First Peoples Hospital of Yichang

Yichang, China

First Peoples Hospital of Yichang

Yichang, China
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Yao Y.-B.,First Peoples Hospital of Yichang | Wang L.,First Peoples Hospital of Jingmen | Xia Y.,First Peoples Hospital of Yichang | Wang Z.,Shanghai University
Chinese Journal of New Drugs | Year: 2010

Drug castration therapy is important in the treatment of advanced and metastatic prostate cancer. Degarelix is a new potent GnRH-receptor antagonist, which has high water solubility, low histamine release, low systemically allergic reactions and no testosterone surge. In this article, we introduced its features of molecule construction, mechanism of action, pharmacokinetics, and clinical efficacy and safety.


Fan T.,First Peoples Hospital of Yichang | Song Y.-J.,First Peoples Hospital of Yichang
Journal of the College of Physicians and Surgeons--Pakistan : JCPSP | Year: 2016

Placement of a central venous catheter (CVC) is a common procedure, often replaced by femoral vein cannulation. The overall complication rate is 12 - 15%. Loss of a complete guide wire into the circulation is a rare and preventable complication. Here we report a case of guide wire loss during femoral venous cannulation and literature review.


Fan T.,First Peoples Hospital of Yichang | Song Y.-J.,First Peoples Hospital of Yichang
Journal of the College of Physicians and Surgeons Pakistan | Year: 2016

Pulmonary sarcomatoid carcinoma (PSC) is a rare malignant cancer composed of sarcoma and sarcoma-like elements with spindle or giant cell features. We report the case of a 60-year-old male with past medical history of right renal cell carcinoma 2 years earlier. A pulmonary nodule was detected in the left upper lobe, 23 months after nephrectomy. Systemic positron emission tomography-computerized tomography (PET-CT) revealed one high metabolic mass shadow in the left upper lobe. Chest CT scan with contrast revealed a left upper lobe mass (2.9 x 2.5 cm). The case was suspected to be a lung metastasis of renal cell carcinoma. After surgery, the pathology revealed PSC-giant cell carcinoma. The tumor's pathology and treatment methods are discussed.


Zhang Y.-Q.,China Three Gorges University | Wan L.-Y.,China Three Gorges University | Wan L.-Y.,First Peoples Hospital of Yichang | He X.-M.,China Three Gorges University | And 4 more authors.
DNA and Cell Biology | Year: 2017

Gremlin1, the antagonist of bone morphogenetic protein-7 and one of the target genes of transforming growth factor (TGF)-β signal pathway, plays an important role in embryonic development and its expression decreases along with aging. To explore the expression of gremlin1 in liver fibrosis and the causal link between gremlin1 and hepatic stellate cell (HSC) activation, we detected the expression of gremlin1 in mice with hepatic fibrosis induced by porcine serum using real time quantitative PCR (RT-qPCR) and immunohistochemical staining. The hepatic fibrosis mice were evaluated by the external feature of the liver, histology, hepatic function, collagen deposition, and the expression of fibrosis-related genes (genes COLIα2 and COLIVα2) in the liver. In the HSC-T6, western blotting was used to analyze the expression of α-smooth muscle actin (α-SMA), COL1α, and TGF-β1 in conditions of overexpression of gremlin1 or gremlin1 being knocked down by specific siRNA, respectively. The results showed that the mRNA expression of the gremlin1 gene was significantly increased consistent with increased expression of COLIα2 and COLIVα2 in the liver tissue of the hepatic fibrosis mice. Increased expression of gremlin1 coincided with the same area of the collagen deposition. Furthermore, the results also showed that the expression of α-SMA, COLIα1, and TGF-β1 was consistent with the expression of gremlin1 not only in the HSC-T6 overexpressing gremlin1 but also in the HSC-T6 that gremlin1 is knocked down by specific siRNA. The findings suggest that gremlin1 might play an important role in the progression of hepatic fibrosis and that it modulates HSC activation. © Copyright 2017, Mary Ann Liebert, Inc. 2017.


Wan L.-Y.,China Three Gorges University | Wan L.-Y.,First Peoples Hospital of Yichang | Zhang Y.-Q.,China Three Gorges University | Li J.-M.,China Three Gorges University | And 9 more authors.
DNA and Cell Biology | Year: 2016

Hepatic fibrosis is a reversible process involving plenty of transcription factors and pathways. Vitamin D receptor (VDR) as a member of ligand-induced transcription factors can interact with 9-cis retinoid X receptor (RXR) and VDR-interacting repressor (VDIR) to mediate transactivation or transrepression in the absence or in the presence of VDR ligand to regulate the expression of VDR target genes. The active form of vitamin D [1α,25(OH)2D3] can downregulate the expression of type I collagen both α1 and α2 (COLIα1 and COLIα2) in hepatic stellate cells (HSC-T6) in a time-dependent fashion, which provides a new direction for hepatic fibrosis therapy. As one of VDR target genes, rat COLIα1 gene contains 1αnVDRE (E-box1 and E-box2) in its promoter, and unliganded VDR/RXR may bind to 1αnVDRE through VDIR to mediate transactivation, whereas liganded VDR/RXR may bind to 1αnVDRE through VDIR for transrepression. The results suggested a sort of relying on each other relationship between VDR/RXR and VDIR in regulating the expression of COLIα1 gene in HSC-T6 cells, which established VDR as a potential target for blocking and even reversing hepatic fibrosis. © Copyright 2016, Mary Ann Liebert, Inc.


Pang X.-M.,Guangxi Medical University | Liu J.-L.,Guangxi Medical University | Li J.-P.,Guangxi Medical University | Huang L.-G.,Guangxi Medical University | And 6 more authors.
Journal of Neurochemistry | Year: 2015

Previous studies have shown that fastigial nucleus stimulation (FNS) reduces tissue damage resulting from focal cerebral ischemia. Although the mechanisms of neuroprotection induced by FNS are not entirely understood, important data have been presented in the past two decades. MicroRNAs (miRNAs) are a newly discovered group of non-coding small RNA molecules that negatively regulate target gene expression and are involved in the regulation of cell proliferation and cell apoptosis. To date, no studies have demonstrated whether miRNAs can serve as mediators of the brain's response to FNS, which leads to endogenous neuroprotection. Therefore, this study investigated the profiles of FNS-mediated miRNAs. Using a combination of deep sequencing and microarray with computational analysis, we identified a novel miRNA in the rat ischemic cortex after 1 h of FNS. This novel miRNA (PC-3p-3469-406), herein referred to as rno-miR-676-1, was upregulated in rats with cerebral ischemia after FNS. In vivo observations indicate that this novel miRNA may have antiapoptotic effects and contribute to neuroprotection induced by FNS. Our study provides a better understanding of neuroprotection induced by FNS. MicroRNA (miRNA) is defined as a small non-coding RNA that fulfills both the expression and biogenesis criteria. Here, we describe a novel miRNA in the rat ischemic cortex expressed after 1 h of fastigial nucleus stimulation (FNS). The miRNA was functionally characterized by secondary structure, quantitative expression, the conservation analysis, target gene analysis, and biological functions. We consider rno-miR-676-1 to be a true microRNA and present evidence for its neuroprotective effects exerted after induction by FNS. MicroRNA (miRNA) is defined as a small non-coding RNA that fulfills both the expression and biogenesis criteria. Here, we describe a novel miRNA in the rat ischemic cortex expressed after 1 h of fastigial nucleus stimulation (FNS). The miRNA was functionally characterized by secondary structure, quantitative expression, the conservation analysis, target gene analysis, and biological functions. We consider rno-miR-676-1 to be a true microRNA and present evidence for its neuroprotective effects exerted after induction by FNS. © 2015 International Society for Neurochemistry.


Wang P.,China Three Gorges University | Wang P.,First Peoples Hospital of Yichang | Fang M.,First Peoples Hospital of Yichang | Zha Y.,First Peoples Hospital of Yichang | And 3 more authors.
Neuroendocrinology Letters | Year: 2014

OBJECTIVES: Dopaminergic signaling in the basolateral amygdala (BLA) is important for emotion-related activity. However, little is known about the influence of dopamine (DA) on excitatory synaptic transmission of pyramidal neurons in BLA at early developmental stage. Here in this study, we observed the effect of DA on excitatory neurotransmission in the pyramidal cells of BLA in acute slices. METHODS: Acute slices from amygdala of rats at the age of 14-16 days were prepared and maintained in vitro using standard method. Whole-cell patch clamp recordings were performed to examine the evoked excitatory postsynaptic current (eEPSC), spontaneous excitatory postsynaptic current (sEPSC) and miniature excitatory postsynaptic current (mEPSC). Drugs including DA and synaptic blockers were added in recording solution due to different experimental designs. RESULTS: We found that bath application of DA at a concentration of 100 μM significantly inhibited the amplitude of evoked EPSC. However, the amplitude and frequency of mEPSC were not affected. We also found increased pair pulse facilitation after DA application, indicating DA inhibited excitatory neurotransmission through suppression of release probability at the pre-synaptic terminals. Importantly, DA was also effective in decreasing activity induced upregulation in sEPSCs. Moreover, the DA effects were not affected by either antagonist of dopamine 1 or dopamine 2-like receptors. CONCLUSION: We studied the effects of DA on excitatory neurotransmission and found that DA inhibited glutamatergic synaptic transmission via modulation of pre-synaptic release probability.


Li Q.,First Peoples Hospital of Yichang | Chen J.,Huazhong University of Science and Technology | Chen Y.,Huazhong University of Science and Technology | Cong X.,Huazhong University of Science and Technology | Chen Z.,Huazhong University of Science and Technology
Molecular Medicine Reports | Year: 2016

In the present study, pathological alterations in neurons of the dorsal root ganglia (DRG) were investigated in a rat model of chronic sciatic nerve compression. The rat model of chronic sciatic nerve compression was established by placing a 1 cm Silastic tube around the right sciatic nerve. Histological examination was performed via Masson's trichrome staining. DRG injury was assessed using Fluoro Ruby (FR) or Fluoro Gold (FG). The expression levels of target genes were examined using reverse transcription-quantitative polymerase chain reaction, western blot and immunohistochemical analyses. At 3 weeks post-compression, collagen fiber accumulation was observed in the ipsilateral area and, at 8 weeks, excessive collagen formation with muscle atrophy was observed. The collagen volume fraction gradually and significantly increased following sciatic nerve compression. In the model rats, the numbers of FR-labeled DRG neurons were significantly higher, relative to the sham-operated group, however, the numbers of FG-labeled neurons were similar. In the ipsilateral DRG neurons of the model group, the levels of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) were elevated and, surrounding the neurons, the levels of collagen type I were increased, compared with those in the contralateral DRG. In the ipsilateral DRG, chronic nerve compression was associated with significantly higher levels of phosphorylated (p)-extracellular signal-regulated kinase 1/2, and significantly lower levels of p-c-Jun N-terminal kinase and p-p38, compared with those in the contralateral DRGs. Chronic sciatic nerve compression likely induced DRG pathology by upregulating the expression levels of TGF-β1, CTGF and collagen type I, with involvement of the mitogen-activated protein kinase signaling pathway.


Ni J.,Georgia Regents University | Ni J.,First Peoples Hospital of Yichang | Ni J.,China Three Gorges University | Dong Z.,Georgia Regents University | And 3 more authors.
Free Radical Biology and Medicine | Year: 2013

Myofibroblast transformation is a key process in the pathogenesis of lung fibrosis. We have previously reported that hyperoxia induces RhoA activation in HFL-1 lung fibroblasts and RhoA mediates collagen synthesis in hyperoxic lung fibrosis. In this study, we investigated the role of RhoA and actin cytoskeleton in hyperoxia-induced myofibroblast transformation. Exposure of HFL-1 lung fibroblasts to hyperoxia stimulated actin filament formation, shift of G-actin to F-actin, nuclear colocalization of myocardin-related transcription factor-A (MRTF-A), recruitment of MRTF-A to the α-smooth muscle actin (α-SMA) gene promoter, myofibroblast transformation, and collagen-I synthesis. Inhibition of RhoA by C3 transferase CT-04 or dominant-negative RhoA mutant T19N, and inhibition of ROCK by Y27632, prevented myofibroblast transformation and collagen-I synthesis. Moreover, inhibition of RhoA by CT-04 prevented hyperoxia-induced actin filament formation, shift of G-actin to F-actin, and nuclear colocalization of MRTF-A. In addition, disrupting actin filaments with cytochalasin D or scavenging reactive oxygen species (ROS) with tiron attenuated actin filament formation, nuclear colocalization of MRTF-A, myofibroblast transformation, and collagen-I synthesis. Furthermore, overexpression of constitutively active RhoA mutant Q63L or stabilization of actin filaments recapitulated the effects of hyperoxia on the actin cytoskeleton and nuclear colocalization of MRTF-A, myofibroblast transformation, and collagen-I synthesis. Interestingly, knocking down MRTF-A prevented hyperoxia-induced increase in the recruitment of MRTF-A to the serum response factor transcriptional complex on the α-SMA gene promoter, myofibroblast transformation, and collagen-I synthesis. Finally, Y27632 and tiron attenuated hyperoxia-induced increases in α-SMA and collagen-I in mouse lungs. Together, these results indicate that the actin cytoskeletal reorganization due to the ROS/RhoA-ROCK pathway mediates myofibroblast transformation and collagen synthesis in lung fibrosis of oxygen toxicity. MRTF-A contributes to the regulatory effect of the actin cytoskeleton on myofibroblast transformation during hyperoxia. © 2013 Elsevier Inc.


Wu J.-f.,China Three Gorges University | Feng G.,First Peoples Hospital of Yichang | Shi H.,China Three Gorges University | Zhang Q.-j.,China Three Gorges University | Wang X.-l.,China Three Gorges University
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2011

BACKGROUND: Studies show that the microencapsulated heterogeneous olfactory bulb cells can reduce the immunological rejection and improve the functional recovery of spinal cord injury. However, the mechanism is unclear. OBJECTIVE: To investigate the effects of the xenotransplantation of microencapsulated olfactory bulb cells into rats on the expression and activity of nuclear factor-kappa B (NF-κB) after spinal cord injury. METHODS: Rabbits were used to prepare the heterogeneous olfactory bulb cell suspension. Sprague Dawley rats were randomly divided into four groups: the sham operation group, the microcapsule group, the cell group and the simple injury group. The rats in the later three groups were prepared for spinal cord hemisection model and transplanted with gelatin sponge sticking 10 μL microencapsulated olfactory bulb cell suspension, 10 μL microencapsulated olfactory bulb cell suspension, and 10 μL physiological saline respectively. The pathological changes of spinal tissues were observed by haematoxylin-eosin staining, and the expressions of NF-κB were observed by immunohistochemical staining. RESULTS AND CONCLUSION: The expressions of NF-κB in the cytoplasm and cytoblast of neurons were increased in rats after spinal cord injury. The expression level reached a peak at 24 hours, gradually decreased after 3 days, and returned to the normal level after 7 days. The NF-κB+ cells in the microcapsule group were obviously fewer than that in the cell and simple injury groups (P < 0.05). The xenotransplantation of microencapsulated olfactory bulb cells can inhibit the expression and activity of NF-κB to mitigate the NF-κB modified inflammatory reaction after spinal cord injury.

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