L. Peters

Pneumonia induced rise in glucagon promotes endothelial damage and vascular thrombogenicity

This study shows that pneumonia increases glucagon levels, which damages endothelial cells and promotes blood clotting, leading to cardiovascular issues.

MicroRNA-26b protects against MASH development in mice and can be efficiently targeted with lipid nanoparticles.

This paper shows that miR-26b deficiency worsens MASH in mice, and that miR-26b mimic-loaded LNPs can reverse these effects.

Human immune phenotyping reveals accelerated aging in type 1 diabetes

The paper uses flow cytometry to show accelerated immune aging and age-adjusted proinflammatory phenotypes in type 1 diabetes.

A metabolomic view on local climate adaptation: Latitudinal divergence of heat and drought responses in a coastal plant

This study examines latitudinal differences in drought and heat stress resistance in Cakile maritima using metabolomics, finding southern populations show reduced growth reduction under stress due to adaptive metabolic and morphological traits.

Sex matters: effects of sex and mating in the presence and absence of a protective microbe

This study examines sex-specific differences in life history traits of C. elegans under pathogen infection with and without microbial protection.

Genomic analysis reveals a polygenic architecture of antler morphology in wild red deer (Cervus elaphus).

The paper investigates the genetic architecture of antler morphology in red deer using genomic data, finding a polygenic structure with heritable traits and pleiotropic effects.

Intestinal inflammation modulates the expression of ACE2 and TMPRSS2 and potentially overlaps with the pathogenesis of SARS-CoV-2 related disease

The paper examines how intestinal inflammation affects ACE2 and TMPRSS2 expression and identifies shared molecular networks between COVID-19 and IBD.

B cell defects observed in Nod2 knockout mice are a consequence of a Dock2 mutation frequently found in inbred strains

The paper identifies a Dock2 mutation in Nod2-/- mice that causes B cell defects, independent of Nod2 deletion, and shows the mutation is common in inbred strains.