Reinforced Path Reasoning for Counterfactual Explainable Recommendation

Counterfactual explanations interpret the recommendation mechanism via exploring how minimal alterations on items or users affect the recommendation decisions. Existing counterfactual explainable approaches face huge search space and their explanations are either action-based (e.g., user click) or aspect-based (i.e., item description). We believe item attribute-based explanations are more intuitive and persuadable for users since they explain by fine-grained item demographic features (e.g., brand). Moreover, counterfactual explanation could enhance recommendations by filtering out negative items. In this work, we propose a novel Counterfactual Explainable Recommendation (CERec) to generate item attribute-based counterfactual explanations meanwhile to boost recommendation performance. Our CERec optimizes an explanation policy upon uniformly searching candidate counterfactuals within a reinforcement learning environment. We reduce the huge search space with an adaptive path sampler by using rich context information of a given knowledge graph. We also deploy the explanation policy to a recommendation model to enhance the recommendation. Extensive explainability and recommendation evaluations demonstrate CERec's ability to provide explanations consistent with user preferences and maintain improved recommendations. We release our code at https://github.com/Chrystalii/CERec

Counterfactual Explanation for Fairness in Recommendation

Fairness-aware recommendation eliminates discrimination issues to build trustworthy recommendation systems.Explaining the causes of unfair recommendations is critical, as it promotes fairness diagnostics, and thus secures users' trust in recommendation models. Existing fairness explanation methods suffer high computation burdens due to the large-scale search space and the greedy nature of the explanation search process. Besides, they perform score-based optimizations with continuous values, which are not applicable to discrete attributes such as gender and race. In this work, we adopt the novel paradigm of counterfactual explanation from causal inference to explore how minimal alterations in explanations change model fairness, to abandon the greedy search for explanations. We use real-world attributes from Heterogeneous Information Networks (HINs) to empower counterfactual reasoning on discrete attributes. We propose a novel Counterfactual Explanation for Fairness (CFairER) that generates attribute-level counterfactual explanations from HINs for recommendation fairness. Our CFairER conducts off-policy reinforcement learning to seek high-quality counterfactual explanations, with an attentive action pruning reducing the search space of candidate counterfactuals. The counterfactual explanations help to provide rational and proximate explanations for model fairness, while the attentive action pruning narrows the search space of attributes. Extensive experiments demonstrate our proposed model can generate faithful explanations while maintaining favorable recommendation performance

Causal Neural Graph Collaborative Filtering

Graph collaborative filtering (GCF) has gained considerable attention in recommendation systems by leveraging graph learning techniques to enhance collaborative filtering (CF) models. One classical approach in GCF is to learn user and item embeddings by modeling complex graph relations and utilizing these embeddings for CF models. However, the quality of the embeddings significantly impacts the recommendation performance of GCF models. In this paper, we argue that existing graph learning methods are insufficient in generating satisfactory embeddings for CF models. This is because they aggregate neighboring node messages directly, which can result in incorrect estimations of user-item correlations. To overcome this limitation, we propose a novel approach that incorporates causal modeling to explicitly encode the causal effects of neighboring nodes on the target node. This approach enables us to identify spurious correlations and uncover the root causes of user preferences. We introduce Causal Neural Graph Collaborative Filtering (CNGCF), the first causality-aware graph learning framework for CF. CNGCF integrates causal modeling into the graph representation learning process, explicitly coupling causal effects between node pairs into the core message-passing process of graph learning. As a result, CNGCF yields causality-aware embeddings that promote robust recommendations. Our extensive experiments demonstrate that CNGCF provides precise recommendations that align with user preferences. Therefore, our proposed framework can address the limitations of existing GCF models and offer a more effective solution for recommendation systems

Mechanistic correlates of the dual tPA-edaravone therapy of tHI injury.

<p>(<b>A–F</b>) Immunostaining of fibrinogen (A–C) and fluorescent images of the Evans Blue dye (D–F) at 4 h after tHI injury in the striatum (St) and cerebral cortex (Ctx) of the ipsilateral hemisphere of vehicle- and E + tPA-treated animals, and the contralateral hemisphere of mice receiving either treatment. This analysis showed that the E + tPA treatment decreased fibrin deposits, perfusion deficits, and extravasation of the Evans Blue dye. (<b>G</b>) Quantification of malondialdehyde (MDA) at 24 h post-tHI showed significant reduction of lipid peroxidation by the E + tPA treatment. (<b>H</b>) MMP zymography at 24 h post-tHI and quantification showed significant reduction of MMP-9 activity by the E + tPA treatment (n = 4 for each). Equal loading of brain extracts was verified by immunoblot detection of β-actin. L: contralateral (left) hemisphere; R: The ipsilateral (right) hemisphere. (<b>I–K</b>) Real time RT-PCR showed that the E + tPA treatment significantly decreased tHI-induced IL-1β, IL-6, and Tspo transcripts at 24 h recovery (n = 4 each).</p

Spontaneous thrombosis and decreased tPA activity following tHI insults.

<p>(<b>A–L</b>) Immunostaining performed at 1 h after tCCAo, tHI or permanent carotid ligation (pCCAo) plus hypoxia showed deposits of fibrin(ogen) and platelets (detected by anti-Integrin α2β/CD41) and P-Selectin-positive blood vessels (a marker for endothelial activation) and in the ipsilateral hemisphere following tHI insults (C, G, K). Permanent carotid ligation plus hypoxia produced the same staining pattern, but with stronger signals of all three markers (D, H, L). This staining pattern was absent in the brain after tCCAo (A, E, I) or on the contralateral hemisphere following tHI (B, F, J) (n>4 for each). (<b>M</b>) Plasminogen-zymogram showed definitive induction of the brain uPA and ∼50% increase of tPA activity in the ipsilateral hemisphere (R) at 4 h post-HI in neonates. No uPA-induction was found in adult brains at 4 h following tCCAo or tHI insults. The tPA activity in the ipsilateral hemisphere (R) following tHI was reduced to ∼67% of the level in unchallenged (UN) brains (p<0.05). The right panel is the quantification of zymogram band intensity (n = 4 for each). (<b>N</b>) The plasminogen-zymogram from plasma showed the lack of tPA activity and a similar degree of uPA activity at 4 h after tCCAo or tHI insults in adult mice. Immunoblot detection of transferrin (Tf) served as the internal control. (<b>O</b>) Direct measurement of tPA activity using a fluorescent substrate kit also showed significant reduction in the ipsilateral hemisphere at 4 h following tHI insult in adult brains (n = 3-4 for each). (<b>P–Q</b>) Immunoblot analysis showed minimal change of the tPA protein level and no sign of plasminogen activator inhibitor-1 (PAI-1) up-regulation after tCCAo or tHI insult in adult brains (n = 4 for each). Scale bar: 200 μm in A–L.</p

Imparied cerebral vascular reperfusion after transient hypoxia-ischemia (tHI).

<p>(<b>A, B</b>) TTC-staining detected no visible infarction at 24 h after 30-min transient occlusion of the right common carotid artery (RCCAo), but exposing mice to 7.5% oxygen during the ischemic period (RCCAo + Hypoxia) produced sizeable infarction in the ipsilateral hemisphere. (<b>C–E</b>) By subjecting Thy1-YFP mice to 30-min unilateral carotid occlusion (tCCAo) or carotid occlusion with hypoxia (tHI), we detected loss of deep cortical neurons and destruction of white matter in the striatum (St), external capsule (EC), and cerebral cortex (Ctx) in the ipsilateral hemisphere following tHI insult (E), but not on the contralateral hemisphere (D) or after the tCCAo insult. (<b>F, H</b>) Laser speckle contrast imaging showed the effects of hypoxia (7.5% oxygen) on cerebral blood flow (CBF) during and after transient unilateral occlusion of the common carotid artery (RCCAo; R indicates the carotid-ligated hemisphere; L, the contralateral hemisphere). When it was under normoxia (F), CBF on the carotid-ligated hemishere was at ∼50% throughout 30-min ischemia, and recovered to >85% within 3 min after the release of vascular occlusion. When it was under hypoxia during carotid occlusion (H), CBF on the ipsilaterla side dropped to <20% of the contralteral value during ischemia-hypoxia, and rarely recovered to above 30% after release of the carotid artery ligation. Shown are representative CBF tracings for n >4 in each group. The 2-dimensional CBF images correspond to the indicated timespoints (also marked by grey lines in the tracing). (<b>G</b>) CBF response to 30 min hypoxia (7.5% oxygen) without carotid artery ligation. During hypoxia, CBF dropped to 76% of the baseline value on both hemispheres, and transiently rebounded to ∼130% at the end of hypoxic stress. (<b>I–L</b>) Detection of vascular perfusion by tail-vein injection of Evans Blue dye at 10 min before sacrificing the mouse. Evans Blue dye filled vessels in the contralateral hemisphere following tHI insult, but was excluded in pocketed areas in the ipsilateral hemisphere at 2 h, and further restricted or leaked in the brain parenchyma at 4 h (n>3 for each time-point). Scale bar: 250 μm in C–E, H–K.</p

Improvement of long-term functional outcome and protection of white-matter from tHI injury by the dual tPA-edaravone therapy.

<p>(<b>A-B</b>) Survival rate (A) and long-term functional outcome (neurological deficits score, B) were monitored for 7 days following tHI in vehicle-treated and dual tPA-edaravone-treated animals (E + tPA; tPA was administered at 0.5 h). E + tPA-treated mice showed a higher survival rate (75%, n = 8) than the vehicle group (40%, n = 10), and conferred fewer neurological deficits. *, p<0.05; **, p<0.01 compared to vehicle control group by t-test. (<b>C</b>) Motor behavior was examined by rotarod testing at 7-day after tHI. The latency on rotarod (seconds) in vehicle-treated animals (n = 4) was significantly shorter than that in E + tPA-treated animals (n = 6), which is similar to the response in unchallenged (UN) animals (n = 9). (<b>D</b>) Representative coronal images of directionally encoded color (DEC) map of the brains from vehicle-treated and E + tPA-treated mice at 24 hours recovery. The directions of color-encoded water diffusion along the x, y, and z axis were indicated. (<b>E–G</b>) Comparison of the fractional anisotropy (FA), axial/longitudinal diffusivity, and radial/horizontal diffusivity in the midline corpus callosum (CC), and contralateral and ipsilateral external capsule (EC) between the vehicle-treated (n = 6) and E + tPA-treated mice (n = 4). (<b>H–M</b>) Electron micrographs of the indicated axonal tracts following tHI insults in vehicle- or E + tPA-treatment. The CC of vehicle-treated, but not E + tPA-treated animals exhibited numerous empty space (asterisks in H) and myelinated axons filled with large vacuoles (arrowheads in H). The contralateral EC in both groups showed minimal ultrastructural abnormality (I, L). The ipsilateral EC in vehicle-treated animals showed near-complete degradation of the cytoplasm in the vast majority of cell bodies and axons (asterisks in J). In contrast, the ipsilateral EC in E + tPA-treated animals showed minimal ultrastructural pathology, and smaller inter-axonal empty space (asterisk in M). Scale bar: 1 μm in H–M.</p

Synergy between edaravone and early tPA-infusion therapies in the tHI model.

<p>(<b>A</b>) Scheme of experimental treatments tested in this study. tPA (10 mg/kg) was injected through the tail vein at 0.5, 1, or 4 h following the tHI insult. The edaravone treatment consists of 3 doses (3 mg/kg, IP) immediately after, and at 1, and 2 h post-tHI. (<b>B</b>) Tabulation of the number of operated animals, dead within 24 h, considered outliers (outside the mean +/−2 SD), and those included for comparison in each treatment group. (<b>C–F, H</b>) Detection of superoxide, indicated by the fluorescent hydroethidine (oxHEt), at 2.5 h after tHI. This assay showed numerous oxHEt positive nuclei along the blood vessel wall and in the cerebral cortex of mice that received the vehicle-treatment. The number of oxHEt-positive nuclei was greatly reduced in both locations in edaravone-treated animals. H is the quantification of oxHEt-positive nuclei (over DAPI-staining) in 4 randomly selected visual fields. The p-value was determined by <i>t</i>-test. (<b>G</b>) Chemical formula, structure and name of edaravone (also called MCI-186). (<b>I</b>) The mean and infarct volume of individual animals in each treatment group. (<b>J</b>). Statistical analysis of the infarct size in each treatment group (shown are the mean and standard error). The p-values are determined by <i>t</i>-test; * p<0.001 compared to the vehicle control group. (<b>K</b>) Representative TTC-stained brain slices at 24 h after tHI insult in each treatment group. Pale staining indicates infarcted tissue. Scale bar: 10 μm in C, D; 20 μm in E, F.</p