Dr. Ibrahim Mohammed is a clinical psychologist and researcher specializing in trauma, somatic symptoms, and psychopathology in conflict-affected populations. He has worked for over a decade with survivors of massacres in the Kurdistan Region, integrating clinical practice with research. He is also a lecturer at the Institute of Psychotherapy and Psychotraumatology at the University of Duhok. His current research focuses on validating psychological instruments for Kurdish communities and exploring genetic and phenomic factors related to trauma-related disorders. In a new study in Frontiers in Psychiatry, he and colleagues showed exceptionally high levels of trauma among survivors of a notorious atrocity: the 1988 chemical attack on Halabja in Kurdistan. In this editorial, he summarizes their findings.

Researchers at Kumamoto University have developed a highly sensitive blood test that can detect subtle differences in how easily blood begins to clot, offering new possibilities for tailoring anticoagulant therapy and understanding disease-specific clotting abnormalities in patients with cardiovascular disease.

Alveolar fibroblasts play a key role in regulation of lung inflammation. Pseudomonas aeruginosa (PAO) is one of the most common pathogens causing lung injury, and the role of PAO-infected alveolar fibroblasts in such a condition remain unclear. Tumor necrosis factor (TNF)-α was significantly upregulated in alveolar fibroblasts with PAO-associated lung injury patients. Alveolar fibroblasts infected with PAO, combined with gene expression profiling, revealed elevated levels of pro-inflammatory cytokines, and this finding was closely linked to neutrophil-mediated inflammatory injury. Gene Ontology and Kyoto Encyclopedia of Genes Genomes enrichment analysis indicated that differentially expressed genes were linked to pro-inflammatory signals, including necroptosis, nuclear factor (NF)-κB inflammatory signaling, pro-inflammatory cytokine production, and neutrophil migration/activation. Furthermore, Western blot and enzyme-linked immunosorbent assay results demonstrate that PAO activated the NF-κB pathway and enhanced the expression and secretion of pro-inflammatory cytokines in alveolar fibroblasts. The study findings suggest that PAO-infected alveolar fibroblasts contribute to the development of pulmonary inflammatory injury.