Nrf2 induces malignant transformation of hepatic progenitor cells by inducing β-catenin expression.

The Nrf2 signaling pathway prevents cancer initiation, but genetic mutations that activate this pathway are found in various types of cancer. The molecular mechanisms underlying this Janus-headed character are still not understood. Here, we show that sustained Nrf2 activation induces proliferation and dedifferentiation of a Wnt-responsive perivenular hepatic progenitor cell population, transforming them into metastatic cancer cells.

Mental health, art, and deinstitutionalization: an aesthetic-poetic-theatrical account of the city's occupation.

This study aimed to report the experience of an aesthetic, poetic, and theatrical production of the city's occupation from a device of the Psychosocial Care Network to offer space for sociability, production, and cultural intervention. This is an account of an experience from the Social and Cultural Center (CECCO) in Natal, Rio Grande do Norte, Brazil, within madness and mental health deinstitutionalization. The intervention "The Little Prince occupies the Ribeira" was inspired by the work of author Saint-Exupéry.

Behavioural characteristics and abdominal obesity among Brazilian shift working women.

Objective: To explore the association between behavioural characteristics with the prevalence of abdominal obesity (AO) among a population of Southern Brazilian shift working women.

Design: A cross-sectional study was conducted. AO was estimated using waist circumference (WC), and it was used to classify women as having AO (WC ≥ 88 cm).

Nrf2 Ameliorates DDC-Induced Sclerosing Cholangitis and Biliary Fibrosis and Improves the Regenerative Capacity of the Liver.

The Nrf2 pathway protects against oxidative stress and induces regeneration of various tissues. Here, we investigated whether Nrf2 protects from sclerosing cholangitis and biliary fibrosis and simultaneously induces liver regeneration. Diet containing 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) was fed to Nrf2-KO mice (Nrf2-/-), mice with liver-specific hyperactivated Nrf2 (HKeap1-/-) and wild-type (WT) littermates to induce cholangitis, liver fibrosis, and oval cell expansion.

Hepatocyte-specific Keap1 deletion reduces liver steatosis but not inflammation during non-alcoholic steatohepatitis development.

Generation of reactive oxygen species (ROS) in response to fatty acids accumulation has been classically proposed as a possible "second hit" triggering progression from simple steatosis to non-alcoholic steatohepatitis (NASH). In this study we challenged hepatocyte-specific Keap1 knockout mice (Keap1(Δhepa)) and littermate Cre- controls (Keap1(fx/fx)) with two different diet models of NASH in order to evaluate the effects of the anti-oxidant transcription factor Nrf2 over-activation on hepatic metabolism and disease progression. After 4 weeks of MCD diet the liver/body weight ratio of Keap1(Δhepa) mice was significantly higher compared to littermate controls with no differences in total body weight.