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Ganzhou, China

Xiong J.,Gannan Medical College | Song T.,Teaching and Research Section of Biochemistry and Molecular Biology
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2010

BACKGROUND: With development of modern science, various high energy rays, which are widely applied for military affairs, communication, medical science, and daily life, directly cause increasing of radiation dose annually. Therefore, image quality and radiation protection attract more and more attention. Radiation protection plays an important role in modern medical science. For protecting human health, protection tools are necessary for shielding varying rays and microwaves. OBJECTIVE: To summarize mechanism, classification, characteristics, and research status of radiation protection materials. METHODS: Articles were retrieved from PubMed database (http://www.ncbi.nlm.nih.gov/ PubMed) and Wanfang database (http://www.wanfangdata.com.cn) with the key words of "shielding materials, shielding mechanism, protection, classification" from 1982 to 2010. Inclusion criteria: Articles related to shielding mechanism, classification, characteristics, and research status were included. Duplicated papers were excluded. Among 23 articles, 16 ones were included in the final analysis. RESULTS AND CONCLUSION: Shielding materials absorbed rays depending on energy absorption and particle absorption. Medical ray protection materials included organic glass, compound protection materials mixed by a certain ratio of lead, wolfram, and barium, and varying radiation protection clothing. With the development of science and technology, adverse effects induced by various radiations should be relieved, so protection materials and techniques need to be further studied for clinical application. Source

Shumei L.,Gannan Medical College
Advances in Experimental Medicine and Biology | Year: 2010

Objective: Mutations in the inosine monophosphate dehydrogenase 1 gene (IMPDH1) have recently been discovered that IMPDH1 gene plays a critical role in pathogenesis of autosomal dominant retinitis pigmentosa (adRP). Aiming towards an understanding of the molecular background of retinitis pigmentosa (RP), this paper investigates the mutation frequency of IMPDH1 genes in the Han patients with adRP in Ganzhou City. Methods: The whole blood samples were collected randomly from 56 adRP patients and 62 unrelated normal controls who were residents of Han population in Ganzhou City, and then their genomic DNA samples were extracted respectively. Genic polymorphism was examined by the polymerase chain reaction and restrictionfragment-length polymorphisms (PCR-RFLP). The statistical significance of the data was further analyzed by SPSS 14.0 software. Results: Mutation rate of IMPDH1 gene had no significance between in adRP patients and in the normal control by exact probabilities in 2 × 2 table (p = 0.232). The mutation frequency of IMPDH1gene in the Han samples was 3.6%. Conclusion: The mutation frequency of IMPDH1 gene of the Han population in Ganzhou city was similar as approximately 2-5% of the adRP cases among Americans of European origin and Europeans. © Springer Science+Business Media, LLC 2010. Source

He W.,Huazhong University of Science and Technology | He W.,Gannan Medical College | Xu X.,Huazhong University of Science and Technology | Lv Q.,Huazhong University of Science and Technology | Guo L.,Huazhong University of Science and Technology
Cellular and Molecular Neurobiology | Year: 2014

Focal cerebral ischemia can impair the induction of activity-dependent long-term potentiation (LTP) in the hippocampus. This impairment of hippocampal synaptic plasticity can be caused by excitotoxicity and subsequent perturbation of hippocampal LTP-relevant transmitter systems, which include NR2B and PSD-95. It has been suggested that hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels may play an important role in the control of membrane excitability and rhythmic neuronal activity. Our previous study has indicated that the selective HCN channel blocker ZD7288 can produce a dose-dependent inhibition of the induction of LTP at the Schaffer collateral-CA1 synapse of hippocampus by reducing the amount of glutamate released. It has also been demonstrated that ZD7288 can protect against neuronal injury caused by oxygen glucose deprivation. In the present study, we investigated the effect of ZD7288 on the induction of activity-dependent LTP and the expression of NR2B and PSD-95 after focal cerebral ischemia/reperfusion injury. The results showed that the induction of LTP was significantly impaired and the levels of NR2B and PSD-95 mRNA and protein were markedly decreased in the CA1 region of hippocampus following focal cerebral ischemia/reperfusion injury. Administration of low dose ZD7288 (0.25 μg) at 30 min and 3 h after the onset of ischemia attenuated the impairment of LTP induction and alleviated the NR2B and PSD-95 mRNA and protein down-regulation commonly induced by cerebral ischemia/reperfusion injury. These results suggest that low dose ZD7288 can ameliorate the ischemia/reperfusion-induced impairment of synaptic plasticity in the hippocampal CA1 region. © 2014 Springer Science+Business Media New York. Source

Shumei L.,Gannan Medical College
Advances in Experimental Medicine and Biology | Year: 2010

Objective: To study the effect of hesperidin on expression of inducible nitric oxide synthase (iNOS) in cultured rabbit retinal pigment epithelial (RPE) cells under the condition of high glucose in vitro. Method: Hesperidin was extracted from Pericarpium Citri Reticulatae by ultrasound and ethanol precipitation and was detected qualitatively by high performance liquid chromatogram. The third to fifth primary cultured rabbit RPE were selected. The cells were divided into 6 groups including the control group cultured in DMEM, the model group cultured in DMEM containing 33 mmol/L glucose without any drug and four experimental groups which were exposed to hesperidin at the concentration of 10, 20, 40 and 80 mg/L at 37°C under 5% CO2 for 2 h and then cultured in DMEM containing 33 mmol/L glucose. The proliferation of RPE was measured by the MTT assay. The levels of NO produced were measured by spectrophotometry. The changes of iNOS expressed in RPE cells were determined with immunohistochemistry. Results: The growth rate of RPE cells was associated with the concentration of hesperidin. NO production induced by high glucose was significantly inhibited by hesperidin. iNOS expression in hesperidin-treated group was decreased compared with the control group (p <0.001). Conclusion: Hesperidin can increase the proliferation of rabbit RPE cells, and inhibit the level of NO and iNOS expression, so hesperidin can protect rabbit RPE cells. © Springer Science+Business Media, LLC 2010. Source

Ji X.-K.,Wenzhou University | Xie Y.-K.,Gannan Medical College | Zhong J.-Q.,Ganzhou Peoples Hospital | Xu Q.-G.,Wenzhou University | And 4 more authors.
Acta Pharmacologica Sinica | Year: 2015

Aim: Glycogen synthase kinase 3β (GSK-3β) plays a crucial role in hepatic biology, including liver development, regeneration, proliferation and carcinogenesis. In this study we investigated the role of GSK-3β in regulation of growth of hepatic oval cells in vitro and in liver regeneration in partially hepatectomized rats. Methods: WB-F344 cells, the rat hepatic stem-like epithelial cells, were used as representative of oval cells. Cell viability was examined using a WST-8 assay. The cells were transfected with a recombinant lentivirus expressing siRNA against GSK-3β (GSK-3βRNAiLV) or a lentivirus that overexpressed GSK-3β (GC-GSK-3βLV). Adult rats underwent partial (70%) hepatectomy, and liver weight and femur length were measured at d 7 after the surgery. The expression of GSK-3β, phospho-Ser9-GSK-3β, β-catenin and cyclin D1 was examined with immunoblotting assays or immunohistochemistry. Results: Treatment of WB-F344 cells with the GSK-3β inhibitor SB216763 (5 and 10 μmol/L) dose-dependently increased the levels of phospho-Ser9-GSK-3β, but not the levels of total GSK-3β, and promoted the cell proliferation. Knockout of GSK-3β with GSK-3βRNAiLV increased the cell proliferation, whereas overexpression of GSK-3β with GC-GSK-3βLV decreased the proliferation. Both SB216763 and GSK-3βRNAiLV significantly increased the levels of β-catenin and cyclin D1 in the cells, whereas GSK-3β overexpression decreased their levels. In rats with a partial hepatectomy, administration of SB216763 (2 mg/kg, ip) significantly increased the number of oval cells, the levels of phospho-Ser9-GSK-3β, β-catenin and cyclin D1 in liver, as well as the ratio of liver weight to femur length at d 7 after the surgery. Conclusion: GSK-3β suppresses the proliferation of hepatic oval cells by modulating the Wnt/β-catenin signaling pathway. © 2015 CPS and SIMM. Source

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