Clinical Characteristics and Outcomes of Cardiac Findings in Young Persons Following SARS-CoV-2 Infection.

We studied cardiac complications in young persons with severe acute respiratory syndrome coronavirus 2. In a prospective cohort of 127 Military Health System beneficiaries 0-22 years old, 3.1% had cardiac abnormalities, all resolved within 6 months.

Clarkson disease in critically and non-critically ill patients: insights from the Italian IRIS-CLS registry.

Idiopathic Systemic Capillary Leak Syndrome (ISCLS) is a poorly understood paroxysmal permeability disorder. This study aimed to characterize the clinical features and severity markers of ISCLS in critically and non-critically ill patients. We analyzed prospectively and retrospectively collected data on ISCLS cases from the Italian IRIS-CLS Registry (January 1995-December 2023).

Recognition of MR1-antigen complexes by TCR Vγ9Vδ2.

The TCR-mediated activation of T cells expressing the TCR Vγ9Vδ2 relies on an innate-like mechanism involving the butyrophilin 3A1, 3A2 and 2A1 molecules and phospho-antigens, without the participation of classical antigen-presenting molecules. Whether TCR Vγ9Vδ2 cells also recognize complexes composed of antigens and antigen-presenting molecules in an adaptive-like manner is unknown. Here, we identify MR1-autoreactive cells expressing the TCR Vγ9Vδ2.

Responses of Arbuscular Mycorrhizal Fungi and Plant Communities to Long-Term Mining and Passive Restoration.

Mining activities cause strong soil alterations, such as heavy metal (HM) pollution, which decreases the diversity of plant communities and rhizospheric microorganisms, including arbuscular mycorrhizal (AM) fungi. The polymetallic Paramillos de Uspallata mine in the Andes Mountains, the first mining exploitation in Argentina, provides a unique scenario to study AM fungal resilience after long-term disturbance following over 40 years of inactivity. This study aimed to analyze mycorrhizal status and AM fungal communities in the mine and a nearby unexploited area and to evaluate their associations with soil parameters to elucidate life history strategies.

Rewriting nuclear epigenetic scripts in mitochondrial diseases as a strategy for heteroplasmy control.

Mitochondrial diseases, caused by mutations in either nuclear or mitochondrial DNA (mtDNA), currently have limited treatment options. For mtDNA mutations, reducing mutant-to-wild-type mtDNA ratio (heteroplasmy shift) is a promising therapeutic option, though current approaches face significant challenges. Previous research has shown that severe mitochondrial dysfunction triggers an adaptive nuclear epigenetic response, characterized by changes in DNA methylation, which does not occur or is less important when mitochondrial impairment is subtle.