PubMed Trending Research Digest — May 31, 2026

Automated digest · 94 articles · 15 research areas · May 31, 2026

Overview

This week’s digest is dominated by immune-focused translational advances: multiple studies tackle how to improve or safely deploy immune checkpoint and immune-cell therapies. In oncology, work on ICI rechallenge in non-clear cell renal cell carcinoma highlights mature tertiary lymphoid structures as a predictive tumor microenvironment marker, while CAR T relapse analyses in B-ALL point to CAR T functional insufficiency and CD19+ B-cell persistence as a key failure mode. Complementing this, several mechanistic and translational efforts use multi-omics and spatial profiling to explain therapy response and resistance—ranging from microbiome-derived metabolite effects that potentiate anti–PD-1 efficacy (butyrate/IPA) to epigenetic regulators that suppress antitumor immunity (e.g., MORC2) and structural biology that refines how receptor dimerization shapes pharmacology.

A second major theme is immune regulation and inflammation across organ systems, linking mechanistic immune pathways to clinical outcomes. Reviews and studies span depression biology (including vitamin intake and immune cytokine pathways), IBD trial design and endpoints (PROs/PROMs and imaging frameworks), and autoimmune disease therapeutics (e.g., CD40L inhibition in SLE; macrophage deubiquitinase control of STAT1 signaling in ulcerative colitis). In parallel, neuroimmune and CNS-focused research emphasizes lysosomal/repair dysfunction and microglial homeostasis (C9orf72/SMCR8–ESCRT/lysosomal repair; neuroproteasome control of tau PHFs), while other work connects environmental exposures (microplastics) to ferroptosis-linked neurotoxicity.

Finally, the digest includes strong signals from metabolism and systems-level risk prediction. Obesity and cardiometabolic research continues to frame GLP-1–based therapies as disease-modifying, with comparative evidence (tirzepatide vs semaglutide) and broader biomarker/risk stratification efforts (multi-omics diabetes prediction; metabolic syndrome and scarring; long COVID endocrine/metabolic biomarker patterns). Across musculoskeletal and regenerative medicine, exercise and mechanobiology studies reinforce modifiable pathways for pain and tissue remodeling, while disease-modifying strategies (continuous DNA repair for disc degeneration; targeted extracellular vesicle or macrophage-based approaches for liver fibrosis) illustrate a shift toward upstream mechanism intervention rather than purely symptomatic treatment.

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Cancer immunotherapy (ICI, CAR-T, bispecifics, checkpoint modulation)

AI-Designed Cyclic Peptides Enable Controllable Modulation of the CD28 Immune Checkpoint.

The study used an AI-guided peptide discovery approach to develop cyclic peptide antagonists targeting the extracellular protein-protein interaction interface of the immune checkpoint receptor CD28, with lead compound CIP-3 tested for binding and functional disruption. CIP-3 bound the CD28 extracellular domain with nanomolar affinity and disrupted CD28–ligand interactions, enabling controllable modulation of CD28 immune checkpoint signaling. This provides a more pharmacologically controllable, synthetic alternative to biologics for tuning T-cell costimulation in immune checkpoint therapy.

Kuncewicz K, Upadhyay S, Zhu R et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Amivantamab in advanced non-small cell lung cancer with epidermal growth factor receptor exon 20 insertion mutations: Real-world data from the Italian ATLAS Registry.

This multicenter retrospective observational study used real-world data from the Italian ATLAS registry to evaluate safety and effectiveness of amivantamab in advanced non-small cell lung cancer (NSCLC) patients with EGFR exon 20 insertion mutations (EGFR ex20ins). The key finding was the characterization of real-world outcomes and adverse events for amivantamab-treated EGFR ex20ins NSCLC patients (numerical results truncated in the abstract). This is clinically significant because it complements trial evidence with real-world effectiveness and tolerability data for a rapidly evolving targeted-therapy standard.

Passiglia F, Passaro A, Gariazzo E et al. · Cancer · (2026) · View on PubMed ↗

Triple M overlap syndrome in the intensive care unit: differential diagnosis and management.

This study examined Triple M overlap syndrome—myasthenia gravis-like disease, inflammatory myositis, and myocarditis—in critically ill patients receiving immune checkpoint inhibitors (ICIs). The authors highlight the syndrome’s diagnostic and management challenges and its status as the most severe, lethal ICI-related multisystem phenotype requiring intensive care. Clinically, recognizing Triple M overlap early can guide urgent differential diagnosis and treatment escalation to reduce mortality in ICI-treated patients.

Shah C, Rajalbandi RS, Seshadri V et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Systemic multi-omics analysis reveals interferon response heterogeneity and links lipid metabolism to immune alterations in severe COVID-19.

This multi-omics study analyzed hospitalized severe COVID-19 patients (n=37) and uninfected controls (n=31) using whole-blood transcriptomics, immune cell deconvolution, plasma proteomics, and standardized plasma metabolomics. The key finding was interferon-response heterogeneity across patients and a link between lipid metabolism and immune alterations associated with severe disease. These results suggest that combining interferon signatures with immunometabolic markers may better stratify risk and guide targeted therapies for severe COVID-19.

Lira-Junior R, Ambikan AT, Cederholm A et al. · Genome medicine · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Unraveling cellular and molecular mechanisms of relapse in CD19/CD22 dual-targeting chimeric antigen receptor T-cell therapy for B-cell acute lymphoblastic leukemia.

This clinical study evaluated relapse mechanisms in 91 B-cell acute lymphoblastic leukemia (B-ALL) patients treated with CD19/CD22 dual-target CAR T cells (CAR19/22) in the ChiCTR-OPN-16008526 trial. Late relapses (>7 months) were predominantly driven by CAR T functional insufficiency, characterized by lack of persistence or recovery of CD19+ B lymphocytes, while early relapses showed greater heterogeneity. These findings identify persistence of CD19+ B cells as a key therapeutic failure mode and can guide next-generation CAR T designs and monitoring strategies to reduce relapse.

Tan J, He F, Hu H et al. · Leukemia · (2026) · View on PubMed ↗

Structural characterization of kappa-opioid receptor dimer in complex with two G proteins.

This structural biology study characterized the kappa-opioid receptor (κOR) dimer in complex with two Gi proteins using cryo-electron microscopy and cellular assays in living cells. It showed stable κOR dimer formation and provided cryo-EM structures of salvinorin A–bound κOR dimers engaging two Gi proteins via a parallel assembly distinct from GPCR dimers that bind a single G protein. These molecular insights clarify how κOR dimerization can shape pharmacology and support rational development of κOR-targeted analgesics.

Zhao Y, Xu C, Wang Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Sacituzumab tirumotecan plus pembrolizumab versus pembrolizumab in PD-L1-positive advanced non-small-cell lung cancer (OptiTROP-Lung05): interim analysis of a randomised, open-label, phase 3 trial.

This interim analysis of the randomized, open-label phase 3 OptiTROP-Lung05 trial compared sacituzumab tirumotecan (TROP2-targeting antibody-drug conjugate) plus pembrolizumab versus pembrolizumab alone as first-line therapy in PD-L1-positive advanced non-small-cell lung cancer without targetable genomic alterations. The key finding was the relative efficacy and safety of the combination regimen in this defined biomarker-positive population. Clinically, these interim results inform whether adding sacituzumab tirumotecan to PD-1 blockade improves outcomes for patients who lack actionable driver mutations.

Xiong A, Yao W, Zheng W et al. · Lancet (London, England) · (2026) · 1 citations · View on PubMed ↗

First human decedent model of orthotopic multi-organ xenotransplantation: Whole liver and bilateral kidneys from a six-gene-edited pig.

The study reported an orthotopic combined whole-liver and bilateral-kidney xenotransplantation (xeno-CLKT) from a six-gene-edited pig into a 53-year-old human decedent recipient. The grafts maintained basic physiological function for nearly 5 days with no hyperacute rejection, and early immune profiling showed expansion of S100A1 (with further host response characterization using single-cell RNA-seq, proteomics, and metabolomics). This is a translational proof-of-concept for multi-organ xenotransplantation using multi-gene editing and multi-omics monitoring to assess early rejection and graft compatibility.

Liao J, An S, Dong J et al. · Med (New York, N.Y.) · (2026) · 1 citations · View on PubMed ↗

Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid.

The study tested whether oat-β-glucan improves anti-PD-1 therapy in murine tumor models and investigated the responsible gut microbiota and metabolites. Oat-β-glucan selectively expanded Faecalibacterium prausnitzii and, together with anti-PD-1, increased intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation, with metabolomics implicating F. prausnitzii-derived butyrate and indole-3-propionic acid (IPA) as key mediators. Mechanistically, butyrate acted via an HDAC8/H3K27ac/NF-κ axis to potentiate immune responses, supporting a microbiome-targeted strategy to enhance checkpoint blockade efficacy.

Yang S, Lu H, Jin M et al. · Cell host & microbe · (2026) · View on PubMed ↗

mRNA-laden LNP-enabled in situ CAR-macrophage alleviates liver fibrosis via inhibiting activated HSCs and modulating the immune microenvironment.

This preclinical study developed an mRNA-laden lipid nanoparticle (LNP) system conjugated with a CD163 antibody to enable in situ CAR-macrophage generation and tested its effects on liver fibrosis. The key finding was that CD163 antibody-conjugated LNPs delivering FAP-specific mRNA alleviated liver fibrosis by inhibiting activated hepatic stellate cells (HSCs) and reshaping the immune microenvironment. This is significant because it provides a targeted, macrophage-based gene delivery strategy to suppress fibrogenic activation and improve the therapeutic landscape for liver fibrosis.

Huang X, Hao J, Wang S et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Teclistamab in Multiple Myeloma with One to Three Previous Lines of Therapy.

This randomized trial evaluated teclistamab, a bispecific antibody targeting B-cell maturation antigen (BCMA) and CD3, in relapsed or refractory multiple myeloma stratified by 1, 2, or 3 prior lines of therapy. The study compared teclistamab against investigator’s choice regimens (pomalidomide/bortezomib/dexamethasone or carfilzomib/dexamethasone) with progression-free survival as the primary endpoint. The results address whether teclistamab can serve as an effective early-line monotherapy option in multiple myeloma beyond later-line settings.

Touzeau C, Mina R, Quach H et al. · The New England journal of medicine · (2026) · 1 citations · View on PubMed ↗

First-Line Sunvozertinib in NSCLC with EGFR Exon 20 Insertion Mutations.

This phase 3 randomized trial studied first-line sunvozertinib versus carboplatin–pemetrexed chemotherapy in patients with advanced nonsquamous non-small-cell lung cancer (NSCLC) harboring EGFR exon 20 insertion mutations. The primary endpoint was progression-free survival assessed by blinded independent central review, with crossover allowed after progression. The trial directly tests whether targeting EGFR exon 20 insertions with sunvozertinib improves outcomes when used upfront rather than only in later lines.

Zhou C, Greillier L, Liu G et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Targeting MORC2 activates transposable element-mediated viral mimicry and potentiates immune checkpoint blockade in triple-negative breast cancer.

This preclinical study identified MORC2 (MORC family CW-type zinc finger 2), an ATP-dependent chromatin remodeler, as an epigenetic suppressor of antitumor immunity in triple-negative breast cancer (TNBC) and tested its role in response to immune checkpoint blockade. Genetic ablation of MORC2 enhanced CD8+ T cell cytotoxicity and M1-like macrophage polarization in immunocompetent mice, and mechanistically MORC2 targeting activated transposable element-mediated viral mimicry that potentiated immune checkpoint blockade. The results position MORC2 as a therapeutic target to overcome immune evasion and improve ICB efficacy in TNBC.

Zhang FL, Yang SY, Zhang YL et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Complete response to immune checkpoint blockade in sarcomatoid renal cell carcinoma with bone marrow metastasis: case report with tumor immune microenvironment profiling.

This case report studied a patient with sarcomatoid renal cell carcinoma with bone marrow metastasis who achieved complete response to immune checkpoint blockade with ipilimumab plus nivolumab. Matched pre- and post-treatment bone marrow samples were profiled with integrative immune profiling, showing pretreatment enrichment of CD14+ MDSC-like myeloid cells alongside CD8+ T cells and post-treatment immune microenvironment changes consistent with response. The report highlights how bone marrow immune contexture may influence and reflect sensitivity to checkpoint therapy in this aggressive RCC subtype.

Miura Y, Jikuya R, Saijo A et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Pretreatment intratumoral mature TLSs in non-clear cell renal cell carcinoma are associated with response to immunotherapy rechallenge.

This study evaluated efficacy, safety, and predictive biomarkers of immune checkpoint inhibitor (ICI) rechallenge in 39 patients with metastatic non-clear cell renal cell carcinoma (nccRCC), using whole exome sequencing, bulk RNA sequencing, and multiplex immunofluorescence (mIF) to characterize tumor microenvironments. Pretreatment intratumoral mature tertiary lymphoid structures (TLSs) were associated with better response outcomes to ICI rechallenge. These findings suggest that mature TLS presence in nccRCC tumors could serve as a predictive marker to guide selection of patients for ICI rechallenge after progression.

Tang Y, Chen J, Hu J et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer genomics/epigenetics & mechanistic tumor biology

Molecular mechanisms of the MLL4 complex in H3K4 methylation and p53-dependent transcription activation.

The study investigated how the MLL4 complex regulates H3K4 methylation and p53-dependent transcription activation using a reconstituted MLL4 fusion complex (MLL4FC) for structural and functional analyses. It revealed three rigid modules (SET-ASH2L-DPY30, RBBP5-WDR5, and PHD-FYR) and showed that the conserved PHD-FYR module is essential for MLL4- and p53-dependent transcription, supported by cryo-EM and crosslinking mass spectrometry models of MLL4FC interactions with p53, with genomic colocalization in HCT116 cells. These mechanistic insights clarify how MLL4 architecture couples enhancer regulation to p53 transcriptional programs, informing epigenetic therapeutic targeting in cancer.

Sun J, Zhang Z, Yu Y et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

Alcohol-Induced Metabolic Stress Sensed by m6A-Modified ChREBP Drives Immune Evasion in Esophageal Carcinogenesis.

This study investigated how alcohol-induced metabolic stress promotes esophageal squamous cell carcinoma (ESCC) by focusing on a germline variant at the MLXIPL locus (encoding ChREBP) and downstream N6-methyladenosine (m6A) regulation. The key finding was that the rs1051921 C>T risk allele increased ESCC risk among alcohol drinkers by enabling m6A modification of ChREBP transcripts, stabilizing them via recognition by the m6A reader YTHDF1, with alcohol further potentiating this effect. This is important scientifically and clinically because it links a specific alcohol–genotype–m6A mechanism to ESCC risk and suggests potential targets in the ChREBP/m6A/YTHDF1 axis for prevention or therapy.

Ma J, Yue X, Wu Y et al. · Cancer research · (2026) · View on PubMed ↗

Comprehensive mutagenesis defines the functional landscape of human α-tubulin.

This study used comprehensive mutagenesis combined with high-content live-cell imaging and automated quantitative analysis to map the functional effects of all 2,683 single-nucleotide coding variants in human α-tubulin TUBA1A. The key finding was that systematic profiling of microtubule assembly revealed distinct mutation classes that disrupt folding, chaperone engagement, or protofilament geometry, defining structural constraints governing tubulin function. This is significant for precision medicine because it creates a functional atlas that improves interpretation of α-tubulin missense variants beyond conservation-based predictions.

Xu K, Guo Z, Chen Z et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

DOT1L Shapes ncPRC1-Target Gene Repression to Maintain Germinal Center B Cell Identity of Diffuse Large B cell Lymphoma.

This study investigated how the histone methyltransferase DOT1L regulates ncPRC1-mediated repression to maintain germinal center B cell identity in germinal center B cell-like diffuse large B cell lymphoma (GCB-DLBCL), using an EZH2 inhibition–anchored genome-wide CRISPR interference screen. The authors identified non-canonical PRC1 complex components—including USP7, KDM2B, RING1, and PCGF1—and found USP7 as a potential direct DOT1L target whose downregulation increased sensitivity to EZH2 inhibition. These findings mechanistically link DOT1L and ncPRC1/USP7 to preserve the GCB transcriptional program, supporting ncPRC1-axis targeting as a potential therapeutic strategy in GCB-DLBCL.

Göbel C, Niccolai R, Gregoricchio S et al. · Blood · (2026) · View on PubMed ↗

IL-16 production is a mechanism of resistance to BTK inhibitors and R-CHOP in lymphomas.

This study examined non-genetic mechanisms of resistance to Bruton tyrosine kinase (BTK) inhibitors in marginal zone lymphoma (MZL) by modeling chronic ibrutinib exposure and integrating transcriptomic, epigenetic, and proteomic analyses. Chronic ibrutinib exposure produced cross-resistance to BTK inhibitors and degraders without BTK/PLCG2 mutations, alongside pathway reprogramming with activation of PI3K/AKT, MAPK, and MYC and repression of apoptosis and oxidative phosphorylation. Clinically, IL-16 production emerged as a resistance mechanism that could inform combination strategies to overcome BTK-inhibitor failure in MZL.

Arribas AJ, Cannas E, Sartori G et al. · Blood · (2026) · View on PubMed ↗

Pharmacological targeting of IRF4 as a therapeutic strategy for multiple myeloma.

The study investigated pharmacological targeting of the transcription factor IRF4 in multiple myeloma, using high-throughput screening to disrupt the SPI1–IRF4 interaction and then engineering a cereblon-based proteolysis-targeting chimera. The authors identified (S)-H1 and converted it into dIRF4-2, which induces selective proteasomal degradation of IRF4 and shows strong cytotoxic effects across multiple myeloma cell lines. This provides a first-in-class strategy to drug an otherwise “undruggable” transcription factor in IRF4-driven hematologic cancer by leveraging cereblon-mediated targeted protein degradation.

Agius MP, Song C, Liu Q et al. · Nature chemical biology · (2026) · 3 citations · View on PubMed ↗ · [Free PDF ↗](https://ashpublications.org/blood/article-pdf/144/Supplement 1/155/2331895/blood-2902-main.pdf)

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Cancer microenvironment & spatial/omics tumor profiling

Multi-Omics Analysis and Mechanistic Validation Reveal RPS8 as a Novel Prognostic Biomarker and Therapeutic Target for Hepatocellular Carcinoma.

This study investigated ribosomal protein S8 (RPS8) as a prognostic biomarker and therapeutic target in hepatocellular carcinoma (HCC) by combining multi-omics analyses of public datasets (TCGA, GEO) with single-cell RNA-seq mapping and mechanistic validation. RPS8 was identified as a novel prognostic marker with tumor microenvironment–linked expression patterns, and mechanistic experiments supported its functional role in HCC progression (validation details truncated in the abstract). These findings support RPS8 as a candidate biomarker and potential therapeutic target for improving HCC risk prediction and treatment strategies.

Zhu L, Liu H, Qian J et al. · BioFactors (Oxford, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Glutathione peroxidase 3 preserves hepatocyte mitochondrial quality control to enhance macrophage pro-regenerative phenotype during liver regeneration.

This mechanistic animal study examined whether hepatocellular glutathione peroxidase 3 (GPX3) preserves mitochondrial quality control during liver regeneration and how this affects macrophage phenotype, using a 70% partial hepatectomy mouse model. The key finding was that GPX3 in hepatocytes supports mitochondrial quality control and promotes a pro-regenerative macrophage phenotype during regeneration, with hepatocyte-specific GPX3 knockout impairing these processes (details truncated in the abstract). This links GPX3-driven mitochondrial regulation to immune remodeling in regeneration, suggesting a potential therapeutic axis for enhancing liver repair.

Wang Y, Xu J, Zhu Z et al. · Clinical and translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Single-cell spatial transcriptional profiling of pancreatic ductal adenocarcinoma uncovers key immune-modulating and pro-metastatic mechanisms.

This study used high-definition single-cell spatial transcriptomics with the Xenium In Situ (5K) platform on formalin-fixed paraffin-embedded matched pancreatic ductal adenocarcinoma primary tumors and hepatic metastases to map tumor microenvironment dynamics in PDAC. The key finding was that spatial single-cell profiling uncovered immune-modulating and pro-metastatic mechanisms associated with progression from primary tumors to liver metastases. This provides mechanistic targets for improving PDAC therapies by linking spatial immune programs to metastatic behavior.

Zhou J, Shi G, Dai S et al. · Cancer letters · (2026) · View on PubMed ↗

Single-cell and spatial transcriptomics reveal Thbs1-CD36 crosstalk between Kupffer and hepatic stellate cells following mesenchymal stem cell-derived small extracellular vesicles transplantation, alleviating liver fibrosis.

In CCl4-induced liver fibrosis mouse models, this study used single-cell RNA sequencing and spatial transcriptomics to investigate how mesenchymal stem cell-derived small extracellular vesicles (MenSC-sEVs) alter Kupffer cell–hepatic stellate cell communication, focusing on Thbs1–CD36 crosstalk. MenSC-sEV treatment reduced fibrosis and was associated with changes in the Thbs1–CD36 signaling axis between Kupffer and hepatic stellate cells, consistent with a mechanistic anti-fibrotic effect. These findings suggest a specific cell–cell molecular pathway that could be targeted to enhance sEV-based therapies for liver fibrosis.

Chen L, Zhang N, Huang Y et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer metabolism & ferroptosis/immunometabolism

Ferroptosis vulnerability of enzalutamide resistant prostate cancer conferred by ACSL4 overexpression and GPX4 antagonism.

This study investigated ferroptosis vulnerability in enzalutamide-resistant prostate cancer using established enzalutamide-resistant cell lines and tested the role of ACSL4 overexpression and GPX4 antagonism. It found that enzalutamide-resistant populations are enriched for stem cell-like and neuroendocrine-like features and that these cells are susceptible to GPX4-targeted ferroptosis, with ACSL4 overexpression contributing to vulnerability. The results suggest a potential therapeutic approach for enzalutamide-resistant prostate cancer by exploiting GPX4-dependent ferroptosis pathways.

Zhou Y, He J, Zhang H et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic characterization of the tumor microenvironment orchestrates therapeutic strategies and clinical outcomes in pancreatic cancer.

This study characterized the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment by integrating single-cell RNA-seq data to infer cell type-specific metabolic fluxomes and pathways, then linked metabolic subtypes to therapeutic strategies and clinical outcomes. Using 460 PDAC samples, the authors defined three tumor microenvironment metabolism subtypes (TMS1–TMS3) with distinct immune-metabolic profiles and associated clinical differences. Scientifically, it provides a metabolism-informed stratification framework that could guide immunometabolism-targeted therapies in PDAC.

Tang R, Li Y, Zhou C et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Biomarkers & predictive modeling (AI/omics/risk stratification)

Multimodal machine learning for early risk stratification of post-stroke cognitive impairment.

This retrospective cohort study developed and validated a stacking-based multimodal machine learning model using clinical, demographic, and neuroimaging features to predict early post-stroke cognitive impairment (PSCI) in 1070 acute ischemic stroke (AIS) patients. The key finding was that integrating multimodal data in a stacking framework improved early risk stratification for PSCI compared with less integrated approaches (details truncated in the abstract). Clinically, this could enable earlier identification of high-risk AIS patients for timely cognitive-preserving interventions.

Zheng X, Zhao P, Wang N et al. · Journal of Alzheimer’s disease : JAD · (2026) · View on PubMed ↗

Associations Between Tattooing and Health Status: A Population-Based Cross-Sectional Study of Adults in Utah, 2020-2022.

This population-based cross-sectional study analyzed associations between tattooing and health status in ~27,000 adults from Utah Behavioral Risk Factor Surveillance System surveys (2020–2022) using multivariable Poisson regression to estimate prevalence ratios. The key finding was that ever receiving a tattoo was associated with differences in physical, oral, and mental health status compared with not tattooed individuals (exact effect sizes truncated in the abstract). Public-health significance lies in clarifying health profiles of tattooed populations to inform targeted screening, counseling, and access-to-care interventions.

McCarty RD, Trabert B, Millar MM et al. · Public health reports (Washington, D.C. : 1974) · (2026) · View on PubMed ↗

Posterior Pole Shape and Its Association With Axial Length and High Myopia.

This dual-center observational study quantified posterior pole shape by measuring retinal curvature from 3D reconstruction of Bruch’s membrane using wide-field swept-source optical coherence tomography angiography (with axial-length magnification correction) in 142 participants (284 eyes). The key finding was that retinal curvature was associated with axial length and high myopia status. Scientifically and clinically, this geometric retinal metric may help characterize high-myopia risk and refine structural assessment beyond axial length alone.

Wang ZX, Wei B, Duan YC et al. · Photodiagnosis and photodynamic therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Comprehensive biochemical and radiological assessment of clinical characterization pertaining to bilateral adrenal masses: a multi-center cross-sectional investigation.

This multi-center cross-sectional investigation retrospectively assessed clinical, biochemical, and radiological characteristics of bilateral adrenal masses in 1,250 patients across multiple medical centers. The study aimed to delineate the heterogeneity of etiologies (including hyperplasia and infiltrative lesions) while focusing on the common finding that many bilateral adrenal masses are ultimately confirmed as adrenocortical adenomas. Clinically, the comprehensive phenotype characterization can improve diagnostic stratification and management planning for patients with bilateral adrenal lesions.

Akkus G, Kolsuz İ, Arslan YK et al. · Endocrine · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial Analysis of Electrode Proximity to Lateral Wall and Its Impact on ECAP Amplitudes: An OTOPLAN-Based Study.

This retrospective cohort study evaluated 44 implanted ears with cochlear lateral wall electrodes to test whether electrode-to-lateral wall distance measured on postoperative high-resolution CT using OTOPLAN correlates with electrically evoked compound action potential (ECAP) amplitudes. Electrode proximity to the lateral wall was associated with differences in ECAP amplitude at overall and channel-specific levels (with correlation analyses performed across channels). These findings support using OTOPLAN-based spatial planning to optimize cochlear implant electrode placement and potentially improve neural responsiveness.

Aljehani M, Malas M, Alsanosi S et al. · Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · (2026) · View on PubMed ↗

Large-scale multi-omics enhance risk prediction for type 2 diabetes.

This UK Biobank analysis tested whether integrating multi-omics biomarkers (metabolomics and proteomics) improves 10-year type 2 diabetes risk prediction beyond single-omics models and the clinical Cambridge Diabetes Risk Score (CDRS) that includes HbA1c. Using 42,840 participants without baseline diabetes, the study fit models in a derivation set and validated them in an independent set to evaluate incremental predictive performance. The work supports multi-omics approaches as a potential next step for more accurate diabetes risk stratification beyond standard clinical risk scores.

Xie R, Herder C, Schöttker B · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Multimodal deep learning model for AI-based functional prognostic risk stratification in patients undergoing radical nephrectomy.

This study developed and evaluated a multimodal deep learning model to predict rapid glomerular filtration rate (GFR) decline after radical nephrectomy (RN) in patients with complex renal cell carcinoma (RCC), using contrast-enhanced CT images and clinical data from 1621 multi-center patients. The model stratified patients by risk of annual GFR decline >3 mL/min/1.73 m² after RN, supporting preoperative identification of those who might benefit from technically challenging partial nephrectomy (PN). Clinically, this could improve surgical decision-making by using AI-based functional risk prediction to better preserve renal function.

Luo Y, Wang Y, Zou X et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular & cardiotoxicity (mechanisms, prevention, risk)

Prevention of heart failure.

This narrative review focused on prevention of heart failure by outlining a multidisciplinary strategy addressing comorbidities and risk factors, with attention to changing HF phenotypes such as increased HF with preserved ejection fraction and the roles of renal and metabolic conditions. The key finding was that effective HF prevention requires coordinated management of major drivers including arterial hypertension, chronic kidney disease, and diabetes (and other risk factors listed in the truncated abstract). Scientifically and clinically, it supports shifting prevention efforts toward broader comorbidity control rather than focusing only on coronary artery disease.

Piepoli M, Rosano G, Abreu A et al. · European heart journal · (2026) · 1 citations · View on PubMed ↗

Cardiotoxicity induced by multiple myeloma therapies: mechanistic convergence across proteasome inhibitors, CAR-T, and bispecific antibodies.

This review synthesized evidence on cardiotoxicity mechanisms across multiple myeloma therapies, focusing on proteasome inhibitors, CAR-T, and CD3-engaging bispecific antibodies. It converges on multi-omics, preclinical, and real-world data implicating mitochondrial dysfunction, unfolded protein response (UPR), endothelial injury, and systemic inflammation as drivers of cardiac damage. The mechanistic framework supports development of prevention strategies to mitigate therapy-induced cardiovascular toxicity in multiple myeloma.

Chatrathi AR, Patel K, Saini N et al. · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗

The effects of angiotensin receptor blockers as prophylactic migraine treatment: A systematic review and meta-analysis.

This systematic review and meta-analysis evaluated randomized controlled trials of angiotensin receptor blockers (ARBs) for migraine prophylaxis in people with episodic or chronic migraine. The study searched multiple databases up to 22 September 2025 to compare any ARB versus placebo or other preventive migraine drugs, aiming to clarify inconsistent global evidence for ARB efficacy. The results are intended to guide evidence-based use of ARBs in migraine prevention and identify where higher-quality RCT data are still needed.

Riise HS, Thorvik H, Øie LR et al. · Cephalalgia : an international journal of headache · (2026) · View on PubMed ↗ · Free PDF ↗

Adiposity and the risk of aortic aneurysm: results from the UK Biobank, Japan-Specific Health Check-ups Study and a systematic review and meta-analysis of cohort studies.

This study analyzed the association between adiposity and aortic aneurysm risk using two large cohort datasets (UK Biobank and Japan Specific Health Checkups) and supplemented these analyses with a systematic review and meta-analysis of cohort studies. Using multivariable Cox proportional hazards regression, the authors assessed how anthropometric measures of overweight/obesity relate to incident aortic aneurysm across more than 1.1 million participants. Scientifically, it aims to resolve inconsistent prior findings and clarify whether excess adiposity is a causal risk factor for aortic aneurysm development.

Aune D, Otaki Y, Mahamat-Saleh Y et al. · European journal of epidemiology · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurodegeneration & brain clearance/lysosomal dysfunction

Neuroproteasomes regulate endogenous tau paired helical filament formation in an APOE genotype- and age-dependent manner.

This study investigated how neuron-specific plasma membrane proteasomes (“neuroproteasomes”) regulate endogenous tau paired helical filament (PHF) formation in an APOE genotype- and age-dependent manner using primary neurons and mouse brain models. Selective neuroproteasome inhibition rapidly induced de novo formation of sarkosyl-insoluble endogenous tau PHFs with biochemical and ultrastructural features resembling human Alzheimer’s disease PHFs. The results link tau proteostasis control to neuroproteasome function and suggest APOE-dependent vulnerability as a mechanistic modifier relevant to Alzheimer’s disease.

Paradise V, Konrad-Vicario KD, Nguyen C et al. · Nature neuroscience · (2026) · View on PubMed ↗

Physiological brain clearance architecture revealed by neuronal protein tracing.

The study developed a non-invasive genetic neuronal protein tracing system to map endogenous neuron-derived protein clearance routes from the brain to cerebrospinal fluid (CSF) and border tissues in vivo. It identified distinct drainage pathways and border “hotspots” missed by standard tracer injections, with pulse-chase kinetics showing slow skull outflow but rapid dural and nasal clearance, supported by bioorthogonal labeling of endogenous neuronal proteins. These findings refine physiological brain waste clearance architecture and provide a framework for targeting meningeal/CSF drainage dysfunction in neurodegenerative disease.

Chayama Y, Rao NR, Perla D et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondria-lysosome coupling contributes to lysosome acidification and aging.

The study examined lysosome acidification mechanisms across yeast to human, focusing on how mitochondria-lysosome membrane contacts contribute to lysosomal/vacuolar pH regulation during aging. It found that lysosomes/vacuoles acidify by taking up H+ pumped out by the mitochondrial electron transport chain through mitochondria-lysosome/vacuole membrane contacts, and that aging/senescence disrupts this coupling. This links organelle cross-talk to a conserved hallmark of aging and suggests new targets to restore lysosomal function in age-related diseases.

Liu Q, Yoo S, Zhang ZA et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

Diagnostic Revision From Primary Lateral Sclerosis to Amyotrophic Lateral Sclerosis: A Cohort Study.

This population-based cohort study applied current primary lateral sclerosis (PLS) diagnostic criteria to identify clinical characteristics associated with diagnostic revision to amyotrophic lateral sclerosis (ALS) in patients initially meeting PLS criteria. The key finding was which baseline/progression clinical features were linked to later reclassification from probable/definite PLS to ALS. This matters clinically because it can improve early risk stratification and diagnostic accuracy in upper motor neuron syndromes where ALS is the most likely alternative diagnosis.

de Boer EMJ, Willemse SW, Veldink JH et al. · Neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Clinical markers of disease progression in the prodromal to overt alpha-synucleinopathy continuum.

This study used the Disease Course Map (DCM) model to derive single-subject clinical progression markers across the prodromal-to-overt alpha-synucleinopathy continuum in 766 idiopathic/isolated rapid-eye-movement sleep behavior disorder (iRBD) patients. The key finding was that DCM-derived clinical progression measures tracked heterogeneous symptom evolution and could be correlated with established and novel neurodegeneration biomarkers. This is significant because it provides clinically usable progression markers for predicting conversion and tracking disease course in iRBD, a major prodromal stage for Parkinson’s disease and related alpha-synucleinopathies.

Roascio M, Antelmi E, Baldelli L et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic variation in antidiabetic drug targets: associations with Parkinson’s disease risk and age at onset.

This study used drug target Mendelian randomization to test whether genetic variation in antidiabetic drug targets is associated with Parkinson’s disease (PD) risk and age at onset (AAO), leveraging GWAS summary statistics for fasting glucose (FG), HbA1c, and GTEx gene expression. Instrumental-variable analyses suggested that, aside from SGLT2 inhibitors, other antidiabetic drug targets could be instrumented and showed associations with PD outcomes, while DPP-4 inhibitors did not show supportive results in the reported positive-control framework. The work provides genetic evidence relevant to PD prevention/repurposing hypotheses for specific antidiabetic target classes.

Vincze K, Szwajda A, Ploner A et al. · NPJ Parkinson’s disease · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroimmunology & immune regulation in CNS/brain

The C9orf72/SMCR8 complex maintains microglial homeostasis via RAB8A ESCRT-mediated lysosomal repair.

This study investigated how the C9orf72/SMCR8 complex regulates microglial homeostasis in mice, focusing on RAB8A and ESCRT-mediated lysosomal repair. The key finding is that loss of C9orf72 or SMCR8 causes age-dependent neuroinflammation and microgliosis with lysosomal damage marked by galectin-3 accumulation, indicating impaired lysosomal membrane repair. Scientifically, it links a major ALS/FTD gene complex to microglial lysosomal maintenance, suggesting potential targets within the RAB8A–ESCRT repair pathway for neuroinflammatory disease modulation.

Li S, Xu S, Li F et al. · The EMBO journal · (2026) · View on PubMed ↗ · Free PDF ↗

DHX36 is a regulatory switch in the interferon-mediated antiviral response.

This cell-based immunology study investigated the RNA helicase DHX36 as a regulator of interferon-mediated antiviral responses under homeostatic versus dsRNA-stimulated conditions. The key finding was that DHX36 acts as a rheostat restraining immune activation at baseline, while dsRNA reduces DHX36 activity and cells lacking DHX36 show constitutive activation with RNA G-quadruplex accumulation, PKR-dependent stress granule formation, and elevated interferon signaling. This is significant because it clarifies how DHX36 prevents inappropriate innate immune activation and modulates antiviral signaling, highlighting a potential control point for immune dysregulation.

Weixler L, Hilbig D, Simon PS et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

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Neuroscience & neurodevelopmental disorders (ASD, synaptopathies, tau, seizures)

Long-term exposure to polystyrene microplastics exacerbates seizure symptoms via lipid metabolic disruption and ferroptosis: insights from multi-omics analyses.

This study investigated how long-term exposure to polystyrene microplastics exacerbates seizure symptoms, using multi-omics analyses to connect lipid metabolic disruption and ferroptosis to neurotoxicity. The key finding is that microplastics drive lipid metabolic changes and ferroptotic pathways that correlate with worsened seizure phenotypes. Scientifically, it supports a mechanistic route from environmental exposure to brain injury and highlights lipid/ferroptosis pathways as potential intervention targets.

Liu Y, Xie R, Zhao W et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Glycine-modulating Slc6a20a-ASO restores NMDA receptor function in SHANK2 and SHANK3-mutant mice and cortical organoids.

This preclinical study tested whether antisense oligonucleotide (ASO)–mediated inhibition of the glycine transporter Slc6a20a (Slc6a20a-ASO) can restore NMDA receptor (NMDAR) function in male Shank2- and Shank3-mutant mice and cortical organoids. Slc6a20a inhibition normalized ASD-related phenotypes and improved NMDAR function by modulating glycine availability at the receptor. The work supports Slc6a20a as a more targeted alternative to GlyT1 inhibition for correcting NMDAR hypofunction in synaptopathies.

Roh JD, Bae M, Oh Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

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Inflammation, autoimmunity & immunology (IBD, SLE, Behçet, depression-immune links)

Patients’ and Healthcare Professionals’ Experiences of Patient-Centeredness in Digital Care: A Qualitative Systematic Review.

This qualitative systematic review synthesized evidence on patients’ and healthcare professionals’ experiences of patient-centeredness in digital care using Joanna Briggs Institute (JBI) qualitative systematic review methods and PRISMA-guided reporting. The key finding was that existing qualitative studies describe both facilitators and barriers to patient-centeredness in digital care, as perceived by patients and professionals (specific themes truncated in the abstract). Scientifically and clinically, the review highlights actionable considerations for designing digital health services that better support patient-centered outcomes.

Kärsämä R, Kuha S, Hammarén M et al. · Scandinavian journal of caring sciences · (2026) · View on PubMed ↗ · Free PDF ↗

Imaging endpoints in inflammatory bowel disease: current evidence and future directions for ultrasound and MRI.

This narrative review evaluated evidence for imaging endpoints in inflammatory bowel disease (IBD), focusing on intestinal ultrasound (IUS) and magnetic resonance imaging/enterography (MRI/MRE) and how they can be used in clinical trials. The key finding is a pragmatic framework for integrating IUS and MRI/MRE to capture transmural inflammation, extraintestinal complications, and small-bowel involvement that endoscopy misses. Scientifically and clinically, standardizing these imaging endpoints could improve trial design and accelerate more precise, non-invasive assessment of IBD activity and treatment response.

Faggiani I, Danese S, Biroulet LP et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

A first-in-class bifunctional antibody targeting CD20 and CD37 remodels the immune microenvironment in relapsed or refractory B-cell malignancies.

This first-in-class phase Ia trial studied PSB202, a bifunctional antibody co-targeting CD20 and CD37, in adults with relapsed or refractory (R/R) CD20+ B-cell non-Hodgkin lymphoma (B-NHL). The key finding is that PSB202 depletes malignant B cells independently of T-cell engagement, aiming to avoid T-cell overactivation and cytokine release seen with CD3-bispecifics. If confirmed in dose escalation, this strategy could provide a safer immunotherapy platform for R/R B-NHL by remodeling the immune microenvironment through dual B-cell targeting.

Wang L, Liu J, Zhou K et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

The impact of metabolic dysfunction-associated steatotic liver disease on non-invasive fibrosis scores in patients with chronic hepatitis B: a multicenter retrospective study.

This multicenter retrospective study assessed how metabolic dysfunction-associated steatotic liver disease (MASLD) affects non-invasive fibrosis scores in chronic hepatitis B (CHB) patients, using liver biopsy as the reference standard. The key finding is that MASLD status changes the diagnostic performance of non-invasive tests (including MASLD-oriented scores such as FIB-8 and FIB-9) for predicting significant fibrosis in CHB. Clinically, it supports recalibrating or selecting fibrosis NITs based on MASLD comorbidity to avoid misclassification in CHB patients.

Gezer Y, Tayşi MR, Tarakçı A et al. · BMC gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

Psychedelic-induced hypomania and mania: a systematic review and meta-analysis.

This systematic review and meta-analysis assessed human evidence for manic or hypomanic symptoms after exposure to serotonergic psychedelics (psilocybin, LSD, mescaline, DMT/ayahuasca) or MDMA, focusing on individuals with bipolar-spectrum vulnerability. Across eligible studies, the review synthesized whether these agents precipitate transient mood switches versus contribute to persistent bipolar illness or diagnostic transition. Clinically, the findings inform risk assessment and monitoring for mood destabilization when considering psychedelic or MDMA exposure in at-risk populations.

Eskinazi M, Nasserdine R, Cusin RM et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Patient-reported Outcomes in Clinical Trials of Inflammatory Bowel Disease: A Systematic Review and Meta-analysis.

This systematic review and meta-analysis assessed patient-reported outcomes (PROs) and patient-reported outcome measures (PROMs) used in randomized controlled trials for inflammatory bowel disease, including placebo response rates and measurement properties. The key finding was that multiple PROMs are used across IBD trials and that placebo outcome rates and effect sizes vary by instrument and outcome definition, with additional evidence summarized on operating properties. This is significant for clinical trial design because selecting and interpreting PROs appropriately can improve sensitivity to treatment effects and patient-centered endpoints in IBD.

Hanzel J, Yuan Y, Goodwin SW et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗

Efficacy and safety of the CD40 ligand inhibitor dapirolizumab pegol in systemic lupus erythematosus (PHOENYCS GO): a randomised, double-blind, placebo-controlled, phase 3 trial.

This phase 3 randomized, double-blind, placebo-controlled trial (PHOENYCS GO) evaluated the CD40 ligand inhibitor dapirolizumab pegol versus placebo in adults (≥16 years) with moderate-to-severe active systemic lupus erythematosus despite standard-of-care therapy. The key finding was the efficacy and safety profile of dapirolizumab pegol added to standard of care over 48 weeks, demonstrating therapeutic benefit relative to placebo in this difficult-to-treat population. This is significant because it supports a CD40L-targeted mechanism as a potential new treatment option for SLE beyond existing immunosuppressive regimens.

Clowse MEB, Isenberg DA, Merrill JT et al. · Lancet (London, England) · (2026) · 1 citations · View on PubMed ↗

Activating an interleukin 4-FLT3-STAT6 axis in multipotent progenitors restores lymphopoiesis in inflammation and aging.

The study tested whether activating an IL-4–FLT3–STAT6 signaling axis in multipotent progenitors can restore lymphopoiesis in models of inflammation and aging. It found that IL-4 shifted multipotent progenitor differentiation away from inflammation-induced myelopoiesis toward the lymphoid lineage by activating a STAT6-dependent transcriptional program, increasing lymphoid-specific gene expression, and that FLT3 was part of the receptor tyrosine kinase signaling pathway. This suggests a cytokine–kinase–transcription factor axis that could therapeutically rebalance hematopoiesis to improve immune function during chronic inflammation and aging.

Yao J, Wang Y, Zhang Y · Immunity · (2026) · View on PubMed ↗

Pharmacovigilance Analysis of Drug-Induced Stomatitis: Insights From Twenty-One Years of Real-World Data.

This pharmacovigilance study analyzed real-world adverse event reports to identify drugs associated with drug-induced stomatitis using the FDA Adverse Event Reporting System (FAERS) from 2004 Q1 to 2025 Q3. It applied disproportionality metrics (ROR, PRR, IC, EBGM) and multivariable logistic regression to characterize high-risk drugs and time-to-onset heterogeneity, and to generate preliminary mechanistic hypotheses for risk management. The results provide evidence to support clinical surveillance and mitigation strategies for patients exposed to identified high-risk medications.

Liu Z, Peng L, Wang S et al. · International dental journal · (2026) · View on PubMed ↗ · Free PDF ↗

Use of High-Efficacy Therapy in Children With Multiple Sclerosis to Prevent Long-Term Disability.

This retrospective cohort study compared long-term disability outcomes in pediatric-onset multiple sclerosis (MS) patients treated with high-efficacy monoclonal antibody therapies before age 18 versus initiation in adulthood. The key finding was that starting high-efficacy monoclonal antibody treatment during childhood was associated with better long-term disability outcomes than delaying initiation until adulthood. This is significant for pediatric MS care because it supports earlier access to effective monoclonal antibody therapy to prevent long-term disability.

Sharmin S, Roos I, Labauge PM et al. · Neurology · (2026) · 1 citations · View on PubMed ↗

SRSF3 determines Treg cell fate in antitumor immunity and autoimmunity.

This study examined how the splicing factor SRSF3 controls regulatory T cell (Treg) fate by regulating FOXP3 exon 2 inclusion. The key finding was that SRSF3 promoted FOXP3 exon 2 inclusion and protein expression, and Treg-specific deletion of Srsf3 in mice caused profound Treg deficiency and lethal systemic inflammation, while SRSF3 was also required for human Treg suppressive function and was highly expressed in human tumor Tregs. This is significant because it identifies SRSF3–FOXP3 exon 2 splicing as a mechanistic lever for Treg function in both autoimmunity and antitumor immunity.

Jia R, Guo J, Yan L et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal Response Trajectories with Dupilumab or Upadacitinib in Moderate-to-Severe Atopic Dermatitis: A Multicentre Real-World Study: IL-AD (Italian Landscape Atopic Dermatitis).

This multicentre real-world observational study characterized longitudinal clinical response trajectories in moderate-to-severe atopic dermatitis patients treated with dupilumab or upadacitinib using the Italian AD-Landscape platform. The key objective was to describe how treatment response evolves over time in routine practice rather than only at fixed trial timepoints. These trajectory insights can support more personalized therapeutic decision-making and optimization of targeted therapy sequencing in atopic dermatitis.

Potestio L, Patruno C, Ferrucci SM et al. · Dermatology and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy and Safety of Anselamimab in Immunoglobulin Light Chain Amyloidosis: Results From the Randomized CARES Trials.

This randomized CARES trial program evaluated anselamimab, an amyloid-fibril–binding monoclonal antibody, in newly diagnosed stage IIIa/IIIb immunoglobulin light chain (AL) amyloidosis. Patients received anselamimab or placebo in combination with cyclophosphamide, bortezomib, and dexamethasone (with or without daratumumab), and the primary endpoint combined time to all-cause mortality and frequency of cardiovascular hospitalizations. The results assess whether accelerating amyloid clearance with anselamimab improves clinically meaningful outcomes in high-risk AL amyloidosis patients.

Wechalekar AD, Dispenzieri A, Sanchorawala V et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Serum inflammatory cytokines in the progression of depression.

This review summarized evidence linking serum inflammatory cytokines—IL-1β, IL-6, TNF-α, IFN-γ, and C-reactive protein (CRP)—to depression progression and treatment response, focusing on immune-to-brain signaling pathways. It highlights mechanisms involving TLR4/NF-κB/MAPK signaling, NLRP3 inflammasome activation, and altered tryptophan–kynurenine metabolism via IDO1 and TDO2 that can impair monoaminergic neurotransmission. Clinically, the work supports inflammatory biomarkers and immune pathway targeting as potential contributors to depression pathophysiology and therapeutic stratification.

Feng Q, Yuan Z, An Q et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Risk of intestinal involvement in mucocutaneous-onset Behçet’s disease: data from the AIDA network registry.

Using the AIDA network registry, this study analyzed 328 patients with Behçet’s disease (BD) presenting with mucocutaneous-only onset to identify factors predicting later intestinal involvement, using Bayesian methods for limited subgroup sizes. Over follow-up, 46 patients (14%) developed intestinal involvement. The results help clinicians risk-stratify early mucocutaneous-onset BD patients for intestinal disease surveillance and earlier intervention.

Vitale A, Caggiano V, Sbalchiero J et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Macrophage USP9X attenuates colitis by restricting oncostatin M production via K27-linked deubiquitination of STAT1.

This study examined how the deubiquitinase USP9X regulates intestinal inflammation in intestinal macrophages, focusing on ulcerative colitis (UC) patient samples and mouse models of DSS- and TNBS-induced colitis. Myeloid-specific USP9X deletion worsened colitis while USP9X overexpression ameliorated disease, and mechanistically USP9X interacted with STAT1 to remove K27-linked polyubiquitin chains, thereby attenuating STAT1-driven inflammatory signaling. These findings identify USP9X as a protective macrophage regulator and suggest that modulating USP9X–STAT1 ubiquitination could be a therapeutic approach for IBD.

Zhang T, Meng F, Zhao W et al. · Cellular & molecular immunology · (2026) · View on PubMed ↗

The endogenous peptide GPR15L shapes the intestinal microbiota to counteract colitis.

This study investigated the endogenous peptide GPR15L in experimental colitis and inflammatory bowel disease by using genetic deletion or overexpression of Gpr15l and rectal administration of recombinant GPR15L. GPR15L shaped the intestinal microbiota and counteracted colitis, with microbiome effects assessed using co-housing/littermate/fecal microbiota transfer experiments plus 16S rRNA sequencing and shotgun metagenomics. The findings position GPR15L–microbiota crosstalk as a mechanistic axis for developing microbiome-targeted therapies in colitis/IBD.

Leggio M, Schramm S, Dietz L et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗

Prevalence of post-traumatic stress disorder among current and former members of the Canadian Armed Forces: a systematic review and meta-analysis of observational studies.

This systematic review and meta-analysis synthesized observational studies to estimate the prevalence of post-traumatic stress disorder (PTSD) among current and former members of the Canadian Armed Forces (CAF). Using database searches through June 2024 and random-effects pooling with Freeman–Tukey transformation, the authors quantified PTSD prevalence and rated evidence certainty with GRADE. The results provide an evidence base for understanding PTSD burden in CAF populations and informing surveillance and mental health service planning.

Bengizi A, Qureshi AR, Incze T et al. · BMJ military health · (2026) · View on PubMed ↗

Associations between vitamin intake and depression severity: A cross-sectional analysis of NHANES 2005-2014.

This cross-sectional analysis used nationally representative NHANES 2005–2014 data to examine associations between individual vitamin intake and depression severity in the general US population, with depression measured by PHQ-9 and intake assessed via 24-hour recall and laboratory assays. The study found specific relationships between certain vitamin intakes and depression severity (direction and magnitude reported in the full text), while results varied by vitamin and analytic approach including a composite nutritional score. Scientifically, it helps clarify inconsistent prior findings and may guide future prospective studies to determine whether any vitamin-related associations are causal.

Mistry N, Cowan LT, Samawi HM et al. · Journal of affective disorders · (2026) · View on PubMed ↗

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Allergy & asthma (eosinophilic disease, microbiota-immune pathways)

Early-life Gut Microbiota and Allergic Diseases: Immune Regulatory Mechanisms and Intervention Progress.

This review examined how early-life gut microbiota dysbiosis influences immune regulatory mechanisms underlying allergic disease development and progression in children. It highlights that gut microbiota regulates mucosal barrier integrity and immune homeostasis, and that abnormalities in microbial composition and function can promote allergic susceptibility. Understanding these immune pathways supports microbiota-targeted interventions as a potential strategy to prevent or modify allergic diseases early in life.

Yu L, Wu M, Leung T et al. · Clinical reviews in allergy & immunology · (2026) · View on PubMed ↗

Asthma exacerbation profile of benralizumab for severe eosinophilic asthma (the BenRex study): a multicentre, prospective cohort study.

This multicentre, prospective cohort study (BenRex) investigated the asthma exacerbation profile in patients with severe eosinophilic asthma treated with benralizumab, an interleukin-5 receptor α antagonist that depletes eosinophils. The key finding was characterization of exacerbations occurring during benralizumab therapy, including associated clinical and biomarker features such as FeNO and lung function measures around exacerbation events. Scientifically and clinically, understanding why exacerbations still occur on benralizumab can guide patient selection, monitoring, and add-on strategies for residual risk.

Logan J, Martin K, Gillespie L et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Musculoskeletal & pain (MSDs, osteoarthritis, disc herniation)

Effect of aerobic exercise of different intensity on articular cartilage metabolism in patients with knee osteoarthritis: A randomized controlled trial.

This randomized controlled trial tested whether aerobic exercise intensity differentially affects articular cartilage metabolism, symptoms, and structural outcomes in 120 knee osteoarthritis patients (Kellgren–Lawrence grade 2–3) over 12 weeks. The key finding was a dose-response effect of treadmill walking or stationary cycling intensity (low 50–60% HRR, moderate 60–70% HRR, high 70–80% HRR) on cartilage metabolism and related clinical/structural measures (specific results truncated in the abstract). Clinically, it informs optimal exercise prescription intensity to better protect cartilage in knee OA.

Song L, Meng Y · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

PIEZO1 mediates orthodontic tension force-induced alveolar bone remodeling via the Ca²⁺/YAP-TAZ pathway in periodontal ligament stem cells.

This in vitro mechanobiology study investigated how PIEZO1 mediates orthodontic tooth movement (OTM) tension-force–induced alveolar bone remodeling in human periodontal ligament stem cells (PDLSCs) via a Ca²⁺/YAP-TAZ pathway. Using cyclic tension (10% strain, 0.5 Hz) with PIEZO1 inhibition by GsMTx4 and siRNA, the key finding was that PIEZO1 activation couples Ca²⁺ signaling to YAP/TAZ and regulates the OPG–RANKL axis to promote osteogenesis while suppressing osteoclastogenesis. This mechanistic insight identifies PIEZO1–Ca²⁺/YAP-TAZ–OPG/RANKL signaling as a potential target to modulate bone remodeling during orthodontic treatment.

Li T, Shen Z, Liu J et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

A continuous DNA repairing system for alleviating intervertebral disc degeneration.

This work studied a continuous DNA-repairing therapeutic strategy for intervertebral disc degeneration (IVDD), targeting ROS-driven DNA damage to prevent senescence in nucleus pulposus cells (NPCs). Using single-cell sequencing of clinical samples and in vitro modeling, the authors found that oxidative stress initiates DNA damage leading to senescence-associated secretory phenotype (SASP), and that continuous DNA repair can promote DNA replication and extracellular matrix synthesis. Clinically, this suggests a disease-modifying approach for IVDD by interrupting the DNA damage–senescence axis rather than only addressing downstream degeneration.

Peng S, Du Y, Wang R et al. · Journal of nanobiotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Global and high-income regional burden and healthcare costs of musculoskeletal diseases, 1990-2023.

This epidemiologic and health-economics study quantified global and high-income regional burden and healthcare costs of musculoskeletal diseases (MSDs) from 1990–2023 using Global Burden of Disease 2023 data across 36 high-income countries. It estimated trends in incidence, prevalence, and years lived with disability (YLDs), and used Bayesian meta-regression to attribute burden to major risk factors and a cross-national transfer model to estimate direct healthcare costs in 2023. The findings identify key drivers of rising MSD burden despite high spending and can inform targeted prevention and resource allocation in high-income settings.

Yao Y, Liu G, Vithran DTA et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗

Effects of Physical Exercise on Pain in Patients With Lumbar Disc Herniation: A Systematic Review and Meta-Analysis of Randomised Controlled Trials.

This systematic review and meta-analysis evaluated the effects of physical exercise interventions on pain in patients with lumbar disc herniation, including both post-surgical and non-surgical populations, using randomized controlled trials. The key finding was that exercise-based therapy improves pain outcomes, with subgroup analyses performed to explain heterogeneity across trial designs and populations. Clinically, these results support exercise as an evidence-based nonpharmacologic option for lumbar disc herniation pain, potentially reducing reliance on more invasive or medication-focused strategies.

Linhares DG, Linhares BG, Cordeiro LS et al. · Musculoskeletal care · (2026) · View on PubMed ↗ · Free PDF ↗

Abnormal Stress Reduced miR-330 Supplementation Alleviates Osteoarthritis Progression by Suppressing Osteochondral Catabolism.

This study investigated how abnormal mechanical stress affects miR-330 and whether miR-330 supplementation modulates osteoarthritis (OA) progression by suppressing osteochondral catabolism. In human synovial fluid from temporomandibular disorder (TMD) patients and in OA cartilage/subchondral bone from clinical specimens and animal models, miR-330 was reduced under abnormal stress, and global or conditional miR-330 knockout worsened OA phenotypes. These findings identify miR-330 as a mechanosensitive regulator and suggest miR-330 supplementation as a potential disease-modifying approach for OA.

Zou L, Yang K, Wang C et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Physical activity reshapes intrapancreatic immune and inflammatory programmes to restrain chronic pancreatitis.

This study assessed whether physical activity (PA) protects against chronic pancreatitis (CP) and explored mechanisms by combining UK Biobank epidemiology (>500,000 participants) with mouse CP models and immune/inflammatory readouts. PA was associated with reduced CP risk in humans and, in mice, exercise interventions restrained pancreatic injury, fibrosis, and inflammatory/immune programs. These results support PA as a potential modifier of CP progression and identify intrapancreatic immune and inflammatory pathways as mediators.

Tong J, Wu JW, Zou WB et al. · Gut · (2026) · View on PubMed ↗

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Metabolic health & obesity pharmacotherapy (GLP-1/GIP, diabetes risk, metabolic syndrome)

AARS1 promotes diabetic kidney disease through rewiring Akt and NF-κB signaling to suppress autophagy and sustain inflammation.

This study examined the role of alanyl-tRNA synthetase 1 (AARS1) in diabetic kidney disease (DKD) by testing kidney-specific Aars1 knockout mice and β-alanine treatment in streptozotocin-induced and db/db diabetic models, with mechanistic focus on lactylation. The key finding is that AARS1 promotes DKD by rewiring Akt and NF-κB signaling to suppress autophagy and sustain inflammation. Scientifically, it identifies AARS1-mediated lactylation as a potential therapeutic lever to restore autophagy and dampen inflammatory signaling in DKD.

Tian L, Wang Y, Guan C et al. · Cellular & molecular biology letters · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolic dysfunction-associated steatotic liver disease: pathogenesis and novel treatment options.

This review summarized the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and discussed novel treatment options, including the context of FDA-approved therapy. The key finding is that MASLD is driven by systemic insulin resistance and metabolic dysregulation and carries major risks beyond liver disease, while current pharmacologic options remain limited for the broader population. Clinically, it frames where emerging therapies—such as resmetirom for advanced fibrosis subsets—may fit and highlights the need for additional treatments for patients without advanced fibrosis.

Ren R, Liang X, Wei X · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Hormonal, metabolic and metabolomic biomarkers in long COVID.

This review synthesized evidence on hormonal, metabolic, and metabolomic biomarkers in people with long COVID (post-acute sequelae after SARS-CoV-2 infection). A central finding was that vitamin D deficiency is common in long COVID and is associated with neurocognitive symptoms, delayed recovery, and poorer physical performance, alongside other reported endocrine/metabolic abnormalities. Scientifically, identifying these biomarker patterns may enable future risk stratification and development of diagnostic or monitoring tools for long COVID.

Petropoulou D, Karampela I, Christodoulatos GS et al. · Advances in clinical chemistry · (2026) · View on PubMed ↗

Updated Results of the POSITIVE (Pregnancy Outcome and Safety of Interrupting Therapy for Women with Endocrine Responsive Breast Cancer) Trial.

This updated pre-planned analysis reported longer follow-up of the POSITIVE trial, a single-arm prospective study in young women (<42 years) with hormone receptor-positive early breast cancer who temporarily interrupted adjuvant endocrine therapy to attempt pregnancy. The key finding was that the approach remained feasible and did not reveal new major safety concerns with additional follow-up (median ~41 months plus 2.5 years). Clinically, these updated results strengthen evidence that carefully selected patients can pursue pregnancy while managing recurrence risk during endocrine therapy interruption.

Pagani O, Niman SM, Ruggeri M et al. · Annals of oncology : official journal of the European Society for Medical Oncology · (2026) · View on PubMed ↗

Metabolic syndrome is associated with excessive scarring: A prospective cohort study from the UK Biobank.

This prospective cohort study used UK Biobank data (466,625 participants) to test whether metabolic syndrome and its components predict excessive scarring, using multivariable Cox regression with stratified analyses by gender, age, and ethnicity. The key finding was that metabolic syndrome was associated with a higher risk of excessive scarring (HR 1.28, 95% CI 1.08–1.52), with increased waist circumference and hypertension also contributing. This is significant because it identifies metabolic syndrome as a modifiable risk factor for scarring severity, informing prevention and risk counseling.

Yang Z, Xiang S, Zhang Y et al. · Journal of the American Academy of Dermatology · (2026) · View on PubMed ↗

Comparative Efficacy and Safety of Tirzepatide versus Semaglutide: A Systematic Review and Meta-Analysis with Cardiometabolic Implications.

This systematic review and meta-analysis compared tirzepatide (a dual GIP/GLP-1 receptor agonist) versus semaglutide (a GLP-1 receptor agonist) for efficacy and safety using randomized and/or comparative studies identified through database searches up to February 2026. Across included studies (n=3), tirzepatide showed greater improvements in cardiometabolic outcomes than semaglutide while safety outcomes were synthesized across trials (with pooled mean differences and risk ratios using random-effects models). The findings inform comparative incretin therapy selection for obesity and type 2 diabetes risk reduction.

Baba AH, Akhtar R, Rawat A et al. · Nepal journal of epidemiology · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting Inflammation and Fibrosis in Lipedema: The Potential Role of Glucagon-like Peptide-1 Receptor Agonist Therapies.

This narrative review evaluated the potential role of glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapies in lipedema, a condition characterized by subcutaneous fat accumulation with pain, inflammation, and fibrosis. It proposes that GLP-1-based agents may modulate inflammation and fibrosis pathways relevant to lipedema pathophysiology, based on evidence from the broader GLP-1 RA literature. Scientifically, the article frames GLP-1 RAs as candidate disease-modifying therapies and motivates targeted clinical studies in lipedema patients.

Mohseni Y, Vazirnia A, Minokadeh A et al. · Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] · (2026) · View on PubMed ↗

The Role of Glucagon-Like Peptide-1 Receptor Agonists in Hair Loss: Clinical Evidence and Proposed Mechanisms.

This scoping review assessed clinical evidence for GLP-1 receptor agonist (GLP-1RA)-associated alopecia, comparing reported prevalence across agents and summarizing proposed mechanisms using PubMed literature through April 2026. The authors report conflicting findings in the literature regarding whether GLP-1RAs increase hair loss risk, while outlining potential biological explanations for alopecia. Clinically, the review highlights the need for better-controlled studies and informs dermatologic monitoring when prescribing GLP-1RAs.

Zarabian N, Farah M, Stines A et al. · Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] · (2026) · View on PubMed ↗

Genotype-Phenotype Spectrum of Non-Syndromic Monogenic Obesity in a National Paediatric Cohort.

This multicentre retrospective cohort study characterized the genotype–phenotype spectrum of non-syndromic monogenic obesity in a national pediatric population in Türkiye, enrolling patients with biallelic (likely) pathogenic variants in LEP, LEPR, POMC, PCSK1, MC4R, ADCY3 and monoallelic (likely) pathogenic MC4R variants. It systematically collected anthropometric and metabolic measures (including HOMA-IR and SPISE index) across monogenic obesity subtypes to examine metabolic correlations by genotype. The results improve clinical understanding of how specific leptin–melanocortin pathway gene defects relate to severity and insulin resistance in children, supporting more tailored management.

Kahveci A, Karauzum SU, Manyas H et al. · Pediatric obesity · (2026) · View on PubMed ↗ · Free PDF ↗

Beyond weight loss: multisystem benefits of obesity medications.

This review synthesized evidence from randomized controlled trials and high-quality meta-analyses on obesity medications, focusing on agents such as phentermine-topiramate, naltrexone-bupropion, GLP-1 receptor agonists (eg, liraglutide and semaglutide), and newer GLP-1–based therapies (eg, tirzepatide, survodutide, retatrutide, and cagrilintide-semaglutide). Across studies, obesity pharmacotherapies showed multisystem benefits beyond weight loss, including improvements in metabolic, cardiovascular, reproductive, neuropsychiatric, and mechanical outcomes. Clinically, the work supports treating obesity as a disease-modifying condition and informs evidence-based selection of specific drug classes for broader health risk reduction.

Savas M, Kuckuck S, Boon MR et al. · The lancet. Diabetes & endocrinology · (2026) · View on PubMed ↗

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Reproductive/developmental biology & developmental atlases (including placenta/meninges/oocytes)

R-loop homeostasis at transposable elements safeguards transcriptional silencing in replication-quiescent oocytes.

This study mapped R-loop dynamics in replication-free oocytes using RTACC-seq to examine how R-loop homeostasis at transposable elements regulates transcriptional silencing. It found that transposable element–associated R-loops accumulate in transcriptionally active stage oocytes and resolve in fully grown oocytes, coinciding with chromatin condensation and silencing. The location-dependent regulatory effects of R-loops at promoters versus transposable elements reveal a mechanism safeguarding genome regulation during replication-quiescent oocyte development.

Liu SY, Tian XY, Fu HF et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Decoding the spatiotemporal development of human meninges.

The study used single-cell spatiotemporal transcriptomics across 6–23 gestational weeks to characterize the cellular and molecular development of human meninges in utero. It found asynchronous development of meningeal layers with pia mater forming earliest and defined layer-specific fibroblast states expressing barrier-related, neurotransmitter transporter/synapse-related, and lipid metabolism-related genes. This provides a high-resolution developmental atlas that can guide mechanistic studies of how meningeal maturation shapes CNS homeostasis and disease susceptibility.

Li Y, Li Z, She Y et al. · Cell · (2026) · View on PubMed ↗

Evolving strategies for lineage tracing: Genetic markers, synthetic barcodes, and natural variants.

The review synthesized current strategies for lineage tracing, focusing on genetic markers, synthetic barcodes, and retrospective tracing using endogenous natural variants, integrating single-cell sequencing, genome engineering, and spatial profiling. It concluded that these three methodological pillars enable prospective tracking, high-throughput mapping, and retrospective reconstruction of cell fate decisions, each with distinct trade-offs in resolution, scalability, and interpretability. This provides a practical framework for selecting lineage-tracing approaches to link lineage history to dynamic phenotypic states in developmental and disease contexts.

Kang Z, Chen H, Li S et al. · Cell stem cell · (2026) · View on PubMed ↗ · Free PDF ↗

H2O2 sulfenylates GRF8 to facilitate jasmonate signaling by relieving MYC2 inhibition in Arabidopsis.

The study investigated how hydrogen peroxide (H2O2) regulates jasmonate (JA) signaling in Arabidopsis by modulating the transcriptional inhibitor GRF8. It showed that GRF8 inhibits JA signaling by interacting with and suppressing MYC2, recruiting JAZ repressors to enhance MYC2 inhibition, while H2O2 relieves this inhibition to promote JA responses during root growth and leaf senescence. This identifies a specific H2O2–GRF8–MYC2 regulatory mechanism that connects redox signaling to plant hormone transduction.

Song RF, Li L, Guo XR et al. · Molecular cell · (2026) · View on PubMed ↗

Dehydration-induced condensation of AGO1 modulates miRNA functionality.

This mechanistic plant study examined how dehydration affects microRNA (miRNA) regulation by altering the structure and phase behavior of ARGONAUTE 1 (AGO1) in Arabidopsis thaliana. The key finding was that the prion-like domain of AGO1 drives dehydration-induced liquid-liquid phase separation (LLPS) and topological changes that modulate AGO1/miRNA regulatory activity, linked to cytoplasmic calcium levels. This is significant because it reveals a physical mechanism (dehydration-triggered AGO1 condensation/LLPS) that tunes miRNA function during water-deficit stress.

Jung HJ, Oh TR, Yang W et al. · The Plant cell · (2026) · View on PubMed ↗

Structural insights into a conserved mechanism of choline translocation through CHT.

This structural biology study identified and characterized a bacterial Na+-dependent choline transporter (sfCHT) with high sequence identity to the human choline transporter SLC5A7 (CHT1) and determined its structure. The key finding was that cryo-EM structures of Na+- and choline-bound sfCHT show a LeuT-fold architecture with Na+ coordination geometry similar to CHT1, captured in an inward-facing state. This is significant because it provides conserved mechanistic insight into choline translocation that can inform understanding of nutrient/osmoprotection transport across species.

Vilchez-Garcia J, Martínez-Jiménez A, Jiang H et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗

Transcription-independent induction of rapid-onset senescence is integral to healing.

The study investigated senescence induction after skin injury, identifying a rapid, transcription-independent senescence program in skin cells at the wound edge. Within minutes to hours, cells used pre-existing Cdkn1a (p21) mRNA by removing nuclear export inhibitors to enable rapid p21 accumulation, leading to stable cell-cycle arrest and secretion of pro-migratory/pro-inflammatory factors that promote re-epithelialization. This reveals a fast wound-healing senescence mechanism that could be targeted to modulate tissue repair and inflammation without relying on new transcription.

Valdivieso K, Rozmaric T, Victorelli S et al. · Nature cell biology · (2026) · 5 citations · View on PubMed ↗ · Free PDF ↗

Neuroprotection Bundles and Intraventricular Hemorrhage Rates in Neonates <29 Weeks’ Gestation.

This multicenter retrospective pre–post cohort study assessed whether implementing an intraventricular hemorrhage–neuroprotection bundle (IVH-NB) reduced intraventricular hemorrhage rates in neonates born at <29 weeks’ gestation in Canadian NICUs. Sites that implemented the IVH-NB showed changes in IVH incidence compared with pre-implementation periods, with the primary outcome defined as a composite of severe IVH measures (as specified in the full abstract). The results are clinically significant because they evaluate a systems-based neuroprotection strategy that could lower severe brain injury risk in extremely preterm infants.

Deshpande P, Goswami I, Mohammad K et al. · The Journal of pediatrics · (2026) · View on PubMed ↗

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Generated automatically on May 31, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.