Once daily Bromelain-based enzymatic debridement of venous leg ulcers versus gel vehicle (placebo) and non-surgical standard of care: a three-arm multicenter, double blinded, randomized controlled study.

Background: Debridement is considered the first step in treatment of chronic wounds, however, current enzymatic and autolytic debridement agents are slow or ineffective. Previous studies have shown positive initial results with EscharEx® (EX-02 formulation), a Bromelain-based enzymatic debridement agent in development for chronic wounds. The main objective of this study was to assess its efficacy in debriding venous leg ulcers (VLU), compared to gel vehicle (GV) as a placebo control and to non-surgical standard of care (NSSOC).

Improving Health Equity Through Health Literacy Education.

Health literacy is the ability to understand and use health information. More than one-third of adults living in the United States have limited health literacy, which is associated with adverse health outcomes. Physicians need education about how to communicate effectively across the range of health literacy levels, but residency programs often fail to provide it.

Philadelphia-like acute lymphoblastic leukemia: Characterization in a pediatric cohort in a referral center in Colombia.

Background: Philadelphia-like (Ph-like) acute lymphoblastic leukemia (ALL) is a subtype of pediatric leukemia with high risk factors and poor outcome. There are few reports of its prevalence in Latin America.

Aim: This study evaluated the frequency and clinical and biological characteristics of Ph-like ALL in a pediatric cancer center in Colombia.

Anti-neuroinflammatory effect of Iresine celosia on lipopolysaccharide-stimulated microglial cells and mouse.

Abnormal inflammatory response in the central nervous system plays a critical role in various neurological disorders such as Parkinson's disease, Alzheimer's disease and Huntington's disease. Therefore, modulation of abnormal neuroinflammation is thought to be a promising therapeutic strategy for these diseases. Based on this idea, we focused on finding a potential candidate material that would regulate excessive neuroinflammation.

Caveolin-1 deletion exacerbates cardiac interstitial fibrosis by promoting M2 macrophage activation in mice after myocardial infarction.

Adverse remodeling following myocardial infarction (MI) leading to heart failure is driven by an imbalanced resolution of inflammation. The macrophage cell is an important control of post-MI inflammation, as macrophage subtypes secrete mediators to either promote inflammation and extend injury (M1 phenotype) or suppress inflammation and promote scar formation (M2 phenotype). We have previously shown that the absence of caveolin-1 (Cav1), a membrane scaffolding protein, is associated with adverse cardiac remodeling in mice, but the mechanisms responsible remain to be elucidated.