[EN] Bipolar disorder (BD)2 implies impairments in executive functions during euthymia that
interfere in psychosocial functioning. Virtual reality assessments may confer advantages
respect to traditional assessments in terms of efficiency and ecological validity. The aim of
this study was to validate a novel Virtual Cooking Task (VCT) for executive functions
assessment in euthymic patients with BD. This is a cross-sectional study in which a group
of BD patients (n=42) and healthy controls (n=42) were assessed with the VCT and a
battery of computerized standard tasks (CST). Additionally, the influence on psychosocial
functioning of both forms of assessment, measured with the FAST, was investigated to
check ecological validity. In BD group significant impairments in interference, working
memory and sustained attention were found in CST and VCT respect to controls. However,
deficits in planning and problem-solving were also revealed with the VCT. With respect to
psychosocial functioning, only VCT variables were able to predict FAST scores at the
assessment time. The VCT showed a greater sensitivity than CST to assess executive
functions and real-life functioning in BD. This provides evidence about the opportunity to
design novel cognitive assessments for diagnostic and therapeutic purposes in BD., This project has been financed by La Fe Health Institute Research and the Polytechnic University of Valencia as a part of the IX Subprogram of Preparatory Actions for Coordinated projects UPV-La Fe 2020. CogSoc-NT (AP2020-34). PI: PN and MA.
This study has been partly financed by Carlos III Health Research Institute (ISCIII) from Science and Innovation Ministry of Spain and cofinanced by the European Union towards Miguel Servet (CP 21/0008) and Juan Rodés (JR22/00030) contracts. Additionally, this project belongs to PI21/00549 and PI22/00543 projects financed by ISCIII and cofinanced by the European Union.
YC acknowledges a Post-Residence Grant financed by La Fe Health Research Institute (2020-616-1).

The growing interest in Vespa velutina venom stems primarily from its impact on human health due to stings and its potential pharmacological applications. Traditionally, venom extraction methods have relied on capturing individual hornets or removing and euthanizing entire nests, followed by dissection of venom sacs—a labor-intensive and disruptive process. In this work, we present a novel, non-invasive approach to venom harvesting. Using a portable electrostimulation device, venom was extracted directly from active Vespa velutina nests in their natural habitat. This method eliminates the need for nest manipulation, significantly reducing disturbance and improving efficiency. These visuals highlight the practicality and potential of this groundbreaking technique, opening new avenues for sustainable and scalable venom collection.

Inborn errors of immunity (IEI) are a group of monogenic diseases that confer susceptibility to infection, autoimmunity, and cancer. Despite the life-threatening consequences of some IEI, their genetic cause remains unknown in many patients. Objective: We investigated a patient with an IEI of unknown genetic etiology. Whole-exome sequencing identified a homozygous missense mutation of the gene encoding ezrin (EZR), substituting a threonine for an alanine at position 129. Ezrin is one of the subunits of the ezrin, radixin, and moesin (ERM) complex. The ERM complex links the plasma membrane to the cytoskeleton and is crucial for the assembly of an efficient immune response. The A129T mutation abolishes basal phosphorylation and decreases calcium signaling, leading to complete loss of function. Consistent with the pleiotropic function of ezrin in myriad immune cells, multidimensional immunophenotyping by mass and flow cytometry revealed that in addition to hypogammaglobulinemia, the patient had low frequencies of switched memory B cells, CD4 + and CD8 + T cells, MAIT, γδ T cells, and central naive CD4 + cells. Autosomal-recessive human ezrin deficiency is a newly recognized genetic cause of B-cell deficiency affecting cellular and humoral immunity.

Background
Inborn errors of immunity (IEI) are a group of monogenic diseases that confer susceptibility to infection, autoimmunity, and cancer. Despite the life-threatening consequences of some IEI, their genetic cause remains unknown in many patients.
Objective
We investigated a patient with an IEI of unknown genetic etiology.
Methods
Whole-exome sequencing identified a homozygous missense mutation of the gene encoding ezrin (EZR), substituting a threonine for an alanine at position 129.
Results
Ezrin is one of the subunits of the ezrin, radixin, and moesin (ERM) complex. The ERM complex links the plasma membrane to the cytoskeleton and is crucial for the assembly of an efficient immune response. The A129T mutation abolishes basal phosphorylation and decreases calcium signaling, leading to complete loss of function. Consistent with the pleiotropic function of ezrin in myriad immune cells, multidimensional immunophenotyping by mass and flow cytometry revealed that in addition to hypogammaglobulinemia, the patient had low frequencies of switched memory B cells, CD4+ and CD8+ T cells, MAIT, γδ T cells, and centralnaive CD4+ cells.
Conclusions
Autosomal-recessive human ezrin deficiency is a newly recognized genetic cause of B-cell deficiency affecting cellular and humoral immunity.