BaYi Childrens Hospital of the General Military Hospital of Beijing PLA

Beijing, China

BaYi Childrens Hospital of the General Military Hospital of Beijing PLA

Beijing, China
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Zhang X.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | Xu J.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | Xu J.,Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region | Wang J.,Shanghai University | And 7 more authors.
PLoS ONE | Year: 2013

Objective:To characterize microRNA-206 (miR-206) in the development of bronchopulmonary dysplasia (BPD).Design/Methods:We assessed the expression of miR-206 in BPD mouse lung tissues and blood samples of BPD patients by quantitative real-time PCR. Then, the role of miR-206 in regulating cell biology were examined by XTT assay, flow cytometry, transwell invasion assay, wound healing assay and adhesion assay in vitro. Furthermore, luciferase reporter assay, real-time PCR, western blot and Immunofluorescence staining were performed to figure out the target gene of miR-206.Results:A reduction in expression of miR-206 was observed in BPD mice compared with controls and in BPD patients compared with controls. miR-206 overexpression significantly induced cell apoptosis, reduced cell proliferation, migration and adhesion abilities, whereas the inhibition of miR-206 expression had the opposite effect. Fibronectin 1 (FN1) is a direct target of miR-206, and fn 1 can be transcriptionally and translationally regulated by miR-206. Down-regulation of miR-206 modulates biological functions of the cells, at least in part, by increasing the level of fn 1. Furthermore, fn 1 expression levels were increased in the BPD mice and BPD patients.Conclusions:The expression of miR-206 and its target gene, fn 1, may contribute to the progression of BPD. © 2013 Zhang et al.


Zhang X.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | Wang H.,The General Military Hospital of Beijing PLA | Shi Y.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | Peng W.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | And 5 more authors.
Cell Biology International | Year: 2012

BPD (bronchopulmonary dysplasia) is predominantly characterized by persistent abnormalities in lung structure and arrested lung development, but therapy can be palliative. While promising, the use of BMSC (bone marrow-derived mesenchymal stem cell) in the treatment of lung diseases remains controversial. We have assessed the therapeutic effects of BMSC in vitro and in vivo. In vitro co-culturing with injured lung tissue increased the migration-potential of BMSC; and SP-C (surfactant protein-C), a specific marker of AEC2 (type II alveolar epithelial cells), was expressed. Following intraperitoneal injection of BMSC into experimental BPD mice on post-natal day 7, it was found that BMSC can home to the injured lung, express SP-C, improve pulmonary architecture, attenuate pulmonary fibrosis and increase the survival rate of BPD mice. This work supports the notion that BMSC are of therapeutic benefit through the production of soluble factors at bioactive levels that regulate the pathogenesis of inflammation and fibrosis following hyperoxia. © The Author(s) Journal compilation © 2012 International Federation for Cell Biology.


Hua S.,BaYi Childrens Hospital of the General Military Hospital of Beijing PLA | Huang J.,BaYi Childrens Hospital of the General Military Hospital of Beijing PLA | Wu Z.,BaYi Childrens Hospital of the General Military Hospital of Beijing PLA | Feng Z.,BaYi Childrens Hospital of the General Military Hospital of Beijing PLA
Turkish Journal of Pediatrics | Year: 2012

In this study, we aimed to investigate the clinical characteristics of Candida parapsilosis sepsis in preterm infants. In this retrospective analysis of the clinical data of 11 cases of Candida parapsilosis sepsis and 13 cases of C. albicans sepsis, the two groups were compared for research using one-way analysis of variance (one-way ANOVA), χ2 test, and non-conditional logistic regression analysis. Compared to the C. albicans sepsis group, the C. parapsilosis group demonstrated a significantly lower birth weight (1331.8±252.41 vs. 1721.2±589.08) and significantly longer hospital stay (69.909±20.782 vs. 38.385±19.923) (t'/t = 2.160, -3.787; p=0.045, 0.01, respectively); the incidences of retinopathy of prematurity (ROP) (72.7% vs. 30.8%), tienam administration (72.7% vs. 23.1%), pneumothorax, and thoracic closed drainage (27.3% vs. 0) were higher (χ2=4.196, 5.916, 4.052; p=0.041, 0.015, 0.044, respectively). Logistic regression analysis indicated only hospital stay and tienam administration in the regression equation (χ2=18.008, p=0.000). Compared with C. albicans sepsis, an average length hospital stay and administration of tienam are the high-risk factors for C. parapsilosis sepsis. With regard to the other predisposing factors of preterm infant fungal sepsis, there were no differences between the two groups.


Yin Y.,Beijing Institute of Biotechnology | Zhang S.,Beijing Institute of Biotechnology | Zhang S.,BaYi Childrens Hospital of The General Military Hospital of Beijing PLA | Cai C.,Beijing Institute of Biotechnology | And 6 more authors.
Immunobiology | Year: 2014

Protective antigen (PA) is one of the major virulence factors of anthrax and is also the major constituent of the current anthrax vaccine. Previously, we found that the 2β2-2β3 loop of PA contains a dominant neutralizing epitope, the SFFD. We successfully inserted the 2β2-2β3 loop of PA into the major immunodominant region (MIR) of hepatitis B virus core (HBc) protein. The resulting fusion protein, termed HBc-N144-PA-loop2 (HBcL2), can effectively produce anthrax specific protective antibodies in an animal model. However, the protective immunity caused by HBcL2 could still be improved. In this research, we removed amino acids 79-81 from the HBc MIR of the HBcL2. This region was previously reported to be the major B cell epitope of HBc, and in keeping with this finding, we observed that the short deletion in the MIR not only diminished the intrinsic immunogenicity of HBc but also stimulated a higher titer of anthrax specific immunity. Most importantly, this deletion led to the full protection of the immunized mice against a lethal dose anthrax toxin challenge. We supposed that the conformational changes which occurred after the short deletion and foreign insertion in the MIR of HBc were the most likely reasons for the improvement in the immunogenicity of the HBc-based anthrax epitope vaccine. © 2013 Elsevier GmbH.


Wang Y.,Bayi Childrens Hospital Of The General Military Hospital Of Beijing Pla | Yin X.-J.,Bayi Childrens Hospital Of The General Military Hospital Of Beijing Pla | Han T.,Bayi Childrens Hospital Of The General Military Hospital Of Beijing Pla | Peng W.,Bayi Childrens Hospital Of The General Military Hospital Of Beijing Pla | And 3 more authors.
Molecular Genetics and Genomics | Year: 2014

Treacher Collins syndrome (TCS) is the most common and well-known craniofacial disorder caused by mutations in the genes involved in pre-rRNA transcription, which include the TCOF1 gene. This study explored the role of TCOF1 mutations in Chinese patients with TCS. Mutational analysis of the TCOF1 gene was performed in three patients using polymerase chain reaction and direct sequencing. Among these three patients, two additional TCOF1 variations, a novel 18 bp deletion and a novel 1 bp insertion mutation, were found in patient 1, together with a novel nonsense mutation (p.Ser476X) and a previously reported 4 bp deletion (c.1872_1875delTGAG) in other patients. Pedigree analysis allowed for prediction of the character of the mutation, which was either pathological or not. The 18 bp deletion of six amino acids, Ser-Asp-Ser-Glu-Glu-Glu (798*803), which was located in the CKII phosphorylation site of treacle, seemed relatively benign for TCS. By contrast, another novel mutation of c.1072_1073insC (p.Gln358ProfsX23) was a frameshift mutation and expected to result in a premature stop codon. This study provides insights into the functional domain of treacle and illustrates the importance of clinical and family TCS screening for the interpretation of novel sequence alterations. © 2014, Springer-Verlag Berlin Heidelberg.


Wang Y.,BaYi Childrens Hospital of the General Military Hospital of Beijing PLA
Molecular genetics and genomics : MGG | Year: 2014

Duchenne/Becker muscular dystrophies are the most frequent inherited neuromuscular diseases caused by mutations of the dystrophin gene. However, approximately 30% of patients with the disease do not receive a molecular diagnosis because of the complex mutational spectrum and the large size of the gene. The introduction and use of next-generation sequencing have advanced clinical genetic research and might be a suitable method for the detection of various types of mutations in the dystrophin gene. To identify the mutational spectrum using a single platform, whole dystrophin gene sequencing was performed using next-generation sequencing. The entire dystrophin gene, including all exons, introns and promoter regions, was target enriched using a DMD whole gene enrichment kit. The enrichment libraries were sequenced on an Illumina HiSeq 2000 sequencer using paired read 100 bp sequencing. We studied 26 patients: 21 had known large deletion/duplications and 5 did not have detectable large deletion/duplications by multiplex ligation-dependent probe amplification technology (MLPA). We applied whole dystrophin gene analysis by next-generation sequencing to the five patients who did not have detectable large deletion/duplications and to five randomly chosen patients from the 21 who did have large deletion/duplications. The sequencing data covered almost 100% of the exonic region of the dystrophin gene by ≥10 reads with a mean read depth of 147. Five small mutations were identified in the first five patients, of which four variants were unreported in the dmd.nl database. The deleted or duplicated exons and the breakpoints in the five large deletion/duplication patients were precisely identified. Whole dystrophin gene sequencing by next-generation sequencing may be a useful tool for the genetic diagnosis of Duchenne and Becker muscular dystrophies.


PubMed | Institute of Health and Environmental medicine, Qingdao University and BaYi Childrens Hospital of The General Military Hospital of Beijing PLA
Type: | Journal: Scientific reports | Year: 2015

Small interfering RNAs (siRNAs) directed against poliovirus (PV) and other viruses effectively inhibit viral replication and have been developed as antiviral agents. Here, we demonstrate that a specific siRNA targeting the region between nucleotides 100-125 (siRNA-100) from the 5-untranslated region (5-UTR) of PV plays a critical role in inhibiting PV replication. Our data demonstrate that siRNA-100 treatment can greatly reduce PV titers, resulting in up-regulation of host microRNA-7 (miR-7), which in turn, leads to enhance inhibition of PV infection further. Moreover, our results suggest that siRNA-100 can also impair the spread of PV to uninfected cells by increasing host resistance to PV, resulting in decreasing necrosis and cytopathic effects (CPE) levels, as well as prolonging the survival of infected cells. Indeed, the active antiviral effect of siRNA-100 was potentially supplemented by the activity of miR-7, and both of them can serve as stabilizing factors for maintenance of cellular homeostasis. Results of this study identify a molecular mechanism of RNAi for antiviral defense, and extend our knowledge of the complex interplay between host and PV, which will provide a basis for the development of effective RNAi-based therapies designed to inhibit PV replication and protect host cells.


PubMed | BaYi Childrens Hospital of the General Military Hospital of Beijing PLA
Type: Journal Article | Journal: Molecular genetics and genomics : MGG | Year: 2014

Duchenne/Becker muscular dystrophies are the most frequent inherited neuromuscular diseases caused by mutations of the dystrophin gene. However, approximately 30% of patients with the disease do not receive a molecular diagnosis because of the complex mutational spectrum and the large size of the gene. The introduction and use of next-generation sequencing have advanced clinical genetic research and might be a suitable method for the detection of various types of mutations in the dystrophin gene. To identify the mutational spectrum using a single platform, whole dystrophin gene sequencing was performed using next-generation sequencing. The entire dystrophin gene, including all exons, introns and promoter regions, was target enriched using a DMD whole gene enrichment kit. The enrichment libraries were sequenced on an Illumina HiSeq 2000 sequencer using paired read 100 bp sequencing. We studied 26 patients: 21 had known large deletion/duplications and 5 did not have detectable large deletion/duplications by multiplex ligation-dependent probe amplification technology (MLPA). We applied whole dystrophin gene analysis by next-generation sequencing to the five patients who did not have detectable large deletion/duplications and to five randomly chosen patients from the 21 who did have large deletion/duplications. The sequencing data covered almost 100% of the exonic region of the dystrophin gene by 10 reads with a mean read depth of 147. Five small mutations were identified in the first five patients, of which four variants were unreported in the dmd.nl database. The deleted or duplicated exons and the breakpoints in the five large deletion/duplication patients were precisely identified. Whole dystrophin gene sequencing by next-generation sequencing may be a useful tool for the genetic diagnosis of Duchenne and Becker muscular dystrophies.


PubMed | PLA Fourth Military Medical University and BaYi Childrens Hospital of The General Military Hospital of Beijing PLA
Type: Journal Article | Journal: PloS one | Year: 2014

In this study, we evaluated the effect of astragaloside IV (Ast IV) post-ischemia treatment on myocardial ischemia-reperfusion (IR) injury (IRI). We also examined whether hypoxia inducible factor-1 (HIF-1) and its downstream gene-inducible nitric oxide (NO) synthase (iNOS) play roles in the cardioprotective effect of Ast IV. Cultured cardiomyocytes and perfused isolated rat hearts were exposed to Ast IV during reperfusion in the presence or absence of the HIF-1 inhibitor 2-methoxyestradiol (2-MeOE2). The post-ischemia treatment with Ast IV protected cardiomyocytes from the apoptosis and death induced by simulated IRI (SIRI). Additionally, in cardiomyocytes, 2-MeOE2 and HIF-1 siRNA treatment each not only abolished the anti-apoptotic effect of post-ischemia treatment with Ast IV but also reversed the upregulation of HIF-1 and iNOS expression. Furthermore, after treatment with Ast IV, post-ischemic cardiac functional recovery and lactate dehydrogenase (LDH) release in the coronary flow (CF) were improved, and the myocardial infarct size was decreased. Moreover, the number of apoptotic cells was reduced, and the upregulation of the anti-apoptotic protein Bcl2 and downregulation of the pro-apoptotic protein Caspase3 were reversed. 2-MeOE2 reversed these effects of Ast IV on IR-injured hearts. These results suggest that post-ischemia treatment with Ast IV can attenuate IRI by upregulating HIF-1 expression, which transmits a survival signal to the myocardium.


PubMed | BaYi Childrens Hospital of the General Military Hospital of Beijing PLA
Type: Case Reports | Journal: Molecular genetics and genomics : MGG | Year: 2014

Treacher Collins syndrome (TCS) is the most common and well-known craniofacial disorder caused by mutations in the genes involved in pre-rRNA transcription, which include the TCOF1 gene. This study explored the role of TCOF1 mutations in Chinese patients with TCS. Mutational analysis of the TCOF1 gene was performed in three patients using polymerase chain reaction and direct sequencing. Among these three patients, two additional TCOF1 variations, a novel 18 bp deletion and a novel 1 bp insertion mutation, were found in patient 1, together with a novel nonsense mutation (p.Ser476X) and a previously reported 4 bp deletion (c.1872_1875delTGAG) in other patients. Pedigree analysis allowed for prediction of the character of the mutation, which was either pathological or not. The 18 bp deletion of six amino acids, Ser-Asp-Ser-Glu-Glu-Glu (798*803), which was located in the CKII phosphorylation site of treacle, seemed relatively benign for TCS. By contrast, another novel mutation of c.1072_1073insC (p.Gln358ProfsX23) was a frameshift mutation and expected to result in a premature stop codon. This study provides insights into the functional domain of treacle and illustrates the importance of clinical and family TCS screening for the interpretation of novel sequence alterations.

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