Problematic Use of the Internet and Cybervictimization: An Empirical Study with Spanish Adolescents.

Background: Adolescence is a critical stage for the development of behaviours related to problematic Internet and social media use, as well as for the experience of cybervictimisation. The literature highlights the need to examine these types of adolescent behaviours.

Method: A field study was designed to analyse the prevalence of problematic Internet and social media use, as well as cybervictimisation, sexting, and grooming.

Negative Online Experiences, Worry, and Risk Perception Among Adolescents: Gender Differences and Implications for Cybercrime Awareness.

The present study aims to explore the negative online experiences in adolescence, as well as examine the associations of those and their interaction patterns with the frequency of worry and risk perception in relation to several types of online victimization. We conducted a cross-sectional survey study conducted between 2022 and 2023. We collected a nonprobabilistic sample of 824 Spanish adolescents.

Prevalence and Quantification of the Effects of Sexual Harassment Victimization of School-Aged Adolescents.

Background/aim: Sexual harassment has become a serious social and public health problem in adolescents, causing adverse effects on mental health. Nevertheless, some behaviours arise that, due to their characteristics, might be misinterpreted as sexual harassment. A field study using a survey with non-probabilistic accidental sampling was designed in order to estimate the prevalence of sexual harassment victimization in the Spanish adolescent population as well as to quantify the harms.

Free DNA in cystic fibrosis airway fluids correlates with airflow obstruction.

Chronic obstructive lung disease determines morbidity and mortality of patients with cystic fibrosis (CF). CF airways are characterized by a nonresolving neutrophilic inflammation. After pathogen contact or prolonged activation, neutrophils release DNA fibres decorated with antimicrobial proteins, forming neutrophil extracellular traps (NETs).

Localization and functionality of the inflammasome in neutrophils.

Neutrophils represent the major fraction of circulating immune cells and are rapidly recruited to sites of infection and inflammation. The inflammasome is a multiprotein complex that regulates the generation of IL-1 family proteins. The precise subcellular localization and functionality of the inflammasome in human neutrophils are poorly defined.

Expression and regulation of interferon-related development regulator-1 in cystic fibrosis neutrophils.

A genome-wide association study identified interferon-related development regulator-1 (IFRD1), a protein expressed by neutrophils, as a key modifier gene in cystic fibrosis (CF) lung disease. Here, we investigated the expression and regulation of IFRD1 in CF neutrophils. IFRD1 expression was quantified in peripheral blood and airway neutrophils from patients with CF, patients with non-CF lung disease, and healthy control subjects.

Neutrophils express distinct RNA receptors in a non-canonical way.

RNAs are capable of modulating immune responses by binding to specific receptors. Neutrophils represent the major fraction of circulating immune cells, but receptors and mechanisms by which neutrophils sense RNA are poorly defined. Here, we analyzed the mRNA and protein expression patterns and the subcellular localization of the RNA receptors RIG-I, MDA-5, TLR3, TLR7, and TLR8 in primary neutrophils and immortalized neutrophil-like differentiated HL-60 cells.

CXCR1 and CXCR2 haplotypes synergistically modulate cystic fibrosis lung disease.

Cystic fibrosis (CF) lung disease severity is largely independent on the CF transmembrane conductance regulator (CFTR) genotype, indicating the contribution of genetic modifiers. The chemokine receptors CXCR1 and CXCR2 have been found to play essential roles in the pathogenesis of CF lung disease. Here, we determine whether genetic variation of CXCR1 and CXCR2 influences CF lung disease severity.

Ultrastructural characterization of cystic fibrosis sputum using atomic force and scanning electron microscopy.

Background: Cystic fibrosis (CF) lung disease is characterized by perpetuated neutrophilic inflammation with progressive tissue destruction. Neutrophils represent the major cellular fraction in CF airway fluids and are known to form neutrophil extracellular traps (NETs) upon stimulation. Large amounts of extracellular DNA-NETs are present in CF airway fluids.

CXCR2 mediates NADPH oxidase-independent neutrophil extracellular trap formation in cystic fibrosis airway inflammation.

Upon activation, neutrophils release DNA fibers decorated with antimicrobial proteins, forming neutrophil extracellular traps (NETs). Although NETs are bactericidal and contribute to innate host defense, excessive NET formation has been linked to the pathogenesis of autoinflammatory diseases. However, the mechanisms regulating NET formation, particularly during chronic inflammation, are poorly understood.

NETs formed by human neutrophils inhibit growth of the pathogenic mold Aspergillus fumigatus.

Neutrophil extracellular traps (NETs) represent a distinct mechanism to control and eliminate microbial infections. Our results show that conidia and germ tubes of the human pathogenic mold Aspergillus fumigatus are able to trigger the formation of NETs. Viable fungal cells are not essentially required for this host-pathogen interaction.

Fibrin mimics neutrophil extracellular traps in SEM.

Neutrophil extracellular traps (NETs) are extracellular web-like structures produced by activated polymorphonuclear neutrophils. NETs kill bacteria extracellularly, but their role in human pathology remains largely unclear. One possible way of studying NETs is through the SEM approach.

Expression, regulation and clinical significance of soluble and membrane CD14 receptors in pediatric inflammatory lung diseases.

Background: Inflammatory lung diseases are a major morbidity factor in children. Therefore, novel strategies for early detection of inflammatory lung diseases are of high interest. Bacterial lipopolysaccharide (LPS) is recognized via Toll-like receptors and CD14.

Infiltrated neutrophils acquire novel chemokine receptor expression and chemokine responsiveness in chronic inflammatory lung diseases.

Various inflammatory diseases are characterized by tissue infiltration of neutrophils. Chemokines recruit and activate leukocytes, but neutrophils are traditionally known to be restricted in their chemokine receptor (CR) expression repertoire. Neutrophils undergo phenotypic and functional changes under inflammatory conditions, but the mechanisms regulating CR expression of infiltrated neutrophils at sites of chronic inflammation are poorly defined.

Cleavage of CXCR1 on neutrophils disables bacterial killing in cystic fibrosis lung disease.

Interleukin-8 (IL-8) activates neutrophils via the chemokine receptors CXCR1 and CXCR2. However, the airways of individuals with cystic fibrosis are frequently colonized by bacterial pathogens, despite the presence of large numbers of neutrophils and IL-8. Here we show that IL-8 promotes bacterial killing by neutrophils through CXCR1 but not CXCR2.

Bronchoalveolar pepsin, bile acids, oxidation, and inflammation in children with gastroesophageal reflux disease.

Introduction: Gastroesophageal reflux has been suggested as an underlying cause of chronic lung disease. The aim of this study was to assess the value of pepsin and bile acids, both components of GI secretions, in the lungs of children with chronic lung diseases as possible markers for gastroesophageal reflux disease and their relation to oxidation and inflammation.

Materials And Methods: BAL was performed in 96 children with different chronic lung diseases.