Zhongshan Hospital Xiamen University

Multi-parametric quantitative mag- netic resonance imaging (mqMRI) provides comprehensive and accurate information about tissue microstructure and holds significant clinical value for the diagnosis and treatment of diseases. However, conventional methods require long scan time, leading to registration errors and physiological variability between different sequence acqui- sitions. This study aims to propose an advanced imaging method that addresses these limitations.

A novel approach called longitudinal magnetization controlled multiple overlapping-echo detachment (LMC-MOLED) imaging was proposed. LMC-MOLED leverages a deep neural network trained on synthetic data generated from Bloch simulation, incorporating non-ideal factors such as B₀ and B₁ inhomogeneities to efficiently reconstruct parametric maps.

LMC-MOLED enables simulta- neous quantification of T₁, T₂, T₂^*, proton density (PD), ΔB₀, and B₁ parameters in approximately 1.2 seconds per slice. Validation experiments using numerical brain, phantom, and human brains demonstrate its excellent performance, particularly in terms of acquisition speed, image quality, and robustness. Additionally, LMC-MOLED effectively corrects distortions introduced by long echo train acquisition.

LMC-MOLED offers a rapid, robust solution for mqMRI, providing multi-parametric mapping in a single scan with signify- cantly reduced acquisition time. It holds potential to improve diagnostic accuracy and alleviate patient burden.

Helicobacter pylori (H. pylori) infection is the primary driver in gastric cancer (GC) development, but the dynamic changes of the gastric mucosal microenvironment during H. pylori-associated GC progression remains elusive. Here, we perform single-cell RNA sequencing (scRNA-seq) on 21 gastric mucosae collected from four typical stages of GC progression under H. pylori infection. Our scRNA-seq analysis delineates the cellular landscape, dissects the dynamic alterations, and characterizes distinct immune cell populations. Notably, H. pylori-associated activated mast cells upregulate CD38 and COX2 expression, leading to increased secretion of adenosine and prostaglandin E₂ (PGE₂). PGE₂ enhances adenosine receptor expression in CD8⁺ T cells, thereby suppressing their cytotoxicity via adenosine signaling. Cellular interactions are more complex at the GC stage than in the premalignant lesions. Collectively, our study offers a comprehensive insight into the evolving gastric mucosal microenvironment and validates the pro-tumor role of activated mast cells under H. pylori infection.