Intracerebral hemorrhage (ICH) is a lethal stroke subtype with limited treatment options, largely due to secondary injury driven by oxidative stress and neuroinflammation. Here, we developed a ruthenium (Ru)-manganese (Mn) composite nanozyme by integrating Ru nanozyme into Mn-doped zeolitic imidazolate framework (Mn-ZIF) to enable cascade catalytic activity for efficient ROS clearance. In vitro, Ru@Mn-ZIF nanozyme reduced LPS-induced microglia activation and H2O2-induced neuronal oxidative damage, showing stronger protective effects than Mn-ZIF nanozyme. In vivo, both intranasal and intravenous administration of Ru@Mn-ZIF nanozyme significantly decreased hematoma volume, preserved blood-brain barrier integrity, suppressed inflammatory responses, and improved neurological recovery in collagenase- and autologous blood-induced ICH models. Biosafety evaluation revealed no pathological or biochemical abnormalities after treatment. These findings highlight Ru@Mn-ZIF nanozyme as a promising therapeutic strategy for mitigating secondary brain injury and improving outcomes after ICH.

Infected bone defects (IBDs), primarily caused by Methicillin-resistant Staphylococcus aureus (MRSA), remain a major clinical challenge due to persistent bacterial colonization, dysregulated immune responses, and disruption of the osteogenic microenvironment. Here, a multifunctional hydrogel system composed of Gelatin methacryloyl (GelMA) and hyperoside (Hyp), Zn2+, Indocyanine green (ICG) self-assembled nanoparticles was developed to achieve a synergistic “antibacterial-immunomodulatory-osteogenic” therapeutic cascade. Upon near-infrared (NIR)-triggered photothermal therapy (PTT), the Hyp/Zn/ICG nanoparticles exhibited potent antibacterial activity against MRSA. Transcriptomic analysis revealed that PTT treatment disrupted bacterial ribosome assembly and protein synthesis pathways, leading to downregulation of MRSA resistance genes. Simultaneously, PTT-assisted therapy promoted macrophage M2 polarization and suppressed M1 polarization, thereby remodeling the osteoimmune microenvironment. Furthermore, the system enhanced osteogenic differentiation by upregulating RUNX2, COL1A1, and OPN, increasing alkaline phosphatase activity, and promoting matrix mineralization through the BMP signaling. In vivo, PTT-assisted treatment effectively eradicated MRSA, induced M2 polarization, and accelerated bone regeneration in infected bone defects. Collectively, this work introduces a safe, antibiotic-free therapeutic strategy for IBDs, leveraging a coordinated antibacterial, immunomodulatory, and osteogenic mechanism for efficient infection control and bone tissue repair.

The increasing frequency of extinctions of biological populations has important implications for related sectors. Consequently, the risks associated with biodiversity are receiving increasing attention and are being recognized as entirely new risk factors. To understand the drivers of biodiversity risk, it is crucial to measure biodiversity risk at multiple levels, especially in developing countries. Using machine learning and text mining methods, we measure the biodiversity risk of the Chinese market from 2000 to 2023 from the perspectives of macro-government, meso‑industry, and micro-firms, by analysing official news media texts, related fund-holding data, and listed firms’ annual reports. We construct a macro-level index derived from the sentiment and frequency of biodiversity-related discourse in official media, including the China Environment News and the CCTV News, from 2013 to 2023. We also construct a meso-level industry risk exposure indicator, calculated as the deviation of biodiversity-themed public funds’ holdings from market portfolio weights across 58 sectors. In addition, we develop micro-level firm-specific metrics, based on the frequency and sentiment analysis of biodiversity sentences in the annual reports of 5606 A-share listed firms, 2000–2023, using an improved BERT model for Chinese text. These indicators provide researchers, policymakers, and financial practitioners with a foundational resource for empirically investigating the economic and financial implications of biodiversity risk in China.

Colorectal cancer remains a major global health challenge, highlighting the need for effective and selective anticancer agents. In the present study, a series of pyrazolone-derived sulfonamide analogues (Keum and Giovannucci, 2019a, 2019b; Morgan et al., 2023; Lee et al., 2026; Capuozzo et al., 2025; Li et al., 2024; Xie et al., 2020; Gavrić et al., 2025 (1-8)) was designed, synthesized, and evaluated for anti-colorectal cancer activity. Structural characterization of the synthesized compounds was accomplished using 1H NMR, 13C NMR, and HREI-MS analyses. The cytotoxic potential of the compounds was investigated against HCT-116 and HT-29 colorectal cancer cell lines, while HEK-293 cells were used to assess selectivity toward normal cells. Among the synthesized derivatives, analogue 7 exhibited the strongest antiproliferative activity with IC₅₀ values of 1.80 ± 0.20 μM and 2.00 ± 0.20 μM against HCT-116 and HT-29 cells, respectively, and showed reduced toxicity toward HEK-293 cells (IC₅₀ = 34.60 ± 0.20 μM). The selectivity index of 19.22 and 17.30 was calculated for potent compound 7. Molecular docking studies revealed that compound 7 exhibited the strongest binding affinity toward carbonic anhydrase IX (CA IX), with a docking score of -12.49 kcal/mol, forming favorable interactions within the enzyme active site. Enzyme kinetic analysis and Lineweaver-Burk plots suggested a competitive inhibition mechanism for the lead compound. Additionally, DFT and ADMET investigations confirmed favorable electronic characteristics, molecular stability, drug-likeness, and low predicted toxicity. These findings suggest that pyrazolone-derived sulfonamides represent promising scaffolds for future colorectal cancer drug development.

Protein tyrosine phosphatase 1B (PTP1B) serves as a key negative regulator of both insulin and leptin signaling pathways, and its inhibition represents a potential dual-mechanism therapeutic strategy for type 2 diabetes and obesity by simultaneously improving insulin sensitivity and leptin signaling. However, the clinical translation of peptide-based therapeutics is often hindered by poor proteolytic stability and short in vivo half-life. To address these challenges, we implemented a rational dual-modification strategy combining fatty acid conjugation and lactam stapling. Specifically, N-terminal fatty acid conjugation was introduced to prolong systemic circulation through reversible albumin binding, while intramolecular lactam stapling at i+3 positions was employed to constrain the peptide backbone, and improve resistance to enzymatic degradation and target binding affinity. In the present study, 19 lactam-stapled lipopeptide analogues of BimBH3 were designed and synthesized aiming to find potent, proteolytically stable peptide PTP1B inhibitors for diabetes therapy. Structure-activity relationship (SAR) studies identified compounds G4 and G14 as the most potent analogues, exhibiting IC50 values of 459.3 nM and 381.5 nM against PTP1B, respectively. Stability studies further demonstrated that the dual-modification strategy significantly improved metabolic stability. In a DPP-IV degradation assay, G4 and G14 displayed extended half-lives of approximately 11 h, corresponding to a 3.5-fold increase compared to the lead compound SM-6 (t1/2 = 3.195 h). Moreover, these compounds showed prolonged in vitro plasma stability with half-lives reaching 96.47 h for G4 and 112.1 h for G14, highlighting their potential for sustained in vivo potency. In cellular assays and in vivo oral glucose tolerance tests, both G4 and G14 showed promising cellular glucose tolerance and glycemic control efficacy in mice. These results highlight the potential of fatty acid conjugation and lactam stapling dual-modification strategy for the development of proteolytically stable, long-acting peptide drugs.

Methicillin-resistant Staphylococcus aureus (MRSA) biofilm-infected wounds remain difficult to treat because persistent biofilm protection, oxidative stress imbalance, and unresolved inflammation jointly hinder tissue repair. Here, we developed a microenvironment-adaptive bilayer composite dressing (OQT/P) by integrating a pH-responsive copper-based nanozyme into a dynamically crosslinked hydrogel and coupling it with an outer electrospun fibrous membrane. This asymmetric structure enables stage-specific regulation of the infected wound microenvironment. In the mildly acidic infection phase, the embedded nanozyme promotes localized reactive oxygen species (ROS) generation to disrupt MRSA biofilms and enhance antibacterial efficacy. As the wound environment gradually returns toward neutrality, the system shifts toward ROS scavenging, thereby alleviating oxidative stress and suppressing inflammatory amplification. In vitro, OQT/P exhibited favorable interfacial stability, pronounced antibacterial and antibiofilm activity, good cytocompatibility, and pro-angiogenic potential. In a full-thickness MRSA biofilm-infected wound model, OQT/P markedly reduced bacterial burden and ROS accumulation, accelerated wound contraction, and achieved approximately 98.07 ± 0.90% wound closure by day 12. Histological and immunofluorescence analyses further demonstrated attenuated inflammation, enhanced collagen deposition, improved neovascularization, and more advanced tissue remodeling. Transcriptomic profiling, supported by ELISA and Western blot validation, showed that these therapeutic effects were associated with coordinated suppression of infection- and inflammation-related pathways, particularly the NF-κB, TNF, and Th17 axes, together with promotion of a repair-associated immune phenotype. Overall, this study presents a non-antibiotic strategy for MRSA biofilm-infected wounds and demonstrates the therapeutic potential of combining bilayer dressing architecture with dynamic redox regulation for infection control and regenerative repair.

The increasing frequency of extinctions of biological populations has important implications for related sectors. Consequently, the risks associated with biodiversity are receiving increasing attention and are being recognized as entirely new risk factors. To understand the drivers of biodiversity risk, it is crucial to measure biodiversity risk at multiple levels, especially in developing countries. Using machine learning and text mining methods, we measure the biodiversity risk of the Chinese market from 20 0 0 to 2023 from the perspectives of macro-government, meso-industry, and microfirms, by analysing official news media texts, related fundholding data, and listed firms' annual reports. We construct a macro-level index derived from the sentiment and frequency of biodiversity-related discourse in official media, including the China Environment News and the CCTV News, from 2013 to 2023. We also construct a meso-level industry risk exposure indicator, calculated as the deviation of biodiversitythemed public funds' holdings from market portfolio weights across 58 sectors. In addition, we develop micro-level firmspecific metrics, based on the frequency and sentiment analysis of biodiversity sentences in the annual reports of 5606 A-share listed firms, 20 0 0-2023, using an improved BERT model for Chinese text. These indicators provide researchers, policymakers, and financial practitioners with a foundational resource for empirically investigating the economic and financial implications of biodiversity risk in China. (c) 2026 Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)

This study investigates how cross-stock information diffusion, driven by both retail and institutional investors, influences excess comovement in the Chinese retail-dominated market and the U.S. institution-dominated market. Using data from 4,533 Chinese stocks and 4,517 U.S. stocks from 2010 to 2022, we identify three key findings. First, the dominant investor group in each market significantly drives excess comovement. Specifically, in China, compared with institution-driven diffusion, retail-driven information diffusion has a notably stronger effect on excess comovement. In contrast, in the U.S., institution-driven diffusion is the primary driver of excess comovement, surpassing the influence of retail-driven diffusion. Second, we identify investors’ trading behavior as the underlying mechanism through which information diffusion affects excess comovement. Third, we observe a lead-lag relationship: stocks with faster retail-driven information diffusion exhibit comovement that precedes those with slower diffusion. Based on this finding, we further demonstrate that the predictive power of information diffusion varies across markets. In China, retail-driven diffusion shows strong and persistent predictability for excess comovement, whereas in the U.S., institution-driven diffusion exhibits similarly robust predictive capacity.

Based on a sample of listed nonfinancial Chinese firms spanning 2012-2022, this study examines whether shadow banking practices lower firms' financing via trade credit. We find evidence for such an effect. Moreover, trade-credit reduction caused by shadow banking engagement is more pronounced for state-owned enterprises, smaller firms, and those with weak internal governance structures. We also find that stronger regional legality can attenuate these adverse effects for firms headquartered in these regions. Further mechanism analysis reveals that shadow banking compromises trade-credit intensity by deteriorating business performance, escalating default risk, and stifling innovation output. For producers, our results suggest they should avoid diverting resources from their main corporate operations toward financial markets. Policymakers, meanwhile, should develop industry regulations to foster real GDP growth and refine rule-of-law frameworks.

AIMS:Diabetes exacerbates periodontitis by intensifying inflammatory responses and impairing tissue regeneration. Hyperglycemia-induced dysfunction of jawbone-derived bone marrow mesenchymal stem cells (BMSCs) contributes to the imbalance of bone remodeling and periodontal homeostasis. This study aimed to reveal the role and regulatory mechanism of stem cell senescence in diabetic periodontitis. MATERIALS AND METHODS:Diabetic periodontitis model was established in mice by high-fat diet, streptozotocin injections and ligation. Following treatment with high glucose (HG) and Porphyromonas gingivalis lipopolysaccharide (Pg-LPS), BMSCs were analyzed for cellular senescence and m6A levels. Functional roles of Mettl3, Foxo3, and Sirt1 were explored by knockdown, overexpression, and pharmacological activation. MeRIP, ChIP, and RNA stability assays were employed to explore m6A-dependent Foxo3 degradation and its interaction with Sirt1. Therapeutic potential of Sirt1 activation was validated in vivo. KEY FINDINGS:Diabetic mice developed alveolar bone degeneration and cellular senescence pathway enrichment. HG + LPS co-stimulation induced BMSCs senescence, elevated m6A levels and Mettl3 expression. Mettl3 knockdown reduced senescence-associated secretory phenotypes. Mechanistically, m6A hypermodification on the Foxo3 coding sequence accelerated mRNA decay and impeded nuclear translocation via Ythdf2 recognition. Through its transcriptional regulation of Sirt1, Foxo3 mitigated senescence when overexpressed and exacerbated oxidative damage when knocked down. Sirt1 activation alleviated senescence in vitro and in vivo, reciprocally stabilizing Foxo3 and maintaining its transcriptional activity via deacetylation. SIGNIFICANCE:Hyperglycemia disrupts alveolar bone homeostasis by driving stem cell senescence through the Mettl3/Foxo3/Sirt1 axis, suggesting a promising therapeutic strategy for regenerative therapy under diabetic conditions.

The increasing frequency of extinctions of biological populations has important implications for related sectors. Consequently, the risks associated with biodiversity are receiving increasing attention and are being recognized as entirely new risk factors. To understand the drivers of biodiversity risk, it is crucial to measure biodiversity risk at multiple levels, especially in developing countries. Using machine learning and text mining methods, we measure the biodiversity risk of the Chinese market from 2000 to 2023 from the perspectives of macro-government, meso‑industry, and micro-firms, by analysing official news media texts, related fund-holding data, and listed firms' annual reports. We construct a macro-level index derived from the sentiment and frequency of biodiversity-related discourse in official media, including the China Environment News and the CCTV News, from 2013 to 2023. We also construct a meso-level industry risk exposure indicator, calculated as the deviation of biodiversity-themed public funds' holdings from market portfolio weights across 58 sectors. In addition, we develop micro-level firm-specific metrics, based on the frequency and sentiment analysis of biodiversity sentences in the annual reports of 5606 A-share listed firms, 2000-2023, using an improved BERT model for Chinese text. These indicators provide researchers, policymakers, and financial practitioners with a foundational resource for empirically investigating the economic and financial implications of biodiversity risk in China.

Background:Large bone defects remain difficult to heal because effective regeneration requires not only osteogenesis but also a favorable immune microenvironment. Layered double hydroxides (LDHs) are promising bioactive nanomaterials, yet the influence of nanoparticle size on osteoimmunomodulation and bone repair remains insufficiently understood. Methods:MgAl-LDH nanoparticles with lateral sizes of 50 and 100 nm were synthesized and characterized, then evaluated for cellular uptake, cytocompatibility, macrophage polarization, and osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs). LDH nanoparticles were further incorporated into GelMA hydrogels and tested in a murine critical-sized calvarial defect model. Transcriptomic profiling was performed to explore the underlying regenerative mechanisms. Data distribution was assessed using the Shapiro-Wilk test, and normally distributed datasets were analyzed by one-way ANOVA followed by Tukey's post hoc test. Results:Both LDH formulations showed well-defined hexagonal morphology, good colloidal stability, and negligible cytotoxicity. Compared with 100 nm LDH, 50 nm LDH exhibited greater cellular internalization and more effectively shifted macrophages from a pro-inflammatory to a pro-regenerative phenotype (p < 0.05). In BMSCs, LDH treatment enhanced alkaline phosphatase activity, matrix mineralization, and osteogenic gene expression, with the 50 nm group showing the strongest effects (p < 0.05). In vivo, GelMA-LDH hydrogels significantly promoted bone regeneration relative to GelMA alone, with superior performance observed for the 50 nm LDH group (p < 0.05). RNA sequencing and qPCR analyses identified a regeneration-associated molecular signature that was consistent with activation of Wnt/β-catenin-associated signaling together with attenuation of NF-κB-related inflammatory pathways. Conclusion:Size-optimized MgAl-LDH nanoplatelets, particularly the 50 nm formulation, act as an effective nano-bio interface to couple immunomodulation with osteogenesis. GelMA-LDH nanocomposite hydrogels therefore represent a promising nanomedicine strategy for critical-sized bone defect repair, although further mechanistic validation is still required.

The escalating incidence of breast cancer threatens to women's health, underscoring the urgent need for the development of new therapies with reduced toxicity and increased efficacy. Combination therapy strategy holds promising potential to improve therapeutic outcomes, however, most chemotherapeutic drugs agents are hindered by poor water solubility and non-specific toxicity. The combination of chemotherapy drugs with targeted therapies represents a reliable approach. In this study, we designed a combination regimen utilizing the chemotherapeutic agent doxorubicin (Dox) alongside the anti-angiogenic drug apatinib (AP) for breast cancer treatment. Methoxy poly(ethylene glycol)-disulfidepoly(lactic acid) (PEG-SS-PLA) and cyclo(Arg-Gly-Asp- D -Tyr-Cys) conjugated PEG-PLA (cRGD-PEG-PLA) were prepared to achieve both reductive response and active targeting for co-delivery of drugs. The self-assembled drug-loaded micelles exhibited an average particle size of 61.50 nm. Our findings indicate that AP significantly enhances Dox uptake in breast cancer cells. Cellular and animal experimental results consistently demonstrated that the AP + Dox/cRGD-m effectively promotes apoptosis of breast cancer cells, while markedly inhibiting tumor growth and pulmonary metastasis. Additionally, AP + Dox/cRGD-m is biodegradable and sustainable, exhibiting a favorable safety profile in vivo . This study suggests that AP + Dox/cRGD-m may have potential clinical application in the treatment of breast cancer. (c) 2026 Published by Elsevier B.V. on behalf of Chinese Chemical Society and Institute of Materia Medica, Chinese Academy of Medical Sciences.

Glioblastoma (GBM) currently still faces the challenges of limited chemotherapy efficacy and high risk of postoperative recurrence, despite the implementation of multimodal treatment approaches. Glioblastoma stem cells (GSCs), characterized by multidirectional differentiation and potent tumorigenic potential, represent the “tumor seeds” contributing to these challenges. The therapeutic bottleneck for GSCs lies in the lack of drugs and treatment strategies that can simultaneously cross the blood-brain barrier (BBB) and target GSCs. In this study, we modified Fe3+ onto the surface of red blood cell nanovesicles (RNVs) to hijack transferrin (Tf) in the blood. The hijacked Tf recognizes Tf receptors highly expressed on brain microvascular endothelial cells and GSCs, thereby simultaneously enabling nanovesicle crossing of the BBB and targeting of GSCs. Fe3+ interacts with endogenous Fe2+ released from hemoglobin in RNVs to create a feedback loop that amplifies ferroptosis effects, enhancing the chemotherapeutic efficacy of temozolomide against GSCs. This Tf-hijacking nanovesicle enables GSC tumoricidal treatment and provides a novel approach for GBM postoperative recurrence inhibition.

We investigate how government borrowing behaviors influence private sectors by exploring the relationship between government debt maturity and credit term structures. Using individual corporate bonds data between 1987 and 2015, we find that a longer government debt maturity is associated with a steeper credit term structure in both the primary and secondary corporate bond markets. An instrumental variable approach and an exogenous event study help us establish a causality. Our findings are more pronounced among riskier corporate bonds, and the influences of Treasury bond supply on credit term spreads are more pronounced near the maturity where this supply shock originates, suggesting that the credit risk and the maturity clientele channels together drive our findings.

Despite the significant potential of photodynamic therapy (PDT) in cancer treatment, further refinement is needed to address challenges such as poor tumor-specific accumulation of photosensitizers and the development of therapeutic resistance, which may be regulated by epigenetics. Here, a novel tumor microenvironment-responsive delivery platform was developed to co-deliver epigenetic protein degraders and photosensitizers, aiming to block the relevant regulatory mechanisms and enhance the effectiveness of combination therapy. Benefiting from the targeting ability, pH-triggered charge reversal, and intracellular glutathione (GSH)-responsive release, the delivery platform exhibited enhanced tumor accumulation and therapeutic effects. The mechanism of action revealed that the precise accumulation and release of drugs via the tumor-orchestrated delivery system not only regulated cell growth and immune activation, but also inhibited the expression of tumor immune escape molecules (PDL1 and CD47) and M2 macrophage polarization, significantly increasing the anti-breast cancer and anti-melanoma effects of PDT in the presence of an epigenetic modifier. More importantly, we found for the first time that photodynamic therapy can generate therapeutic resistance through the upregulation of CCL5, and confirmed that this resistance can be reduced by the epigenetic degradation of bromodomain-containing protein 4 (BRD4). These findings underscore the potential of integrating PDT with epigenetic protein degraders through a programmed delivery platform, offering a promising strategy for improving cancer treatment outcomes.

Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high mortality and poor prognosis among survivors. Neuroinflammation after ICH plays a critical role in both secondary brain injury and repair. In the early stages of ICH, excessive activation of microglia triggers pro-inflammation, leading to the release of various pro-inflammatory cytokines that exacerbate neuronal damage and worsen neurological deficits. Pterostilbene (PTE), a natural polyphenol with potent anti-inflammatory and antioxidant properties, is an ideal neuroprotective agent. However, its clinical application is limited by poor bioavailability and low blood-brain barrier (BBB) penetrability following oral administration. Here, we developed PTE-loaded methoxy poly(ethylene glycol)-poly( epsilon-caprolactone) (mPEG-PCL) nanoparticles (PTE-NPs) to enhance the bioavailability of PTE and performed an intranasal delivery strategy for non-invasive and efficient transport to the ICH lesion. PTE-NPs significantly suppressed pro-inflammatory microglia activation and cytokine release, thereby reducing inflammation-mediated neuronal damage in the peri-hematomal region. In the two ICH mouse models, PTE-NPs demonstrated significant therapeutic efficacy in improving neurological function with good biosafety. This study provides a potential therapeutic strategy for the treatment of ICH and its future clinical translation. (c) 2026 Published by Elsevier B.V. on behalf of Chinese Chemical Society and Institute of Materia Medica, Chinese Academy of Medical Sciences.

Functional reconstruction of periodontal tissue defects remains a clinical challenge, primarily owing to sustained proinflammatory responses. Endoplasmic reticulum stress (ERS) and mitochondrial dysfunction have been identified as pivotal regulators driving macrophage proinflammatory activation, yet their pathological link remains unclear. In this study, transcriptomic analyses revealed that ERS and mitochondrial dysfunction were mutually reinforced via dysregulated intracellular Ca2+ transport. To target this mechanism, we designed dual-functional polydopamine nanoparticles (PDAB NPs) by leveraging the metal ion-chelating property of polydopamine to scavenge excessive Ca2+, while loading the osteogenic peptide bone morphogenetic protein 9 (BMP9) to confer pro-osteogenic activity. Considering the anatomical constraints of periodontal tissues that hinder nanotherapeutic delivery, we strategically constructed an osteoimmunomodulatory microneedle (OIMN) integrated with decellularized extracellular matrix (dECM) for localized PDAB NPs delivery. Results demonstrated that OIMN not only restored ERS and mitochondrial homeostasis, but also remodeled macrophage polarization, thereby mitigating periodontal inflammation. Moreover, the improved osteoimmune microenvironment further promoted the osteogenic differentiation of bone mesenchymal stem cells (BMSCs) and accelerated periodontal bone regeneration. Collectively, this study presents a novel therapeutic strategy for periodontitis via regulating ER-mitochondrial Ca2+ crosstalk and establishes a translational paradigm for treating other inflammatory bone diseases.

This paper proposes a new agent-based model grounded in the minority‑game framework to reveal the underlying mechanism of excess comovement. We model two key information diffusion behaviors of investors on social media: common attention to different stocks and information interaction about a single stock. The simulation results show that both behaviors significantly influence excess comovement, but their roles differ contextually. For stock pairs with historically positive return correlations, the impact of common attention dominates excess comovement when information interactions are infrequent, and a higher ratio of co-investors amplifies this effect. In contrast, for pairs with historically negative correlations, information interaction becomes the dominant driver of excess comovement when the ratio of co-investors is low, especially during periods of high market herding. Furthermore, the model provides accurate forecasts of excess comovement for both the next day and week.