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A scoping review of artificial intelligence-enabled wearables for medication adherence
npj Digital Medicine, Published online: 14 September 2026; doi:10.1038/s41746-026-03246-5
A scoping review of artificial intelligence-enabled wearables for medication adherenceIntegrated Metabolomic and Transcriptomic Analysis Suggests Potential Therapeutic Mechanism of Shengxian Decoction in Hypobaric Hypoxia-Induced Pulmonary Hypertension in SD Rats
Drug Des Devel Ther. 2026 Sep 5;20:603123. doi: 10.2147/DDDT.S603123. eCollection 2026.
ABSTRACT
BACKGROUND: High-altitude hypoxia can trigger maladaptive cardiopulmonary responses, with hypoxia-induced pulmonary hypertension (HPH) representing a major clinical challenge with limited therapeutic options. Shengxian Decoction (SXT), a classical traditional Chinese medicine formula for treating "qi deficiency and sinking", has shown clinical benefits, but the molecular pathways associated with its effects remain incompletely understood.
METHODS: Male Sprague-Dawley rats were exposed to simulated high altitude (5000 m; 404 mmHg, 10.8% O2) for 28 days and treated with SXT at three doses (1.8, 3.6, or 7.2 g/kg/day; n = 6/group). Integrated serum metabolomics (UHPLC-Q-TOF-MS) and lung transcriptomics (RNA-seq) were applied. Multivariate analysis, pathway enrichment, weighted gene co-expression network analysis, and cross-omics correlation were used for data integration. After randomization, allocation concealment and blinding were strictly implemented throughout all experimental procedures, with all interventions and outcome assessments performed by personnel blinded to group assignment until completion of data analysis.
RESULTS: Chronic hypoxia induced HPH with elevated mPAP, RVHI, RVWI and pulmonary vascular remodeling (increased WT% and WA%), while SXT dose-dependently ameliorated these abnormalities and restored hypoxia-disrupted metabolomic and transcriptomic profiles, with the high-dose group showing the most pronounced effect. Chronic hypoxia induced pronounced metabolic and transcriptional remodeling, with model animals clearly separated from controls in principal component analysis. Most differentially expressed genes exhibited downregulated expression, indicating global transcriptional suppression. SXT treatment dose-dependently restored both metabolomic and transcriptomic profiles, with the high-dose group most closely resembling controls. These pyruvate-proximal nodes may represent potential points of convergence through which SXT-associated metabolic and transcriptional alterations are coordinated. The relationships reported here are based on cross-omics associations, and causal inference will require further functional validation.
CONCLUSION: These findings suggest that SXT may ameliorate HPH partly through coordinated regulation of metabolic pathways and gene networks, particularly those related to energy metabolism, rather than fully explaining disease pathogenesis. The study provides multi-omics evidence supporting the traditional concept of "replenishing qi and elevating sunken qi" and identifies candidate metabolic biomarkers for further investigation. However, the results should be interpreted cautiously because of the relatively small sample size, the lack of functional validation experiments, and the exploratory nature of the biomarker findings. Further mechanistic and clinical studies are required to confirm these observations.
PMID:42719424 | PMC:PMC13557172 | DOI:10.2147/DDDT.S603123
Multi-Omics-Enabled Precision Strategies for Overcoming CAR-T Therapy Limitations in Gastrointestinal Malignancies
Biofactors. 2026 Sep-Oct;52(5):e70150. doi: 10.1002/biof.70150.
ABSTRACT
Gastrointestinal malignancies, including gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic ductal adenocarcinoma, remain major causes of cancer-related morbidity and mortality worldwide. Although chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of hematologic malignancies, its efficacy in gastrointestinal solid tumors remains limited by antigen heterogeneity, insufficient trafficking and infiltration, immunosuppressive tumor microenvironments, on-target off-tumor toxicity, and adaptive resistance. In this review, we summarize the current landscape of CAR-T therapy in gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic cancer, with a focus on representative target antigens and emerging biomarker strategies. We further discuss two major categories of biomarkers: target antigen-related biomarkers and conventional dynamic biomarkers, including serum tumor markers, cytokine changes, CAR-T expansion kinetics, and antigen-loss monitoring. In addition, we highlight how single-cell ribonucleic acid sequencing and spatial transcriptomics provide complementary insights into cellular states, immune exhaustion, stromal barriers, and spatially restricted immune exclusion. By integrating these multi-omics approaches with biomarker-guided patient stratification and next-generation CAR-T engineering, gastrointestinal solid tumor CAR-T therapy may evolve from empirical optimization toward mechanism-driven and precision-guided clinical translation.
PMID:42717494 | PMC:PMC13558850 | DOI:10.1002/biof.70150
Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma
Clin Exp Med. 2026 Jul 26;26(1):329. doi: 10.1007/s10238-026-02264-7.
ABSTRACT
KANSL2, a core component of the NSL histone acetyltransferase complex, has been implicated in tumorigenesis. However, its pan-cancer relevance and functional role in liver hepatocellular carcinoma (LIHC) remain unclear. Multi-omics data from TCGA, GEO, and HPA were integrated to systematically evaluate KANSL2 expression, clinical significance, genomic alterations, and immune associations across cancers. Functional enrichment, immune infiltration analyses, and single-cell transcriptomics were performed. In vitro assays were conducted to validate the biological effects of KANSL2 in LIHC cells. KANSL2 is broadly upregulated across cancers and exhibits strong diagnostic performance. Elevated KANSL2 expression correlates with unfavorable prognosis, particularly in LIHC. Mechanistically, KANSL2 and its co-expressed genes are enriched in cell-cycle progression. KANSL2 expression is also closely associated with immune infiltration and immunoregulatory signaling within the tumor microenvironment, with single-cell data indicating preferential expression in proliferative T-cell subsets. Functional experiments demonstrate that KANSL2 silencing suppresses proliferation, migration, and invasion, and induces G2/M phase arrest in LIHC cells. Notably, its effects on apoptosis are limited, suggesting that KANSL2 primarily drives tumor progression through cell-cycle-dependent mechanisms. This study identifies KANSL2 as a key regulator of tumor progression and immune remodeling in LIHC. By promoting malignancy predominantly via cell-cycle control, KANSL2 represents a promising biomarker for diagnosis and prognosis, and a potential therapeutic target.
PMID:42726304 | PMC:PMC13569553 | DOI:10.1007/s10238-026-02264-7
Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma
Clin Exp Med. 2026 Jul 26;26(1):329. doi: 10.1007/s10238-026-02264-7.
ABSTRACT
KANSL2, a core component of the NSL histone acetyltransferase complex, has been implicated in tumorigenesis. However, its pan-cancer relevance and functional role in liver hepatocellular carcinoma (LIHC) remain unclear. Multi-omics data from TCGA, GEO, and HPA were integrated to systematically evaluate KANSL2 expression, clinical significance, genomic alterations, and immune associations across cancers. Functional enrichment, immune infiltration analyses, and single-cell transcriptomics were performed. In vitro assays were conducted to validate the biological effects of KANSL2 in LIHC cells. KANSL2 is broadly upregulated across cancers and exhibits strong diagnostic performance. Elevated KANSL2 expression correlates with unfavorable prognosis, particularly in LIHC. Mechanistically, KANSL2 and its co-expressed genes are enriched in cell-cycle progression. KANSL2 expression is also closely associated with immune infiltration and immunoregulatory signaling within the tumor microenvironment, with single-cell data indicating preferential expression in proliferative T-cell subsets. Functional experiments demonstrate that KANSL2 silencing suppresses proliferation, migration, and invasion, and induces G2/M phase arrest in LIHC cells. Notably, its effects on apoptosis are limited, suggesting that KANSL2 primarily drives tumor progression through cell-cycle-dependent mechanisms. This study identifies KANSL2 as a key regulator of tumor progression and immune remodeling in LIHC. By promoting malignancy predominantly via cell-cycle control, KANSL2 represents a promising biomarker for diagnosis and prognosis, and a potential therapeutic target.
PMID:42726304 | PMC:PMC13569553 | DOI:10.1007/s10238-026-02264-7
Key Experimental Therapeutics and Knowledge Gaps in Metabolic Dysfunction-Associated Steatohepatitis (MASH)
Drug Des Devel Ther. 2026 Sep 5;20:543657. doi: 10.2147/DDDT.S543657. eCollection 2026.
ABSTRACT
Metabolic dysfunction-associated steatohepatitis (MASH) is not solely a disorder of hepatocellular lipid accumulation, but a multicellular disease driven by coordinated metabolic stress, sterile inflammation, fibrogenesis, and niche remodeling. Recent therapeutic progress with the provisional approval of resmetirom and semaglutide has validated MASH as a tractable clinical target. However, many experimental agents have shown limited or inconsistent efficacy, particularly for regression of hepatic fibrosis or cirrhosis, reflecting the biological heterogeneity and dynamic cellular architecture of the disease. Distinct from conventional pathway- or drug class-based reviews, we summarize emerging therapeutics through a liver cell-centered framework, integrating hepatocyte-directed metabolic therapies, immune-cell modulation, hepatic stellate cell-targeted antifibrotic strategies, niche-directed approaches involving liver sinusoidal endothelial cells and cholangiocytes, systemic multi-cell modulators, and precision-delivery technologies. We further compare how these interventions reshape pathogenic communication among hepatic and extrahepatic compartments, while emphasizing unresolved challenges in drug target selection, cellular specificity, disease-stage dependency, safety, and patient stratification. This perspective emphasizes the need to move from isolated pathway targeting toward cell- and network-informed therapeutic strategies supported by spatial multi-omics, human-relevant models, and precision delivery.
PMID:42719321 | PMC:PMC13557022 | DOI:10.2147/DDDT.S543657
Multi-Omics-Enabled Precision Strategies for Overcoming CAR-T Therapy Limitations in Gastrointestinal Malignancies
Biofactors. 2026 Sep-Oct;52(5):e70150. doi: 10.1002/biof.70150.
ABSTRACT
Gastrointestinal malignancies, including gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic ductal adenocarcinoma, remain major causes of cancer-related morbidity and mortality worldwide. Although chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of hematologic malignancies, its efficacy in gastrointestinal solid tumors remains limited by antigen heterogeneity, insufficient trafficking and infiltration, immunosuppressive tumor microenvironments, on-target off-tumor toxicity, and adaptive resistance. In this review, we summarize the current landscape of CAR-T therapy in gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic cancer, with a focus on representative target antigens and emerging biomarker strategies. We further discuss two major categories of biomarkers: target antigen-related biomarkers and conventional dynamic biomarkers, including serum tumor markers, cytokine changes, CAR-T expansion kinetics, and antigen-loss monitoring. In addition, we highlight how single-cell ribonucleic acid sequencing and spatial transcriptomics provide complementary insights into cellular states, immune exhaustion, stromal barriers, and spatially restricted immune exclusion. By integrating these multi-omics approaches with biomarker-guided patient stratification and next-generation CAR-T engineering, gastrointestinal solid tumor CAR-T therapy may evolve from empirical optimization toward mechanism-driven and precision-guided clinical translation.
PMID:42717494 | PMC:PMC13558850 | DOI:10.1002/biof.70150
Multi-Omics-Enabled Precision Strategies for Overcoming CAR-T Therapy Limitations in Gastrointestinal Malignancies
Biofactors. 2026 Sep-Oct;52(5):e70150. doi: 10.1002/biof.70150.
ABSTRACT
Gastrointestinal malignancies, including gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic ductal adenocarcinoma, remain major causes of cancer-related morbidity and mortality worldwide. Although chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of hematologic malignancies, its efficacy in gastrointestinal solid tumors remains limited by antigen heterogeneity, insufficient trafficking and infiltration, immunosuppressive tumor microenvironments, on-target off-tumor toxicity, and adaptive resistance. In this review, we summarize the current landscape of CAR-T therapy in gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic cancer, with a focus on representative target antigens and emerging biomarker strategies. We further discuss two major categories of biomarkers: target antigen-related biomarkers and conventional dynamic biomarkers, including serum tumor markers, cytokine changes, CAR-T expansion kinetics, and antigen-loss monitoring. In addition, we highlight how single-cell ribonucleic acid sequencing and spatial transcriptomics provide complementary insights into cellular states, immune exhaustion, stromal barriers, and spatially restricted immune exclusion. By integrating these multi-omics approaches with biomarker-guided patient stratification and next-generation CAR-T engineering, gastrointestinal solid tumor CAR-T therapy may evolve from empirical optimization toward mechanism-driven and precision-guided clinical translation.
PMID:42717494 | PMC:PMC13558850 | DOI:10.1002/biof.70150
Inhaled nanosilica orchestrates a pulmonary macrophage-NK cell axis for memory-like NK programming toward synergistic cancer immunotherapy
ACC1 inhibition enhances BCG-induced trained immunity by reprogramming acetyl-CoA metabolism
Developmental deviations of association-network structural connectivity in youths with ADHD predict symptom and treatment outcomes
Nature Biomedical Engineering, Published online: 31 August 2026; doi:10.1038/s41551-026-01779-4
This large-scale study of white matter structural connectivity during development reveals biomarkers associated with attention deficit hyperactivity disorder in youth that track symptom trajectories and predict differential treatment response.Publisher Correction: Edge-sharing RuO<sub>2</sub> single layer for stable and low overpotential acidic water electrolysis
Nature Nanotechnology, Published online: 08 September 2026; doi:10.1038/s41565-026-02288-w
Publisher Correction: Edge-sharing RuO2 single layer for stable and low overpotential acidic water electrolysisStructural Process Supervision for Latent Chain-of-Thought Reasoning
CS-Guard: Benchmarking LLM Guardrails for Code Generation Security
A Trust-Network-Based Federated Learning Framework for Multi-Center Aging Clock Prediction
LightNav-0: Eliciting VLM Spatial Intelligence for Generalist Embodied Navigation
Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells
Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01221-3
Chen and colleagues report that the neuropeptide galanin impairs antitumor immunity in glioblastoma by interacting with its receptor GALR3 on monocytic myeloid-derived suppressor cells, promoting their infiltration and ferroptosis resistance.