Cryopreserved human alternatively activated macrophages promote resolution of acetaminophen-induced liver injury in mouse.

Acute liver failure is a rapidly progressing, life-threatening condition most commonly caused by an overdose of acetaminophen (paracetamol). The antidote, N-acetylcysteine (NAC), has limited efficacy when liver injury is established. If acute liver damage is severe, liver failure can rapidly develop with associated high mortality rates.

BMP6 participates in the molecular mechanisms involved in APAP hepatotoxicity.

Given the lack of accurate diagnostic methods of acetaminophen (APAP)-induced acute liver failure (ALF), the search for new biomarkers for its diagnosis is an urgent need. The aim of this study was to evaluate the role of bone morphogenetic protein 6 (BMP6) in APAP-induced ALF progression and its potential value as a biomarker of ALF. Hepatic and circulating BMP6 expression was assessed in APAP-treated mice and in serum samples from patients with APAP overdose.

Case report: Clinical and immunohistochemical manifestations of suspected Sjogren's disease in a dog.

Sjogren's disease, well-described in people, is rarely identified in veterinary species. In people, Sjogren's disease is one of the most common systemic autoimmune disorders with an incidence of 0.5% in the female population.

Macrophage Therapy for Acute Liver Injury (MAIL): a study protocol for a phase 1 randomised, open-label, dose-escalation study to evaluate safety, tolerability and activity of allogeneic alternatively activated macrophages in patients with paracetamol-induced acute liver injury in the UK.

Introduction: Acute liver failure (ALF) has no effective treatment other than liver transplantation and is commonly caused by paracetamol overdose. New treatments are needed to treat and prevent ALF. Alternatively-activated macrophages (AAMs) can promote resolution of liver necrosis and stimulate hepatocyte proliferation.