Improving the Therapeutic Relationship When Prescribing Antidepressants: A Pilot Study.

Studies indicate that the quality of the doctor-patient relationship moderates the effect of pharmacotherapy. To enhance the quality of the therapeutic relationship in the pharmacotherapy of depression, we developed a brief manual with interactive materials for residents in psychiatry and their patients. In a pilot study at a psychiatric university hospital's outpatient department, we compared patient-centered treatment parameters of a first patient group treated as usual and a second patient group treated using the manual. The study had no influence on the choice of medication. In the manual group, patient satisfaction with the doctor-patient relationship increased significantly at the three-month follow-up. Depression parameters declined in both groups, without group differences. Continuation of antidepressant medication at six months was higher in the manual group. In conclusion, a simple intervention using written materials for doctors prescribing antidepressants improved doctors' and patients' satisfaction with treatment

Projeto de regulamentação da formatação de percursos pedestres de curta e longa distância no Brasil

É notável que a procura de atividades pedestres ao ar livre tem aumentado e mediante a isso a oferta de passeios acompanhados se justifica e vem crescendo cada vez mais. Percebe-se a crescente implantação de percursos pedestres que permitem a livre e orientada circulação dos turistas e população local. O pedestrianismo é o exercício que consiste em fazer caminhadas com diferentes níveis de dificuldade. É uma prática desportiva e turística, competitiva ou não, muito praticada em ambientes naturais, o que oferece aos praticantes diversos benefícios inerentes à prática de atividades ao ar livre. Muito se ouve que atividades ao ar livre junto à natureza propiciam uma forma de escapar do stress e sedentarismo vividos diariamente nas grandes cidades. Estudos comprovam que o contato com a natureza promove vitalidade, alivia o estresse e a ansiedade, fortalece o sistema imunológico, melhora o desempenho e o humor, e ameniza e diminui chances de desenvolvimento de doenças mentais, de pressão arterial e a frequência cardíaca (McDonald, Bearley e Elmqvist, 2018; Parque et al, 2010)

IgG in the control of FcεRI activation: a battle on multiple fronts.

The rising global incidence of IgE-mediated allergic reactions poses a significant challenge to the quality of life of affected individuals and to healthcare systems, with current treatments being limited in effectiveness, safety, and disease-modifying capabilities. IgE acts by sensitizing the high-affinity IgE receptor FcεRI expressed by mast cells and basophils, tuning these cells for inflammatory degranulation in response to future allergen encounters. In recent years, IgG has emerged as an essential negative regulator of IgE-dependent allergic inflammation. Mechanistically, studies have proposed different pathways by which IgG can interfere with the activation of IgE-mediated inflammation. Here, we briefly summarize the major proposed mechanisms of action by which IgG controls the IgE-FcεRI inflammatory axis and how those mechanisms are currently applied as therapeutic interventions for IgE-mediated inflammation

IgE glycans promote anti-IgE IgG autoantibodies that facilitate IgE serum clearance via Fc Receptors.

BACKGROUND Recent studies have shown that IgE glycosylation significantly impacts the ability of IgE to bind to its high-affinity receptor FcεRI and exert effector functions. We have recently demonstrated that immunizing mice with IgE in a complex with an allergen leads to a protective, glycan-dependent anti-IgE response. However, to what extent the glycans on IgE determine the induction of those antibodies and how they facilitate serum clearance is unclear.Therefore, we investigated the role of glycan-specific anti-IgE IgG autoantibodies in regulating serum IgE levels and preventing systemic anaphylaxis by passive immunization. METHODS Mice were immunized using glycosylated or deglycosylated IgE-allergen-immune complexes (ICs) to induce anti-IgE IgG antibodies. The anti-IgE IgG antibodies were purified and used for passive immunization. RESULTS Glycosylated IgE-ICs induced a significantly higher anti-IgE IgG response and more IgG-secreting plasma cells than deglycosylated IgE-ICs. Passive immunization of IgE-sensitized mice with purified anti-IgE IgG increased the clearance of IgE and prevented systemic anaphylaxis upon allergen challenge. Anti-IgE IgG purified from the serum of mice immunized with deglycosylated IgE-ICs, led to a significantly reduced elimination and protection, confirming that the IgE glycans themselves are the primary drivers of the protectivity induced by the IgE-immune complexes. CONCLUSION IgE glycosylation is essential for a robust anti-IgE IgG response and might be an important regulator of serum IgE levels

Glycan-specific IgG anti-IgE autoantibodies are protective against allergic anaphylaxis in a murine model.

BACKGROUND IgE causes anaphylaxis in type-1 hypersensitivity diseases by activating degranulation of effector cells such as mast cells and basophils. The mechanisms that control IgE activity and prevent anaphylaxis under normal conditions are still enigmatic. OBJECTIVE We aimed to unravel how anti-IgE autoantibodies are induced and understand their role in regulating serum IgE level and allergic anaphylaxis. METHODS We immunized mice with different forms of IgE and tested anti-IgE autoantibody responses and their specificities. We then analysed the effect of those antibodies on serum kinetics and their in vitro and in vivo impact on anaphylaxis. Finally, we investigated anti-IgE autoantibodies in human sera. RESULTS Immunization of mice with IgE-immune complexes induced glycan-specific anti-IgE autoantibodies. The anti-IgE autoantibodies prevented effector cell sensitization, reduced total IgE serum levels, protected mice from passive and active IgE sensitization, and resulted in cross-protection against different allergens. Furthermore, glycan-specific anti-IgE autoantibodies were present in sera from allergic and non-allergic subjects. CONCLUSION In conclusion, we provide first evidence that in the murine model the serum level and anaphylactic activity of IgE may be down-regulated by glycan-specific IgG anti-IgE autoantibodies