First Peoples Hospital of Nanning

Nanning, China

First Peoples Hospital of Nanning

Nanning, China
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Li K.,Guangxi Medical University | Du Y.,Guangxi Medical University | Jiang B.-L.,First Peoples Hospital of Nanning | He J.-F.,Guangxi Medical University
Medical Science Monitor | Year: 2014

Graves' ophthalmopathy is an inflammatory autoimmune disease of the orbit, characterized by inflammation and proliferation of the orbital tissue caused by CD4+T cells and orbital fibroblasts. Despite recent substantial findings regarding its cellular and molecular foundations, the pathogenesis of Graves' ophthalmopathy remains unclear. Accumulating data suggest that microRNAs play important roles in the pathophysiology of autoimmunity and proliferation. Specifically, microRNA-155 (miR-155) can promote autoimmune inflammation by enhancing inflammatory T cell development. In contrast to miR-155, microRNA-146a (miR-146a) can inhibit the immune response by suppressing T cell activation. Furthermore, miR-155 and miR-146a are involved in cell proliferation, differentiation, and many other life processes. Thus, miR-155 and miR-146a, with opposite impacts on inflammatory responses carried out by T lymphocytes, appear to have multiple targets in the pathogenesis of Graves' ophthalmopathy. Our previous work showed that the expression of miR-146a was significantly decreased in peripheral blood mononuclear cells from Graves' ophthalmopathy patients compared with normal subjects. Accordingly, we proposed that the expression of miR-155 increased and the expression of miR-146a decreased in the target cells (CD4+T cells and orbital fibroblasts), thus promoting ocular inflammation and proliferation in Graves' ophthalmopathy. The proposed hypothesis warrants further investigation of the function of the differentially expressed microRNAs, which may shed new light on the pathogenesis of Graves' ophthalmopathy and lead to new strategies for its management. © Med Sci Monit, 2014.


Duan M.-C.,Eighth Peoples Hospital of Nanning | Zhong X.-N.,Guangxi Medical University | Liu G.-N.,Guangxi Medical University | Wei J.-R.,First Peoples Hospital of Nanning
Journal of Immunology Research | Year: 2014

Pathogenic mechanisms underlying the development of lung cancer are very complex and not yet entirely clarified. T lymphocytes and their immune-regulatory cytokines play a pivotal role in controlling tumor growth and metastasis. Following activation by unique cytokines, CD4+ T helper cells differentiate into Th1, Th2, Th17, and regulatory T cells (Tregs). Traditionally, research in lung cancer immunity has focused almost exclusively on Th1/Th2 cell balance. Recently, Th17 cells and Tregs represent an intriguing issue to be addressed in lung cancer pathogenesis. Tregs play an important role in the preservation of self-tolerance and modulation of overall immune responses against tumor cells. Th17 cells directly or via other proinflammatory cytokines modulate antitumor immune responses. Notably, there is a close relation between Tregs and Th17 cells. However, the possible interaction between these subsets in lung cancer remains to be elucidated. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent a useful tool for lung cancer treatment in the future. The purpose of this review is to discuss recent findings of the role of these novel populations in lung cancer immunity and to highlight the pleiotropic effects of these subsets on the development and regulation of lung cancer. © 2014 Min-Chao Duan et al.


Li Z.,Kunming Medical University | Yang Y.,First Peoples Hospital of Nanning | Gao Y.,Kunming Medical University | Wu X.,Kunming Medical University | And 6 more authors.
American Journal of Cancer Research | Year: 2016

Accumulating evidence has revealed that the expression of the lipid raft protein flotillin-1 is elevated in various human cancers, but the role flotillin-1 plays in the carcinogenesis of cervical cancer remains unclear. The expression profile of flotillin-1 was assayed using real-time PCR, western blotting, and immunohistochemical (IHC) staining in cervical cancer cell lines and cancer tissues with paired adjacent noncancerous cervical tissues. The expression of flotillin-1 protein was detected by IHC staining in a large cohort of 308 paraffin-embedded cervical cancer tissues. Ectopic expression and the short hairpin RNA interference approach were employed to determine the role of flotillin-1 in cervical cancer cell metastasis and the possible mechanism involved. Flotillin-1 expression protein and mRNA were significantly upregulated in cervical cancer cell lines and cancer tissues; elevated expression of flotillin-1 protein in early-stage cervical cancer was significantly associated with pelvic lymph node metastasis (P < 0.001), and was an independent predictive factor of poor overall survival. Moreover, flotillin-1 up- and downregulation remarkably affected cervical cancer cell motility and invasion, respectively, through epithelial-mesenchymal transition (EMT) regulated by the Wnt/β-catenin and nuclear factor-κB (NF-κB) pathways. Our results suggest that flotillin-1 facilitates cervical cancer cell metastasis through Wnt/β-catenin and NF-κB pathway-regulated EMT and that the flotillin-1 expression profile serves not only as novel predictor of pelvic lymph node metastasis, but also as neoteric risk factor for patients with early-stage cervical cancer.


Gu R.,Jinan University | Gu R.,First Peoples Hospital of Nanning | Liu N.,Jinan University | Luo S.,Jinan University | And 3 more authors.
Medicine (United States) | Year: 2016

It has been suggested that microRNA-9 (miR-9) is associated with the development of knee osteoarthritis (OA). This study was aimed to investigate the association between the mechanism of miR-9 targeting nuclear factor kappa-B1 (NF-kB1) and the proliferation and apoptosis of knee OA chondrocytes. Cartilage samples were collected from 25 patients with knee OA and 10 traumatic amputees, and another 15 OA rat models, together with 15 rats without knee OA lesions were also established. MiR-9 expressions in both knee OA cartilage and normal cartilage samples were detected using quantitative real-time PCR. The expressions of related genes (NF-kB1, IL-6, and MMP-13) in the two groups were also detected. Dual luciferase reporter gene assay was employed to examine the effect of miR-9 on the luciferase activity of NF-kB1 30UTR. Knee OA chondrocytes were transfected with miR-9 mimics, miR-9 inhibitor, and NF-kB1 siRNA, respectively, and changes in cellular proliferation and apoptosis were detected via MTT assay and flow cytometric analysis, respectively. Western blotting assay was used to detect the expressions of NF-kB1, interleukin-6 (IL-6), and matrix metalloproteinase-13 (MMP-13). According to results from human OA samples and rat OA models, miR-9 was significantly downregulated in knee OA cartilage tissues compared with normal cartilage tissues (P<0.01). The expressions of NF-kB1, IL-6, and MMP-13 in knee OA cartilage tissues were significantly higher than those in normal cartilage tissues (P<0.01). Dual luciferase reporter gene assay showed that miR-9 could bind to the 30UTR of NF-kB1 and significantly inhibit the luciferase activity by 37% (P<0.01). Upregulation of miR-9 or downregulation of NF-kB1 could promote cell proliferation and suppress cell apoptosis. Conclusively, downregulated miR-9 can facilitate proliferation and antiapoptosis of knee OA chondrocytes by directly binding to NF-kB1, implying that stimulating miR-9 expressions might assist in treatment of knee OA. Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All.


Qin Y.,Guangxi Medical University | Li L.,Guangxi Medical University | Chen J.,Guangxi Medical University | Tang X.,First Peoples Hospital of Nanning | And 3 more authors.
Oncology Research | Year: 2012

Fentanyl is used as an analgesic to treat pain in a variety of patients with cancer. Moreover, fentanyl may affect tumor growth in many cell lines. To gain better insight into the interaction between fentanyl and tumor, we investigated the effects of fentanyl on the growth of gastric carcinoma cells and the expression of some apoptosis-related genes including NF-κB and PTEN. A human gastric cancer cell line MGC-803 was used. The viability and proliferation of gastric cancer MGC-803 cells were detected by MTT assay and colony formation assay. The cell cycle progression and apoptosis were assessed by flow cytometry and the ultrastructure of cells was examined with transmission electron microscope. The migration of cells was investigated by wound healing assay. The expression of NF-κB and PTEN was evaluated by semiquantitative RT-PCR and Western blot. Our data showed that fentanyl could inhibit cell growth and proliferation and made cell cycle arrest at G2/M phase. Compared with control cells, MGC-803 cells that were incubated with fentanyl also had a higher apoptotic rate. Fentanyl could lead to morphological changes of gastric cancer cells and reduce the motility of MGC-803 cells. Moreover, fentanyl could downregulate NF-κB and upregulate PTEN, which might be the mechanism of fentanyl inhibiting gastric cancer progression in vitro. Copyright © 2012 Cognizant Comm. Corp.


Su S.Y.,Guangxi Medical University | Zhou X.,Guangxi Medical University | Pang X.M.,First Peoples Hospital Of Nanning | Chen C.Y.,Guangxi Medical University | And 2 more authors.
Genetics and Molecular Research | Year: 2016

Neurofibromatosis type 1, also known as NF1 or von Recklinghausen’s disease, is a common neurocutaneous syndrome that presents with multiple café-au-lait patches, skinfold freckling, dermatofibromas, neurofibromas, and Lisch nodules. The mutations of the gene NF1, encoding the protein neurofibromin, have been identified as the cause of this disease. Here, we report a clinical and molecular study of a Chinese patient with multiple café-au-lait skin freckles, dermatofibroma, central and peripheral nervous system tumors, and bone abnormalities attributed to NF1. The patient showed >6 café-au-lait spots on the body and multiple dermatofibromas. A brain glioma and multiple nerve sheath tumors inside and outside the vertebral canal were identified by magnetic resonance imaging, which also showed multiple intercostal nerve schwannomas and hydrocephalies above the cerebellar tentorium. Talipes equinus was also apparent. A mutation analysis of the NF1 gene revealed a novel frameshift mutation in exon 43, consisting of a heterozygous deletion of four nucleotides (GAGA) between positions 6520 and 6523. No NF1 mutations were detected in the patient’s parents or younger brother. These results extend the list of known mutations in this gene. The absence of the NF1 mutation in the healthy family members suggests that it is responsible for the NF1 phenotype. To our knowledge, this frameshift mutation represents a novel NF1 case, and may be associated with nervous system tumors and bone abnormalities. © FUNPEC-RP.


Duan M.,Eighth Peoples Hospital of Nanning | Duan M.,First Peoples Hospital of Nanning | Ning Z.,Eighth Peoples Hospital of Nanning | Fu Z.,First Peoples Hospital of Nanning | And 4 more authors.
Mediators of Inflammation | Year: 2015

The presence of Th17 cells and IL-27 is observed in a variety of inflammatory associated cancers. However, there are some data on the role of Th17 cells and IL-27 in the regulation of immune reactions in non-small-cell lung cancer (NSCLC). The aim of this study is to assess the variation of Th17 cells and IL-27 in the peripheral blood (PB) of patients with NSCLC. The proportion of Th17 cells in peripheral blood mononuclear cells (PBMCs) was evaluated by flow cytometry. The serum concentrations of IL-27 and IL-17 were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expression of RORγt and IL-27 in the peripheral blood was examined by real-time quantitative polymerase chain reaction (QPCR). Expression of IL-27 was lower in NSCLC patients compared with normal controls. The frequency of Th17 cells was increased in NSCLC patients, accompanied by the upregulation of IL-17 and RORγt. IL-27 negatively correlated with the number of Th17 cells and the RORγt mRNA. Our results indicate that IL-27 might inhibit Th17 differentiation in NSCLC patients and better understanding of the regulatory effects of IL-27 on Th17 cells may shed light on potential new targets in cancer prevention and therapy. © 2015 Minchao Duan et al.


Huang H.,First Peoples Hospital of Nanning | Huang F.,First Peoples Hospital of Nanning | Huang J.-P.,Hangzhou Normal University
Molecular Medicine Reports | Year: 2013

Delta-like-4 (Dll-4) prevents excess angiogenic sprouting and promotes the formation of a well-differentiated vascular network. Therefore, transplantation of Dll-4-overexpressing endothelial progenitor cells (EPCs) was hypothesized to be superior to transplantation of EPCs in the treatment of ischemic heart disease. In the current study, EPCs harvested from C57BL/6 mouse bone marrow were infected in vitro with Dll-4 (EPCDll-4+) or Dll-4 knockdown (EPCDll-4-) with recombinant lentiviral vectors and the control cells were non-transfected or transduced with mock vectors (EPCnull). Eight-week-old C57BL/6 mice underwent ligation of the left anterior descending artery to establish a myocardial infarction (MI) model. The ligated animals were randomly divided into 5 groups, which, following one week, were intravenously injected with EPCs, EPCnull, EPCDll-4+, EPC Dll-4-or medium. Two weeks later, echocardiographic assessment, western blotting, fluorescent microsphere and histological studies were performed. The results demonstrated that the number of mature vessels and blood flow in ischemic myocardium were increased in the EPCDll-4+ group, but were markedly decreased in the EPCDll-4-group compared with the control groups. The expression levels of Dll-4, hairy/enhancer of split (Hes)-related protein 1 (Hey-1), phosphorylation of mammalian target of rapamycin (mTOR) and p70S6 kinase (p70S6K) were significantly increased in the EPCDll-4+ group, while they were markedly decreased in the EPC Dll-4-group. Furthermore, for EPCDll-4+-treated animals, an enhanced cardiac function was observed as assessed by echocardiography. Thus, the transplantation of Dll-4-overexpressing EPCs stimulates neovascularization effectively, increases the blood flow to the ischemic zone and improves cardiac function. These effects may be due to the activation of Notch/Hey-1/mTOR/p70S6K signaling pathways, which are initiated by Dll-4.


PubMed | Guangxi Medical University and First Peoples Hospital of Nanning
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2016

Neurofibromatosis type 1, also known as NF1 or von Recklinghausens disease, is a common neurocutaneous syndrome that presents with multiple caf-au-lait patches, skinfold freckling, dermatofibromas, neurofibromas, and Lisch nodules. The mutations of the gene NF1, encoding the protein neurofibromin, have been identified as the cause of this disease. Here, we report a clinical and molecular study of a Chinese patient with multiple caf-au-lait skin freckles, dermatofibroma, central and peripheral nervous system tumors, and bone abnormalities attributed to NF1. The patient showed >6 caf-au-lait spots on the body and multiple dermatofibromas. A brain glioma and multiple nerve sheath tumors inside and outside the vertebral canal were identified by magnetic resonance imaging, which also showed multiple intercostal nerve schwannomas and hydrocephalies above the cerebellar tentorium. Talipes equinus was also apparent. A mutation analysis of the NF1 gene revealed a novel frameshift mutation in exon 43, consisting of a heterozygous deletion of four nucleotides (GAGA) between positions 6520 and 6523. No NF1 mutations were detected in the patients parents or younger brother. These results extend the list of known mutations in this gene. The absence of the NF1 mutation in the healthy family members suggests that it is responsible for the NF1 phenotype. To our knowledge, this frameshift mutation represents a novel NF1 case, and may be associated with nervous system tumors and bone abnormalities.


PubMed | Sun Yat Sen University, Kunming Medical University and First Peoples Hospital of Nanning
Type: Journal Article | Journal: American journal of cancer research | Year: 2016

Accumulating evidence has revealed that the expression of the lipid raft protein flotillin-1 is elevated in various human cancers, but the role flotillin-1 plays in the carcinogenesis of cervical cancer remains unclear. The expression profile of flotillin-1 was assayed using real-time PCR, western blotting, and immunohistochemical (IHC) staining in cervical cancer cell lines and cancer tissues with paired adjacent noncancerous cervical tissues. The expression of flotillin-1 protein was detected by IHC staining in a large cohort of 308 paraffin-embedded cervical cancer tissues. Ectopic expression and the short hairpin RNA interference approach were employed to determine the role of flotillin-1 in cervical cancer cell metastasis and the possible mechanism involved. Flotillin-1 expression protein and mRNA were significantly upregulated in cervical cancer cell lines and cancer tissues; elevated expression of flotillin-1 protein in early-stage cervical cancer was significantly associated with pelvic lymph node metastasis (P < 0.001), and was an independent predictive factor of poor overall survival. Moreover, flotillin-1 up- and downregulation remarkably affected cervical cancer cell motility and invasion, respectively, through epithelial-mesenchymal transition (EMT) regulated by the Wnt/-catenin and nuclear factor-B (NF-B) pathways. Our results suggest that flotillin-1 facilitates cervical cancer cell metastasis through Wnt/-catenin and NF-B pathway-regulated EMT and that the flotillin-1 expression profile serves not only as novel predictor of pelvic lymph node metastasis, but also as neoteric risk factor for patients with early-stage cervical cancer.

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