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01.
arXiv (CS.CV) 2026-06-25

Brevity is the Soul of Inference Efficiency: Inducing Concision in VLMs via Data Curation

Inference efficiency is typically pursued by shrinking the model: distillation, pruning, quantization, and sparse routing each lower per-token cost while treating token count as fixed. But output length has been inflating, and it is precisely the component the standard toolkit leaves untouched. Here, we argue that brevity is the missing inference-efficiency lever, and that pretraining data curation is a practical way to pull it: a model trained on concise, correct data learns to answer in fewer tokens; i.e. it has a lower Cost-of-Pass. We apply our VLM curation pipeline to the MAmmoTH-VL single-image subset, and compare models trained on our curated data, the standard MAmmoTH-VL data, and external open-weight frontier VLMs. On a controlled 20-evaluation set and 14 VLMs at 1B-4B activated parameters, we hold output length fixed with a per-model regression, separating brevity from quality, and price models in FLOPs per correct answer. Curation buys a 35x Cost-of-Pass advantage over the most verbose 4B comparator (Qwen3.5-4B) within $\sim$1 pp of accuracy (0.41 vs 14.58 TFLOPs per correct answer; 0.691 vs 0.704 mean accuracy). Curation also buys a +17.55-percentage-point matched-length accuracy gain over the uncurated baseline that grows with model scale (from +16.7 pp at 1B to +21.2 pp at 4B). This brevity improvement concedes no quality: generic verbosity buys no accuracy at any capability or scale, and the window where reasoning-structured verbosity still earns its tokens shrinks from 4 of 8 capability groups at 2B to 1 of 8 at 4B. Per example, the concise model even reaches correct answers the verbose reasoning model misses, marking reasoning as a distinct curation target rather than something brevity gives up. Inference efficiency in this regime is a tokens-per-correct problem, and brevity is the lever that targets it directly.

02.
medRxiv (Medicine) 2026-06-12

An integrative multi-omics framework identifies epigenetic dysregulation of HAND2 as a potential primary driver of impaired enteric neural crest cell differentiation in Hirschsprung Disease

Hirschsprung disease (HSCR) is a congenital neurodevelopmental disorder characterized by segmental aganglionosis due to impaired developmental processes of enteric neural crest cells (NCCs). Despite being the leading genetic cause of functional intestinal obstruction in early childhood, HSCR represents a paradigmatic challenge in precision medicine: its multifactorial etiology, complex gene-environment interactions and limited resolution of single-modality analyses have long hindered mechanistic understanding and therapeutic translation. Here, we applied an integrative multi-omics approach combining genetic, phenotypic, epigenomic and transcriptomic analyses of matched ganglionic and aganglionic formalin-fixed paraffin-embedded (FFPE) patient tissues, complemented by patient-specific in vitro models. Beyond established genetic contributors, our integrative approach reveals novel regulatory pathways predominantly affecting enteric NCC differentiation, with convergent evidence pointing to epigenetic dysregulation as a primary disease mechanism. Notably, we identified over 1,300 differentially methylated positions between ganglionic and aganglionic FFPE samples, with HAND2 emerging as a key candidate due to multiple hypermethylated sites and consistently reduced expression levels in aganglionic tissues and in vitro models, suggesting a potential role in HSCR pathophysiology. We propose that our multi-omics approach offers a powerful and comprehensive framework for dissecting disease mechanisms. Beyond advancing biological understanding, this strategy holds promise for paving the way for molecularly informed patient stratification and supporting the development of personalized treatment and postoperative management strategies.