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GC-C deficient mice on the mixed genetic background nearly all died (median survival of 5 days) following carbon tetrachloride injection while WT littermates experienced only 35% mortality.
For example, K18 R89C mice are predisposed to Fas but not TNF-induced apoptosis and the same mice develop more pronounced liver fibrosis after thioacetamide, but not after carbon tetrachloride injection (Ku et al. 2003b; Strnad et al. 2008).
Survival was followed for 14 days after carbon tetrachloride injection in wild type and GC-C deficient mice on both a mixed genetic background and on an inbred C57BL6/J background.
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Upon transplantation in vivo, they ameliorated severe acute liver damage in SCID mice caused by carbon tetrachloride (CCl4) injection.
Similarly, it has been reported that a small number of hepatocytes in the adult liver can change their fate to that of biliary cells, even after PH and induction of acute hepatic injury by carbon tetrachloride (CCl4) injection (Yanger et al. 2013; Sekiya & Suzuki 2014).
To analyze the functional relevance of this pathway, two models of experimental liver fibrosis were applied to wildtype (WT) and CX3CR1-deficient mice, namely repetitive carbon tetrachloride (CCl4) injections as well as surgical ligation of the biliary duct (BDL, bile duct ligation) [ 48].
dBDPCs have cytochrome P450 activity and express specific hepatic transcription factors, such as hepatic nuclear factor 1α. To demonstrate liver regenerative activity, dBDPCs were injected into mice with severe acute liver damage caused by a high-dose injection of carbon tetrachloride (CCl4).
The positive ion mobility spectra of the extracted malathion were obtained after direct injection of carbon tetrachloride or methanol solutions.
Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl4) with or without curcumin for 6 weeks.
Injection of carbon tetrachloride (CCl4) can induce hepatic fibrosis [ 43] and necrosis of hepatocytes around the central vein and connective tissue septa linking portal canals and central veins [ 66, 67].
In animal studies, adiponectin-knockout mice developed more severe carbon tetrachloride-induced liver fibrosis compared with wild type mice, and adiponectin injection prior to carbon tetrachloride treatment could prevent it [ 14].
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