SofaGym: An Open Platform for Reinforcement Learning Based on Soft Robot Simulations.

OpenAI Gym is one of the standard interfaces used to train Reinforcement Learning (RL) Algorithms. The Simulation Open Framework Architecture (SOFA) is a physics-based engine that is used for soft robotics simulation and control based on real-time models of deformation. The aim of this article is to present , an open-source software to create OpenAI Gym interfaces, called environments, out of soft robot digital twins.

Acetaminophen inhibits NF-kappaB activation by interfering with the oxidant signal in murine Hepa 1-6 cells.

A toxic dose of acetaminophen (APAP) reduces the activity of NF-kappaB in mouse liver. NF-kappaB inactivation may be important for APAP toxicity, as this transcription factor can play a central role in maintaining hepatic viability. We recently reported that APAP likewise inhibits serum growth factor activation of NF-kappaB in a mouse hepatoma cell line (Hepa 1-6 cells).

Intraocular and intraorbital compartment pressure changes following orbital bone grafting: a clinical and laboratory study.

Visual loss is an uncommon but catastrophic complication after intraorbital bone grafting for the reconstruction of acute traumatic defects or long-standing enophthalmos. Increased intraocular or intraorbital compartment pressure may be pathogenic in this setting. A two-part study was designed to test the null hypothesis that intraocular and intraorbital compartment pressure values remain constant despite orbital volume reduction with graft material.

Modulation of serum growth factor signal transduction in Hepa 1-6 cells by acetaminophen: an inhibition of c-myc expression, NF-kappaB activation, and Raf-1 kinase activity.

Acetaminophen (APAP) is a widely used analgesic and antipyretic that can lead to severe liver damage when taken at excessive doses. APAP toxicity results when cytochrome P450-generated APAP metabolites trigger an oxidative stress and covalently modify target proteins. APAP has also been reported to inhibit cells from completing S-phase through a cytochrome P450-independent mechanism, raising the possibility that APAP may directly suppress liver regeneration and repair.

Inhibition of protein phosphatase activity and changes in protein phosphorylation following acetaminophen exposure in cultured mouse hepatocytes.

Protein phosphorylation was determined in cultured mouse hepatocytes exposed to an hepatotoxic concentration of acetaminophen (APAP) for selected times up to 12 h. Cultures were radiolabled with 32P-orthophosphoric acid and the cell extracts were analyzed by 2D gel electrophoresis and autoradiography. APAP exposure selectively increased the phosphorylation state of proteins of molecular weight 22, 25, 28, and 59 kDa and decreased the phosphorylation of a 26-kDa protein.