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Because epigenetic alterations, including losses and gains of DNA methylation, have been increasingly recognized to occur during carcinogenesis, 32, 33 we speculate that epigenetically regulated genes might serve as signatures of distinctive modes of liver tumor formation.
We simulated the extended model over a wide range of parameter values and identified parameter sets giving rise to distinct modes of liver regeneration and common or unique molecular regulation of liver regeneration dynamics.
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The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved.
Necrosis represents the main mode of liver cell death following warm/cold I-R [ 21– 23], but other modes of cell death, namely, apoptosis [ 2, 24, 25] and autophagy [ 26– 48], also play an important role.
Our work highlights the fact that diverse modes of acute liver injury have differing requirements for RIP1 and RIP3; moreover, within a single injury model, RIP1 and RIP3 blockade can have diametrically opposite effects on tissue damage, suggesting that interference with distinct components of the necrosome must be considered separately.
Open image in new window Fig. 1 B-mode ultrasound of liver and right kidney.
The mode of progression of liver metastases is by direct expansion of the metastatic site within the liver parenchyma.
Similar results for comparison between metabolic modes of kidney and liver are also shown in Figure S3.
Lineage-stage-specific effects of TCDD on rHpSC and rHB colonies provide insight into a mode-of-action for TCDD-induced liver tumorigenesis.
This work was followed by intensive research to establish an in vitro system combining liver cells and metabolomics for the identification of liver toxicity and modes of action.
Reported additional modes of action [9] include liver damage [10], [11], [12], [13], [14], disrupted pancreatic Beta-cell function [15], thyroid hormone disruption [16] and obesity promoting effects [17].
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