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Hepatocyte growth factor (HGF) or scatter factor (SF) is a paracrine cellular growth, motility and morphogenic factor. It is secreted by mesenchymal cells and targets and acts primarily upon epithelial cells and endothelial cells , but also acts on haemopoietic progenitor cells and T cells .
Risk factors known as of 2010 are: Quantity of alcohol taken: Consumption of 60–80 g per day (14 g is considered one standard drink in the US, e.g. 1 + 1 ⁄ 2 US fl oz or 44 mL hard liquor, 5 US fl oz or 150 mL wine, 12 US fl oz or 350 mL beer; drinking a six-pack of 5% ABV beer daily would be 84 g and just over the upper limit) for 20 years or more in men, or 20 g/day for women ...
Liver regeneration is the process by which the liver is able to replace damaged or lost liver tissue. The liver is the only visceral organ with the capacity to regenerate. [1] [2] The liver can regenerate after partial hepatectomy or injury due to hepatotoxic agents such as certain medications, toxins, or chemicals. [3]
Undifferentiated hepatocyte-like cells appear in small, individualized, colonies The cells are available as undifferentiated growth-stage cells that can be grown in-house with the possibility of cell manipulation and amplification; or as fully differentiated cells that are ready and easy-to-use cells with high inter-assay reproducibility and ...
Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency [11] and glycogen storage disease type II. [12] In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative or cardiopathic effects. Liver transplantation can be curative.
The cytotoxic effects of chemotherapy are currently being studied in the modulation of the G2/M transition, concerning both checkpoint abrogation or checkpoint arrest. [19] Many therapies focus on inactivating the checkpoint in order to force cells with excess DNA damage to proceed through mitosis and induce cell death.
Similar to S Phase, G2 experiences a DNA damage checkpoint. The cell is once more examined for sites of DNA damage or incomplete replication, and the kinases ATR and ATM are recruited to damage sites. Activation of Chk1 and Chk2 also transpire, as well as p53 activation, to induce cell cycle arrest and halt progression into mitosis.