Recollection & Traumatic Growth: Unique Mediational Pathways Through Traumatic Stress Components

Although the severity of the COVID-19 outbreak varies from time to time, pandemic has affected larger audiences all around the world. Given the increasingly severe measures taken by the authorities, healthcare professionals have experienced positive and negative effects of the events, both personally and vicariously. The main aim is to examine how remembering influences vicarious traumatization and post-traumatic growth in a sample of healthcare workers. We proposed a multiple mediation model testing of distinct roles of stress components (hypervigilance, avoidance, intrusion) on the link between recollective features of remembering and post-traumatic growth, which allows to characterize memory-linked mechanisms underlying the effects of traumatic stress on growth. We demonstrated unique pathways by which remembering influenced traumatic growth. For the links of emotional intensity and imagery with growth, we found full mediation through avoidance and intrusion Individuals recalling events with high emotional intensity and imagery tend to experience more intrusions of trauma, which then resulted in traumatic growth. On the other hand, the opposite pattern was found for avoidance. Emotionally intense and vivid recall of events increased avoidance responses, but high avoidance reduced traumatic growth. With respect to reliving, while the pattern was similar, we found a partial mediation, showing significant role reliving has in supporting traumatic growth

Recollection & traumatic growth: unique mediational pathways through traumatic stress components

Although the severity of the COVID-19 outbreak varies from time to time, the pandemic has affected larger audiences worldwide. Given the increasingly severe measures taken by the authorities, healthcare professionals have experienced positive and negative effects of the events, both personally and vicariously. The main aim is to examine how remembering influences vicarious traumatization and post-traumatic growth in a sample of healthcare workers. We proposed a multiple mediation model testing of distinct roles of stress components (hypervigilance, avoidance, intrusion) on the link between recollective features of remembering and post-traumatic growth, which allows characterizing memory-linked mechanisms underlying the effects of traumatic stress on growth. We demonstrated unique pathways by which remembering influenced traumatic growth. For the links of emotional intensity and imagery with growth, we found full mediation through avoidance and intrusion Individuals recalling events with high emotional intensity and imagery tend to experience more intrusions of trauma, which then resulted in traumatic growth. On the other hand, the opposite pattern was found for avoidance. Emotionally intense and vivid recall of events increased avoidance responses, but high avoidance reduced traumatic growth. With respect to reliving, while the pattern was similar, we found a partial mediation, showing the significant role reliving has in supporting traumatic growth.DuolingoEuropean Office of Aerospace Research and DevelopmentFindingFiveMIT-IBM Watson AI LabThe Robert J. Glushko and Pamela Samuelson FoundationToyota Research Institute2-s2.0-85139390184Temmu

Immune reconstitution inflammatory syndrome after hematopoietic stem cell transplantation in a FOXN1-deficient patient

The FOXN1 gene mutation is a unique disorder that causes the nude severe combined immunodeficiency phenotype. In patients with severe combined immunodeficiency, hematopoietic stem cell transplantation (HSCT) is life-saving if performed earlier. Thymic transplantation is the curative treatment for FOXN1 deficiency because the main pathology is thymic stromal changes. In this report, we describe the clinical features of a Turkish patient with a homozygous FOXN1 mutation treated with HSCT from his human leukocyte antigen-matched sibling. On follow-up, he showed Bacille Calmette Guerin adenitis and was evaluated as having immune reconstitution inflammatory syndrome. By presenting our patient, we aimed to draw attention to the development of HSCT and subsequent immune reconstitution inflammatory syndrome as a treatment option in patients with FOXN1 deficiency

Two patients with chronic mucocutaneous candidiasis caused by TRAF3IP2 deficiency

Background: TRAF3 interacting protein 2 (TRAF3IP2) (Act1) is an adapter protein that interacts with IL-17R via its similar expression to fibroblast growth factor genes and IL-17R domain and coordinates 2 separate proinflammatory pathways following IL-17 cytokine stimulation. Objective: We sought to elucidate the immunologic consequences of TRAF3IP2 homozygous mutations to improve treatments for immunodeficiency patients with chronic mucocutaneous candidiasis. Methods: We describe 2 patients presenting with chronic mucocutaneous candidiasis who harbor biallelic nonsense mutations in TRAF3IP2. The cellular and molecular features of this genetic defect were assessed using in vitro cytokine assays and protein analysis. Results: We show that the homozygous mutation causes complete loss of protein expression. We also show that the absence of TRAF3IP2 was associated with a defective response to combined IL-2/IL-25 (IL-17E) stimulation. Conclusions: Failure to initiate normal signaling downstream of IL-17R engagement likely contributes to the patients & rsquo; recurrent fungal infections. These findings add to our molecular understanding of genetic defects affecting this critical pathway of antifungal immunity. (J Allergy Clin Immunol 2021;148:256-61.

Inflammatory bowel disease and guillain barre syndrome in FCHO1 deficiency

To the Editor: FCH And Mu Domain Containing Endocytic Adaptor 1 (FCHO1) gene encodes a protein that plays a critical role in clathrin-mediated endocytosis, a biological process that maintains cellular functions in signaling, nutrient- and growth factor- uptake, and diferentiation [1–3]. Recently, biallelic mutations in FCHO1 were linked to a combined immunodefciency that is characterized by recurrent infections caused by bacteria, viruses, mycobacteria, fungi, T cell lymphopenia, and hypogammaglobulinemia [4, 5].Sidra Precision Medicine Progra

Diagnostic Modalities Based on Flow Cytometry forChronic Granulomatous Disease: A MulticenterStudy in a Well-Defined Cohort

TARAMAWOSWOS:000588386800037TARAMAPUBMEDTARAMASCOPUSBackground: Chronic granulomatous disease (CGD) is characterized by defective microbial killing due to mutations affecting subunits of thenicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex. Definitive genetic identificationof disease subtypes may be delayed or notreadily available. Objective: We sought to investigate the role of intracellular staining of NADPH oxidase enzyme subunits in predicting the respective genetic defectsin CGD patients and carriers. Methods: Thirty-fourgenetically inherited CGD patients, including twelve patients with X-linked CGD (gp91phoxdeficiency due to CYBB mutations) and 22 patients with autosomal recessive CGD (p22phox, p47phox and p67phoxdeficiency due toCYBA, NCF1 and NCF2mutations, respectively)were recruited from different immunology centers and followed up prospectively.Dihydrorhodamine (DHR) testingand NADPH oxidase subunit expression in white blood cells were determined by flow cytometry. Results:gp91phoxand p22phoxdefects, which result in simultaneous loss of both proteins due to their complex formation, were only differentiated by comparative analysis ofpatients’and mothers’ intracellular staining. p47phox and p67phox protein expression was almost undetectable in patients compared to carrier mothers and healthy controls. The expression values of the respective subunits were found to be significantly higherin all controlsas compared to carrier mothers, which in turn were higher than those of patients. Conclusion: Analysis of NADPH oxidase enzyme subunits byflow cytometry in patients and carriers is useful in the rapid predictionof the genetic defect of patients with CGD,thus guiding targeted sequencing and aiding in their early diagnosis