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PAR$^2$-RAG: Planned Active Retrieval and Reasoning for Multi-Hop Question Answering

arXiv:2603.29085v1 Announce Type: new Abstract: Large language models (LLMs) remain brittle on multi-hop question answering (MHQA), where answering requires combining evidence across documents through retrieval and reasoning. Iterative retrieval systems can fail by locking onto an early low-recall trajectory and amplifying downstream errors, while planning-only approaches may produce static query sets that cannot adapt when intermediate evidence changes. We propose \textbf{Planned Active Retrieval and Reasoning RAG (PAR$^2$-RAG)}, a two-stage framework that separates \emph{coverage} from \emph{commitment}. PAR$^2$-RAG first performs breadth-first anchoring to build a high-recall evidence frontier, then applies depth-first refinement with evidence sufficiency control in an iterative loop. Across four MHQA benchmarks, PAR$^2$-RAG consistently outperforms existing state-of-the-art baselines, compared with IRCoT, PAR$^2$-RAG achieves up to \textbf{23.5\%} higher accuracy, with retrieval gains of up to \textbf{10.5\%} in NDCG.
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Pathogenesis and immune regulation of rheumatoid arthritis-associated interstitial lung disease: from basic research to clinical implications

Front Immunol. 2026 Mar 13;17:1770348. doi: 10.3389/fimmu.2026.1770348. eCollection 2026.

ABSTRACT

Interstitial lung disease (ILD) is one of the most common extra-articular manifestations of rheumatoid arthritis (RA). Some patients with RA-ILD may develop progressive pulmonary fibrosis, leading to severe impairment of lung function and respiratory failure, which impacts quality of life and can even be life-threatening. This review identified genetic susceptibility, environmental factors, and immune dysregulation as key contributors to the etiology and pathogenesis of RA-ILD. We highlight that autoantibodies, adaptive immune abnormalities, and tertiary lymphoid organ formation significantly drive pulmonary inflammation and fibrosis, while pro-inflammatory cytokines and epithelial-mesenchymal transition (EMT) further contribute to lung tissue injury. Current treatment options, including glucocorticoids, immunosuppressants, and antifibrotic agents such as nintedanib and pirfenidone, are often limited by substantial side effects. Additionally, emerging therapies like JAK inhibitors, CAR-T cells, and the upcoming phosphodiesterase-4B inhibitor, nerandomilast, show promise, but no curative treatment exists to date. Future research could focus on multi-omics technologies and conducting multicenter clinical trials to establish therapeutic targets and advance precision medicine for RA-ILD.

PMID:41909710 | PMC:PMC13021622 | DOI:10.3389/fimmu.2026.1770348

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