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2.
China Occupational Medicine ; (6): 153-156, 2021.
Artículo en Chino | WPRIM | ID: wpr-923228

RESUMEN

OBJECTIVE: To analyze the funding status of the National Natural Science Fund(NNSF) in the field of occupational respiratory disease(ORD) research in China. METHODS: Through the NNSF Committee Science Foundation sharing service network database, we collected the information of funded projects in the field of ORD research in China from 1987 to 2018, and analyzed the funding expenditure, funding categories, supporting units and research contents. RESULTS: A total of 106 NNSF funded projects were obtained in the research field of ORD in China in the period 1987-2018, and the total amount of funding was 37.945 million yuan. The number of funded projects, the average and the total amounts of fundings showed an increasing trend year by year(all P<0.05). The main types of funded projects were general projects and Youth Science Foundation projects(97.2%). The funded projects and funds were mainly concentrated in colleges and universities, accounting for 79.2% and 83.4% respectively. Beijing(29 items, 27.4%), Hebei(13 items, 12.3%) and Jiangsu(11 items, 10.4%) were the top three provinces and municipalities in the number of funded projects. Silicosis, pulmonary fibrosis, quartz, alveolar macrophages and acute lung injury were the top five keywords of funded project items, and the research types mainly focused on the mechanism of diseases. CONCLUSION: The NNSF funding is imbalanced in the types of funding, supporting units, and regional distribution on ORD research field in China. It is suggested that the funding structure of NNSF should be optimized, interdisciplinary research should be encouraged and expanded, and cooperation among different institutions and regions should be promoted.

3.
Chinese journal of integrative medicine ; (12): 676-682, 2012.
Artículo en Inglés | WPRIM | ID: wpr-347127

RESUMEN

<p><b>OBJECTIVE</b>To investigate the inhibitory activities of norcantharidin (NCTD), a demethylated analogue of cantharidin, on Hep3B cells (a human hepatoma cell line) with deficiency of p53.</p><p><b>METHODS</b>The survival rate of the Hep3B cells after treating with NCTD was measured by MTT assay. Cell cycle of treated cells was analyzed by flow cytometry, and DNA fragmentation was observed by electrophoresis. The influence of inhibitors for various caspases and anti-death receptors antibodies on the NCTD-induced apoptosis in the cells was determined.</p><p><b>RESULTS</b>NCTD treatment resulted in growth inhibition of Hep3B cells in a dose- and time-dependent manner. Cell cycle analysis of the cells after treatment with NCTD for 48 h shows that NCTD induced G(2)M phase arrest occurs at low concentration ([Symbol: see text] 25 μmol/L) but G(0)G(1) phase arrest at high concentration (50 μmol/L). The addition of both caspase-3 and caspase-10 inhibitors completely inhibited DNA fragmentation. Addition of anti-TRAIL/DR5 antibody significantly inhibited DNA fragmentation.</p><p><b>CONCLUSION</b>NCTD may inhibit the proliferation of Hep3B cells by arresting cell cycle at G(2)M or G(0)G(1) phase, and induce cells apoptosis via TRAIL/DR5 signal transduction through activation of caspase-3 and caspase-10 by a p53-independent pathway.</p>


Asunto(s)
Humanos , Anticuerpos Antineoplásicos , Farmacología , Anticuerpos Neutralizantes , Farmacología , Apoptosis , Compuestos Bicíclicos Heterocíclicos con Puentes , Farmacología , Carcinoma Hepatocelular , Patología , Caspasa 10 , Metabolismo , Caspasa 3 , Metabolismo , Inhibidores de Caspasas , Farmacología , Puntos de Control del Ciclo Celular , Línea Celular Tumoral , Proliferación Celular , Fragmentación del ADN , Inmunohistoquímica , Neoplasias Hepáticas , Patología , Receptores del Ligando Inductor de Apoptosis Relacionado con TNF , Metabolismo , Transducción de Señal , Ligando Inductor de Apoptosis Relacionado con TNF , Metabolismo , Proteína p53 Supresora de Tumor , Metabolismo
4.
Neuroscience Bulletin ; (6): 271-276, 2007.
Artículo en Inglés | WPRIM | ID: wpr-264714

RESUMEN

<p><b>OBJECTIVE</b>To investigate lipopolysaccharide (LPS) induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B (BN52021).</p><p><b>METHODS</b>Thirty Sprague-Dawley rats were randomly divided into 3 groups (n = 10 for each group): Control group, Model group and Treatment group (treated with BN52021). LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method.</p><p><b>RESULTS</b>The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly.</p><p><b>CONCLUSION</b>LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.</p>


Asunto(s)
Animales , Ratas , Conducta Animal , Encefalopatías , Patología , Fibrinolíticos , Usos Terapéuticos , Ginkgólidos , Usos Terapéuticos , Hipocampo , Inmunohistoquímica , Inflamación , Patología , Lactonas , Usos Terapéuticos , Lipopolisacáridos , Toxicidad , Aprendizaje por Laberinto , Microglía , Metabolismo , Microscopía Electrónica de Transmisión , Neuronas , Factor de Activación Plaquetaria , Metabolismo , Glicoproteínas de Membrana Plaquetaria , Ratas Sprague-Dawley , Receptores Acoplados a Proteínas G
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