastric cancer cells BGC, human colorectal cancer cells LS180, human cervical cancer cells HeLa, human hepatoma cells HepG2, and human breast cancer cells MCF-7 were divided into normal control group, positive control cisplatin, doxorubicin, teniposide, etoposide, 5-fluorouracil groups and JR6 group. The effect of JR6 and positive drugs on inhibition in 10 tumor cell lines for 48 h was measured using MTT method and the values of IC 50 were calculated by the methods of curvilinear regression. After EJ cells were cultured with JR6 3.02, 9.07, 27.2, 81.7 and 245 μmol·L -1 for 48 h, the activities of superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), and catalase (CAT) as wall as the content of malondialdehyde (MDA) in EJ cells were detected. EJ cells were divided into exogenous SOD +doxorubicin 9.19 μmol·L -1 and exogenous SOD + JR6 3.02, 9.07, 27.2, 81.7 and 245 μmol·L -1 groups. Proliferation of sensitive cells was measured by MTT method. After EJ cells were cultured with doxorubicin 9.19 μmol·L -1 and JR6 12.3 , 49.0 and 196 μmol·L -1 for 24 h, the generation of reactive oxygen species in JR6-sensitive tumor cells was measured by laser scanning confocal microscopy. RESULTS: MTT assay results showed EJ cells were sensitive to JR6, and IC 50 of JR6 in EJ cells was 57.1 μmol·L -1, while IC 50 of JR6 in other tumor cells ranged from 71.3 to 124 μmol·L -1. Compared with normal control group, doxorubicin 9.19 μmol·L -1 decreased activities of SOD by (64.3 ± 2.1)%, GSH-Px by (66.5 ± 3.5)% and CAT by (49.6 ± 1.9)%, but increased the content of MDA by (432 ± 5.4)% in EJ cells (P < 0.01). JR6 3.02, 9.07, 27.2, 81.7 and 245 μmol·L -1 significantly decreased activities of SOD (7.28 ± 0.3)%, (57.1 ± 3.2)%, (66.5 ± 4.7)%, (72.1 ± 5.5)% and (78.7 ± 2.4)%, decreased GSH-Px (20.3 ± 1.6)%, (32.8 ± 2.3)%, (45.3 ± 3.6)%, (59.3 ± 4.5)% and (71.9 ± 4.2)%, decreased CAT (10.1 ± 0.6)%, (15.9 ± 0.7)%, (25.9 ± 2.3)%, (38.8 ± 3.5)%, (52.4 ± 3.9)% in EJ cells, respectively; and JR6 3.02, 9.07, 27.2, 81.7 and 245 μmol·L -1 raised the content of MDA (24.4 ± 1.3)%, (90.2 ± 8.7)%, (217.0 ± 19.0)%, (356.0 ± 24.0)% and (539.0 ± 32.0)%, respctively. Exogenous SOD could protect against the inhibition effect of doxorubicin 9.19 μmol·L -1 and JR6 3.02, 9.07, 27.2, 81.7 and 245 μmol·L -1 on EJ cells, compared with no exogenous SOD group (P < 0.05). Compared with normal control group, doxorubicin 9.19 μmol·L -1 increased content of reactive oxygen species by (43.0 ± 2.1)%, JR6 12.3, 49.0 and 196 μmol·L -1 increased contents of reactive oxygen species by (40.7 ± 0.7)%, (84.1 ± 6.3)% and (151.0 ± 2.9)%, respectively. CONCLUSION: The human bladder cancer cell line EJ is JR6-sensitive. JR6 interferes the intracellular balance of redox system to inhibit proliferation of EJ cells. Exogenous SOD can protect against the inhibition effect of JR6 in EJ cells.


Zhou G.,Xijing Hospital | Zhou G.,Affiliated Bayi Childrens Hospital | Feng Z.,Affiliated Bayi Childrens Hospital | Xiong H.,Central Hospital of xiAn | And 2 more authors.
Journal of Cardiothoracic and Vascular Anesthesia | Year: 2013

Objective: To investigate the clinical effects of a combined ultrafiltration strategy on the surgical treatment of pediatric patients with congenital heart diseases. Design: A prospective, randomized, controlled study. Setting: A single-institution study in an affiliated hospital of a university. Participants: Sixty-five pediatric patients who underwent open heart surgery with cardiopulmonary bypass (CPB) to treat congenital heart disease were enrolled. The participants were randomized into 2 groups: conventional + modified ultrafiltration (MUF) (CM) group and prime + zero-balanced + MUF (PZM) group. Interventions: In the CM group (n = 33), conventional ultrafiltration was performed after removal of the aortic clamp, and MUF was performed after the completion of CPB. In the PZM group (n = 32), ultrafiltration was performed for the circuit prime solution, zero-balance ultrafiltration was performed after removal of the aortic clamp, and MUF was performed after the completion of CPB. Measurements and Main Results: The blood gas parameters and tumor necrosis factor alpha content in the priming solution and perioperative blood samples were analyzed. Postoperative parameters, including mechanical ventilation time, respiratory indices, intensive care unit time, and hospital time, also were recorded. One hospital death occurred in each group. No severe complications occurred in either group. The lactic acid, glucose, and tumor necrosis factor alpha contents in the priming solution and perioperative blood samples were significantly lower in the PZM group compared with the CM group. The respiratory indices were statistically significantly better in the PZM group compared with the CM group in the early postoperative period. No significant differences were found between the 2 groups regarding the postoperative ventilation time, inotropic support, homologous blood transfusion, drainage, intensive care unit time, or postoperative hospital time. Conclusion: The combined use of ultrafiltration of prime solution, zero-balance ultrafiltration, and MUF strategy is associated with a modest improvement in pulmonary function compared with the combination of conventional and MUF strategies in the early postoperative period, but the principal clinical outcomes are similar. © 2013 Elsevier Inc. All rights reserved.


Yin X.,Affiliated Bayi Childrens Hospital | Li L.,Affiliated Bayi Childrens Hospital | Zhang X.,Affiliated Bayi Childrens Hospital | Yang Y.,Affiliated Bayi Childrens Hospital | And 3 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2013

Objective: This study aimed to investigate the development of neural stem cells (NSCs) in fetal brain, which may provide experimental evidence for the clinical treatment of brain injury in children. Methods: A total of 60 fetuses were collected after labor induction and divided into 6 groups according to the gestational age (16 w, 20 w, 24 w, 28 w, 32 w and 36 w; n=10 per group). The hippocampus, striatum, subventricular zone, frontal lobe, temporal lobe, occipital lobe and parietal lobe were harvested. In situ hybridization, immunohistochemistry and light microscopy were done to determine the morphology and quantity of NSCs. Results: NSCs were identified in the brain of fetuses with different gestational age. NSCs were round, oval, spindle-shaped, starlike, triangular or polygonal. NSC colony was also observed with symmetrical or asymmetrical division. Single NSC, group-like NSCs and cluster-like NSCs were found in the different sites of fetal brain, and NCSs interacted with each other via synapses. However, the distribution, morphology, growth and quantity of NSCs were different in the brain of fetuses with different gestational age. The number of NSCs reduced with the increase in gestational age, but they were always observed. Conclusion: The morphology of NSCs in fetal brain is variable and they are widely distributed in the hippocampus, subventricular zone, striatum and cortex. The number of NSCs reduced with the increase of gestational age.


Yin X.,Affiliated Bayi Childrens Hospital | Meng F.,The No302 Hospital Of Pla | Wang Y.,Affiliated Bayi Childrens Hospital | Wei W.,Affiliated Bayi Childrens Hospital | And 3 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2013

Objective: To investigate the mechanism underlying the effect of hyperbaric oxygen (HBO) on hypoxic/ischemic brain damage (HIBD) in a neonatal rat model. Methods: A total of 30 neonatal SD rats aged 7 days were randomly assigned into control group, HIBD group and HBO group (n=10 per group). Following HIBD modeling in neonatal rats, HBO treatment was performed for consecutive 7 days. Immunohistochemistry was done to measure the expression of bone morphogenetic protein-4 (BMP-4) and nestin in the hippocampus. In situ hybridization was employed to detect the mRNA expression of BMP-4 and nestin in the hippocampus. TUNEL staining was done to detect the apoptosis of nerve cells. Results: HIBD was successfully established in the present study. Among three groups, the protein expression of BMP-4 in the hippocampus was the highest in the HBO group, and the smallest in the HIBD group. The BMP-4 expression in the HIBD group was significantly lower than that in the control group. The protein expression of nestin in the hippocampus was the highest in the HBO group, and the smallest in the HIBD group. The nestin protein expression in the hippocampus of HIBD group was significantly lower than that in the control group. The mRNA expression of BMP-4 in the hippocampus was the highest in the HBO group, and the smallest in the HIBD group. The mRNA expression of nestin in the hippocampus was the highest in the HBO group, and the smallest in the HIBD group. The number of apoptotic cells was the largest in the HIBD group, and the number of apoptotic cells in the HBO group was still larger than that in the control group (P<0.01). Conclusion: HBO may promote the neurological recovery in neonatal rats with HIBD, which may be attributed to the increased protein and mRNA expression of BMP-4 and nestin in the hippocampus and the inhibition of neural apoptosis.


Chai Y.,Affiliated Bayi Childrens Hospital | Yin X.,Affiliated Bayi Childrens Hospital
Acta Medica Mediterranea | Year: 2014

Neonatal hypoxic-ischemic(H/I) brain damage is a serious complication of intrauterine asphyxia during perinatal period, eventually leading to severe long-term neurodevelopmental disability or even death. Survival babies would experience cerebral palsy, epilepsy, mental retardation, cognitive, sensory and motor dysfunctions. However, there has no proven effective treatment available to protect the brain against injury after H/I occurs, because the exact timing of the hypoxic-ischemic event is unknown and we hardly identify the phase of injury or recovery in an individual patient precisely. In recent years, much effort has been made on the understandings of the H/I damages in the brain and underlying mechanisms of neural dysfunction, expecting the intervention of targeted neuroprotection in the newborn stage. We briefly summarize recent findings of the pathogenesis of hypoxic-ischemic injury with an emphasis on the disturbed neurogenesis process in the brain; the potential role of neural regeneration in basic and clinical research, including the endogenous stem cells mobilization and cell transplantation aiming to enhance the brain function.


PubMed | Affiliated Bayi Childrens Hospital and PLA Fourth Military Medical University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Patients with essential hypertension undergo endothelial dysfunction, particularly in the conduit arteries. Cilostazol, a type III phosphodiesterase inhibitor, serves a role in the inhibition of platelet aggregation and it is widely used in the treatment of peripheral vascular diseases. Previous studies have suggested that cilostazol suppresses endothelial dysfunction; however, it remains unknown whether cilostazol protects the endothelial function in essential hypertension. The aim of the present study was to investigate whether, and how, cilostazol suppresses angiotensin II (angII)induced endothelial dysfunction. Human umbilical vein endothelial cells (HUVECs) and Sprague Dawley rats were exposed to angII and treated with cilostazol. Endothelial cell apoptosis and function, nitric oxide and superoxide production, phosphorylation (p) of Akt, and caspase3 protein expression levels were investigated. AngII exposure resulted in the apoptosis of endothelial cells in vitro and in vivo. In vitro, cilostazol significantly suppressed the angIIinduced apoptosis of HUVECs; however, this effect was reduced in the presence of LY294002, a phosphoinositide 3 kinase (PI3K) inhibitor. Furthermore, cilostazol suppressed the angIIinduced pAkt downregulation and cleaved caspase3 upregulation. These effects were also alleviated by LY294002. In vivo, cilostazol suppressed the angIIinduced endothelial cell apoptosis and dysfunction. Cilostazol was also demonstrated to partially reduced the angIIinduced increase in superoxide production. The results of the present study suggested that cilostazol suppresses endothelial apoptosis and dysfunction by modulating the PI3K/Akt pathway.


PubMed | Affiliated Bayi Childrens Hospital
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2014

To investigate value of amplitude-integrated electroencephalograph (aEEG) in early diagnosis and prediction of long-term prognosis of neonatal hypoxic-ischemic encephalopathy (HIE), 120 HIE Children were randomly assigned into aEEG group and control group (n = 60 per group). Children in each group were sub-divided into mild, moderate and severe HIE groups (n = 20 per group). 1, 3, 14 and 28 days after birth, aEEG was performed in aEEG group; 3, 14 and 28 days after birth, neonatal behavioral neurological assessment (NBNA) was done in both groups. Children who discharged were followed up at adjusted gestational age of 12 months with Denver Developmental Screening Test (DDST) and prognosis evaluation.aEEG manifestation was positively related to clinical severityb of HIE (r = 0.843, P < 0.01). On day 3 and 14, NBNA score was comparable between two groups (P > 0.05), but significant difference in NBNA score was noted on day 28 (P < 0.05). On day 3, 14 and 28, aEEG manifestation was positively associated with prognosis at adjusted gestational age of 12 months (r = 0.832, 0.857, 0.778, 0.743, P < 0.01). In aEEG group, disability rate was 13.8%, which was significantly lower than that in control group (23.2%); cure rate in aEEG group (60%) was significantly higher than that in control group (40%). Moreover, long-term prognosis was also dramatically different between aEEG group and control group ((2) = 4.107, P < 0.05).aEEG manifestation is significantly associated with clinical severity of HIE and may be helpful for early diagnosis of HIE. aEEG may be used to predict long term prognosis of HIE children.


PubMed | Affiliated Bayi Childrens Hospital
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2013

This study aimed to investigate the development of neural stem cells (NSCs) in fetal brain, which may provide experimental evidence for the clinical treatment of brain injury in children.A total of 60 fetuses were collected after labor induction and divided into 6 groups according to the gestational age (16 w, 20 w, 24 w, 28 w, 32 w and 36 w; n=10 per group). The hippocampus, striatum, subventricular zone, frontal lobe, temporal lobe, occipital lobe and parietal lobe were harvested. In situ hybridization, immunohistochemistry and light microscopy were done to determine the morphology and quantity of NSCs.NSCs were identified in the brain of fetuses with different gestational age. NSCs were round, oval, spindle-shaped, starlike, triangular or polygonal. NSC colony was also observed with symmetrical or asymmetrical division. Single NSC, group-like NSCs and cluster-like NSCs were found in the different sites of fetal brain, and NCSs interacted with each other via synapses. However, the distribution, morphology, growth and quantity of NSCs were different in the brain of fetuses with different gestational age. The number of NSCs reduced with the increase in gestational age, but they were always observed.The morphology of NSCs in fetal brain is variable and they are widely distributed in the hippocampus, subventricular zone, striatum and cortex. The number of NSCs reduced with the increase of gestational age.


PubMed | Affiliated Bayi Childrens Hospital
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2015

To investigate the relationship between Surfactant protein B (SP-B) gene polymorphisms and bronchopulmonary dysplasia (BPD) development in preterm infants of China Han ethnic population.SP-B gene polymorphisms were studied in 134 neonates who were born at <32 weeks of gestation, with the diagnosis of BPD and in a control group of 168 preterm infants without BPD. Genotyping for SP-B was performed by polymerase chain reaction (PCR) and gene sequencing.In this study, three of the SNP genotypes, -18C/A, 1580C/T and 4564T/C were common identified in SP-B gene. The -18C/A genotype was found to be significantly associated with BPD (2=10.741, P<0.01), with P<0.01 for the dominant model (OR=1.712, 95% CI=1.228-2.3894) and the allelic model (OR=1.787, 95% CI=1.276-2.502). The 1580C/T genotype was found to be associated with BPD (2=7.014, P<0.05), with P<0.05 for the dominant model (OR=0.752, 95% CI=0.593-0.954) and P<0.01 for the allelic model (OR=0.706, 95% CI=0.548-0.909). The 4564T/C genotypes and alleles were found not to be associated with BPD (2=3.399 and 3.227, P>0.05).SP-B -18C/A and 1580C/T polymorphisms are associated with BPD. The 1580C/T polymorphism was protective while the -18C/A polymorphism increased the risk for BPD. SP-B 4564T/C polymorphism is not associated with BPD.

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