No abstract

The administration of hypertonic saline solution in experimental AP attenuated hemodynamic alterations, decreased inflammatory cytokines, diminished systemic lesions and pancreatic acinar necrosis, prevented pancreatic infection, and reduced the mortality rate.

Objectives To assess the prevalence of antibodies to Toxoplasma gondii and Neospora caninum in a population of dogs with a diagnosis of suspected inflammatory meningoencephalitis. Materials and Methods Medical records of three referral centres were reviewed from 2008 to 2016 to identify a cohort of dogs diagnosed and treated for suspected inflammatory meningoencephalitis after testing for evidence of exposure to these pathogens. Results In our sample of 400 dogs the prevalence for exposure (IgG>1:50) to Toxoplasma gondii was 8/201 (3∙98%). Active infection (IgG titre >1:400 or/and an IgM titre >1:64 and/or positive PCR in CSF) was suspected in 1/400 (0∙25%). The prevalence for exposure [Indirect fluorescent antibody (IFA) titre >1:50] and active infection (IFA titres ≥⃒1:400 and/or positive PCR in CSF) with Neospora caninum were 14/201 (6∙96%) and 9/400 (2∙25%), respectively. Clinical Significance In view of the low prevalence of protozoan infections, the risk associated with starting immunosuppressive medication in dogs with evidence of inflammatory meningitis or encephalitis in the UK appears low.

Liver fibrosis occurring as an outcome of non-alcoholic steatohepatitis (NASH) can precede the development of cirrhosis. We investigated the effects of sorafenib in preventing liver fibrosis in a rodent model of NASH. Adult Sprague-Dawley rats were fed a choline-deficient high-fat diet and exposed to diethylnitrosamine for 6 weeks. The NASH group (n=10) received vehicle and the sorafenib group (n=10) received 2.5 mg·kg-1·day-1 by gavage. A control group (n=4) received only standard diet and vehicle. Following treatment, animals were sacrificed and liver tissue was collected for histologic examination, mRNA isolation, and analysis of mitochondrial function. Genes related to fibrosis (MMP9, TIMP1, TIMP2), oxidative stress (HSP60, HSP90, GST), and mitochondrial biogenesis (PGC1α) were evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Liver mitochondrial oxidation activity was measured by a polarographic method, and cytokines by enzyme-linked immunosorbent assay (ELISA). Sorafenib treatment restored mitochondrial function and reduced collagen deposition by nearly 63% compared to the NASH group. Sorafenib upregulated PGC1α and MMP9 and reduced TIMP1 and TIMP2 mRNA and IL-6 and IL-10 protein expression. There were no differences in HSP60, HSP90 and GST expression. Sorafenib modulated PGC1α expression, improved mitochondrial respiration and prevented collagen deposition. It may, therefore, be useful in the treatment of liver fibrosis in NASH.