Shanghai Childrens Medical Center

Shanghai, China

Shanghai Childrens Medical Center

Shanghai, China
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Xu Z.W.,Shanghai Childrens Medical Center | Shen J.,Shanghai JiaoTong University
Journal of Cardiac Surgery | Year: 2010

Objective: To find a better method of right ventricular-pulmonary artery (RV-PA) reconstruction in repairing truncus arteriosus (TA). Basic studies design: Retrospective clinical study, contrast study. Clinical setting: Shanghai Children's Medical Center. Participants: 23 patients with truncus arteriosus. Intervention: To decrease the man-made interference, all of the exams during the follow-up period were carried out at our center. Main outcome measurements: Hospital death, survival rate, the later outcomes during follow-up including the growth of pulmonary artery, the later heart function, and reintervention. Results: There were two early hospital deaths, with no deaths during follow-up. The overall survival rate was 91.30%. One patient underwent reintervention for RVOTO. In Group 1, the difference between the diameters of RV-PA anastomosis was statistically significant. The early diameter was 1.01 ± 0.26 cm, the later was 1.32 ± 0.45 cm, p = 0.019. The velocity of flow at the position of anastomosis and the orifice of RPA/LPA was acceptable. There was a significant difference between the growth ratio of the RV-PA anastomosis of two groups, with a p value of 0.048. The later ejection fraction was higher than the early one in both groups. There was no reintervention for truncal valve regurgitation. Conclusions: The postoperative survival and follow-up results were satisfactory. A direct anastomosis of RV-PA continuity has the potential for RVOT growth and is associated with a low ratio of pulmonary artery and bifurcation obstruction. The myocardial function improved during follow-up period. IAA was a major risk factor associated with hospital death. © 2010 Wiley Periodicals, Inc.


Deng Z.H.,Shanghai Childrens Medical Center
Zhonghua er ke za zhi. Chinese journal of pediatrics | Year: 2012

To explore an innovative technique that is aided by multi-disciplinary hybrid approach in identification and treatment of tracheoesophageal fistula (TEF) in children intraoperatively. From April 2008 to October 2011, 4 patients with isolated TEF were presented with 2 H-type fistulas and 2 recurrent TEF. For all the four cases, with the cooperation of the gastroenterologists, respiratory physician and surgeon, methylene blue was first injected into the trachea for detecting the dye in the esophagus by the gastroscopy. Bronchoscopy was performed where the fistula tract was shown by the methylene blue and a guide wire was passed through the fistula. The patients underwent rigid gastroscopy and the guide wire was identified and brought out through the mouth by biopsy pliers. This created a wire loop through the fistula. X-ray was then used to identify the level of the fistula. According to the level of the fistula it was determined whether surgical incision and approach should be used. The fistula was then repaired successfully by surgery. In the 4 patients, with the aid of gastroscopy and bronchoscopy, identification of the fistula intraoperatively was then facilitated by traction on the loop. The fistula was identified and repaired. There were no fistula recurrences. Multi-disciplinary hybrid therapy for tracheoesophageal fistula in children is beneficial for the precise localization of the fistula. This new technique is an effective and definitive method in identification and treatment of TEF in children.


Chou F.-S.,Cincinnati Childrens Hospital Medical Center | Griesinger A.,Cincinnati Childrens Hospital Medical Center | Wunderlich M.,Cincinnati Childrens Hospital Medical Center | Lin S.,Cincinnati Childrens Hospital Medical Center | And 8 more authors.
Blood | Year: 2012

AML1-ETO (AE) is a fusion product of translocation (8;21) that accounts for 40% of M2 type acute myeloid leukemia (AML). In addition to its role in promoting preleukemic hematopoietic cell self-renewal, AE represses DNA repair genes, which leads to DNA damage and increased mutation frequency. Although this latter function may promote leukemogenesis, concurrent p53 activation also leads to an increased baseline apoptotic rate. It is unclear how AE expression is able to counterbalance this intrinsic apoptotic conditioning by p53 to promote survival and self-renewal. In this report, we show that Bcl-xL is up-regulated in AE cells and plays an essential role in their survival and self-renewal. Further investigation revealed that Bcl-xL expression is regulated by thrombopoietin (THPO)/MPL-signaling induced by AE expression. THPO/MPL-signaling also controls cell cycle reentry and mediates AE-induced self-renewal. Analysis of primary AML patient samples revealed a correlation between MPL and Bcl-xL expression specifically in t(8;21) blasts. Taken together, we propose that survival signaling through Bcl-xL is a critical and intrinsic component of a broader self-renewal signaling pathway downstream of AML1-ETO-induced MPL. © 2012 by The American Society of Hematology.


Duan C.-W.,Shanghai JiaoTong University | Shi J.,Sixth People Hospital | Chen J.,Shanghai Childrens Medical Center | Wang B.,Shanghai JiaoTong University | And 13 more authors.
Cancer Cell | Year: 2014

Residence of cancer-propagating cells (CPCs) within preferential microenvironmental niches has a major part in evading therapy. However, the nature of niches involved and the mechanisms protecting CPCs remain largely unknown. We addressed these issues in mouse transplantation models of acute lymphoblastic leukemia (ALL). When the engrafted leukemic cells substantially damaged adjacent microenvironment in the bone marrow (BM), after chemotherapy small foci of CPCs were retained, surrounded by sheaths of supporting cells that comprise a protective niche. We investigated patients' BM biopsies and found evidence of a similar process in patients receiving induction therapy. The efficacy of chemotherapy was enhanced by interfering with the niche formation or function. We therefore identified a therapy-induced niche that protects CPCs. © 2014 Elsevier Inc.


Hu C.-E.,Fudan University | Liu Y.-C.,Fudan University | Zhang H.-D.,Shanghai Childrens Medical Center | Huang G.-J.,Fudan University
Biochemical and Biophysical Research Communications | Year: 2014

Gastric carcinoma is the fourth most common cancer worldwide, with a high rate of death and low 5-year survival rate. However, the mechanism underling gastric cancer is still not fully understood. Here in the present study, we identify the RNA-binding protein PCBP2 as an oncogenic protein in human gastric carcinoma. Our results show that PCBP2 is up-regulated in human gastric cancer tissues compared to adjacent normal tissues, and that high level of PCBP2 predicts poor overall and disease-free survival. Knockdown of PCBP2 in gastric cancer cells inhibits cell proliferation and colony formation in vitro, whereas opposing results are obtained when PCBP2 is overexpressed. Our in vivo subcutaneous xenograft results also show that PCBP2 can critically regulate gastric cancer cell growth. In addition, we find that PCBP2-depletion induces apoptosis in gastric cancer cells via up-regulating expression of pro-apoptotic proteins and down-regulating anti-apoptotic proteins. Mechanically, we identify that miR-34a as a target of PCBP2, and that miR-34a is critically essential for the function of PCBP2. In summary, PCBP2 promotes gastric carcinoma development by regulating the level of miR-34a. © 2014 Elsevier Inc. All rights reserved.


Cheng X.,Anhui Medical University | Huang Y.,Shanghai Childrens Medical Center | Zhao Q.,Anhui Medical University | Gu E.,Anhui Medical University
Journal of Anaesthesiology Clinical Pharmacology | Year: 2014

Background: Children with obstructive sleep apnea (OSA) are particularly at risk under anesthesia after uvulopalatopharyngoplasty (UPPP). This prospective randomized double-blind study focused on the comparison of dexmedetomidine- ketamine and sevoflurane-sufentanil anesthesia on children with respect to safety, feasibility, and clinical effects. Materials and Methods: A total of 60 children, aged 2-10 years, classified as American Society of Anesthesiologists (ASA) status I and II scheduled for UPPP were prospectively studied. Patients were randomly allocated to receive either dexmedetomidine-ketamine-based anesthesia (group DK, n = 30) or sevoflurane-sufentanil-based anesthesia (group SS, n = 3 0). Heart rate (HR) and systolic blood pressure during the first 60 min of the procedure, Ramsay sedation score, the Pediatric Anesthesia Emergence Delirium (PAED) scale and a 5-point scale used to evaluate emergence agitation (EA) in postanesthesia care unit (PACU) and postoperative outcomes data were recorded. Results: During the first 60 min of anesthesia, mean HR, and mean diastolic noninvasive arterial blood pressure (NIBP) were not statistically different in the two groups (P > 0.05) Compared with group SS, the patients in group DK had lower rescue tramadol requirement and lower pain score, PAED score, and EA score at 5, 10, 15, and 30 min in PACU; but had a higher Ramsay scale at 10, 15, 30, 45, and 60 min in PACU and the incidence of SpO 2 below 95%, also the time of first bowel movement and ambulation in group DK was shorter. Conclusions: The dexmedetomidine-ketamine combination was not superior to a sevoflurane-sufentanil combination because of late awake time and a high potential for adverse respiratory events in PACU, the benefit of dexmedetomidine administration being a decreased incidence of EA and a lower recovery time of bowel movement and ambulation.


Hu C.-E.,Fudan University | Liu Y.-C.,Fudan University | Zhang H.-D.,Shanghai Childrens Medical Center | Huang G.-J.,Fudan University
Biochemical and Biophysical Research Communications | Year: 2014

A number of JmjC domain-containing histone demethylases have been identified and biochemically characterized in mammalian. JMJD2A is a transcriptional cofactor and enzyme that catalyzes demethylation of histone H3 lysines 9 and 36. Here in this study, we aim to explore the role of JMJD2A in human gastric cancer. Quantitative real-time PCR, Western blot and immunohistochemistry analyses reveal higher expression of JMJD2A in clinical gastric cancer tissues than that in normal gastric mucosa. JMJD2A expression is associated with tumor stage and nodal status, and high level of JMJD2A predicts poor overall and disease-free survival. Univariate and multivariate survival analyses demonstrate that JMJD2A could serve as an independent prognostic factor. Furthermore, we show that inhibition the expression of JMJD2A attenuates the growth and transformation of three lines of gastric cancer cells. Mechanically, JMJD2A knockdown induces apoptosis of gastric cancer cells by up-regulating the expression of pro-apoptotic proteins and by down-regulating anti-apoptotic protein. Finally, we show that JMJD2A level is correlated with the level of the pro-apoptotic microRNA miR-34a in gastric cancer tissues and JMJD2A represses the expression of miR-34a by decreasing its promoter activity. Those findings demonstrate that JMJD2A regulates gastric cancer growth and serves as an independent prognostic factor, and implicate that JMJD2A may be a promising target for intervention. © 2014 Elsevier Inc. All rights reserved.


Sun J.,Shanghai Childrens Medical Center | Zhong L.,Shanghai First Peoples Hospital | Zhu Y.,Shanghai First Peoples Hospital | Liu G.,Shanghai First Peoples Hospital
Journal of Reproduction and Development | Year: 2011

The aim of this study was to establish a novel method for isolating and purifying Leydig cells from mice testes. Testes of postpuberal mice were harvested and digested in a low concentration of collagenase NB4 for 15 min 2 times. Cells obtained were cultured in low glucose DMEM with 10% FBS. Immunofluorescence was used to detect the expression of Leydig cell biomarkers including 3β-hydroxysteroid dehydrogenase, cholesterol side-chain cleaving enzyme (CYP11A1) and 17α-hydroxylase/17,20-lyase (CYP17A1). It was found that the purity of the isolated Leydig cells was 69.6 ± 4.16%. After 7 days in primary culture, it increased to 90%. The testosterone synthase spectrum could be detected at the primary culture. In conclusion, the application of a low concentration of collagenase for differential digestion allows isolation of large quantities of viable Leydig cells. © 2011 by the Society for Reproduction and Development.


Hu C.-E.,Fudan University | Gan J.,Fudan University | Zhang R.-D.,Shanghai Childrens Medical Center | Cheng Y.-R.,Fudan University | Huang G.-J.,Fudan University
Scandinavian Journal of Gastroenterology | Year: 2011

Objective: Defective immune function is an important cause of tumor development. Accumulation of myeloid-derived suppressor cell (MDSC) associated with inhibition of dendritic cell (DC) function is one of the major immunological abnormalities in cancer. However, the molecular mechanism of the phenomenon remains unclear. Material and methods. We evaluated T cell stimulatory activity and interleukin (IL)-12 production of DC in a mouse model of liver cancer (hepatocellular carcinoma [HCC] mice). Then we detected the frequency of MDSC in spleen, peripheral blood (PB), lymph node (LN) and tumor tissue of HCC mice and its potential mechanisms. We also evaluated IL-10 production of MDSC and mechanism by which MDSC inhibit DC function. Results. Toll-like receptor (TLR)-ligand (LPS, CpG, poly(I:C))-induced IL-12 production of DC was decreased in HCC mice compared with control. The T cell stimulatory activity of DC was lower in HCC mice than in controls. Meanwhile, an increase in the frequency of MDSC in tumor development was detected in spleen, PB, LN and tumor, and the IL-10 levels were higher in HCC mice derived MDSC than in control. Furthermore, the MDSC inhibited TLR-ligand-induced IL-12 production of DC by IL-10 production and suppressed T cell stimulatory activity of DC. Finally, we demonstrated that the increase in the frequency of MDSC was mediated by MyD88-NF-kB pathway. Conclusions. Our study suggests a new role for MDSCs in HCC development by suppressing host immune responses, and these findings have important implications when designing immunotherapy protocols. © 2011 Informa Healthcare.


Li X.,Cincinnati Childrens Hospital Medical Center | Li X.,South China Normal University | Erden O.,Cincinnati Childrens Hospital Medical Center | Li L.,Cincinnati Childrens Hospital Medical Center | And 3 more authors.
Antioxidants and Redox Signaling | Year: 2014

Aims: A component of the base excision repair pathway, poly(ADP-ribose) polymerase-1 (PARP1) functions in multiple cellular processes, including DNA repair and programmed cell death. We previously showed that Salidroside, a phenylpropanoid glycoside isolated from medicinal plants, prevented the loss of hematopoietic stem cells (HSCs) in native mice and rescued HSCs repopulating in transplanted recipients under oxidative stress. The aim of this study was to investigate the mechanism by which PARP1 activation by Salidroside maintains HSCs under oxidative stress. Results: We found that although there were no spontaneous defects in hematopoiesis in Parp1-/- mice, oxidative stress compromised the repopulating capacity of Parp1-/- HSCs in transplanted recipient mice. A biochemical study using truncated proteins lacking the defined functional domains of PARP1 showed that the tryptophan-glycine-arginine-rich (WGR) domain of PARP1 was critical for Salidroside binding and subsequent PARP1 activation under oxidative stress. Functionally, complementation of Parp1-/- HSCs with full-length PARP1WT, but not the PARP1R591K mutant in WGR domain restored Salidroside-stimulated PARP1 activation in vitro. Mechanistically, activated PARP1 by Salidroside enhanced the repopulating capacity of the stressed HSCs by accelerating oxidative DNA damage repair. Innovations and Conclusion: Our findings reveal the action of mechanism for Salidroside in PARP1 stimulation and a novel role of PARP1 activation in maintaining HSC function under oxidative stress. Antioxid. Redox Signal. 20, 1853-1865. © Copyright 2014, Mary Ann Liebert, Inc. 2014.

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