Publications by authors named "Xiaoyang Gong"

4 Publications

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[Analysis of efficacy of coblation assisted endoscope system for the treatment of parapharyngeal space tumors with transoral approach].

Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2021 Mar;35(3):204-208

Department of Otorhinolaryngology,the First Affiliated Hospital,Nanjing Medical University,Nanjing,210029,China.

To summarize and analyze the feasibility, safety and efficacy of parapharyngeal space surgery assisted by coblation and endoscopic system with transoral approach. The data of 20 patients with parapharyngeal space tumors were retrospectively analyzed. All the patients underwent CT and/or MRI examination before surgery, and all underwent transoral approach assisted by coblation and endoscopic systems. The patients were followed up strictly after the operation, with a follow-up time of 8-56 months and the median follow-up time of 28 months. Among the 20 patients, 18 (90%) were pathologically benign tumors and 2 (10%) were malignant tumors. The maximum tumor diameter was (4.4±1.6) cm, the operative time was (79.00±30.03) min, the intraoperative blood loss was (23.63±22.20) mL, and the postoperative pain VAS score was 2.8±1.4. There were 17 cases complete resection, and 3 cases of relapse, including 1 patient who died after distant metastasis of synovial sarcoma postoperative complications occurred in 2 cases, hoarseness in 1 case of neurofibroma and tongue extension deflection in 1 case of schwannoma. Coblation assisted endoscopic system for the treatment of parapharyngeal space tumors with transoral approach has no cervical scar, which is a satisfaction for the patients, less intraoperative bleeding, short operative time, mild postoperative reaction and quick recovery. However, external approach is still recommended for primary malignant lesions, extensive or highly vascularized lesions, tumors located on the lateral side of the internal carotid artery, less than 2 cm from the skull base, or lateral invasion of the deep lobe of the parotid gland, or a pleomorphic adenoma is considered or is found to be too large to be completely resected preoperatively or intraoperatively.
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http://dx.doi.org/10.13201/j.issn.2096-7993.2021.03.003DOI Listing
March 2021

Neuroprotective effects of ginsenoside Rg1 through the Wnt/β-catenin signaling pathway in both in vivo and in vitro models of Parkinson's disease.

Neuropharmacology 2016 Feb 23;101:480-9. Epub 2015 Oct 23.

Department of Physiology, Dalian Medical University, Da'lian 116044, China. Electronic address:

Ginsenoside Rg1 (Rg1) is a major bioactive ingredient in Panax ginseng that has low toxicity and has been shown to have neuroprotective effects. The objectives of the present study were to explore the potential of the application of Rg1 for the treatment of Parkinson's disease (PD) and to determine whether its neuroprotective effects are exerted through the Wnt/β-catenin signaling pathway by using in vivo and in vitro models of PD. In the in vivo study, Rg1 treatment ameliorated the behavioral deficits of "Pole test", and reduced dopaminergic cell loss that were induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) in a dose-dependent manner in an in vivo model of PD. In the in vitro study, cell viability was increased and cell apoptosis induced by 1-methyl-4-phenylpyridinium(MPP+) was decreased by Rg1 pretreatment. Rg1 induced protective effects on the protein and mRNA expression levels of markers of the Wnt/β-catenin signaling pathway in both the in vivo and the in vitro studies, and these neuroprotective effects were blocked by DKK1 in the in vitro study. Our results provide evidence that Rg1 has neuroprotective effects in both in vivo and in vitro PD models, and these effects act through the Wnt/β-catenin signaling pathway. Taken together, these results indicate that Rg1 may exert therapeutic effects on PD via the Wnt/β-catenin signaling pathway and may therefore provide a novel approach for the treatment of PD.
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http://dx.doi.org/10.1016/j.neuropharm.2015.10.024DOI Listing
February 2016

Rat hippocampal proteomic alterations following intrahippocampal injection of amyloid beta peptide (1-40).

Neurosci Lett 2011 Aug 14;500(2):87-91. Epub 2011 Jun 14.

Department of Traditional Chinese Medicine, The Second Affiliated Hospital, Dalian Medical University, Dalian 116023, China.

Amyloid beta peptide 1-40 (Aβ(1-40)) is closely associated with the progressive neuronal loss and cognitive decline observed in Alzheimer's disease (AD). This study aimed to establish a proteomic strategy for the profiling of AD tissues for disease-specific changes in protein abundance. Intrahippocampal injection of Aβ(1-40) induced spatial memory and learning decline in rats. Proteomic analysis revealed the changes in protein expression in the rat hippocampus treated with Aβ(1-40). Four proteins of interest which was in abundance was significantly altered in Aβ(1-40)-treated rats were identified by peptide mass fingerprint (PMF). These proteins corresponded to synapsin Ib, protein disulfide-isomerase A3 precursor, tubulin β chain and ATP synthase β subunit. Our results provide new insights into the relationship between Aβ and the pathogenesis of AD, and suggest potential targets for the therapy of AD.
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http://dx.doi.org/10.1016/j.neulet.2011.06.009DOI Listing
August 2011

Role of the SNK-SPAR pathway in the development of Alzheimer's disease.

IUBMB Life 2010 Mar;62(3):214-21

Department of Traditional Chinese Medicine, The First Affiliated Hospital, Dalian Medical University, Liaoning Province, China.

Alzheimer's disease (AD) is characterized by the presence of senile plaques and neurofibrillary tangles in the brain. The beta-amyloid peptide (Abeta) is the primary constituent of the senile plaques, and has been proposed to be a key contributor to the neurodegeneration observed in AD. The molecular mechanisms underlying dendritic spine damage that is induced by Abeta toxicity in AD patients remain largely unknown. It has been suggested previously that the SNK-SPAR signaling pathway is involved in activity-dependent remodeling of synapses. The relationship between the SNK-SPAR pathway and Abeta-induced excitotoxicity, however, is poorly understood. The present study investigated the effects of bilateral intrahippocampal injection of Abeta peptide 1-40 (Abeta(1-40)) on learning and memory in the rat, and explored the mechanisms underlying the effects of this injection. We reported that bilateral injection of Abeta(1-40) in rats resulted in impaired performance in the step-down passive avoidance and Morris water maze tasks. Then we examined mRNA and protein expression levels in the different brain regions one week after injection with Abeta(1-40) and found that the SNK-SPAR signaling pathway was possibly involved in dendritic spine damage in the different brain regions of Abeta-treated rats. These results demonstrate that the SNK-SPAR pathway may possibly play a crucial role in Abeta-induced excitotoxic damage in the central nervous system by regulating synaptic stability.
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http://dx.doi.org/10.1002/iub.308DOI Listing
March 2010