Jiangxi Childrens Hospital
Jiangxi Childrens Hospital
Wang M.,Capital Medical University |
Yang W.,Jiangxi Childrens Hospital |
Li M.,Peking University |
Li Y.,Capital Medical University
Experimental and Molecular Pathology | Year: 2014
Background: Burkitt lymphoma (BL) is a highly aggressive B-cell lymphoma with rapid proliferation. It has become evident that miRNAs are involved in hematopoietic malignancies. This study was undertaken to investigate the miRNA expression patterns of pediatric intestinal BL tissues. Methods: We collected 28 BL and 8 reactive lymphoid hyperplasia (RLH) samples. miRNA expression profiling was performed in BL and RLH tissues to identify BL-related miRNAs, which were further analyzed by qRT-PCR and miRNA-ISH. In addition, immunohistochemistry (IHC) and western blot were used to define the protein targets of the BL-related miRNAs. Furthermore, we evaluated cell growth status by using methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay in Raji cell line, which was transected with the BL-related miRNA mimics or inhibitors. Results: miRNA expression profiling showed that miR-150 had extremely decreased expression levels in BL patients. In both ISH and qRT-PCR analyses, BL had reduced levels of miR-150 expression compared with RLH. However, there is no significant correlation of miR-150 expression and EBV status in BL. Moreover, IHC and western blotting defined that c-Myb and Survivin are the protein targets of miR-150. Re-expression of miR-150 reduced the proliferation of Raji cells. Conclusions: Deregulation of miR-150 may be useful as a diagnostic tool in BL, based on miRNA profile screening, qRT-PCR and miRNA-ISH. miR-150 plays an important role in BL by targeting c-Myb and Survivin. Re-expression of miR-150 reduced the proliferation of Raji cells, which suggests it to be a promising novel candidate for tumor treatment. © 2014 Elsevier Inc.
Huang M.,Jiangxi Childrens Hospital |
Huang G.-D.,Nanchang University |
Peng D.,Jiangxi Childrens Hospital
Biomedical Research (India) | Year: 2017
The role of angiotensin-converting enzyme (ACE) I/D polymorphism in psoriasis have not been determined. Thus, in this study, we aimed to analyse ACE I/D polymorphism for the association with the risk of psoriasis in a Chinese Han population. A total of 161 cases (72 men and 89 women; mean age, 43.8 ± 5.5 years) and 256 controls (119 men and 137 women; mean age, 42.1 ± 6.9 years) were included in the study. The observed frequencies of all tested genotypes in controls did not deviate from Hardy-Weinberg equilibrium (HWE). Compared with the II genotype, the DD frequency of ACE I/D polymorphism among cases was significantly different from controls (DD versus II: OR=2.94; 95% CI=1.61-5.42; p<0.05). In addition, compared with the I allele, the D allele among cases was significantly associated with psoriasis risk (D versus I: OR=1.61; 95% CI=1.21-2.21; p<0.05). In conclusion, the current study showed that ACE I/D polymorphism may influence the risk of psoriasis in a Chinese Han population. © 2017, Scientific Publishers of India. All rights reserved.
PubMed | Fudan University, Chinese Academy of Sciences, Shanghai JiaoTong University and Jiangxi Childrens Hospital
Type: | Journal: Biochemical and biophysical research communications | Year: 2016
Neuroblastoma (NB) is the most common extracranial solid tumor of childhood. In this study, we examined the expression of bone morphogenetic protein receptor 2 (BMPR2) in primary NB and adjacent non-tumor samples (adrenal gland). BMPR2 expression was significantly downregulated in NB tissues, particularly in high-grade NB, and was inversely related to the expression of the NB differentiation markers ferritin and enolase. The significance of the downregulation was further explored in cultured NB cells. While enforced expression of BMPR2 decreased cell proliferation and colony-forming activity, shRNA-mediated knockdown of BMPR2 led to increased cell growth and clonogenicity. In mice, NB cells harboring BMPR2 shRNA showed significantly increased tumorigenicity compared with control cells. We also performed a retrospective analysis of NB patients and identified a significant positive correlation between tumor BMPR2 expression and overall survival. These findings suggest that BMPR2 may play an important role in the development of NB.
PubMed | BGI, Nan Jing Childrens Hospital, Zhe Jiang Childrens Hospital, Duke University and 2 more.
Type: | Journal: Scientific reports | Year: 2017
Genetic factors play a major role in the etiology of epilepsy disorders. Recent genomics studies using next generation sequencing (NGS) technique have identified a large number of genetic variants including copy number (CNV) and single nucleotide variant (SNV) in a small set of genes from individuals with epilepsy. These discoveries have contributed significantly to evaluate the etiology of epilepsy in clinic and lay the foundation to develop molecular specific treatment. However, the molecular basis for a majority of epilepsy patients remains elusive, and furthermore, most of these studies have been conducted in Caucasian children. Here we conducted a targeted exome-sequencing of 63 trios of Chinese epilepsy families using a custom-designed NGS panel that covers 412 known and candidate genes for epilepsy. We identified pathogenic and likely pathogenic variants in 15 of 63 (23.8%) families in known epilepsy genes including SCN1A, CDKL5, STXBP1, CHD2, SCN3A, SCN9A, TSC2, MBD5, POLG and EFHC1. More importantly, we identified likely pathologic variants in several novel candidate genes such as GABRE, MYH1, and CLCN6. Our results provide the evidence supporting the application of custom-designed NGS panel in clinic and indicate a conserved genetic susceptibility for epilepsy between Chinese and Caucasian children.
PubMed | Nanchang University, Jiangxi Childrens Hospital and Jiangxi Provincial Maternal and Child Health Hospital
Type: | Journal: International immunopharmacology | Year: 2016
The precision-cut kidney slice (PCKS) model appears to be a useful ex vivo model of renal fibrosis. However, little in-depth molecular investigation on the PCKS model has been performed. Therefore, the aim of this study will be to investigate and validate the molecular validity of this model.The PCKS model was constructed in male C57BL/6 mice. To induce renal fibrosis, PCKS were incubated in recombinant human TGF-1 for 48 h. Protein expression of phosphorylated Smad2 (p-Smad2, cytosolic and nuclear), Smad7, phosphorylated ERK1 (p-ERK1), phosphorylated ERK2 (p-ERK2), and phosphorylated p38 MAPK (p-p38 MAPK) was measured using Western blotting. To assess Smad2/3 heteromeric complex formation and phosphorylated Smad3 (p-Smad3) expression, immunoprecipitation was performed with an anti-Smad2 or an anti-Smad3 antibody, respectively, prior to Western blotting.p-Smad2 and p-Smad3 were significantly upregulated in the PCKS model relative to control (p<0.05). However, we found no significant difference in Smad7 expression between the PCKS model and control (p>0.05). The PCKS model demonstrated significantly greater Smad2/3 complex formation and nuclear translocation relative to control (p<0.05). The PCKS model showed significantly greater expression of p-ERK1, p-ERK2, and p-p38 MAPK relative to control (p<0.05).The PCKS model displays several well-established molecular markers of renal fibrosis. However, the PCKS model failed to display Smad7 downregulation and appears to display over-activation of p-Smad2 and p-Smad3 as well as under-activation of ERK1/2 and p38 MAPK signaling vis--vis the well-established in vivo unilateral ureteric obstruction model of renal fibrosis.
Xiao J.,Jiangxi Maternal and Child Health Hospital |
Zhang S.,Jiangxi Childrens Hospital |
Wang F.,Nanchang University |
Wang Y.,Jiangxi Maternal and Child Health Hospital |
And 4 more authors.
American Journal of Obstetrics and Gynecology | Year: 2014
Objective The aim of this preliminary study was to investigate whether ultrasound-guided high-intensity focused ultrasound (HIFU) can play a role in treating cesarean scar pregnancy (CSP). Study Design Between November 2011 and December 2012, 16 patients with CSP were treated with ultrasound-guided HIFU ablation. Successful treatment was defined as disappearance of CSP mass, undetectable serum beta human chorionic gonadotropin, and no serious complications such as severe bleeding, uterine rupture, or hysterectomy.Results All patients were successfully treated in the outpatient department and none required readmission. After 2-5 treatment sessions, the mean time for achieving undetectable serum beta human chorionic gonadotropin was 4.94 ± 2.32 weeks, and the mean time for CSP mass disappearance was 6.69 ± 3.36 weeks. Three patients experienced moderate abdominal pain that subsided in 1-2 days, and nine patients experienced mild vaginal bleeding (<30 mL) that resolved within 2-3 days. All 16 patients had recovered their normal menstruation function at follow-up.Conclusion These preliminary results suggest that ultrasound-guided HIFU ablation is a noninvasive, feasible, and effective method for the treatment of CSP. © 2014 Elsevier Inc. All rights reserved.
Zhou X.,Tulane University |
Hao Q.,Tulane University |
Zhang Q.,Tulane University |
Liao J.-M.,Tulane University |
And 5 more authors.
Cell Death and Differentiation | Year: 2015
Over the past decade, a number of ribosomal proteins (RPs) have been found to have a role in activating the tumor suppressor p53 by directly binding to MDM2 and impeding its activity toward p53. Herein, we report that RPL5 and RPL11 can also enhance the transcriptional activity of a p53 homolog TAp73, but through a distinct mechanism. Interestingly, even though RPL5 and RPL11 were not shown to bind to p53, they were able to directly associate with the transactivation domain of TAp73 independently of MDM2 in response to RS. This association led to perturbation of the MDM2-TAp73 interaction, consequently preventing MDM2 from its association with TAp73 target gene promoters. Furthermore, ectopic expression of RPL5 or RPL11 markedly induced TAp73 transcriptional activity by antagonizing MDM2 suppression. Conversely, ablation of either of the RPs compromised TAp73 transcriptional activity, as evident by the reduction of p21 and Puma expression, in response to 5-fluorouracil (5-FU). Consistently, overexpression of RPL5 or RPL11 enhanced, but knockdown of either of them hampered, TAp73-mediated apoptosis. Intriguingly, simultaneous knockdown of TAp73 and either of the RPs was required for rescuing the 5-FU-triggered S-phase arrest of p53-null tumor cells. These results demonstrate a novel mechanism underlying the inhibition of tumor cell proliferation and growth by these two RPs via TAp73 activation. © 2015 Macmillan Publishers Limited All rights reserved.
Nakhoul H.,Tulane University |
Ke J.,Tulane University |
Ke J.,Jiangxi Childrens Hospital |
Zhou X.,Tulane University |
And 3 more authors.
Clinical Medicine Insights: Blood Disorders | Year: 2014
Ribosomopathies are diseases caused by alterations in the structure or function of ribosomal components. Progress in our understanding of the role of the ribosome in translational and transcriptional regulation has clarified the mechanisms of the ribosomopathies and the relationship between ribosomal dysfunction and other diseases, especially cancer. This review aims to discuss these topics with updated information. © the authors, publisher and licensee Libertas Academica Limited.
Zhang D.-G.,Jiangxi Childrens Hospital
Journal of Leukemia and Lymphoma | Year: 2012
MicroRNA (miRNA) is a recently discovered class of new noncoding small RNA molecules, they play key regulatory roles in the genesis,development and prognosis of lymphatic and hematopoietic tumours. This review presents the update on miRNA biogenesis,functionary mechanism and their role in pediatric B-cell lymphoblastic leukemia and lymphoma.
Zhong J.-M.,Jiangxi Childrens Hospital
Chinese Journal of Contemporary Pediatrics | Year: 2014
Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a new category of severe, potentially treatable autoimmune encephalitis and can appear in patients of all ages, but more frequently in children. It is a highly characteristic syndrome evolving in five stages: the prodromal phase (viral infection-like symptoms), psychotic phase, unresponsive phase, hyperkinetic phase, and gradual recovery phase. The treatment for this disorder includes firstline immunotherapy (steroids, intravenous immunoglobulin, plasmapheresis), second-line immunotherapy (rituximab, cyclophosphamide), and tumor removal. Hereby the progresses, selections and shortcomings of the treatment protocols for this disease are introduced.