A Novel In Vivo Method Using to Evaluate α-Glucosidase Inhibition by Natural Products for Type 2 Diabetes Treatment.

Background: Non-insulin-dependent diabetes mellitus, or type 2 diabetes, is one of the diseases of greatest concern worldwide, and research into natural compounds that are capable of regulating glycemia and insulin resistance is therefore gaining importance. In the preclinical stages, is considered a promising in vivo model for research into this disease. Most studies have been carried out using mutant strains and observing changes in their phenotype rather than directly measuring the effects within the worms.

Myeloproliferative Neoplasm-like Mutations of Calreticulin Induce Phenotypes Associated with Calreticulin Dysfunction in .

In previous research, we created a model with homozygous mutations in calreticulin similar to those found in patients with essential thrombocythemia (ET) and primary myelofibrosis (PMF), two myeloproliferative neoplasms (MPNs). This model, lacking JAK orthologs, enabled us to examine the transcriptomic effects caused by mutant calreticulin without the influence of JAK/STAT activation, the primary pathogenic mechanism associated with calreticulin mutations known to date. Most of the gene expression changes observed seemed to be due to a partial loss of protein function, with the alteration of the extracellular matrix being particularly notable.

but Not Mutations Are Associated with an Overexpression of Retinoid X Receptor Alpha in Essential Thrombocythemia.

Essential thrombocythemia (ET) is a blood cancer caused by mutations in and . It is widely recognized that both mutations lead to the constitutive activation of JAK2/STAT signaling, although other JAK/STAT-independent pathogenic mechanisms triggered by these alterations have also been described in ET. In an attempt to study JAK2/STAT-independent mechanisms derived from mutations, our research group created a model with patient-like mutations in calreticulin that lacks JAK counterparts.

Mucus-penetrating and permeation enhancer albumin-based nanoparticles for oral delivery of macromolecules: Application to bevacizumab.

The oral administration of therapeutic proteins copes with important challenges (mainly degradation and poor absorption) making their potential therapeutic application extremely difficult. The aim of this study was to design and evaluate the potential of the combination between mucus-permeating nanoparticles and permeation enhancers as a carrier for the oral delivery of the monoclonal antibody bevacizumab, used as a model of therapeutic protein. For this purpose, bevacizumab was encapsulated in PEG-coated albumin nanoparticles as a hydrophobic ion-pairing complex with either sodium deoxycholate (DS) or sodium docusate (DOCU).