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arXiv:2505.15435공식 코드 · Papers with Code

TimeCausality: Evaluating the Causal Ability in Time Dimension for Vision Language Models

Reasoning about temporal causality, particularly irreversible transformations of objects governed by real-world knowledge (e.g., fruit decay and human aging), is a fundamental aspect of human visual understanding. Unlike temporal perception based on simple event sequences, this form of reasoning requires a deeper comprehension of how object states change over time. Although the current powerful Vision-Language Models (VLMs) have demonstrated impressive performance on a wide range of downstream tasks, their capacity to reason about temporal causality remains underexplored. To address this gap, we introduce \textbf{TimeCausality}, a novel benchmark specifically designed to evaluate the causal reasoning ability of VLMs in the temporal dimension. Based on our TimeCausality, we find that while the current SOTA open-source VLMs have achieved performance levels comparable to closed-source models like GPT-4o on various standard visual question answering tasks, they fall significantly behind on our benchmark compared with their closed-source competitors. Furthermore, even GPT-4o exhibits a marked drop in performance on TimeCausality compared to its results on other tasks. These findings underscore the critical need to incorporate temporal causality into the evaluation and development of VLMs, and they highlight an important challenge for the open-source VLM community moving forward. Code and Data are available at \href{https://github.com/Zeqing-Wang/TimeCausality }{TimeCausality}.

arXiv:2305.06808공식 코드 · Papers with Code

Modelling disease impact: lifespan reduction is greatest for young adults in an exogenous damage model of disease

We model the effects of disease and other exogenous damage during human aging. Even when the exogenous damage is repaired at the end of acute disease, propagated secondary damage remains. We consider both short-term mortality effects due to (acute) exogenous damage and long-term mortality effects due to propagated damage within the context of a generic network model (GNM) of individual aging that simulates a U.S. population. Across a wide range of disease durations and severities we find that while excess short-term mortality is highest for the oldest individuals, the long-term years of life lost are highest for the youngest individuals. These appear to be universal effects of human disease. We support this conclusion with a phenomenological model coupling damage and mortality. Our results are consistent with previous lifetime mortality studies of atom bomb survivors and post-recovery health studies of COVID-19. We suggest that short-term health impact studies could complement lifetime mortality studies to better characterize the lifetime impacts of disease on both individuals and populations.

arXiv:2007.11113공식 코드 · Papers with Code

Early life imprints the hierarchy of T cell clone sizes

The adaptive immune system responds to pathogens by selecting clones of cells with specific receptors. While clonal selection in response to particular antigens has been studied in detail, it is unknown how a lifetime of exposures to many antigens collectively shape the immune repertoire. Here, through mathematical modeling and statistical analyses of T cell receptor sequencing data we demonstrate that clonal expansions during a perinatal time window leave a long-lasting imprint on the human T cell repertoire. We demonstrate how the empirical scaling law relating the rank of the largest clones to their size can emerge from clonal growth during repertoire formation. We statistically identify early founded clones and find that they are indeed highly enriched among the largest clones. This enrichment persists even after decades of human aging, in a way that is quantitatively predicted by a model of fluctuating clonal selection. Our work presents a quantitative theory of human T cell dynamics compatible with the statistical laws of repertoire organization and provides a mechanism for how early clonal dynamics imprint the hierarchy of T cell clone sizes with implications for pathogen defense and autoimmunity.

arXiv:2003.09764공식 코드 · Papers with Code

Lifespan Age Transformation Synthesis

We address the problem of single photo age progression and regression-the prediction of how a person might look in the future, or how they looked in the past. Most existing aging methods are limited to changing the texture, overlooking transformations in head shape that occur during the human aging and growth process. This limits the applicability of previous methods to aging of adults to slightly older adults, and application of those methods to photos of children does not produce quality results. We propose a novel multi-domain image-to-image generative adversarial network architecture, whose learned latent space models a continuous bi-directional aging process. The network is trained on the FFHQ dataset, which we labeled for ages, gender, and semantic segmentation. Fixed age classes are used as anchors to approximate continuous age transformation. Our framework can predict a full head portrait for ages 0-70 from a single photo, modifying both texture and shape of the head. We demonstrate results on a wide variety of photos and datasets, and show significant improvement over the state of the art.

arXiv:1807.04709공식 코드 · Papers with Code

Inferring Multidimensional Rates of Aging from Cross-Sectional Data

Modeling how individuals evolve over time is a fundamental problem in the natural and social sciences. However, existing datasets are often cross-sectional with each individual observed only once, making it impossible to apply traditional time-series methods. Motivated by the study of human aging, we present an interpretable latent-variable model that learns temporal dynamics from cross-sectional data. Our model represents each individual's features over time as a nonlinear function of a low-dimensional, linearly-evolving latent state. We prove that when this nonlinear function is constrained to be order-isomorphic, the model family is identifiable solely from cross-sectional data provided the distribution of time-independent variation is known. On the UK Biobank human health dataset, our model reconstructs the observed data while learning interpretable rates of aging associated with diseases, mortality, and aging risk factors.