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OpenRouter more than doubles valuation to $1.3B in a year
Large Language Model–Generated Patient Instructions for Prescriptions in Primary Health Care: Preclinical Algorithm Validation
Safety of Telemedicine Versus In-Person Care for Patients With Tracheal Devices: Propensity Score–Matched Cohort Study
Amazon fulfillment competitor Stord raises $250M at $3B valuation
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.
ABSTRACT
Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.
PMID:42189071 | DOI:10.1002/advs.75839
Multi-Omics Identification of Biomarkers for High-Altitude Pulmonary Hypertension
J Cardiovasc Dev Dis. 2026 Apr 30;13(5):195. doi: 10.3390/jcdd13050195.
ABSTRACT
(1) Aim: The incidence of high-altitude pulmonary hypertension (HAPH) has risen in recent years and is expected to continue increasing; however, its diagnosis remains challenging. In this study, we employed proteomics and metabolomics to identify the proteins and metabolic biomarkers that contribute to the development of HAPH. (2) Methods: We applied integrated proteomics and metabolomics to match blood samples from 40 HAPH patients and 40 healthy controls in Yunnan's high-altitude regions to characterize molecular profiles, identify biomarkers, and develop a predictive model. (3) Results: Proteomic analysis identified four proteins (A2IPH7, K1C14, PSME2, SERPINE2) commonly dysregulated in HAPH patients from two high-altitude regions. SERPINE2 was notably downregulated and showed a negative correlation with clinical severity, which was further validated in HAPH rat lung tissues and supported by UK Biobank data for idiopathic PAH. Concurrent metabolomics uncovered 11 shared metabolites, largely acyl fatty acids, enriched in pathways such as unsaturated fatty acid synthesis. Integration of these multi-omics data enabled the development of a robust predictive model. (4) Conclusion: Our study identified key protein and metabolic biomarkers involved in HAPH development, which were validated in animal models. Based on these findings, a predictive model was developed, highlighting SERPINE2 and 11 metabolites as promising targets for the prediction and prevention of HAPH.
PMID:42188081 | DOI:10.3390/jcdd13050195
A visual analysis of the research dynamics of biomarkers for lung cancer screening
Clin Epigenetics. 2026 May 26;18(1):90. doi: 10.1186/s13148-026-02084-2.
ABSTRACT
BACKGROUND: Non-invasive biomarkers offer potential to improve risk stratification and early diagnosis of lung cancer, complementing low-dose computed tomography (LDCT) screening. This study employed bibliometric analysis to identify global research trends, collaborative networks, and future directions in lung cancer biomarker research. Publications on lung cancer biomarkers for screening were retrieved from the Web of Science Core Collection (WoSCC). Data processing and visualisation were performed using Citespace, VOSviewer, KH Coder, Latent Dirichlet Allocation (LDA) topic modelling, and the online bibliometric analysis platform. Burst detection analysis was performed to predict emerging research trends.
RESULTS: Analysis of 3636 publications revealed exponential growth in research output since 2014. International collaboration demonstrated a dual-core structure centred on China and the United States, with Chinese institutions showing high publication volumes and American institutions demonstrating greater citation influence. Journal citation mapping revealed three evolutionary phases: basic mechanisms-clinical translation-intelligent integration. LDA topic modelling identified 22 topics grouped into five core research directions: imaging and pathological diagnostic techniques; molecular and omics marker research; liquid biopsy and new detection technologies; clinical and translational medicine research; and tumour biology and treatment mechanisms. Burst detection analysis predicted future four priority areas: epigenetic studies centred on DNA methylation for risk prediction; treatment resistance and invasion mechanisms; liquid biopsy technology development; and targeted therapy clinical trials.
CONCLUSIONS: Lung cancer biomarker research has evolved towards multimodal, intelligent screening approaches. Future research priorities include DNA methylation-based markers, circulating microRNA signatures, and artificial intelligence-assisted diagnostic platforms to improve early detection accuracy and complement LDCT screening.
PMID:42185923 | DOI:10.1186/s13148-026-02084-2
Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation
J Transl Med. 2026 May 25. doi: 10.1186/s12967-026-08312-w. Online ahead of print.
ABSTRACT
BACKGROUND: Liver fibrosis is a dynamic and reversible pathological process underlying chronic liver diseases, characterized by excessive extracellular matrix deposition and progressive hepatic architectural distortion. It acts as a critical precursor to cirrhosis, hepatic decompensation, and hepatocellular carcinoma, imposing a substantial global disease burden.
MAIN BODY: Accumulating evidence indicates that liver fibrosis is a highly plastic process governed by multicellular crosstalk, immune microenvironment remodeling, epigenetic-metabolic coupling, and mechanotransduction. This review outlines core cellular effectors and their heterogeneity revealed by single-cell omics, and highlights key regulatory layers including circadian rhythm, epigenetic imprinting, metabolic reprogramming, and the gut-liver axis, as well as etiology-specific differences in fibrosis progression, reversibility, and therapeutic response. We also summarize advances in non-invasive diagnosis and clinical translation of anti-fibrotic therapies, and discuss key bottlenecks leading to clinical trial failures.
CONCLUSION: A deeper understanding of cell fate regulation and multicellular ecosystem remodeling will facilitate the development of precise strategies to achieve meaningful fibrosis regression and improve long-term clinical outcomes in chronic liver diseases.
PMID:42185911 | DOI:10.1186/s12967-026-08312-w
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.
ABSTRACT
Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.
PMID:42189071 | DOI:10.1002/advs.75839
Multi-Omics Identification of Biomarkers for High-Altitude Pulmonary Hypertension
J Cardiovasc Dev Dis. 2026 Apr 30;13(5):195. doi: 10.3390/jcdd13050195.
ABSTRACT
(1) Aim: The incidence of high-altitude pulmonary hypertension (HAPH) has risen in recent years and is expected to continue increasing; however, its diagnosis remains challenging. In this study, we employed proteomics and metabolomics to identify the proteins and metabolic biomarkers that contribute to the development of HAPH. (2) Methods: We applied integrated proteomics and metabolomics to match blood samples from 40 HAPH patients and 40 healthy controls in Yunnan's high-altitude regions to characterize molecular profiles, identify biomarkers, and develop a predictive model. (3) Results: Proteomic analysis identified four proteins (A2IPH7, K1C14, PSME2, SERPINE2) commonly dysregulated in HAPH patients from two high-altitude regions. SERPINE2 was notably downregulated and showed a negative correlation with clinical severity, which was further validated in HAPH rat lung tissues and supported by UK Biobank data for idiopathic PAH. Concurrent metabolomics uncovered 11 shared metabolites, largely acyl fatty acids, enriched in pathways such as unsaturated fatty acid synthesis. Integration of these multi-omics data enabled the development of a robust predictive model. (4) Conclusion: Our study identified key protein and metabolic biomarkers involved in HAPH development, which were validated in animal models. Based on these findings, a predictive model was developed, highlighting SERPINE2 and 11 metabolites as promising targets for the prediction and prevention of HAPH.
PMID:42188081 | DOI:10.3390/jcdd13050195
TamboUI Promises to Bring Better Capabilities to Build TUIs in Java

The call to action “to make 2026 the year of Java in the terminal” was quickly responded to by the launch of TamboUI. Inspired by Ratatui, the library used in Claude CLI, it promises support ranging from low-level terminal drawing to high-level APIs such as components and event handling. Currently at version 0.3.0, it has already been adopted by major projects such as Maven and Spring.
By Olimpiu PopSTAT+: How Kyle Diamantas defied expectations as he rose to lead the FDA
WASHINGTON — People in the food world didn’t know what to expect when the Trump administration appointed a little-known Florida attorney as the FDA’s top food official in 2025.
They knew Kyle Diamantas worked at Jones Day representing food, beverage, and tobacco-industry clients. They saw the picture of him and Donald Trump Jr. holding giant, dead wild turkeys after a hunt. He had no experience in public health, in medicine or science, or in government.
The credentials didn’t scream qualified. And Diamantas was stepping into a center rocked by DOGE layoffs and a defiant resignation by former leader Jim Jones.
Continue to STAT+ to read the full story…


© Camille MacMillin/STAT
Opinion: The Ebola outbreak will lead to devastating violence against women and girls
The World Health Organization has declared a new public health emergency. Bundibugyo, an Ebola strain for which we have no vaccine and no treatment, is now spreading across the eastern Democratic Republic of Congo. So far, there have been more than 900 suspected cases and about 220 suspected deaths, according to the World Health Organization. Centered in a region with active conflict and fragile health systems, the outbreak has already crossed the borders into Uganda.
Public health advocates will spend the next several months talking about transmission, case fatality, contact tracing, and vaccine development. But one critical topic will go largely undiscussed: what this outbreak will do to women and girls.


© ALEXIS HUGUET/AFP via Getty Images
Opinion: 8 former CDC directors: Reform PEPFAR, don’t dismantle it
On Sunday, the World Health Organization (WHO) declared an Ebola outbreak in the Democratic Republic of the Congo and Uganda to be a public health emergency. This outbreak is deadly, with hundreds of cases across at least two countries, including, by report, one American who was working in the area.
At the same time, a cluster of hantavirus cases linked to a Dutch cruise ship in the South Atlantic has killed three and exposed hundreds more.


© Hajarah Nalwadda/Getty Images