Spores of filamentous fungi are common biological particles in indoor air that can negatively impact human health, particularly among immunocompromised individuals and patients with chronic respiratory conditions. Airborne viruses represent an equally pervasive threat, with some carrying the potential for pandemic spread, affecting both healthy individuals and the immunosuppressed alike. This study investigated the abundance and diversity of airborne fungal spores in both hospital and residential environments, using custom designed air samplers with or without the presence of negative air ions (NAIs) inside the sampler. The main purpose of investigation was the assessment of biological effects of NAIs on fungal spore viability, deposition, mycelial growth, and sporulation, as well as airborne viral load. The precise assessment of mentioned biological effects is otherwise difficult to carry out due to low concentrations of studied specimens; therefore, specially devised and designed, ion-bioaerosol interaction air samplers were used for prolonged collection of specimens of interest. The total fungal spore concentrations were quantified, and fungal isolates were identified using cultural and microscopic methods, complemented by MALDI-TOF mass spectrometry. Results indicated no significant difference in overall spore concentration between environments or treatments; however, presence of NAIs induced a delay in the sporulation process of Cladosporium herbarum, Aspergillus flavus, and Aspergillus niger within 72 h. These effects of NAIs are for the first time demonstrated in this work; most likely, they are mediated by oxidative stress mechanisms. A parallel experiment demonstrated a substantially reduced concentration of aerosolized equine herpesvirus 1 (EHV-1) DNA within 10–30 min of exposure to NAIs, with more than 98% genomic load reduction beyond natural decay. These new results on the NAIs interaction with a virus, as well as new findings regarding the fungal sporulation, resulted in part from a novel interaction setup designed for experiments with the bioaerosols. Our findings highlight the potential of NAIs as a possible approach for controlling fungal sporulation and reducing airborne viral particle quantities in indoor environments.

The first allogeneic identical sibling donor hematopoietic stem cell transplantation at the Institute for Mother and Child Health Care of Serbia ?Dr. Vukan Cupic? (Institute) was performed in the seventies of the last century. Almost twenty years later, the first allogeneic transplant from sibling haploidentical donor was performed in an infant suffering from severe combined immunodeficiency. After several years of efforts, the bone marrow transplant unit was opened in April 1997 at the Institute. Over the 25 years, the transplant team performed 360 hematopoietic stem cell transplantations, 175 autologous and 185 allogeneic (103 from identical sibling donor, 43 from haploidentical sibling donor, 36 from matched unrelated donor, 2 from identical sibling cord blood and 1 from unrelated identical cord blood).

Oxidative stress (OS) has long been recognized as a central driver of malignant transformation and progression. In leukemia, disrupted redox balance and metabolic reprogramming critically shape cell proliferation, differentiation, and survival, while also influencing response to therapy. An excess of reactive oxygen species (ROS) over the antioxidant defense system (AOS) not only promotes leukemogenesis but also contributes to the cytotoxic activity of many chemotherapeutics. In this study, we investigated the effects of two drugs, busulfan and melphalan, used as conditioning therapy for hematopoietic stem cell transplantation, on OS and metabolism in HL-60 (promyelocytic) and K562 (erythroleukemic) cell lines, two different in vitro models with distinct metabolic profiles. In multiple myeloma cells, melphalan has been reported to induce ROS production, deplete glutathione (GSH), enhance protein and lipid oxidation, and activate the Nuclear factor erythroid 2 (Nrf-2)-mediated antioxidant response, underscoring its impact on redox regulation. Here, we compared basal redox markers in HL-60 and K562 cells and assessed how busulfan and melphalan modulate ROS generation and cytotoxicity. Importantly, we complemented these analyses with metabolomic profiling to capture drug-induced changes in key metabolic pathways, including glycolysis, the tricarboxylic acid (TCA) cycle, amino acid metabolism, and glutathione metabolism. Our results indicate that chemotherapy leads to redox imbalance and metabolic remodeling in leukemia cell models, representing potential biomarkers of chemosensitivity that can be exploited to develop improved therapeutic strategies for myeloid leukemias.