Coronavirus disease 2019 (COVID-19) patients can develop interstitial pneumonia, which, in turn, can evolve into acute respiratory distress syndrome (ARDS). This is accompanied by an inflammatory cytokine storm. severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) has proteins capable of promoting the cytokine storm, especially in patients with comorbidities, including obesity. Since currently no resolutive therapy for ARDS has been found and given the scientific literature regarding the use of adenosine, its application has been hypothesized. Through its receptors, adenosine is able to inhibit the acute inflammatory process, increase the protection capacity of the epithelial barrier, and reduce the damage due to an overactivation of the immune system, such as that occurring in cytokine storms. These features are known in ischemia/reperfusion models and could also be exploited in acute lung injury with hypoxia. Considering these hypotheses, a COVID-19 patient with unresponsive respiratory failure was treated with adenosine for compassionate use. The results showed a rapid improvement of clinical conditions, with negativity of SARS-CoV2 detection.

Some COVID-19 patients develop interstitial pneumonia that can evolve into Acute Respiratory Distress Syndrome (ARDS). This is accompanied by an inflammatory cytokine storm. SarS-CoV has proteins capable of promoting cytokine storm, especially in patients with comorbidities, including obesity. Since there is currently no resolutive therapy for ARDS and given the scientific literature regarding the use of adenosine, its application has been hypothesized. Adenosine through its receptors is able to inhibit the acute inflammatory process, increase the protection capacity of the epithelial barrier and reduce the damage due to an overactivation of the immune system, such as in cytokine storms. These features are known in ischemia / reperfusion models and could also be exploited in acute lung injury, with hypoxia. In light of these hypotheses, for compassionate use, a COVID-19 patient, with unresponsive respiratory failure, was treated with adenosine. The results showed a rapid and clear improvement in clinical conditions, with the negative effect of detection of SarS-CoV2.

Nakaseomyces glabratus (formerly Candida glabrata) is a high-priority fungal pathogen with marked stress adaptability and a well-documented capacity to acquire antifungal resistance. This critical narrative review examines how environmental and host-imposed stress responses intersect with antifungal tolerance, persistence, heteroresistance, and stable resistance. Literature was identified through targeted PubMed and publisher-site searches and citation tracking through 5 September 2026, prioritizing primary mechanistic and longitudinal studies. Hsp90–calcineurin signaling, MAPK/cell wall integrity pathways, Gcn2–eIF2α–Gcn4-mediated translational control, mitochondrial function, efflux regulation, genomic plasticity, and chromatin-associated regulation are considered. Experimental evidence shows that calcineurin regulates echinocandin tolerance and persistence, cell wall integrity-dependent tolerance can influence resistance emergence, and high echinocandin persistence is associated with preferential emergence of resistant populations under defined experimental and in vivo conditions. Heteroresistance is a distinct population state from which stable resistance can emerge experimentally. These findings support a framework in which stress-responsive survival may increase evolutionary opportunity without implying inevitable progression to resistance. A direct causal link between contemporary climate change and N. glabratus antifungal resistance remains unproven. Future studies should test whether realistic environmental or host stress histories reproducibly alter subsequent resistance trajectories across strains and clinical settings.