The First Peoples Hospital of Shangqiu
The First Peoples Hospital of Shangqiu
PubMed | Neurosurgery Institute, Panorama Medical Imaging Center, The First Peoples Hospital of Shangqiu, Shanghai University and Pudong Special Education School
Type: | Journal: Psycho-oncology | Year: 2016
Patient-oncologist alliance and psychosocial well-being have strong associations with adherence to cancer management. For patients with cancer of unknown primary (CUP), adherence is crucial to treatment or occult primary screening plans. There has been no study investigating the relationship between alliance, psychosocial factors, and adherence in such patients or in Chinese sociocultural settings.The measures of alliance, psychosocial well-being, and adherence willingness were administered to patients with CUP, with a mean age of 58.33 11.24 years. Multiple linear regression models were applied to investigate the independent relationship between alliance and adherence by controlling for socioeconomic and psychosocial confounders.Alliance was found to be independently and positively associated with greater adherence willingness and adherence to treatment and follow-up screening after controlling for significant confounders, including medical conditions, psychosocial well-being variables, and socioeconomic factors.Stronger patient-oncologist alliance may foster enhanced adherence to treatment and follow-up screening in patients with CUP. Patient-oncologist alliance seems affected by socioeconomic factors and psychosocial well-being in the Chinese sociocultural settings.
PubMed | The Peoples Hospital of Anyang City, The First Peoples Hospital of Shangqiu and Tangyin County Peoples Hospital
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2016
The aim of this study was to explore the inhibition of subcutaneously implanted human pituitary tumor cells in nude mice by LRIG1 and its mechanism. For this study, athymic nude mice were injected with either normal pituitary tumor RC-4B/C cells or LRIG1-transfected RC-4B/C cells. We then calculated the volume inhibition rate of the tumors, as well as the apoptosis index of tumor cells and the expression of Ras, Raf, AKt, and ERK mRNA in tumor cells. Tumor cell morphological and structural changes were also observed under electron microscope. Our data showed that subcutaneous tumor growth was slowed or even halted in LRIG1-transfected tumors. The tumor volumes were significantly different between the two groups of mice (2 = 2.14, P < 0.05). The tumor apoptosis index was found to be 8.72% in the control group and 39.7% in LRIG1-transfected mice (2 = 7.59, P < 0.05). The levels of Ras, Raf, and AKt mRNA in LRIG1-transfected RC-4B/C cells were significantly reduced after transfection (P < 0.01). Transfected subcutaneous tumor cells appeared to be in early or late apoptosis under an electron microscope, while only a few subcutaneous tumor cells appeared to be undergoing apoptosis in the control group. In conclusion, the LRIG1 gene is able to inhibit proliferation and promote apoptosis in subcutaneously implanted human pituitary tumors in nude mice. The mechanism of LRIG1 may involve the inhibition of the PI3K/ Akt and Ras/Raf/ERK signal transduction pathways.
Cao J.,Nanjing Agricultural University |
Feng C.,The First Peoples Hospital of Shangqiu |
Liu Y.,The First Peoples Hospital of Shangqiu |
Wang S.,Nanjing University of Science and Technology |
Liu F.,Nanjing Agricultural University
Biosensors and Bioelectronics | Year: 2014
Since many diseases are caused by pathogenic bacterial infections, accurate and rapid detection of pathogenic bacteria is in urgent need to timely apply appropriate treatments and to reduce economic costs. To end this, we designed molecular beacon-Au nanoparticle hybrid nanoprobes to improve the bacterial detection efficiency and sensitivity. Here, we show that the designed molecular beacon modified Au nanoparticles could specifically recognize synthetic DNAs targets and can readily detect targets in clinical samples. Moreover, the hybrid nanoprobes can recognize Escherichia coli within an hour at a concentration of 102cfu/ml, which is 1000-folds sensitive than using molecular beacon directly. Our results show that the molecular beacon-Au nanoparticle hybrid nanoprobes have great potential in medical and biological applications. © 2014 Elsevier B.V.
Liu Y.,Zhengzhou University |
Liu Y.,The First Peoples Hospital of Shangqiu |
Song L.,Zhengzhou University
International Journal of Clinical and Experimental Pathology | Year: 2015
Neuroblastoma inflicts mostly on children, and the pathogenesis remains elusive. Clinical diagnosis and therapeutic approaches are still on the incipient stage, so further understanding of the molecular and cellular mechanisms of the disease is necessary. Inflammation has been commonly regarded as a hallmark in tumorigenesis and development, and we identified a new inflammatory factor, HMGB1, is considerably increased in neuroblastoma. Our study shows that HMGB1 induces autophagy in Schwann cells through activation of TLR4, and knockdown of TLR4 obviates the HMGB1-induced autophagy. The HMGB1-induced autophagy is through classical pathway, as deficiency of Beclin 1 deprived autophagy in Schwann cells. Coculture of neuroblastoma with Schwann cells pretreated with HMGB1 promoted the proliferation of neuroblastoma cells, and if Beclin 1 is knocked down in Schwann cells, no promotion effects is observed. Taken together, our study demonstrates that HMGB1-induced autophagy in Schwann cells contributes to neuroblastoma cell proliferation, thus providing a potential therapeutic approach on neuroblastoma development.
Yang Y.-X.,The First Peoples Hospital of Shangqiu |
Zhu Y.-H.,The First Peoples Hospital of Shangqiu
International Journal of Clinical and Experimental Pathology | Year: 2016
Objective: The receptor for activated protein kinase C (RACK1) has been implicated in the development and progression of several human malignancies, but its role in human laryngeal squamous cell carcinoma (LSCC) has not been investigated. Methods: We performed quantitative real-time PCR (qRT-PCR) and western blot to analyze the expression of RACK1 in LSCC tissues and their matched adjacent non-tumor tissues. Immunohistochemistry (IHC) was carried out to analyze the expression levels of RACK1 in 72 paraffin-embedded LSCC tissues. The correlation between RACK1 expression and clinicopathological features was assessed by Chi-square analysis. The survival data of LSCC patients was analyzed by the Kaplan-Meier and log rank tests. Results: Expression levels of RACK1 mRNA and protein were increased in LSCC tissues than that in adjacent non-tumor tissues (P < 0.05). RACK1 expression was significantly correlated with T classification, clinical stage and lymph nodes metastasis (P < 0.05). LSCC patients with high RACK1 expression exhibited shorter survival time compared to those with low RACk1 expression (P < 0.05). Moreover, multivariate analysis further demonstrated that upregulated expression of RACK1 was an independent prognostic factor for LSCC patients (P < 0.05). Conclusions: RACK1 play an important role in the progression of LSCC, and present as a useful prognostic marker and a potential therapeutic target for LSCC patients.
PubMed | Shandong University and The First Peoples Hospital of Shangqiu
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2016
MicroRNA-590 (miR-590) shows oncogenic functions in various tumor types, but little is known about biological functions of miR-590 in lung adenocarcinoma. In this study, we observe that miR-590 is not only overexpressed in lung adenocarcinoma tissues and metastatic lymph nodes, but also significantly increased in lung adenocarcinoma cell lines. Moreover, gain-of-function and loss-of-function studies show miR-590 serve as a tumor suppressor regulating lung adenocarcinoma cells migration and invasion. Furthermore, OLFM4 is proved to as a functional target for miR-590 to regulate lung adenocarcinoma cells migration and invasion. In conclusion, miR-590 regulates lung adenocarcinoma metastasis through directly modulating functional target OLFM4.
PubMed | Cangzhou Center Hospital and The First Peoples Hospital of Shangqiu
Type: | Journal: Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology | Year: 2017
The establishment and maintenance of successful pregnancy mainly depends on trophoblast cells. Their dysfunction has been implicated in recurrent spontaneous abortion (RSA), a major complication of pregnancy. However, the underlying mechanisms of trophoblasts dysfunction remain unclear. DNA-damage-induced cell apoptosis has been reported to play a vital role in cell death. In this study, we identified a novel microRNA (miR-520) in RSA progression via regulating trophoblast cell apoptosis. Microarray analysis showed that miR-520 was highly expressed in villus of RSA patients. By using flow cytometry analysis, we observed miR-520 expression was correlated with human trophoblast cell apoptosis in vitro, along with decreased poly (ADP-ribose) polymerase-1 (PARP1) expression. With the analysis of clinic samples, we observed that miR-520 level was negatively correlated with PARP1 level in RSA villus. In addition, overexpression of PARP1 restored the miR-520-induced trophoblast cell apoptosis in vitro. The status of chromosome in trophoblast implied that miR-520-promoted DNA-damage-induced cell apoptosis to regulate RSA progression. These results indicated that the level of miR-520 might associate with RSA by prompting trophoblast cell apoptosis via PARP1 dependent DNA-damage pathway.
Zhu L.,The First Peoples Hospital of Shangqiu
Zhonghua nan ke xue = National journal of andrology | Year: 2013
To investigate the incidence and spermatogenesis of cryptorchid testes induced by postnatal injection of estradiol. Ninety male newborn Balb/C mice were randomly divided into an experimental (n = 60), a solvent control (n = 20) and a normal control group (n = 10). The experimental mice were again assigned to a 4-week, a 6-week, an 8-week, and a 10-week subgroup, and injected subcutaneously with 17-beta estradiol (5 microg/d) from 3 to 28, 3 to 42, 3 to 56 and 3 to 70 days after birth, respectively. The incidence of cryptorchidism and morphological changes of the testes were observed at 2 weeks after drug withdrawal. The incidence rates of cryptorchidism in the 4-, 6-, 8- and 10-week groups were 0%, 26.7%, 60% and 60%, respectively, but no cryptorchidism occurred in the solvent and normal control groups. The 4- and 6-week groups showed autonomous descent of the cryptorchid testes and recovery of spermatogenesis after drug withdrawal. The models became stable and no spermatogenesis recovery was observed after 8 weeks of continuous medication. Stable cryptorchid infertile models can be established in mice by postnatally continuous injection of estradiol for over 8 weeks.
PubMed | Zhengzhou University and The First Peoples Hospital of Shangqiu
Type: Journal Article | Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico | Year: 2016
The strategy of dual inhibiting epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) pathways has been extensively investigated in advanced non-small-cell lung cancer (NSCLC), but the benefit-to-risk ratio of dual-targeted regimen versus EGFR-tyrosine kinase inhibitors (TKIs) alone is still unclear. We thus perform this meta-analysis to assess the efficacy and safety of this regimen versus EGFR-TKIs alone in those patients.Databases from PubMed, Web of Science and the Cochrane Library up to March 31, 2015 were searched to identify relevant studies. Eligible studies included prospective randomized controlled trials (RCTs) evaluating dual inhibiting EGFR and VEGF pathways versus EGFR-TKIs alone in advanced NSCLC. The endpoints were overall survival (OS), progression-free survival (PFS), objective response rate (ORR) and grade 3 or 4 adverse events. Statistical analyses were conducted by using either random effects or fixed effect models according to the heterogeneity of included studies.A total of 1918 patients with advanced NSCLC from 4 RCTs were identified for the analysis. The pooled results demonstrated that dual inhibiting EGFR and VEGF pathways significantly improved the PFS (HR 0.71, 95% CI 0.58-0.86, p<0.001) and ORR (OR 1.54, 95% CI 1.14-2.08, p=0.005) in unselected NSCLC when compared to EGFR-TKIs alone, but it did not translate into OS benefit (HR 0.94, 95% CI 0.84-1.05, p=0.24). No evidence of publication bias was observed.Our study suggests that dual inhibition of EGFR and VEGF pathways significantly improves PFS and ORR, but it does not translate into survival benefit in unselected NSCLC patients. Prospective clinical trials investigating the role of this regimen in EGFR mutation-positive NSCLC are still warranted.
PubMed | Henan Provincial Peoples Hospital and The First Peoples Hospital of Shangqiu
Type: Journal Article | Journal: Oncology reports | Year: 2016
The aim of this study was to verify whether anti-miR-101 participates in the treatment of hepatocellular carcinoma(HCC) as a small-molecule antitumor agent, and to explore the effect on phosphatase and tensin homolog deleted on chromosome10(PTEN). Patients who received consecutive hepatectomies were followed-up, and miR-101 expressions in their tumor and paracancerous tissues were detected. Correlation between miR-101 expression and clinical pathological factors and prognosis was studied. Highthroughput sequencing was used to detect the genetic and microRNA(miRNA) levels of tumor tissues. Expression of anti-miR-101 in different HCC cell lines was determined, and those of desired genes and proteins were detected by qRT-PCR and western blotting to obtain the target gene. miR-101 was significantly upregulated in HCC patients compared with that in paracancerous tissues. High miR-101 expression, vascular invasion, tumor size 7cm and late pathological stage were the risk factors of recurrence-free survival rate. High miR-101 expression was the independent prognostic factor of total and recurrence-free survival rates. CXCL12, IL6R, FOXO3 and PTEN were screened as desired genes, and only PTEN was expressed significantly differently in three cell lines. miR-101 could bind 3-UTR of WT-PTEN with reduced fluorescent intensity, suggesting that PTEN was the target gene. SMMC-7721, HepG2 and Huh7 were eligible cell lines for miR-101 studies. miR-101 was an applicable molecular marker of HCC. Anti-miR-101 regulated the transcription of PTEN and may promote cell proliferation, differentiation and apoptosis by regulating downstream genes with PTEN. The regulatory effects of anti-miR-101 on PTEN provide valuable evidence for finding novel miRNA drugs.