|1.||Nagashima, Hitoshi: 5 articles (11/2015 - 08/2002)|
|2.||Iwashita, Keiko: 2 articles (10/2011 - 05/2007)|
|3.||Goto, Tetsuhisa: 2 articles (05/2007 - 11/2003)|
|4.||Inoue, Hiroyuki: 1 article (03/2010)|
|5.||Usami, Ihomi: 1 article (03/2010)|
|6.||Someno, Tetsuya: 1 article (03/2010)|
|7.||Ikeda, Daishiro: 1 article (03/2010)|
|8.||Wada, Shun-ichi: 1 article (03/2010)|
|9.||Ohba, Shun-ichi: 1 article (03/2010)|
|10.||Umezawa, Yoji: 1 article (03/2010)|
01/01/1977 - "The lesions in animals injected with 1.0 mg/kg rubratoxin B consisted of mild hepatic necrosis and degenerative changes in renal tubular epithelium. "
05/01/1988 - "In a fourth study, rubratoxin B was administered ip at a dose of 75% of the ip LD50 daily for 1 wk. Histopathological alterations included hepatic congestion and mild sinusoidal ectasia, multifocal necrosis of hepatocytes, splenic congestion and mild renal tubular degeneration. "
08/30/2002 - "Bromobenzene and rubratoxin B are known to induce necrosis and apoptosis of cells, respectively. "
03/01/1978 - "Rubratoxin B, a metabolite of Penicillium rubrum, is a potent mycotoxin that produces hepatic mid-zonal necrosis. "
|2.||Hepatocellular Carcinoma (Hepatoma)
11/30/2003 - "The induction of cytokine secretion by rubratoxin B was investigated using human hepatoma cell lines HepG2 and HuH-7. "
05/01/2007 - "Induced secretion of insulin-like growth factor binding protein-1 (IGFBP-1) in human hepatoma cell HepG2 by rubratoxin B."
11/30/2003 - "Rubratoxin B induced the secretion of hepatic injury-related colony stimulating factors in human hepatoma cells."
11/30/2003 - "To our knowledge, this is the first report that an exogenous stimulus induced the secretion of M-CSF and GM-CSF in hepatocyte-derived hepatoma cells, suggesting that rubratoxin B is an excellent model compound to study the mechanisms of M-CSF and GM-CSF secretion. "
05/01/2007 - "The induction of insulin-like growth factor binding protein-1 (IGFBP-1) secretion by rubratoxin B was investigated using human hepatoma cell line HepG2; we also documented the involvement of stress-activated MAP kinases [c-Jun-N-terminal kinases (JNKs) and p38s] in this process. "
|5.||Pathologic Dilatation (Ectasia)
|1.||Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)
|2.||Macrophage Colony-Stimulating Factor
|4.||Dimethyl Sulfoxide (DMSO)
|5.||Protein Phosphatase 2 (Protein Phosphatase 2A)
|6.||Tissue Inhibitor of Metalloproteinase-1
|8.||Aflatoxin B1 (Aflatoxin B)