Inflammatory cytokines in leprosy reactions and periodontal diseases.

The inflammatory cytokines involved in the immune response to chronic periodontal disease (CPD) in the context of leprosy reactions (LR) were analyzed in 57 new cases of multibacillary leprosy (MBL). They were stratified by the presence of CPD and LR. Messenger RNA (mRNA) expression of inflammatory mediators was determined by qRT-PCR using skin biopsy and by ELISA using serum samples, maintaining 5% of significance level in ANOVA and correlation analyses.

Pretreatment with fish oil attenuates heart ischaemia consequences in rats.

What is the central question of this study? We investigated whether pretreatment with fish oil could prevent the major consequences of ischaemic injury to the heart. What is the main finding and its importance? Fish oil pretreatment attenuated the consequences of ischaemic injury as indicated by the small infarction area and the preservation of systolic function and coronary blood flow. These findings support the use of fish oil in order to reduce the impact of heart ischaemia.

Glucose and fatty acid metabolism in infarcted heart from streptozotocin-induced diabetic rats after 2 weeks of tissue remodeling.

Background: The effects of streptozotocin (STZ)-induced diabetes on heart metabolism and function after myocardial infarction (MI) remodelling were investigated in rats.

Methods: Fifteen days after STZ (50 mg/kg b.w.

Impact of conditioning hyperglycemic on myocardial infarction rats: Cardiac cell survival factors.

While clinical data have suggested that the diabetic heart is more susceptible to ischemic heart disease (IHD), animal data have so far pointed to a lower probability of IHD. Thus, the aim of this present review is to look at these conflicting results and discuss the protective mechanisms that conditioned hyperglycemia may confer to the heart against ischemic injury. Several mechanisms have been proposed to explain the cardioprotective action of high glucose exposure, namely, up-regulation of anti-apoptotic factor Bcl-2, inactivation of pro-apoptotic factor bad, and activation of pro-survival factors such as protein kinase B (Akt), vascular endothelial growth factor (VEGF), hypoxia inducible factor-1α and protein kinase C-ε.