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Yue B.,Qingdao University | Ren Q.-X.,Peoples Hospital of Rizhao | Su T.,Peoples Hospital of Rizhao | Zhang L.,Qingdao Women and Childrens Hospital
European Review for Medical and Pharmacological Sciences | Year: 2014

OBJECTIVE: ERK5 is over expressed in a many of human cancers and this overexpression has been associated with metastasis and invasion. Furthermore, ERK5 silencing inhibits aggressive phenotypes of cancer cells. However, mechanisms by which ERK5 regulates tumour progression or metastasis have not been elucidated. In this study, using human osteosarcoma cell lines U2OS as a model, we explored the involvement of ERK5 silencing on invasiveness of U2OS cells. MATERIALS AND METHODS: ERK5 siRNA targeting ERK5 was stably transfected into the human osteosarcoma cell lines U2OS. ERK5 knocked-down U2OS cells was then transfected with Slug cDNAorMMP-9 cDNA plasmidtore-express Slug or MMP-9. Cell proliferation was detected by MTT assay. Cell invasion and metastasis was detected by Matrigel invasion and wound healing assay. An orthotopic nude mouse model of U2OS was applied for in vivo lung metastasis experiments. ERK5, Slug, MMP-9 and E-cadherin were analyzed by realtime PCR, and Western blotting. RESULTS: ERK5 silencing by siRNA in U2OS cells decreased Slug and MMP-9 expression. Compared with the vector-transfected cells, ERK5 knocked-down cells showed reduced migration and invasion in vitro, as well as decreased metastatic potential in experimental metastasis. Re-expression of Slug or MMP-9 in ERK5 knocked-down cells restored the invasive phenotypes. We also discovered that Re-expression of Slug in ERK5 knocked-down cells restored the MMP-9 expression, and re-expression of MMP-9 in ERK5 knocked-down cells did not affect Slug and ERK5 expression. CONCLUSIONS: Our data suggest that ERK5 knockdown inhibits aggressive behaviour of human U2OS cells through modulating Slug signaling and MMP-9 expression.


PubMed | Ningbo Women and Childrens Hospital, Zhengzhou Childrens Hospital, Capital Medical University, Ningxia Medical University and 20 more.
Type: Journal Article | Journal: Chinese medical journal | Year: 2016

Globally, the proportion of child deaths that occur in the neonatal period remains a high level of 37-41%. Differences of cause in neonate death exist in different regions as well as in different economic development countries. The specific aim of this study was to investigate the causes, characteristics, and differences of death in neonates during hospitalization in the tertiary Neonatal Intensive Care Unit (NICU) of China.All the dead neonates admitted to 26 NICUs were included between January l, 2011, and December 31, 2011. All the data were collected retrospectively from clinical records by a designed questionnaire. Data collected from each NICU were delivered to the leading institution where the results were analyzed.A total of 744 newborns died during the 1-year survey, accounting for 1.2% of all the neonates admitted to 26 NICUs and 37.6% of all the deaths in children under 5 years of age in these hospitals. Preterm neonate death accounted for 59.3% of all the death. The leading causes of death in preterm and term infants were pulmonary disease and infection, respectively. In early neonate period, pulmonary diseases (56.5%) occupied the largest proportion of preterm deaths while infection (27%) and neurologic diseases (22%) were the two main causes of term deaths. In late neonate period, infection was the leading cause of both preterm and term neonate deaths. About two-thirds of neonate death occurred after medical care withdrawal. Of the cases who might survive if receiving continuing treatment, parents concern about the long-term outcomes was the main reason of medical care withdrawal.Neonate death still accounts for a high proportion of all the deaths in children under 5 years of age. Our study showed the majority of neonate death occurred in preterm infants. Cause of death varied with the age of death and gestational age. Accurate and prompt evaluation of the long-term outcomes should be carried out to guide the critical decision.


PubMed | Oregon Health And Science University, Qingdao Women and Childrens Hospital and Qingdao University
Type: | Journal: Clinica chimica acta; international journal of clinical chemistry | Year: 2016

Asymmetric dimethylarginine (ADMA) has been associated with an increased risk of cardiovascular disease. We investigated the role of serum ADMA concentrations in early-onset coronary artery disease (EOCAD).Candidates for coronary artery angiography (age<50y for men and <55y for women) who met the inclusion criteria were enrolled in this study. Serum concentrations of ADMA were determined using ELISA. Severity of coronary atherosclerosis was estimated by number of diseased vessels.A total of 601 subjects (286 with EOCAD patients and 315 controls) were included in the study. ADMA concentrations were found to be significantly higher in the EOCAD group (0.4800.110mol/l) than in the control group (0.4570.091, P=0.007). ADMA concentrations significantly increased with the number of diseased vessels (P<0.001). In addition, serum ADMA concentrations were affected by diabetes mellitus and smoking status, and were positively correlated with serum creatinine and body mass index (BMI).Our results show that serum ADMA concentrations were associated with the presence and severity of EOCAD, suggesting that ADMA may be involved in the progression of EOCAD.


Zhang B.-B.,Mie University | Wang D.-G.,Guangxi University | Guo F.-F.,Qingdao Women And Childrens Hospital | Xuan C.,Qingdao University
Familial Cancer | Year: 2015

Cancer stem cells (CSCs) are believed as the initiators of the occurrence, development and recurrence of malignant tumors. Targeting this unique cell population would provide a less toxic approach than regular chemotherapeutic agents that kill bulk rapid proliferating tumor cells and also normal cells which divide rapidly. To date, major research effort has been aimed at identifying and eradicating CSC population. The metabolism heterogeneity of mitochondria in CSCs shows a big promise for cancer research. Of them, mitochondrial membrane potential (Δψm), reflecting the functional status of the mitochondrion is proved to be highly related to cancer malignancy. Reactive oxygen species, mainly produced from mitochondria, are also increased in many types of cancer cells. However, their statuses in CSCs remain poorly understood. Here we shall review the mitochondrial membrane potential and reactive oxygen species of CSCs and propose the novel potential targets for cancer therapy. © 2014, Springer Science+Business Media Dordrecht.


PubMed | China Medical University at Heping and Qingdao Women and Childrens Hospital
Type: | Journal: Diabetes research and clinical practice | Year: 2016

The aim of the present study was to investigate the probable pathogenesis of gestational diabetes mellitus (GDM) by analyzing the correlation between sex hormone-binding globulin (SHBG) secreted by the placenta during pregnancy and insulin signaling components and glucose transporter proteins (GLUTs) in the placental tissue.Placental tissue was collected from full-term and non-obese [body mass index <25kg/m(2)] pregnant women; 10 diagnosed with GDM and 10 with normal pregnancy. We used real-time polymerase chain reaction (PCR), immunohistochemistry and western blotting to detect expression of protein and mRNA of SHBG and insulin signaling components and GLUTs in placental tissue.In the placental tissue of non-obese women, there was a decrease in expression of SHBG protein and mRNA, with a concurrent decrease in expression of GLUT-4 protein and mRNA in women with GDM compared with normal controls. There was a decrease in GLUT-3 and insulin receptor substrate (IRS)-1 protein expression and lower IRS-2 mRNA expression was also observed in GDM placental tissue. Linear correlation analyses showed a positive correlation between SHBG and IRS-2 mRNA (P=0.038, R(2)=0.2178, y=0.249x+1.4208); positive correlation between SHBG and phosphatidylinositol 3-kinase (PI3K) p85 mRNA (P=0.035, R(2)=0.224, y=0.3506x+0.7433); positive correlation between SHBG and GLUT-4 mRNA (P=0.000, R(2)=0.5174, y=1.3822+1.7811x); positive correlation between IRS-2 and GLUT-4 mRNA (P=0.002, R(2)=0.4064, y=-0.8272+2.9592x); negative correlation between IRS-1 and PI3K p85 mRNA (P=0.005, R(2)=0.366, y=2.4492-0.1929x); negative correlation between IRS-1 and GLUT-3 mRNA (P=0.027, R(2)=0.243, y=0.9254-0.0714x); and positive correlation between IRS-2 and GLUT-1 mRNA (P=0.004, R(2)=0.3794, y=0.0225+0.6298x).The results confirm that defective receptors for insulin signal transduction and GLUT proteins are present in GDM placental tissue. Decreasing expression of SHBG may participate in regulation of insulin signaling, leading to a concomitant decrease in expression of relevant insulin signaling components in placental tissue, implying insulin resistance and eventual development of GDM.


Dong H.,Qingdao University | Qian D.,Qingdao University | Wang Y.,Qingdao Women and Childrens Hospital | Meng L.,Peoples Hospital of Zhangqiu | And 3 more authors.
World Journal of Surgical Oncology | Year: 2015

Background: Survivin, an inhibitor of apoptosis, is overexpressed in pancreatic ductal adenocarcinoma (PDAC). Its expression is known to be associated with poor clinical outcome. However, to our knowledge, there has been no study to characterize its usefulness as a serum marker for human pancreatic cancer. Furthermore, the relation between survivin expression and the serum level of survivin has not been widely studied in PDAC. We performed this study to investigate the expression and serum level of survivin in PDAC and its clinical significance as a prognostic factor. Methods: We performed immunohistochemical staining for survivin in formalin-fixed, paraffin-embedded blocks from 80 PDAC tissues. The serum level of survivin from the patients (n = 80) and age-matched healthy volunteers (n = 80) were analyzed by enzyme-linked immunosorbent assays (ELISAs) prior to surgical resection. Levels of expression were correlated with clinicopathological parameters. Results: Serum survivin concentrations were significantly elevated in patients with PDAC when compared with healthy sera (P < 0.001). High serum survivin levels were significantly associated with perineural invasion, venous invasion, lymph node status (N stage), cell differentiation, and recurrence but not with the tumor size, age, gender of the patients, or tumor location. The median overall survival time of the group with normal serum survivin levels was longer than that of the group with elevated serum survivin. The independent factors associated with overall survival were advanced pancreatic cancer and elevated serum survivin level. Of the 80 cases of PDAC, 65 (81.25 %) were positive for survivin expression. There were significant associations between survivin expression and perineural invasion, venous invasion, and lymph node status. A significant difference in overall survival was associated with survivin expression. Conclusions: Patients with elevated serum survivin level and high survivin expression at diagnosis demonstrated a poor outcome. Detection of serum survivin or tissue survivin expression may predict the prognosis of patients with PDAC. © 2015 Dong et al.


PubMed | Qingdao Women and Childrens Hospital and Qingdao University
Type: Journal Article | Journal: Stem cell research & therapy | Year: 2017

Stem cells provide a promising candidate for the treatment of the fatal pediatric dilated cardiomyopathy (DCM). This study aimed to investigate the effects of intramuscular injection of human umbilical cord-derived mesenchymal stem cells (hUCMSCs) on the cardiac function of a DCM rat model.A DCM model was established by intraperitoneal injections of doxorubicin in Sprague-Dawley rats. hUCMSCs at different concentrations or cultured medium were injected via limb skeletal muscles, with blank medium injected as the control. The rats were monitored for 4weeks, meanwhile BNP, cTNI, VEGF, HGF, GM-CSF, and LIF in the peripheral blood were examined by ELISA, and cardiac function was monitored by echocardiography (Echo-CG). Finally, the expression of IGF-1, HGF, and VEGF in the myocardium was examined by histoimmunochemistry and real-time PCR, and the ultrastructure of the myocardium was examined by electron microscopy.Injection of hUCMSCs markedly improved cardiac function in the DCM rats by significantly elevating left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS). The BNP and cTNI levels in the peripheral blood were reduced by hUCMSCs, while HGF, LIF, GM-CSF, and VEGF were increased by hUCMSCs. Expression of IGF-1, HGF, and VEGF in the myocardium from the DCM rats was significantly increased by hUCMSC injection. Furthermore, hUCMSCs protected the ultrastructure of cardiomyocytes by attenuating mitochondrial swelling and maintaining sarcolemma integrity.Intramuscular injection of UCMSCs can improve DCM-induced cardiac function impairment and protect the myocardium. These effects may be mediated by regulation of relevant cytokines in serum and the myocardium.


Wang K.,Qingdao Women And Childrens Hospital | Li Y.T.,Qingdao Women And Childrens Hospital | Hou M.,Qingdao Women And Childrens Hospital
Genetics and Molecular Research | Year: 2016

Angelman syndrome (AS) is a neurogenetic disorder caused by a defect in the expression of the maternally inherited ubiquitin protein ligase E3A (UBE3A) gene in chromosome 15. The most common genetic defects include maternal deletions in chromosome 15q11-13; however, paternal uniparental disomy and imprinting defects allow for the identification of mutations in UBE3A in 10% of patients with AS. The aim of this study was to validate the clinical features and genetic polymorphisms of AS, and to discuss the relationship between functional language lateralization and the arcuate fasciculus in the Broca’s and Wernicke’s areas. Six children with AS (mean age = 32.57 months) presenting characteristic behavioral patterns of AS (frequent laughter and happy demeanor, hand flapping, and hypermotor behavior) were recruited to this study. The patients underwent a clinical evaluation (clinical history, dysmorphological and neurological examinations, and psychological evaluations) and paraclinical investigations [genetic tests (fluorescence in situ hybridization and methylation polymerase chain reaction), electroencephalogram, and magnetic resonance imaging]. We conclude that AS diagnosis cannot rely solely on genetic testing for polymorphisms in UBE3A and must consider its clinical characteristics. Moreover, functional language lateralization and the arcuate fasciculus in the Broca’s and Wernicke’s areas were found to be closely correlated. Therefore, UBE3A gene mutation analysis combined with comprehensive clinical evaluations may be suitable for the diagnosis of AS. © FUNPEC-RP.


Ding Z.,Qingdao Women and Childrens Hospital
Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery | Year: 2012

To investigate the clinical pathological features of tracheobronchial foreign bodies and to improve the diagnosis and treatment. A retrospective study was conducted on 1050 cases with suspected tracheobronchial foreign bodies. Each patient was analyzed for age, sex, history, complication and location of the foreign body. Nine hundred and forty-nine out of 1050 cases were diagnosed as tracheobronchial foreign body, in which 13 patients coughed out the foreign bodies before operation and the rest 936 cases were given operation by bronchoscope under general anesthesia. Among the 949 cases, 936 cases were given operation, with successful removal of foreign bodies in 932 cases (99.6%). One patient suffered from complication (0.1%). For the diagnosis of tracheobronchial foreign bodies, it is very important to collect the detailed history of foreign body inhalation, physical examination and chest roentgenoscopy. Spiral CT with 3-D reconstruction of trachea and bronchus is performed in patients with suspected foreign bodies. Complete surface anesthesia of respiratory tract mucosa is the key procedure in the removal of foreign bodies from respiratory tract by bronchoscope.


PubMed | Qingdao Women and Childrens Hospital
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2016

Angelman syndrome (AS) is a neurogenetic disorder caused by a defect in the expression of the maternally inherited ubiquitin protein ligase E3A (UBE3A) gene in chromosome 15. The most common genetic defects include maternal deletions in chromosome 15q11-13; however, paternal uniparental disomy and imprinting defects allow for the identification of mutations in UBE3A in 10% of patients with AS. The aim of this study was to validate the clinical features and genetic polymorphisms of AS, and to discuss the relationship between functional language lateralization and the arcuate fasciculus in the Brocas and Wernickes areas. Six children with AS (mean age = 32.57 months) presenting characteristic behavioral patterns of AS (frequent laughter and happy demeanor, hand flapping, and hypermotor behavior) were recruited to this study. The patients underwent a clinical evaluation (clinical history, dysmorphological and neurological examinations, and psychological evaluations) and paraclinical investigations [genetic tests (fluorescence in situ hybridization and methylation polymerase chain reaction), electroencephalogram, and magnetic resonance imaging]. We conclude that AS diagnosis cannot rely solely on genetic testing for polymorphisms in UBE3A and must consider its clinical characteristics. Moreover, functional language lateralization and the arcuate fasciculus in the Brocas and Wernickes areas were found to be closely correlated. Therefore, UBE3A gene mutation analysis combined with comprehensive clinical evaluations may be suitable for the diagnosis of AS.

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