A potentially important tumor-host interaction is increased tumor-cell invasiveness in response to motility factors derived from stromal and lymphoid cells. Conditioned medium of IL-2-stimulated lymphocytes and fractions enriched in either T cells, natural killer (NK) cells, or monocytes induced mot
Possible roles of nonparenchymal cells in hepatocyte proliferation induced by lead nitrate and by tumor necrosis factor α
✍ Scribed by H Shinozuka; T Ohmura; S L Katyal; A I Zedda; G M Ledda-Columbano; A Columbano
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 474 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
proliferative response of the liver to mitogens, de-A single intravenous injection of lead nitrate (LN) to pending on the capacity of the mitogens to stimulate rats induces liver cell proliferation without causing cell TNF-a production. (HEPATOLOGY 1996;23:1572-1577.) necrosis (direct hyperplasia). We suggested that liver cell proliferation in this model may be triggered by the induction of liver tumor necrosis factor a (TNF-a). Be-Abbreviations: LN, lead nitrate; mRNA, messenger RNA; TNF-a, tumor that TNF-a may be involved in triggering cell proliferanecrosis factor a; NAF, nafenopin; BrdU, 5-bromo-2-deoxyuridine; ABC, avition in this type of direct hyperplasia. This suggestion din-biotin-peroxidase.
📜 SIMILAR VOLUMES
Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members w
Injection of bacterial endotoxin or granulocyte/macrophage colony-stimulating factor (GM-CSF) into exhypoxic polycythemic mice simultaneously with erythropoietin (EPO) suppressed erythroid cell formation, as monitored by 59Fe incorporation into circulating red blood cells. This effect was dose-depen