1.An analysis of the impact factors of hepatology journals in SCI.
Chun-guang WENG ; Xiao-min YU ; Meng HUANG
Chinese Journal of Hepatology 2006;14(6):477-478
OBJECTIVETo analyze the status of liver disease research in China.
METHODHepatology and gastroenterology journals in the Science Citation Index were searched and their impact factors were analyzed.
RESULTS19 periodicals in this field were published in 6 countries. Among them 11 (61%) were published in the USA. Eleven of the 19 were full text embodied in the ScienceDirect (Elsevier), Blackwell and Wiley. The impact factor of the journal Gastroenterology was 13.092, the highest or the 19, and Hepatology, with an impact factor of 10.416, was in the second position. Of the 19 periodicals, 12 had an impact factor over 2.822. Articles published in those journals from 1001 through 2005 were written by mainland Chinese authors.
CONCLUSIONThe 12 periodicals with an impact factor over 2 can be regarded as core periodicals in this field. The medical periodicals in China need to be further improved in order to reach top international standards.
Bibliometrics ; Databases, Bibliographic ; Gastroenterology ; Humans ; Liver Diseases ; Periodicals as Topic
2.Induction of robust senescence-associated secretory phenotype in mouse NIH-3T3 cells by mitomycin C.
Wei-Xing HUANG ; Xiao-Xuan GUO ; Zhong-Zhi PENG ; Chun-Liang WENG ; Chun-Yan HUANG ; Ben-Yan SHI ; Jie YANG ; Xiao-Xin LIAO ; Xiao-Yi LI ; Hui-Ling ZHENG ; Xin-Guang LIU ; Xue-Rong SUN
Acta Physiologica Sinica 2017;69(1):33-40
Senescence-associated secretory phenotype (SASP) is often a concomitant result of cell senescence, embodied by the enhanced function of secretion. The SASP factors secreted by senescent cells include cytokines, proteases and chemokines, etc, which can exert great influence on local as well as systemic environment and participate in the process of cell senescence, immunoregulation, angiogenesis, cell proliferation and tumor invasion, etc. Relative to the abundance of SASP models in human cells, the in vitro SASP model derived from mouse cells is scarce at present. Therefore, the study aimed to establish a mouse SASP model to facilitate the research in the field. With this objective, we treated the INK4a-deficient mouse NIH-3T3 cells and the wildtype mouse embryonic fibroblasts (MEF) respectively with mitomycin C (MMC), an anticarcinoma drug which could induce DNA damage. The occurring of cell senescence was evaluated by cell morphology, β-gal staining, integration ratio of EdU and Western blot. Quantitative RT-PCR and ELISA were used to detect the expression and secretion of SASP factors, respectively. The results showed that, 8 days after the treatment of NIH-3T3 cells with MMC (1 μg/mL) for 12 h or 24 h, the cells became enlarged and the ratios of β-gal-positive (blue-stained) cells significantly increased, up to 77.4% and 90.4%, respectively. Meanwhile, the expression of P21 protein increased and the integration ratios of EdU significantly decreased (P < 0.01). Quantitative RT-PCR detection showed that the mRNA levels of several SASP genes, including IL-6, TNF-α, IL-1α and IL-1β increased evidently. ELISA detection further observed an enhanced secretion of IL-6 (P < 0.01). On the contrary, although wildtype MEF could also be induced into senescence by MMC treatment for 12 h or 24 h, embodied by the enlarged cell volume, increased ratios of β-gal-positive cells (up to 71.7% and 80.2%, respectively) and enhanced expression of P21 protein, the secretion of IL-6 displayed no significant change. Our study indicated that, although MMC could induce senescence in both mouse NIH-3T3 cells and wildtype MEF, only senescent NIH-3T3 cells displayed the canonical SASP phenomena. Current study suggested that senescent NIH-3T3 cells might be an appropriate in vitro SASP model of mouse cells.
Animals
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Cell Proliferation
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Cellular Senescence
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drug effects
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Cyclin-Dependent Kinase Inhibitor p21
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genetics
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metabolism
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Cytokines
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genetics
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metabolism
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DNA Damage
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Fibroblasts
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drug effects
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Interleukin-6
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secretion
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Mice
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Mitomycin
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pharmacology
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NIH 3T3 Cells
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Phenotype