Guizhou Province Peoples Hospital

Guiyang, China

Guizhou Province Peoples Hospital

Guiyang, China
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Zeng X.-J.,GuiZhou Province Peoples Hospital
European review for medical and pharmacological sciences | Year: 2017

OBJECTIVE: Pulmonary carcinoma is one common malignant tumor with a high risk of recurrence and metastasis. Non-small cell lung cancer (NSCLC) is the most common subtype. As one tumor biomarker, microRNA (miR) has tissue sensitivity and can facilitate oncogene or inhibit tumor suppressor gene. MiR-218 has abnormal expression and can work as one molecular marker for tumors. However, its expression and function mechanism in lung cancer cells have not been fully illustrated.MATERIALS AND METHODS: In vitro cultured pulmonary adenoma A549 cells and normal bronchial epithelial cell line 16HBE were tested for miR-218 expression. A549 cells were transfected with miR-218 mimic or negative controls, followed by real-time PCR quantifying for miR-218. MTT method was used to test cell proliferation, whilst Transwell chamber was adopted for measuring cell invasion. Dual luciferase reporter gene assay (DLRGA) was used to test target relationship between miR-218 and CDCP1. Western blot was used to test CDCP1 expression.RESULTS: MiR-218 was down-regulated in A549 cells compared to 16HBE (p<0.05). Transfection of miR-218 mimic significantly facilitated miR-218 expression, inhibited tumor proliferation or invasion. As the target gene of miR-218, CDCP1 expression was suppressed by miR-218 over-expression (p<0.05 compared to control group).CONCLUSIONS: MiR-218 inhibits NSCLC proliferation or metastasis via down-regulating CDCP1, and can work as one novel molecular target for lung cancer diagnosis.


Li X.,The General Hospital of Jinan Military Region | Yang Y.,Guizhou Province Peoples Hospital | Fang J.,The General Hospital of Jinan Military Region | Zhang H.,The General Hospital of Jinan Military Region
International Journal of Clinical and Experimental Pathology | Year: 2013

Found in inflammatory zone (FIZZ1), also known as hypoxia-induced mitogenic factor (HIMF), is a secreted protein formed by 111 amino acid residues. FIZZ1 is mainly located in alveolar epithelial cells, white adipose tis-sue and the heart. This study aimed to explore the effects of FIZZ1 on the angiogenic ability of cultured rat aortic endothelial cells (RAECs) and the potential mechanism. The RAECs were cultured in the extracellular matrix (ECM) supplemented with 10% fetal bovine serum (FBS). Matrigel assay was used to detect the angiogenic ability of the RAECs and Agilent Rat Microarray containing 41,000 genes/ESTs was used to screen the differentially expressed genes of the RAECs after they were treated with FIZZ1 (5 × 10-9~2 × 10-8 mol/L). The results were verified using RT-PCR method. We found that FIZZ1 markedly enhanced the angiogenic ability of RAECs (22.6 ± 2.94 vs. 19.7 ± 2.57, P < 0.01; 28.5 ± 3.32 vs. 19.7 ± 2.57, P < 0.01; 36.9 ± 5.01 vs. 19.7 ± 2.57, P < 0.01) in a dose-dependent manner (5 × 10-9~2 × 10-8 mol/L). 440 genes (Gng8, Atg9a, Gdf6, etc.) were found to be up-regulated and 497 genes (Hbb-b1, Camk1g, etc.) down-regulated in the experimental group. Changes in Gng8 and Atg9a were revealed by RT-PCR. FIZZ1 could enhance angiogenesis of RAECs by up-regulating Gng8 and Atg9a.


Li X.,Chongqing Medical University | Li X.,Guizhou Province Peoples Hospital | Shao X.,Guizhou Province Peoples Hospital | Wang N.,Guizhou Province Peoples Hospital | And 3 more authors.
Brain Research | Year: 2010

This study was aimed to examine the changes in auditory event-related potentials (AERPs) and their relationship with brain metabolic changes in mild cognitive impairment (MCI). 34 MCI patients and 34 healthy elderly controls were subjected to auditory stimulus oddball task, and then post-stimulus potentials (P50, N100, P200, N200, and P300) were obtained, levels of N-acetylaspartate (NAA), creatine (Cr) and the ratio of NAA/Cr were measured by proton magnetic resonance spectroscopy (1H-MRS) in left frontal, left temporal and right parietal cortex. Compared with the control group, the MCI group had significantly increased P50 amplitudes and P300 latency, and the NAA/Cr was abnormal. Linear progression analysis revealed a strong negative correlation between P50 amplitudes and NAA/Cr in left frontal cortex, and negative correlation between P300 latency and NAA/Cr in left frontal and left temporal, as well as correlation of AERP components and MRS metabolites with clinical scores of cognitive tests. These findings suggest that metabolic abnormalities of different brain regions may reflect the changes of underlying brain activities that are instrumental in the MCI. Therefore AERPs and MRS measurements may offer a mean to track changes of brain activities associated with functional changes, and to assess early cognitive impairment in MCI. © 2010 Elsevier B.V.


Huang D.,Guizhou Province Peoples Hospital | Fang F.,Guizhou Province Peoples Hospital | Xu F.,Guizhou Province Peoples Hospital
Chinese Critical Care Medicine | Year: 2011

Objective: To examine the correlation between the hyperoxia-induced reactive oxygen species (ROS) production and Toll-like receptors (TLRs) expression in cultured alveolar epithelial cells in order to understand the role of TLRs signaling in inflammatory response during acute lung injury. Methods: Three groups of cultured human lung adenocarcinoma cell line A549 were exposed to: Circled digit oneair, Circled digit twohyperoxia (95%O 2 + 5%CO 2) and Circled digit three N-acetylcysteine (NAC) pretreatment + hyperoxia. The level of intracellular ROS, TLR2/4 mRNA, TLR2/4 protein and cytokin interleukin-6/8 (IL-6/8) concentrations in the culture supernatant were measured by flow cytometry, reverse transcription-polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA) in cells harvested at different time points into the treatment. Results: A549 cells were found to have a baseline (mainly intracellular) TLR2/4 expression. Continued exposure to hyperoxia caused Circled digit one a progressive increase in intracellular ROS, which became significantly higher than the air treated cells after 2 hours of exposure (11.820±3.123 vs. 7.223±1.170, P<0.01), and reached a peak after 48 hours of exposure (113.837±5.247, P<0.01): Circled digit two an increase in intracellular TLR2/4 mRNA which peaked after 2 hours of exposure (TLR2 mRNA: 1.820±0.056 vs. 1.263±0.023; TLR4 mRNA: 2.080±0.220 vs. 1.317±0.107, both P<0.01); Circled digit three significant increase in TLR2/4 protein expression (mainly intracellular), both peaked after exposure for 6 hours (TLR2 protein: 8.370±1.548 vs. 3.930±0.277; TLR4 protein: 25.803±5.783 vs. 8.867±2.230, both P<0.01). Circled digit four a progressive increase in culture supernatant IL-6 (ng/L), IL-8 (ng/L) concentration, both peaked at 48 hours (IL-6: 2 213.41±69.99 vs. 9.76±1.47; IL-8: 11 520.38±429.93 vs. 159.56±20.80, both P<0.01). NAC pre-treatment significantly supressed the hyperoxia induced intracellular ROS (14.050±1.257 vs. 31.180±2.336, P<0.01) production, the hyperoxia induced expression of TLR2/4 (TLR2 mRNA: 1.270±0.061 vs. 1.683±0.025; TLR4 mRNA: 1.587±0.058 vs. 1.650±0.139; TLR2 protein: 3.458±0.258 vs. 8.371±1.548; TLR4 protein, 11.611±3.403 vs. 25.803±5.783, all P<0.05), and the hyeroxia induced increase in IL-6 and IL-8 in supernatant level (IL-6: 8.42±0.70 vs. 73.51±16.70; IL-8: 134.94±5.19 vs. 772.82±96.05, both P<0.05), as seen in the hyperoxia treated groups. Conclusion: Hyperoxia induced intracellular ROS production can up-regulate TLR2/4 expression in A549 cells, leading to the release pro-inflammatory cytokines IL-6 and IL-8 from these cells.


Wang Y.Q.,Guizhou Province Peoples Hospital
Zhonghua er ke za zhi. Chinese journal of pediatrics | Year: 2013

Omenn syndrome is a rare autosomal recessive hereditary severe combined immunodeficiency. The purpose of this study was to understand clinical characteristics and genetic mutation type of Omenn syndrome and to improve the recognition of Omenn syndrome among pediatric clinicians. One suspected case of severe combined immunodeficiency was found to have pneumonia repeatedly, intractable diarrhea, poor antibiotic treatment effect, lymphadenopathy, hepatosplenomegaly and erythroderma. The patient was diagnosed as having Omenn syndrome by RT-PCR, and the expression of RAG1/RAG2 and gene analysis of RAG1/RAG2 were performed. The classification of lymphocyte was CD3(+) cells (35.3%), CD19(+) cells (0.4%), CD16(+) cells (57.6%). After stimulation with phytohemagglutinin (PHA), lymphocyte proliferation of the child was extremely low. Genetic studies showed RAG1 homozygous deletion mutation (2302 del T). He had detectable activated T-lymphocytes with low circulating B-lymphocytes and no evidence of maternal T-cell engrafment as indicated by the short tandem repeat (STR) analysis. Omenn syndrome is a severe combined immunodeficiency disease caused by mutations in the RAG1/RAG2 gene. The disease has been reported rarely in China. The clinical manifestations of the disease is early postnatal repeated infections and erythroderma. Mutation analysis of RAG1/RAG2 gene may help to confirm the diagnosis and may be useful in early immune reconstitution and genetic counseling.


Luo L.,Guizhou Province Peoples Hospital | Sun Z.,Guizhou Province Peoples Hospital | Luo G.,Guizhou Province Peoples Hospital
Journal of Surgical Research | Year: 2013

Background: Cyclosporin A (CsA) is associated with significant chronic nephrotoxicity, which typically manifests as renal fibrosis. In contrast, rapamycin (RAPA) has been shown to inhibit fibrosis. This study sought to determine the effect of CsA and RAPA on the expression of connective tissue growth factor (CTGF) and E-cadherin in a rat kidney model of chronic allograft nephropathy. Materials and methods: Left renal grafts from male Fisher (F344, RT11v1) rats were orthotopically transplanted into Lewis (LEW, RT11) rats. After transplantation, all recipients were given CsA 10 mg/kg-1 d-1 for 10 d and divided into three groups (n = 9/group): (1) vehicle, administered orally; (2) CsA, 6 mg/kg-1 d -1; (3) RAPA, 0.8 mg/kg-1 d-1. At 4, 8, and 12 wk posttransplantation, the kidney allografts were harvested and serum creatinine levels were measured. Connective tissue growth factor expression was determined using real-time polymerase chain reaction and Western blot. Kidney allografts sections also underwent hematoxylin-eosin and Masson trichrome staining, in addition to CTGF and E-cadherin immunostaining. Results: The serum creatinine levels were increased at 8 and 12 wk posttransplantation and were significantly lower in the RAPA group (P < 0.05). The Banff score also showed a significant decrease at 4, 8, and 12 wk (P < 0.05). CTGF messenger ribonucleic acid and protein levels were significantly lower in the RAPA group (P < 0.05), whereas E-cadherin expression was higher in the RAPA group at 4, 8, and 12 wk (P < 0.05). Masson's trichrome staining showed a significant decrease in collagen deposition at 8 and 12 wk after RAPA treatment. Conclusion: RAPA can ameliorate fibrogenesis in kidney allografts by inhibiting epithelial-mesenchymal transition process, whereas CsA did not have this effect. © 2013 Elsevier Inc. All rights reserved.


Luo G.H.,Guizhou Province Peoples Hospital
Zhonghua yi xue za zhi | Year: 2010

To determine whether urinary connective tissue growth factor (CTGF) can be a molecular marker for chronic allograft nephropathy (CAN) in a rat model. F344 rat renal grafts were orthotopically transplanted into Lewis rats (n = 24). Lewis rats underwent sham operation as control group (n = 12). Kidney grafts were harvested at Weeks 4, 8, 12 and 16 respectively. Serum creatinine (SCr) was measured. The CAN grades were evaluated according to the Banff 97 schema. The expressions of CTGF in kidney, serum and urine were determined by Western blot and competitive indirect ELISA. Spearman correlation analysis was used to compare CTGF expression and the development of CAN. The expression of CTGF in the graft group was markedly elevated in comparison with the control group. Statistics analysis of CTGF protein in kidney detected by Western blot showed significant differences between these five groups (0.33 ± 0.05 for control, 0.55 ± 0.02 for Week 4, 0.80 ± 0.03 for Week 8, 0.90 ± 0.03 for Week 12 and 1.14 ± 0.11 for Week 16, P < 0.01). Both urine and serum CTGF increased by Week 4 and maintained a high level up to Week 16. The urinary CTGF of renal allografts was (2.9 ± 0.7), (12.9 ± 3.6), (32.3 ± 11.4) and (31.0 ± 8.9) ng/mg creatinine for Weeks 4, 8, 12 and 16 respectively. The urinary levels were positively correlated with SCr, Banff scores and expression of CTGF in the graft kidney (r = 0.848, 0.874, 0.747, all P < 0.01). CTGF plays a significant role in the pathological changes of CAN after kidney transplantation. Urinary CTGF has the potential as a biomarker for predicting the clinical course of CAN.


Luo L.,Guizhou Province Peoples Hospital | Sun Z.,Guizhou Province Peoples Hospital | Wu W.,Guizhou Province Peoples Hospital | Luo G.,Guizhou Province Peoples Hospital
BMC Nephrology | Year: 2012

Background: Tacrolimus (FK506) is associated with renal fibrosis in long-term use. Mycophenolatemofetil (MMF) can also inhibit or attenuate the progression of renal fibrosis. This study aimed to determine the different effects of FK506 and MMF on fibrosis-associated genes in the kidney in rats that underwent chronic allograft nephropathy (CAN). Methods: Fisher (F344) kidneys were orthotopically transplanted into Lewis rat recipients. All recipients were given Cyclosporin A (CsA) 10 mg/kg-1·d-1 × 10 day and were then randomly divided into three oral treatment groups (n = 9 in each group): (1) the vehicle group was given vehicle orally; (2) the FK506 group was given 0.15 mg/kg-1·d-1 FK506; and (3) the MMF group was given 20 mg/kg-1.d-1 MMF. At 4, 8, and 12 weeks post-transplantation, serum creatinine (SCr), collagen deposition, Connective tissue growth factor (CTGF), alpha smooth muscle actin (α-SMA) and E-cadherin expressions were determined and hematoxylin-eosin (HE) and Periodic acid-Schiff (PAS) stains were performed. Results: Renal function progressively deteriorated and showed typical CAN morphology in the vehicle and FK506 groups, while SCr and inflammatory infiltration (Banff score) showed a significant decrease in the MMF group after 8 weeks post-transplantation compared with those in the other groups (p<0.05). Furthermore, expression levels of CTGF and α-SMA in the MMF group were significantly reduced, and the down-regulated expression of E-cadherin was abated (p<0.05). Conclusions: MMF showed favorable effects on renal interstitial fibrosis, thus efficiently retarding the progression of CAN. © 2012 Luo et al.; licensee BioMed Central Ltd.


Luo L.,Guizhou Province Peoples Hospital | Sun Z.,Guizhou Province Peoples Hospital | Cheng H.,Guizhou Province Peoples Hospital | Luo G.,Guizhou Province Peoples Hospital
Immunology Letters | Year: 2012

Many means in inbred rodent models promoted long-term graft survival or donor-specific tolerance, but less so in nonhuman primates, outbred rodents or human patients. A diverse repertoire of memory T cells, derived from heterologous immunity or prior to exposure to alloantigen, has been believed to be an important part of this barrier. Memory T cells have a unique capacity to generate effector functions quickly upon re-exposure to antigen, and this capacity is achieved by reduced activation thresholds, and expressed high level trafficking and adhesion molecules, which is likely responsible for their exhibiting differential susceptibility to immune therapeutics compared with naïve T cells. This review outlines recent progress on characteristics of memory T cells and focuses on these potential therapies targeting memory T cells which are likely to ameliorate allograft rejection by inducing transplant tolerance. © 2012 Elsevier B.V.


Luo L.,Guizhou Province Peoples Hospital | Luo G.,Guizhou Province Peoples Hospital | Fang Q.,Guizhou Province Peoples Hospital | Sun Z.,Guizhou Province Peoples Hospital
Transplantation Proceedings | Year: 2014

Background Late kidney allograft dysfunction is becoming a significant problem and tubular atrophy and interstitial fibrosis are main causes. It was reported that hypoxia could induce epithelial - mesenchymal transition (EMT) in renal tubular epithelial cells (TECs), and hypoxia-inducible factor-1 (HIF-1) is one of the important regulators of cellular adaptive to hypoxia. Methods In this study, we used an HIF-1αΔODD-expressing adenovirus, which could stably and functionally express HIF-1α under normoxia conditions, and used a hypoxia/reoxygenation cell model to simulate ischemia/reperfusion (I/R) injury in vitro, to investigate the effect of HIF-1α on EMT-related gene expressions. Results Our results demonstrated that HIF-1α could significantly upregulate α-smooth muscle actin expression, and reduced the E-cadherin expression in HK-2 cells during I/R injury. Moreover, miR-21 expression had a positive correlation with HIF-1α in this process. Conclusion These results suggest that HIF-1α may promote the EMT development through regulating fibrotic gene expression during I/R injury in human renal TECs, and miR-21 could be among the important regulatory pathways in the process. © 2014 by Elsevier Inc. All rights reserved.

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