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What Are We Actually Decoding? Source Attribution for Non-Invasive Brain-to-Language Retrieval

arXiv:2605.24524v1 Announce Type: cross Abstract: In non-invasive neural language decoding, results can be inflated by sources that are not stimulus-evoked neural evidence: decoder priors, embedding-based metrics, and non-neural structural nuisances such as signal duration. The methodological challenge is therefore attribution: a reported gain is more informative when it can be traced to a specific source. We recast stimulus-locked MEG-to-audio retrieval as an auditing framework that separates apparent performance into three sources - structural shortcuts, window-level stimulus-locked evidence, and cross-window contextual aggregation - and provides a diagnostic for each. Signal-blind Gaussian noise reaches 66.3% Rank@1 (R@1) under variable-length decoding but collapses to near chance once fixed-duration windows and stimulus-identity splits are enforced, isolating structural leakage. Under these controls, fixed-window retrieval recovers measurable MEG-audio discriminability, while an oracle sentence-bucket diagnostic shows that 95.7% of Top-1 errors select the wrong sentence, localising the residual bottleneck to sentence-level competition. We audit this contextual source with Group Context Bias (GCB), an inference-time additive logit bias that pools sentence-consistent evidence across windows while leaving the base retrieval scores and candidate pool fixed. Used as a score-space intervention, GCB makes the contextual source measurable: R@1 shifts from 44% to 52% on Gwilliams and from 22% to 29% on MOUS under the same fixed setting. GCB is auditable under this design: its effect collapses under random-grouping perturbations and vanishes when local evidence is attenuated in MEG or is near chance in EEG, supporting its use as a controlled source-attribution intervention. These results suggest that brain-to-language performance should be source-attributed, not merely reported.

EBV strain interacts with host HLA to drive nasopharyngeal carcinoma risk

Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10416-8

A genome-to-genome association study identifies host and viral risk factors that interact to drive nasopharyngeal carcinoma endemicity in southern China.

Mechanisms of Xinwei Tang in stress-induced gastric dysmotility: evidence from rat and In Vitro models

In Vitro Cell Dev Biol Anim. 2026 Mar 18. doi: 10.1007/s11626-026-01151-5. Online ahead of print.

ABSTRACT

Stress is a key trigger of gastric dysmotility, partly via mitochondrial dysfunction and disordered gut-brain hormonal signaling. Xinwei Tang (XWT) is a multi-herb formula used empirically for upper gastrointestinal symptoms, but its mechanisms remain unclear. This study aimed to determine whether XWT alleviates water-immersion restraint stress (WIRS)-induced gastric dysmotility and to delineate underlying mitochondrial and metabolic pathways using integrated in vivo, in vitro and multi-omics approaches. Male rats underwent 7-d WIRS and received vehicle, domperidone (3 mg/kg) or XWT (3, 6, 12 g/kg). Gastric emptying, serum motilin/gastrin, oxidative stress indices and PINK1/Parkin-LC3/p62 proteins were assessed, and H₂O₂-injured GES-1 cells were treated with XWT-medicated serum. Gastric antra from MOD and XWT-H rats were analyzed by RNA-seq and DIA proteomics (n = 3/group). WIRS reduced gastric emptying by roughly half and lowered motilin/gastrin, increased ROS/MDA and disrupted PINK1/Parkin-LC3/p62 profiles; XWT dose-dependently reversed these changes, with XWT-H approximating domperidone. Omics revealed XWT-associated downregulation of inflammatory/protease and acute-phase genes/proteins and enrichment of oxidative phosphorylation, tricarboxylic-acid cycle and other metabolic pathways, without global activation of canonical autophagy/mitophagy gene sets. These preclinical data indicate that XWT ameliorates stress-induced gastric dysmotility via mitochondria- and metabolism-centred protection with selective tuning of mitophagy-related proteins.

PMID:41851413 | DOI:10.1007/s11626-026-01151-5

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