Loss of Hepatic Leucine-Rich Repeat-Containing G-Protein Coupled Receptors 4 and 5 Promotes Nonalcoholic Fatty Liver Disease.

The roof plate-specific spondin-leucine-rich repeat-containing G-protein coupled receptor 4/5 (LGR4/5)-zinc and ring finger 3 (ZNRF3)/ring finger protein 43 (RNF43) module is a master regulator of hepatic Wnt/β-catenin signaling and metabolic zonation. However, its impact on nonalcoholic fatty liver disease (NAFLD) remains unclear. The current study investigated whether hepatic epithelial cell-specific loss of the Wnt/β-catenin modulator Lgr4/5 promoted NAFLD.

How does social evaluation influence Hot and Cool inhibitory control in adolescence?

The aim of the present study is to examine whether in Hot, i.e., affectively charged contexts, or cool, i.

Peers' Choices Influence Adolescent Risk-taking Especially When Explicit Risk Information is Lacking.

This study examines the impact of peers' previous cautious versus risky choices on adolescents' risk-taking depending on the level of information about the risk. Adolescents completed an adaptation of the BART that manipulated social influence (cautious and risky) and risk information (i.e.

Development of a Shock and Detonation Velocity Measurement System Using Chirped Fiber Bragg Gratings.

Dynamic measurements of shock and detonation velocities are performed using long chirped fiber Bragg gratings (CFBGs). Such thin probes, with a diameter of typically 125 µm or even 80 µm can be directly inserted into high-explosive (HE) samples or simply glued laterally. During the detonation, the width of the optical spectrum is continuously reduced by the propagation of the wave-front, which physically shortens the CFBG.

Farnesoid X Receptor Agonism, Acetyl-Coenzyme A Carboxylase Inhibition, and Back Translation of Clinically Observed Endpoints of Lipogenesis in a Murine NASH Model.

A promising approach for the treatment of nonalcoholic steatohepatitis (NASH) is the inhibition of enhanced hepatic lipogenesis (DNL), which is the synthesis of fatty acids from nonlipid sources. This study assesses three approaches to DNL suppression in a newly developed dietary NASH mouse model: i) dietary intervention (switch from NASH-inducing diet to normal diet); ii) inhibition of acetyl-coenzyme A carboxylase (ACC), the enzyme catalyzing the rate-limiting step in DNL; and iii) activation of farnesoid X receptor (FXR), a major transcriptional regulator of DNL. C57BL/6J mice on a high-fat diet combined with consumption of a fructose-sucrose solution developed several of the liver histologic features seen in human disease, including steatosis, inflammation, and fibrosis, accompanied by elevated fibrosis biomarkers and liver injury enzymes.