Animal studies of fatty liver disease over-estimate the benefit of drugs due to publication bias and are confounded by off-target weight loss, illustrating the challenge of successful translational across species.
Circadian neutrophil infiltration in the liver modulates liver clock-gene expression and daily hepatic metabolism through the secretion of elastase and activation of JNK-FGF21-Bmal1 axis in the hepatocyte.
TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.
Statistical analysis and LASSO regression modeling provide insights into pathogen-specific host response patterns in cerebrospinal fluid from different disease etiologies to support future classification of pathogen type based on host response patterns in meningitis.