A. Barros

Semaphorin 4B is an ADAM17-cleaved inhibitor of adipocyte thermogenesis

This study identifies SEMA4B as an ADAM17-cleaved inhibitor of adipocyte thermogenesis, showing it dampens thermogenic responses and protects against obesity.

DNA damage independent inhibition of NF-κB transcription by anthracyclines

This study shows anthracyclines inhibit NF-κB transcription without DNA damage, affecting inflammation independently of their DNA-damaging effects.

Host-dependent induction of disease tolerance to infection by tetracycline antibiotics

This study shows tetracycline antibiotics protect against sepsis by inducing disease tolerance through mitochondrial protein synthesis inhibition, independent of their direct antibiotic effects.

Trem-2 promotes emergence of restorative macrophages and endothelial cells during recovery from hepatic tissue damage.

This study shows Trem-2 promotes the transition of liver macrophages to restorative phenotypes and influences endothelial cell de-differentiation during liver recovery from injury.

Th2 cytokine profile in appendicular lavage fluid is compatible with allergy as an etiology for acute appendicitis

The study finds elevated Th2 cytokines in appendicitis patients, supporting allergy as a potential cause of acute appendicitis.

CXCL5-mediated recruitment of neutrophils into the peritoneal cavity of Gdf15-deficient mice protects against abdominal sepsis

This study shows that GDF15 deficiency in mice protects against abdominal sepsis by enhancing CXCL5-mediated neutrophil recruitment to the peritoneum, improving bacterial control.

Comparison Between Normobaric Hypoxia Altitude Simulation Test and Altitude Hypoxia Predictive Equations in Cystic Fibrosis Patients

The paper compares normobaric hypoxia altitude simulation test results with five predictive equations in cystic fibrosis patients to assess their accuracy in predicting in-flight hypoxia.

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.