The potential of autologous patient-derived circulating extracellular vesicles to improve drug delivery in rheumatoid arthritis.

Recognizing the need for innovative therapeutic approaches in the management of autoimmune diseases, our current investigation explores the potential of autologous extracellular vesicles (EVs), derived from the blood of rheumatoid arthritis patients, to serve as therapeutic vectors to improve drug delivery. We found that circulating EVs derived from arthritic mice (collagen-induced arthritis model) express the joint/synovia homing receptor, αVβ3 integrin. Importantly, both autologous labeled EVs, derived from the blood of arthritic mice (collagen antibody-induced arthritis model) and healthy mice-derived EVs, exhibit targeted migration toward inflamed synovia without infiltrating healthy joints, as demonstrated by an in vivo imaging system.

Intrarenal Anti-Leptin Treatment Attenuates Ischemia and Reperfusion Injury.

Introduction: Renal ischemia and reperfusion (IR) injury introduces cellular stress and is the main cause of acute kidney damage. Renal cells exposed to noxious stress induce the expression of the pleiotropic hormone leptin. As we have previously revealed a deleterious stress-related role for leptin expression, these results suggested that leptin is also involved in pathological renal remodeling.

[TEST FOR NEUTRALIZING ANTIBODIES IN UROLOGIC PATIENTS WITH NO RESPONSE TO INTRAVESICAL BOTULINUM TOXIN INJECTIONS].

Botulinum toxin has been at the center of attention in the last decades as a treatment option in several urologic diseases related to lower urinary tract function. Intravesical injection of the toxin is recommended for two main indications: neurogenic detrusor over-activity and idiopathic detrusor over-activity, resistant to oral therapy. In certain cases, clinical response to treatment is less than ideal, despite previous response.

Autoimmune Concept of Schizophrenia: Historical Roots and Current Facets.

Background: The review analyzes the possible role of autoimmune processes in the pathogenesis of schizophrenia and the evolution of concepts on this issue from its origin to the present.

Results: Risks of autoimmune processes causing schizophrenia are associated with several factors: an impaired functioning of dopaminergic and glutamatergic systems in the brain, kynurenine pathway disorder with overproduction of quinolinic, anthranilic, and kynurenic acids (possibly altering both neurons and T-regulators), increased intestinal permeability, as well as food antigens' effects, stress and infections with various pathogens at different stages of ontogenesis. An increase in the levels of proinflammatory cytokines and chemokines as well as a decrease in the levels of anti-inflammatory ones also may contribute to schizophrenia risks.