J. Jimenez

CD40 is an immune checkpoint regulator that potentiates myocardial inflammation through activation and expansion of CCR2+ macrophages and CD8 T-cells

This study shows CD40 agonists promote myocardial inflammation by activating CCR2+ macrophages and CD8 T-cells, leading to heart failure.

Prenatal VEGF Nano-Delivery Reverses Congenital Diaphragmatic Hernia-Associated Pulmonary Abnormalities

This paper investigates VEGF supplementation as a treatment for congenital diaphragmatic hernia (CDH)-associated lung abnormalities using an ex vivo model and nanoparticle-based delivery in vivo.

The HCM-Linked Mutation Arg92Leu in TNNT2 Allosterically Alters the cTnC-cTnI Interface and Disrupts the PKA-mediated Regulation of Myofilament Relaxation

This paper investigates how the HCM-linked mutation Arg92Leu in TNNT2 alters the cTnC-cTnI interface, impairing PKA access and causing early diastolic dysfunction.

Expansion of Disease Specific Cardiac Macrophages in Immune Checkpoint Inhibitor Myocarditis

This study identifies an inflammatory macrophage population expanded in ICI myocarditis, driven by IFN-γ signaling and T-cell interactions, suggesting IFN-γ blockade as a potential therapeutic strategy.

BiFCo: Visualising cohesin assembly/disassembly cycle in living cells.

The paper introduces BiFCo, a system for visualizing cohesin assembly/disassembly in living cells using bimolecular fluorescent complementation in fission yeast.

Prospective Motion Correction and Automatic Segmentation of Penetrating Arteries in Phase Contrast MRI at 7 T

This paper develops a prospective motion correction method for 7 T phase contrast MRI of penetrating arteries and evaluates its effectiveness using CNN-based segmentation.

The finger 2 tip loop of Activin A is required for the formation of its non-signaling complex with ACVR1 and type II Bone Morphogenetic Protein receptors

The paper shows that the non-signaling complex formed by Activin A and ACVR1 reduces disease severity in FOP by tempering heterotopic ossification.

Multimodal memory T cell profiling identifies a reduction in a polyfunctional Th17 state associated with tuberculosis progression

The paper uses multimodal single-cell profiling to identify a reduction in a polyfunctional Th17-like memory T cell state associated with tuberculosis progression.