Childrens Hospital of Zhengzhou
Childrens Hospital of Zhengzhou
Huo Y.,The Sixth Peoples Hospital of Zhengzhou |
Zheng L.,The Sixth Peoples Hospital of Zhengzhou |
Chen X.,The Sixth Peoples Hospital of Zhengzhou |
Ge L.,Childrens Hospital of Zhengzhou |
Wang Y.,Zhengzhou University
Microbial Pathogenesis | Year: 2017
The objective of this study was to express and characterize the major capsid protein (VP1) of a GII.6 Norovirus (NoV)strain isolated in China. The newly identified GII.6 NoV strain was isolated from a five-year old boy presenting acute gastroenteritis. The genome of the GII.6 strain was 7550 nucleotides in length, excluding the poly-adenylation tail. Multiple sequence alignment and phylogenetic analysis based on deduced VP1 amino acid sequences from different genotypes indicated close relationship between GII.3 and GII.6 NoVs, as demonstrated by the presence of a short sequence insertion in the P2 domain and clustering in the same subgroup. Expression of GII.6 VP1 led to assembly of virus like particles (VLPs). In vitro VLP-salivary histo-blood group antigens (HBGAs) binding assay demonstrated wide-spectrum binding activities of assembled VLPs to blood type A, B, AB and O salivary HBGAs with highest binding capacity to type A salivary HBGAs and lowest to type AB and O salivary HBGAs. In vitro VLP-salivary HBGAs binding blockade assay indicated absence of cross-blocking effects for hyperimmune sera produced against different genotypes. In conclusion, our results suggest a rational VLPs-based multivalent NoV vaccine should contain capsid proteins of a GII.6 strain. © 2017 Elsevier Ltd
Mi G.-L.,Shandong University |
Mi G.-L.,Shandong Mental Health Center |
Zhao L.,Childrens Hospital Of Zhengzhou |
Qiao D.-D.,Shandong University |
And 4 more authors.
Antonie van Leeuwenhoek, International Journal of General and Molecular Microbiology | Year: 2015
Infant colic, excessive crying of unknown cause, is a major burden to families and effects about 10–30 % of infants. Despite decades of research, the exact cause and treatment of infant colic has remained elusive. The use of Lactobacillus reuteri (DSM 17938) in infant colic is somewhat controversial and hence, we designed this study to evaluate its efficacy in infantile colic. We recruited predominantly or exclusively breastfed infants, aged less than 4 months in a placebo controlled observational randomized study. Participants’ were assigned to receive L. reuteri at a dose 108 colony forming units (n = 21) and placebo (n = 21). Placebo was an identical formulation without live micro-organisms. Treatment was given to subjects for 21 days and they were followed for 4 weeks. Treatment success (primary outcome), daily reduction in crying time, parent satisfaction and reduction in maternal depression (secondary outcomes) were assessed at the end of study period. Treatment success was observed in all infants (100 %) of the probiotic group while it was seen in 15.7 % of the placebo group. Mean daily crying time was more significantly reduced to 32.1 ± 8.3 min/day (P < 0.01) from 200.9 ± 6.3 min/day in the probiotic group as compared to the placebo group (120.6 ± 20.0 min/day). Moreover, throughout the study period, parent’s satisfaction and improvement in maternal depression (Edinburgh postnatal depression scale) was also significantly higher in the probiotic group. In our study population, reduction in crying time was significant (P < 0.01) even during first week of initiation of therapy. We conclude that L. reuteri (DSM 17938) reduces daily crying time and maternal depression during infantile colic. We suggest L. reuteri may be a safe and efficacious option for reducing infant colic. © 2015, Springer International Publishing Switzerland.
Hou L.-L.,Henan University |
Gao C.,Childrens Hospital of Zhengzhou |
Chen L.,Henan University |
Hu G.-Q.,Henan University |
Xie S.-Q.,Henan University
Acta Pharmacologica Sinica | Year: 2013
Aim: To investigate the effects and the molecular mechanisms of fucoxanthin, a major carotenoid found in edible seaweed, on HeLa cells. Methods: The cytotoxicity of fucoxanthin was evaluated using MTT assay. Cell cycle and apoptosis were evaluated using flow cytometric analysis. Autophagy was detected with acridine orange staining and transient transfection of the GFP-LC3 plasmid into the cells. Protein expression was detected with Western blotting. Results: Treatment of HeLa cells with fucoxanthin (10-80 μmol/L) for 48 h caused dose-dependent cytotoxicity with an IC50 value of 55.1±7.6 μmol/L. Fucoxanthin (10, 20, and 40 μmol/L) dose-dependently induced G0/G1 arrest, but did not change the apoptosis of HeLa cells. The same concentrations of fucoxanthin dose-dependently increased the protein expression of LC3 II (the autophagosome marker) and Beclin 1 (the initiation factor for autophagosome formation) in HeLa cells. Moreover, fucoxanthin dose-dependently decreased the levels of phosphorylated Akt and its downstream proteins p53, p70S6K, and mTOR, and increases the expression of PTEN in HeLa cells. Pretreatment of HeLa cells with 3-methyladenine (5 mmol/L) blocked the cytotoxic effect of fucoxanthin as well as fucoxanthin-induced autophagy. Conclusion: Fucoxanthin exerts autophagy-dependent cytotoxic effect in HeLa cells via inhibition of Akt/mTOR signaling pathway. © 2013 CPS and SIMM.
Tian M.,Childrens Hospital of Zhengzhou |
Liu C.,Childrens Hospital of Zhengzhou
Renal Failure | Year: 2015
Aim: To explore the underlying mechanism of low-molecular-weight heparin calcium therapy on Henoch-Schönlein purpura nephritis (HSPN). Methods: Eighty-nine children with severe HSPN were randomized into control group (treated with conventional therapy, n = 45) and treatment group (treated with conventional therapy plus low-molecular-weight heparin calcium, n = 44). The concentrations of plasma fibrinogen (Fg), d-dimer and fibrin degradation products (FDPs) were detected before and after treatment. The urinary red blood cell (RBC) and 24 h proteinuria were determined weekly for assessing the childrens kidney function. Results: Two groups were well-matched at baseline. After 8 weeks of treatment, the clinical outcomes of HSPN and outcome of proteinuria of the treatment group were better than the control group (p < 0.05); the content of Fg, d-dimer and FDP in plasma of the treatment group were lower than the control group (p < 0.05); but there was no difference about the curative effect of hematuria and the coagulation function between the two groups (p > 0.05). Conclusions: Fibrinolytic system may participate in the kidney injury of HSPN children and low-molecular-weight heparin calcium could correct blood hypercoagulability through inhibiting hyperfibrinolysis, and thus improving the blood supply of kidney. © 2015 Informa Healthcare USA, Inc.
Geng X.,Childrens Hospital Of Zhengzhou |
Xie L.,Hospital of Chinese Medicine |
Xing H.,Peoples Hospital Of Weifang
Technology in Cancer Research and Treatment | Year: 2016
Activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is a novel poor prognostic indicator of neuroblastoma (NB), and the positive effects of chemotherapy on NB have been confirmed. In this study, we investigated the effect of small molecule PI3K inhibitor PI103 on chemosensitivity. The PI3K inhibitor cooperates with doxorubicin to synergistically induce apoptosis and to reduce tumor growth of NB in in vitro and in vivo models. Human NB cells, SH-SY5Y and SK-N-BE(2), were treated with PI103 combined doxorubicin-enhanced Bid cleavage, activated Bax, and caspase 3. Activation of caspase 3 was also observed in xenografts of NB in nude mice upon combination of doxorubicin with the specific PI3K inhibitor PI103. Cell viability was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. Both PI103 and doxorubicin inhibited growth of NB in vitro and PI103 induced a G1 arrest of NB cells. PI103 combined doxorubicin significantly inhibits the growth of established NB tumors, induced apoptosis of tumor cells, and improved the survival of mice in vivo. Taken together, our findings suggest that PI3K inhibition seems to be a promising option to sensitize tumor cells for chemotherapy in NB, which may be effective in the treatment of NBs. © 2015, © The Author(s) 2015.
Sun X.-M.,Childrens Hospital of Zhengzhou |
Kang P.,Childrens Hospital of Zhengzhou |
Tao K.,PLA Fourth Military Medical University
Asian Pacific Journal of Tropical Medicine | Year: 2015
Objective: To explore the causes of immune dysfunction in neonatal rats with hyperbilirubinemia. Methods: A total of 60 newborn SD rats were equally randomized into normal saline (NS) group, LPS control group, bilirubin control group, low-dose group and high-dose group. After anesthesia, 0.1 mL NS was given to the NS and LPS control group and different doses of bilirubin for the other groups; 1 h later, the NS and bilirubin control group received the intraperitoneal injection of 0.05 mL NS and 1mg/kg LPS for the other groups. After 5 or 24 hours of model establishment, spleens were collected for detecting the expression levels of MyD88 and p-TAK1 protein and the spleen cells apoptosis by immunohistochemmistry and TUNEL method. After 24 hours of model establishment, serum inflammatory factors levels and T cell subsets distribution were determined by ELISA and flow cytometry. Results: In contrast to low-dose bilirubin, high-dose bilirubin could induce spleen cells apoptosis in coordination with LPS. After 5 hours of model establishment, compared with NS group, MyD88 expression level in low-dose group elevated while p-TAK1 level in high-dose group reduced (P<0.05). In high-dose group, inflammotory factors levels and CD8+ T cells percentage were all higher than LPS control and NS group (P<0.05), while CD4+ T cells percentage was lower than NS group (P<0.05). Conclusions: High-concentration plasma bilirubin in coordination with LPS could inhibit NF-κB signal pathways activation and aggravate inflammatory reaction, thus caused immunosuppression with inflammation cascade, which resulted in the immune dysfunction. © 2015 Hainan Medical College.
Ding D.,China Medical University at Heping |
Zhao A.,Childrens Hospital of Zhengzhou |
Qiu B.,China Medical University at Heping |
Xing D.,China Medical University at Heping |
And 2 more authors.
Journal of Neurosurgery: Pediatrics | Year: 2014
Ependymoblastoma is a rare and devastating primitive neuroectodermal tumor with ependymal differentiation. This tumor occurs very early in life and shows rapid growth and a diffuse infiltration through the leptomeningeal space. This neoplasm is characterized by uniform neuroepithelial cells, multilayered ependymal rosettes, perivascular pseudorosettes, and numerous mitotic figures. In this article, the authors report on a 4-year-old girl who was diagnosed as having an ependymoblastoma with cystic change. After a series of laboratory and imaging examinations, the left frontal solid-cystic lesion was surgically excised. Histological examinations confirmed the diagnosis of ependymoblastoma. The patient's intracranial hypertension symptoms were alleviated, and postoperative chemotherapy was performed. At the 6-month follow-up visit, MRI demonstrated evidence of relapse, and the girl died of tumor recurrence 14 months after surgery. Databases (PubMed, MEDLINE, Embase, and Web of Science) were searched for relevant articles published from 1970 to 2012; 71 eligible cases of ependymoblastoma were obtained, and 42 provided complete clinical details. Prognosis of children with ependymoblastoma is poor, and data on clinical behavior and optimal treatment strategies are lacking, but sustained remissions have been achieved after multimodal treatment according to existing literature. In this report, the clinical and histopathological features and therapeutic options of this tumor are discussed in the light of the published data. Further studies, especially those examining multimodality therapy, are needed to improve survival of children with this rare malignant CNS tumor. ©AANS, 2014.
Ren H.,Childrens Hospital Of Zhengzhou |
Shi X.,Women and Infants Hospital of Zhengzhou |
Li Y.,Childrens Hospital Of Zhengzhou
Experimental and Therapeutic Medicine | Year: 2016
Human laryngeal papilloma (LP) is a human papillomavirus-induced hyperplastic tumor of the respiratory tract, which is characterized by rapid growth and apoptosis resistance. Isoflurane (ISO) inhibits proliferation and elicits apoptosis in cancer cells. The results of the present study found that the mRNA and protein levels of cyclooxygenase-2 (COX2) were higher in LP tissues than in normal laryngeal samples, and prostaglandin E2 (PGE2) production was increased in LP cells, as determined by quantitative polymerase chain reaction, western blot and radioimmunoassay analyses. Notably, the increase in COX2 and PGE2 levels was significantly abrogated in the ISO-treated LP cells. The inhibitory effects of ISO on COX2 expression and activity depended on the inactivation of p38 mitogen-activated protein kinase (MAPK) in LP cells. By inhibiting the COX2 activity of LP cells, ISO treatment markedly suppressed cell viability and proliferation, as determined using Cell Counting Kit-8, flow cytometry and 5-ethynyl-20-deoxyuridine incorporation assays. Furthermore, ISO treatment promoted cell apoptosis, as demonstrated by flow cytometry, nucleosomal fragmentation and caspase-3 activity assays. Collectively, the present results suggest that COX2 is critical in the progression of LP, and ISO is a potential agent for LP therapy by impeding p38 MAPK/COX2 signaling. © 2016, Spandidos Publications. All rights reserved.
PubMed | Childrens Hospital of Zhengzhou, Henan University of Traditional Chinese Medicine, Women and Infants Hospital of Zhengzhou and Henan Eye Hospital
Type: Journal Article | Journal: Experimental and therapeutic medicine | Year: 2017
The effect of glucocorticoid on cytokines Toll-like receptor (TLR)9 and TLR7 in peripheral blood of patients with uveitis was explored. Forty-six patients with uveitis admitted to our hospital from April 2014 to April 2015 were selected as the research observational group. Thirty-five able-bodied individuals in the same period were selected as the control group. To treat uveitis, the observational group was injected with glucocorticoid (1-2 mg/kg/day) daily, while the control group did not receive any treatment. The quantity of expression of peripheral blood cytokines TLR9 and TLR7 were detected by the methods of fluorescence quantitative PCR, enzyme-linked immunosorbent assay and western blotting. The content of peripheral blood TLR9 and TLR7 (0.210.01, 0.190.01) decreased significantly (P<0.05) in observational group after glucocorticoid treatment. Compared with data of control group (0.210.01, 0.190.01), TLR9 and TLR7 content in peripheral blood after glucocorticoid treatment on the patients with uveitis from observation group (0.190.01, 0.170.01) did not show any significant difference, for correlation between TLR9 and TLR7 in observation group before and after treatment. It was observed that the cytokine content of TLR9 was associated with TLR7 positively (r=0.653, P=0.012). In conclusion, glucocorticoid can improve uveitis by reducing the content of cytokines TLR9 and TLR7 in peripheral blood.
PubMed | Childrens Hospital of Zhengzhou, Northwest University for Nationalities, Nanjing Medical University, Nanchang University and 3 more.
Type: | Journal: Genetics in medicine : official journal of the American College of Medical Genetics | Year: 2017
The aim of this study was to investigate the genetic basis and pathogenic mechanism of variable maculopathies, ranging from mild photoreceptor degeneration to central areolar choroidal dystrophy, in a five-generation family.Clinical characterizations, whole-exome sequencing, and genome-wide linkage analysis were carried out on the family. Zebrafish models were used to investigate the pathogenesis of GUCA1A mutations.A novel mutation, GUCA1A p.R120L, was identified in the family and predicted to alter the tertiary structure of guanylyl cyclase-activating protein 1, a photoreceptor-expressed protein encoded by the GUCA1A gene. The mutation was shown in zebrafish to cause significant disruptions in photoreceptors and retinal pigment epithelium, together with atrophies of retinal vessels and choriocapillaris. Those phenotypes could not be fully rescued by exogenous wild-type GUCA1A, suggesting a likely gain-of-function mechanism for p.R120L. GUCA1A p.D100E, another mutation previously implicated in cone dystrophy, also impaired the retinal pigment epithelium and photoreceptors in zebrafish, but probably via a dominant negative effect.We conclude that GUCA1A mutations could cause significant variability in maculopathies, including central areolar choroidal dystrophy, which represents a severe pattern of maculopathy. The diverse pathogenic modes of GUCA1A mutations may explain the phenotypic diversities.Genet Med advance online publication 26 January 2017Genetics in Medicine (2017); doi:10.1038/gim.2016.217.