PubMed Trending Research Digest — July 28, 2026

Automated digest · 96 articles · 15 research areas · July 28, 2026

Overview

Across this week’s set of studies, a dominant theme is precision targeting—either by identifying actionable molecular vulnerabilities (e.g., metabolic-to-signaling links in metastasis, UPS remodeling driven by tumor mutations, KRAS-pathway targeting in pancreatic cancer) or by refining patient selection using increasingly scalable biomarkers (plasma phospho-tau for early-onset dementia differentiation, blood proteomics for dementia subtype/stage, and tissue checkpoint profiling in metastatic ccRCC). Several papers also emphasize how resistance evolves and can be anticipated: 5-FU resistance via an S1PR2 β-arrestin1–DPD axis, EGFR TKI resistance frameworks, and tumor evolution reviews that integrate multi-omics and lineage concepts to guide evolution-informed therapy.

A second major thread is immune modulation through non-classical routes. This includes next-generation immunotherapies beyond checkpoint blockade (CAR T for claudin 18.2 gastric cancer, CSF-1R inhibition for TGCT, CD47-directed NK engagers, and T cell engagers like ImmTAC), as well as mechanistic immune biology that can be therapeutically exploited (complement activation in early synucleinopathy, NOD1/2 macrophage signaling as adaptive immune resistance, and microglia/sEV-mediated heart-to-brain inflammation in HFpEF). Complementing these are cell-free and delivery-focused advances—lyophilized platelet EVs for TBI bleeding reduction, bispecific antibody–LNPs for targeted mRNA delivery, and exosome-focused perspectives on the “exosome paradox” in cancer drug resistance.

Finally, multiple studies connect cellular stress and organ-system physiology to disease progression and outcomes. Examples include mitochondria/lysosome quality control and innate immune signaling (mitophagy/mtDNA–cGAS–STING in osteoarthritis, lysosomal renewal under hypoxia–reoxygenation), RNA biology and epitranscriptomics as regulators of genome stability and anti-tumor immunity (REXO4 and m6A-marked R-loops), and neurodegeneration mechanisms (Aβ seeding by specific molecular-weight fractions, “big tau” isoform mapping). Together, these works reflect a broader shift toward mechanistic, multi-scale interventions—spanning molecules, cells, systems, and clinical trial design—to improve both efficacy and safety.

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Cancer metabolism & metastasis mechanisms

α-fluoro-β-alanine functions as a β-arrestin1-biased ligand of S1PR2 to upregulate DPD expression in cancer cells.

This work identified α-fluoro-β-alanine (FBAL), a catabolite of the chemotherapeutic 5-fluorouracil (5-FU), as a β-arrestin1-biased ligand of sphingosine-1-phosphate receptor 2 (S1PR2) in cancer cells, focusing on colorectal cancer. The key finding was that FBAL activates β-arrestin1-biased S1PR2 signaling to upregulate dihydropyrimidine dehydrogenase (DPD), thereby promoting 5-FU resistance, with mechanistic involvement of GRK6-mediated phosphorylation of S1PR2. Clinically, this links a 5-FU metabolite to acquired resistance via the S1PR2–β-arrestin1–DPD axis, suggesting potential targets to overcome resistance.

Tan M, Shao H, Zhang X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Loss of ATP-Dependent Citrate Lyase Drives Left Ventricular Dysfunction by Metabolic Remodeling.

This study investigated how loss of ATP-dependent citrate lyase (ACLY/ATP-dependent citrate lyase, Acly) affects cardiac metabolism and function by using human heart tissue samples from healthy donors and patients with nonischemic cardiomyopathy and applying CRISPR-based approaches to model ACLY loss. The key finding was that ACLY loss drives left ventricular dysfunction through metabolic remodeling, consistent with disrupted acetyl-CoA production and downstream lipid synthesis programs. Scientifically, it identifies ACLY as a metabolic regulator of cardiac adaptation and suggests metabolic targeting as a potential therapeutic direction in nonischemic cardiomyopathy.

Liu S, Gammon ST, Tan L et al. · Circulation · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Precision Medicine in Pancreatic Cancer: Targeting KRAS and Beyond.

This review assessed the emerging precision-medicine strategy for advanced/metastatic pancreatic cancer focused on targeting mutant KRAS and related pathways, contextualizing results from recent clinical trials including RASolute 302. It concludes that KRAS inhibition has demonstrated clinically meaningful activity in metastatic pancreatic cancer, expanding the theoretical eligibility for targeted therapeutics beyond previously small subgroups. The scientific significance is that KRAS-directed therapy is moving pancreatic cancer toward biomarker-driven treatment, potentially improving outcomes where conventional chemotherapy has had limited impact.

Schürmann H, Park W, O’Kane GM et al. · Targeted oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Mitochondrial SLC25A46 Rewires Fatty Acid Oxidation to Promote Cell Proliferation and Ferroptosis Evasion in Ovarian Cancer by Stabilizing CACT.

This study characterized the role of mitochondrial SLC25A46 in ovarian cancer by showing it is upregulated in ovarian tumors and promotes proliferation and ferroptosis evasion. Mechanistically, SLC25A46 enhanced fatty acid oxidation by stabilizing CACT (carnitine-acylcarnitine translocase) from MARCHF5-mediated degradation, increasing ATP and NADPH production to support tumor growth. The significance is that the SLC25A46–CACT axis may represent a metabolic vulnerability and a therapeutic target to counter ferroptosis resistance in ovarian cancer.

Gao Y, Hao J, Zhang X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Tailored strategies to overcome third-generation TKI resistance in EGFR-mutated non-small cell lung cancer.

This review article summarized evidence for tailored strategies to overcome third-generation EGFR TKI resistance in EGFR-mutated non-small cell lung cancer (NSCLC). It organizes resistance mechanisms including on-target EGFR alterations such as C797S and other kinase domain mutations, off-target pathway activation (e.g., MET or HER2 amplification, RAS-MAPK signaling, oncogenic fusions), and neuroendocrine transformation to small-cell lung cancer, and discusses corresponding clinical evidence (truncated). The significance is that it provides a framework for selecting next-line approaches based on tumor molecular profiling to improve outcomes after resistance to third-generation EGFR inhibitors.

Saporita I, Farinea G, Lombardi E et al. · Expert opinion on therapeutic targets · (2026) · View on PubMed ↗

Inhibition of the Metalloproteinase ADAMTS5 Suppresses Colorectal Cancer Metastasis via the PEDF/Wnt/β-Catenin Pathway.

This study investigated the role of the metalloproteinase ADAMTS5 in colorectal cancer (CRC) metastasis and tested whether its effects involve the PEDF/Wnt/β-catenin pathway. It found that ADAMTS5 is upregulated in CRC tissues and that inhibiting ADAMTS5 suppresses CRC metastasis through modulation of PEDF/Wnt/β-catenin signaling. These findings position ADAMTS5 as a mechanistic driver and potential therapeutic target for limiting metastatic progression in CRC.

Sun X, Zhang H, Hu Y et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Pan-cancer proteogenomic interrogation of the ubiquitin-proteasome system.

This study used harmonized pan-cancer proteogenomic data from up to 11 CPTAC cohorts to interrogate how somatic cancer-driver alterations remodel the ubiquitin-proteasome system (UPS) at the protein level, focusing on UPS protein dysregulation, prognostic associations, and mutation-driven remodeling (with emphasis on TP53 loss). It found that mRNA levels poorly predict UPS protein abundance, that a recurrent set of E3 ligases is dysregulated across cancers, and that somatic mutations—especially TP53 loss—produce coherent UPS protein quantitative trait locus (pQTL) signatures. These findings support mutation-informed, proteome-level targeting of UPS components as a route to improve prognostic stratification and therapeutic design across tumor types.

González-Robles TJ, Khan M, Sastourné P et al. · Cell death and differentiation · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.

This review synthesized current knowledge on tumor evolution, emphasizing signaling pathways, molecular mechanisms, and therapeutic targets, and describing how modern technologies (high-throughput sequencing, single-cell and spatial omics, lineage tracing, computational modeling, and noninvasive biopsy) enable dynamic tracking of tumor heterogeneity. The key finding is that evolutionary framing plus multi-omics/lineage approaches can better explain adaptive plasticity and guide identification of evolution-informed therapeutic targets. The significance is that it supports a framework for developing therapies that anticipate and counter tumor evolutionary trajectories.

Zhang KY, Zhu XZ, Yan YX et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

ADSL drives fumarate mediated scrib-rictor complex formation to promote metastasis dissemination in triple-negative breast cancer.

This study investigated how the metabolic enzyme ADSL drives fumarate-mediated formation of the SDC1/Rictor (Scrib-Rictor) complex to promote metastasis dissemination in triple-negative breast cancer (TNBC) using untargeted metabolomics, chemoproteomic succination profiling, and in vivo metastasis models. ADSL-driven fumarate signaling promoted SDC1/Rictor complex assembly and enhanced metastatic dissemination. These findings identify a specific metabolic-to-signaling mechanism that could be targeted to limit TNBC metastasis.

Fan Y, He X, Deng W et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell-free therapies & extracellular vesicles (EVs)

Targeted mRNA Delivery Using Bispecific Antibody-Lipid Nanoparticle Complexes.

This study developed targeted mRNA delivery using bispecific antibody–lipid nanoparticle complexes (TbsAb-LNPs) to improve extrahepatic, tissue-specific uptake beyond conventional lipid nanoparticles. The key finding was that antibody-based bispecific targeting enabled targeted LNP binding and uptake in vitro as a platform for modeling targeted delivery prior to in vivo testing. This advances the engineering of next-generation RNA therapeutics toward cellular- and tissue-specific delivery for individualized treatments.

Hickey JC, Roach T, Cassaidy B et al. · Molecular pharmaceutics · (2026) · View on PubMed ↗

Cigarette Smoke-Exposed Alveolar Epithelial Cell-Derived Exosomes Exacerbate Skeletal Muscle Dysfunction Through HDAC2 Signalling.

This study investigated whether cigarette smoke–exposed alveolar epithelial cell–derived exosomes drive skeletal muscle dysfunction in the context of COPD, with emphasis on histone deacetylase 2 (HDAC2) signaling. Using the exosome inhibitor GW4869 in a cigarette smoke exposure model, it found that exosomes exacerbate skeletal muscle dysfunction by regulating HDAC2-dependent inflammatory transcriptional control. Scientifically, it links lung-derived extracellular vesicle signaling to systemic muscle impairment and identifies the exosome–HDAC2 axis as a potential therapeutic target for COPD-related sarcopenia.

Li C, Ou M, Jiang G et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Exosomes in cancer drug resistance: dual roles in therapy failure and emerging precision therapeutics.

This review discussed exosomes in cancer drug resistance, focusing on their dual roles as mediators of therapy failure and as emerging tools for precision therapeutics, including transfer of resistance-associated cargo such as P-gp and PD-L1 and nucleic acids like miR-21 and lncRNA H19. The key finding is the “exosome paradox”: exosomes can promote drug resistance and immune evasion while also being engineered or leveraged for targeted therapeutic delivery. The significance is that understanding exosome cargo and signaling pathways (e.g., PI3K/AKT and MAPK) may enable new precision interventions to overcome resistance.

Tegegne BA, Belew H, Teffera ZH et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

Lyophilized platelet derived extracellular vesicles promote hemostasis and attenuate intracranial hemorrhage following traumatic brain injury.

This study evaluated whether lyophilized platelet-derived extracellular vesicles (LPEVs) promote hemostasis and reduce intracranial hemorrhage (ICH) after traumatic brain injury (TBI) using characterization by flow cytometry, scanning electron microscopy, and Nanosight plus in vitro human brain endothelial barrier assays and a murine TBI model. LPEVs improved hemostatic outcomes, attenuated ICH, and preserved blood–brain barrier (BBB) integrity after TBI. The results support LPEVs as a potential cell-free therapeutic approach to reduce fatal bleeding complications in TBI.

Trivedi A, Miyazawa B, Fields AT et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Targeted small molecules & natural products (mechanism-focused)

A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death.

This study investigated a chemically induced proximity (CIP) strategy using lysine acetyltransferase (KAT)-based TCIPs (transcriptional/epigenetic chemical inducers of proximity) to induce oncogene-induced cell death in diffuse large B-cell lymphoma (DLBCL). The lead KAT-TCIP redirected p300/CBP to activate cell-death networks repressed by the oncogenic driver BCL6, reprogramming the epigenome to initiate apoptosis. This mechanistic approach is clinically significant as a small-molecule alternative to immunotherapy for selectively killing BCL6-driven lymphoma cells.

Nix MN, Gourisankar S, Bowman KJ et al. · Cell · (2026) · View on PubMed ↗

Unlocking Sulforaphane’s Potential in Friedreich Ataxia: Further Evidence from Preclinical Investigations Using Induced Pluripotent Stem Cell-Derived Sensory Neurons.

This preclinical study tested sulforaphane (SF) against omaveloxolone (Omav) and dimethyl fumarate (DMF) in induced pluripotent stem cell (iPSC)-derived sensory neurons from Friedreich ataxia patients with expanded GAA repeats in the FXN gene (e.g., 550 GAA1 repeats). It provides further evidence that SF can increase frataxin (FXN) expression and modulate epigenetic, inflammatory, and oxidative stress pathways in this patient-derived neuronal model. Scientifically, the results strengthen SF as a candidate therapeutic approach for FRDA alongside the only approved therapy, Omav, and support continued development using human iPSC-derived systems.

Yang W, Thompson B, Miellet S et al. · Antioxidants & redox signaling · (2026) · View on PubMed ↗

Peptide LKLKLL is a more effective component of Akkermansia muciniphila which regulate glucolipid metabolism through GLP-1/GIP dual modulation.

This preclinical study examined the Akkermansia muciniphila–derived hexapeptide LKLKLL and its effects on glucolipid metabolism via GLP-1/GIP dual modulation in cell and mouse models. It found that LKLKLL reduced body weight in high-fat diet obese mice, improved glucose tolerance in diabetic models, and enhanced GLP-1 secretion (with GLP-1/GIP dual modulation supported by STC-1 cell findings). These results support LKLKLL as a defined, translational alternative to live A. muciniphila for obesity and diabetes interventions.

Li Y, Ye D, Fu C et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗

Evaluating the pharmacokinetics, efficacy and safety of low-dose cannabidiol.

This article reviewed pharmacokinetics, pharmacodynamics, and safety evidence for low-dose cannabidiol (CBD) at doses ≤2.5 mg/kg or ≤175 mg/day (including oral doses ≤150 mg). It found that low-dose CBD produces peak concentration (Cmax) and exposure (AUC) levels 5- to 100-fold lower than typical Epidiolex (20 mg/kg) dosing, with very limited evidence of physical or neurological effects in healthy volunteers. The review is significant for interpreting real-world low-dose CBD use and for guiding expectations about efficacy and safety relative to approved higher-dose formulations.

Warren WG, Osborn M, Yates A et al. · British journal of clinical pharmacology · (2026) · View on PubMed ↗

Dual-targeting pharmacological UFMylation inhibition reprograms tumor and immune microenvironments to achieve long-term glioblastoma regression.

This study reported two small-molecule UFMylation inhibitors that target the UFMylation E3 ligase complex core protein DDRGK1—osimertinib (via a covalent mechanism) and CP-24 (non-covalent)—and tested their effects on tumor and immune microenvironments in glioblastoma models. The key finding is that both compounds disrupt the DDRGK1–UFL1 interaction, globally suppress UFMylation, inhibit ER-phagy, and induce ER stress, leading to long-term glioblastoma regression with microenvironment reprogramming. Scientifically, it establishes DDRGK1-dependent UFMylation as a druggable vulnerability and provides a mechanistic rationale for combining ER-stress/immune microenvironment modulation in glioblastoma therapy.

Tan P, Liu Z, Hu X et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Activity-based proteomics analysis revealed that DNJ directly targeted ATP5F1 to alleviate high glucose induced cardiomyocyte injury.

This study used activity-based protein profiling (ABPP) to identify direct molecular targets of the natural alkaloid 1-deoxynojirimycin (DNJ) in cardiomyocytes under high-glucose–induced injury conditions. DNJ directly targeted ATP5F1 (a mitochondrial ATP synthase subunit) and alleviated high-glucose–triggered cardiomyocyte injury. Targeting ATP5F1 via DNJ provides a mechanistic basis for developing more specific therapies for diabetic cardiomyopathy.

Li X, Chen Y, Yang H et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗

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Immunotherapy beyond classic checkpoint blockade

First CAR T-Cell Therapy Approved for Solid Tumors.

China studied satricabtagene autoleucel (satri-cel), a claudin 18.2–targeting CAR T-cell therapy, in patients with claudin 18.2-positive, HER2-negative gastric or gastro-esophageal junction cancer. In a phase II trial, the CAR T cells increased progression-free survival and overall survival. This first solid-tumor CAR T approval supports claudin 18.2 as a therapeutic target but highlights the need for further work to improve efficacy in solid tumors.

Cancer discovery · (2026) · View on PubMed ↗

Phase 1/2 study of IMC-C103C, a T cell receptor bispecific (MAGE-A4×CD3) ImmTAC targeting MAGE-A4-expressing malignancies.

This phase 1/2 study evaluated IMC-C103C, a T cell receptor bispecific ImmTAC (MAGE-A4×CD3) targeting MAGE-A4 peptide presented by HLA-A02:01, in advanced solid tumors. In HLA-A02:01+ patients receiving weekly intravenous IMC-C103C with step-up dosing, the trial assessed safety and preliminary anti-tumor activity using dose escalation guided by the mTPI-2 method, alongside pharmacokinetics/pharmacodynamics and biomarker analyses. The study design and early results support clinical development of MAGE-A4-directed T cell engagement for HLA-A*02:01–restricted malignancies.

Sweis RF, Melero I, Davar D et al. · Journal for immunotherapy of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Beyond immune checkpoint blockade: T cell engagers and antibody-drug conjugates in cancer and autoimmune disease.

This review studied next-generation immunotherapies beyond immune checkpoint blockade, focusing on T cell engagers (TCEs) and antibody–drug conjugates (ADCs) in cancer and immune-mediated inflammatory disorders (IMIDs). It found that TCEs can redirect cytotoxic T cells to kill targets independently of MHC restriction, while ADCs deliver cytotoxic payloads via receptor-mediated internalization, potentially addressing resistance and toxicity limitations of checkpoint inhibitors. These mechanistic insights are clinically significant for designing and selecting therapies that better match tumor/immune biology in both oncology and autoimmune disease.

Abdelaziz AM, Shokr MM · Biochemical pharmacology · (2026) · View on PubMed ↗

Therapeutic targeting of CD47 using a tri-specific NK cell engager to inhibit multiple myeloma.

This preclinical study investigated a tri-specific NK cell engager designed to therapeutically target CD47 signaling to inhibit multiple myeloma, focusing on CD47–SIRPα immune escape biology. By blocking CD47, the engager aimed to restore macrophage phagocytosis and NK cell activity, thereby suppressing multiple myeloma growth and overcoming resistance mechanisms. The significance is translational: it supports CD47-directed tri-specific NK engagers as a potential next-generation immunotherapy for refractory multiple myeloma.

Sumankan R, Sungwan P, Boonsatit N et al. · Cancer immunology, immunotherapy : CII · (2026) · View on PubMed ↗ · Free PDF ↗

TANGENT study design: a phase III, randomized study of emactuzumab for the treatment of tenosynovial giant cell tumors.

The TANGENT phase III randomized study evaluated emactuzumab, a CSF-1R inhibiting monoclonal antibody, in patients with tenosynovial giant cell tumors (TGCT) who were not adequately treatable with surgery or had high post-surgical recurrence risk. The trial design targets tumor-associated macrophage reduction by binding the CSF-1R dimerization interface, aiming to improve outcomes while addressing the limitations of long-term CSF-1R pathway inhibitor therapy. If successful, this would support a more durable, mechanism-driven systemic option for TGCT patients who face debilitating local disease and recurrence after surgery.

Gelderblom H, Palmerini E, van de Sande M et al. · Future oncology (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Biomarkers & precision diagnostics (blood/tissue/omics)

Incidence, risk factors and tumor spectrum of second primary cancers after gastric cancer: a multicenter cohort study with long-term follow-up.

This multicenter cohort study evaluated long-term incidence, risk factors, and tumor spectrum of second primary cancers (SPCs) in gastric cancer survivors who underwent curative-intent radical gastrectomy (2007–2021) in the MAGIS cohort. The key findings were not fully visible in the provided abstract text, but the study was designed to quantify SPC risk over time and identify clinical factors associated with SPC occurrence. Clinically, defining SPC detection patterns and stage distribution after gastrectomy could guide long-term surveillance strategies for gastric cancer survivors.

Gao X, Han W, Lu L et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Circulating alpha-1 antitrypsin and its c-terminal peptides differentiate bacterial from viral community-acquired pneumonia.

Researchers studied whether circulating alpha-1 antitrypsin (AAT) and its C-terminal peptides can distinguish bacterial from viral community-acquired pneumonia in 81 prospectively enrolled adults at hospital admission (day 0) and day 3. Using ELISA for AAT and LC–based quantification of nine AAT-derived C-terminal peptides, they tested whether these biomarkers discriminate bacterial versus viral CAP. If validated, this approach could reduce inappropriate antimicrobial use by improving early etiologic diagnosis.

Pashai Fakhri M, Börner FR, Held J et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Genome-wide association analyses of borderline personality disorder identify 11 loci and highlight shared risk with mental and somatic disorders.

This study performed the largest genome-wide association study meta-analysis of borderline personality disorder (BPD) in individuals of European ancestry, using 12,339 BPD cases and 1,041,717 controls for discovery and 685 cases and 107,750 controls for replication. It identified 11 independent associated genomic loci, 9 risk genes in gene-based analyses, and estimated SNP-heritability of 17.3% with polygenic scores predicting 4.6% of BPD liability-scale variance. These findings improve genetic risk mapping for BPD and highlight shared genetic architecture with both mental and somatic disorders, supporting cross-disorder biology for future mechanistic work and risk prediction.

Streit F, Awasthi S, Hall ASM et al. · Nature genetics · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Plasma proteome profiling identified biomarkers for the differential diagnosis and molecular staging of neurodegenerative dementias.

This study used large-scale plasma proteomics to identify blood-based biomarkers for differential diagnosis and molecular staging across major neurodegenerative dementias in 1,318 samples from international cohorts. It found >200 dysregulated proteins across Alzheimer’s disease, dementia with Lewy bodies, and frontotemporal dementia, with glial fibrillary acidic protein most increased along the Alzheimer’s continuum and integrin alpha-V and integrin alpha-M consistently reduced. These proteomic signatures could enable scalable, blood-based stratification of dementia subtype and disease stage, potentially improving clinical diagnosis and monitoring.

Bellomo G, Vermunt L, In ‘t Veld S et al. · Nature aging · (2026) · View on PubMed ↗ · Free PDF ↗

Single-Cell Analysis of Residual Esophageal Squamous Cell Carcinoma After Neoadjuvant Immunochemotherapy Reveals TFAM-Mediated Immunoregulation in Dendritic Cells.

This study performed single-cell analysis on tumor microenvironments from 14 patients with esophageal squamous cell carcinoma (ESCC) undergoing neoadjuvant immunochemotherapy (nICT) to identify cellular programs associated with treatment response. The key finding was that a TFAM-mediated immunoregulation program in dendritic cells emerged as linked to differential residual disease after nICT, with nonnegative matrix factorization (NMF) revealing coordinated immunosuppressive programs associated with minimal or no pathological tumor regression. Scientifically and clinically, these single-cell biomarkers could help predict nICT responsiveness and point to dendritic-cell TFAM pathways as targets to improve outcomes.

Chen L, Feng T, Zhou J et al. · Cancer research · (2026) · View on PubMed ↗

Use of blood-based neurofilament light chain as an endpoint in clinical trials of neurodegenerative conditions: a scoping review.

This scoping review examined interventional neurodegenerative clinical trials (2013–2024) that used blood-based neurofilament light chain (serum or plasma NfL) as an endpoint, summarizing evidence across diseases and study designs. The review found that blood NfL is increasingly used to quantify neuroaxonal injury and can serve as a feasible trial endpoint, with variability in sampling matrices and analytical approaches. Scientifically, consolidating how blood NfL is applied helps standardize endpoint selection and improves interpretability of neurodegeneration trial outcomes.

Zheng Y, Bhalala OG, Chin KS et al. · Journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

Multiomics integrative bioinformatics analysis of gene expression characteristics and molecular mechanisms in preeclampsia placental tissue.

This bioinformatics study integrated multiple placental transcriptome and single-cell RNA-seq datasets from GEO to characterize molecular mechanisms and gene expression features associated with preeclampsia (PE) placental tissue. Using differential expression, Weighted Gene Co-expression Network Analysis (WGCNA), and machine learning to define molecular subtypes and pathways (details truncated), it aimed to identify key dysregulated gene networks driving placental dysfunction. The scientific significance is that it provides candidate PE biomarkers and mechanistic targets that could guide future experimental validation and precision approaches to PE.

Li N, Tian L, Wei H · Artificial cells, nanomedicine, and biotechnology · (2026) · View on PubMed ↗ · Free PDF ↗

Medical Students’ Attitudes, Perceptions, and Self-Reported Familiarity With Artificial Intelligence in Healthcare: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis synthesized studies reporting medical students’ attitudes, perceptions, and self-reported familiarity with artificial intelligence (AI) in healthcare and medical education. It focused on harmonizing constructs across heterogeneous survey instruments and examined heterogeneity, prediction intervals, risk of bias, and certainty of evidence (methods truncated). The clinical/educational significance is that it clarifies how AI literacy and perceptions vary across settings, informing curriculum design and assessment strategies for future clinicians.

Zhang W, Han J, Han X et al. · JMIR medical education · (2026) · View on PubMed ↗ · Free PDF ↗

Associations of viral infections and antiviral vaccinations with anti-NMDAR and other forms of autoimmune encephalitis.

This systematic literature review assessed reported associations between viral infections and antiviral vaccinations and the development of autoimmune encephalitis (AIE), including anti-NMDAR and other AIE subtypes. The key finding was that specific viral infection and vaccination triggers are reported across AIE subtypes with subtype-dependent frequencies rather than a single uniform association. Clinically, the review helps refine immunological trigger hypotheses and supports more informed risk–benefit counseling when evaluating suspected AIE after infections or immunization.

Bamberg S, Schulte-Frankenfeld PM, Kreye J · Brain, behavior, & immunity - health · (2026) · View on PubMed ↗ · Free PDF ↗

Immune checkpoint profiling of B7-H proteins predicts survival and treatment response in metastatic clear cell renal cell carcinoma.

This retrospective cohort study profiled immune checkpoint B7-H family proteins (B7-H3, B7-H4, B7-H5, B7-H7) by immunohistochemistry in primary tumors from 145 patients with metastatic clear cell renal cell carcinoma (ccRCC). The key finding was that B7-H expression patterns—showing intratumoral heterogeneity and compartmentalized localization—predicted survival and treatment response. Scientifically and clinically, it suggests that B7-H checkpoint profiling could help stratify metastatic ccRCC patients for prognosis and potential immunotherapy responsiveness.

Emaldi M, Rey-Iborra E, Mosteiro L et al. · The journal of pathology. Clinical research · (2026) · View on PubMed ↗ · Free PDF ↗

Anatomical and Histologic Response to Neoadjuvant Therapy: Recurrence Patterns Among Poor Responders. A Multi-institutional Observational Cohort Study.

This multi-institutional observational cohort study evaluated how anatomical response to neoadjuvant therapy (NAT), quantified by the Tumor Burden Score ratio (TBSr), and histologic response, assessed by Tumor Regression Grade (TRG), predict recurrence patterns after hepatectomy for colorectal liver metastases (CRLM). It found that integrating TBSr with TRG improves characterization of recurrence patterns among poor responders following NAT. Clinically, this combined macroscopic–histologic response framework could refine post-hepatectomy risk stratification and guide follow-up or additional therapy decisions for CRLM patients.

Baldo A, Akabane M, Elemosho A et al. · Annals of surgery · (2026) · View on PubMed ↗

Sustainable miniaturized smartphone-coupled TLC platform for innovative cleaning validation: application to tizanidine combinations under challenging concentration ratios.

This work developed a sustainable, miniaturized smartphone-coupled thin-layer chromatography (TLC) platform for at-line cleaning validation and applied it to quantify tizanidine (TZN) carryover in the presence of aceclofenac (ACF), ibuprofen (IBF), and paracetamol (PRC) under challenging concentration ratios. The key finding is that the smartphone-coupled miniaturized TLC approach enables rapid, portable determination of TZN in multi-drug mixtures to support routine monitoring of cross-contamination risk. Clinically and operationally, this provides a practical analytical tool to strengthen pharmaceutical cleaning validation for high-risk, narrow-therapeutic-index drugs like tizanidine.

Abd El-Aziz MO, Nadim AH, Monir HH et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Blood-based multimodal biomarker models for differentiating early-onset Alzheimer’s disease from frontotemporal dementia: a longitudinal study of early-onset dementia and family members (LEAF) study.

This longitudinal LEAF study assessed blood-based multimodal biomarker models to differentiate early-onset Alzheimer’s disease (EOAD) from early-onset frontotemporal dementia (EOFTD) in 185 participants (EOAD n=150, EOFTD n=35, age ≤65) using plasma immunoassays for p-tau217, p-tau181, neurofilament light (NfL), and GFAP. Plasma p-tau217 and p-tau181 showed high discriminative performance (AUC 0.831 and 0.862, respectively) for distinguishing EOAD from EOFTD. These data support plasma phospho-tau–based biomarker models for earlier and more accurate diagnosis in early-onset dementia populations.

Kwon HS, Moon SY, Hwang M et al. · Journal of neurology · (2026) · View on PubMed ↗

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Neurodegeneration & protein aggregation/seeding

Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.

This study investigated whether soluble high-molecular-weight amyloid-β (Aβ) species (>150 kDa) isolated from amyloid-β-laden brains can act as aggregation seeds to initiate spreading of Aβ pathology. Intrahippocampal injection of these soluble >150 kDa Aβ species accelerated cerebral β-amyloidosis in amyloid precursor protein transgenic mice compared with controls. Scientifically, it identifies a specific Aβ molecular-weight fraction capable of driving in vivo seeding, informing mechanistic models of Alzheimer’s disease progression.

Kashiwagi-Hakozaki M, Uchigami H, Naka Y et al. · Brain communications · (2026) · View on PubMed ↗ · Free PDF ↗

Distribution of Big Tau Isoforms in the Human Central and Peripheral Nervous System.

This study characterized the distribution and disease relevance of “big tau” isoforms (including exon 4a inclusion) across the human central and peripheral nervous system using mass spectrometry–based sequencing and mapping. It found distinct anatomical patterns of big tau isoform composition in CNS and PNS tissues and assessed changes in postmortem samples from Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and controls. The work is significant because it provides isoform-level neuroanatomical evidence that could improve biomarker development and mechanistic understanding of tau pathology beyond canonical “small” tau.

Koppisetti RK, Barthélemy NR, Horie K et al. · Annals of neurology · (2026) · View on PubMed ↗

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Neuroinflammation & glial/immune mechanisms

Microglial states revisited: from homeostasis to disease.

This review studied microglial state biology across development, brain region, sex, age, genotype, and environment, focusing on how modern omics approaches redefine microglial phenotypes. It found that single-cell/single-nucleus transcriptomics, chromatin accessibility profiling, and spatial multi-omics eliminate simple “resting vs activated” or “M1 vs M2” binaries and instead reveal a multidimensional microglial state space. Scientifically, this reframing supports more precise interpretation of homeostatic versus disease-associated microglial signatures in neurodegeneration and other CNS disorders.

Eggen BJL, Kooistra SM · Nature reviews. Neuroscience · (2026) · View on PubMed ↗

Complement dysregulation during the early phases of synucleinopathy.

This study investigated complement dysregulation during early synucleinopathy, focusing on how pathological aggregated α-syn (alpha-synuclein) may activate complement before overt neurodegeneration in Parkinson’s disease. The key finding (not fully shown in the truncated abstract) is that the work was designed to determine whether complement activation is directly triggered by α-syn pathology rather than only as a secondary response to neuronal loss, using a rat α-syn preclinical model. Clinically, clarifying early complement involvement could identify new immunomodulatory targets to slow progression in synucleinopathies.

Khan H, Gifford M, Kordbacheh A et al. · Acta neuropathologica · (2026) · View on PubMed ↗ · Free PDF ↗

Small Extracellular Vesicles From Cardiomyocytes Activate Microglia Aggravating HFpEF.

The study investigated whether small extracellular vesicles (sEVs) released from cardiomyocytes activate hypothalamic microglia and worsen HFpEF using a mouse model combining a long-term high-fat diet with the nitric oxide synthase inhibitor L-NAME. sEV-driven microglial activation and hypothalamic inflammation were observed, and microglial depletion with the CSF1R inhibitor PLX3397 suppressed downstream sympathetic activation (as reported in the truncated abstract). These findings support a heart-to-brain inflammatory mechanism in HFpEF and suggest that targeting microglia or sEV signaling could be a therapeutic strategy.

Men L, Wang Q, Ren B et al. · Circulation research · (2026) · View on PubMed ↗

Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.

This review synthesized evidence linking gut microbiota-driven metabolites to the development of stress-related mental disorders (e.g., depression, anxiety, and post-traumatic stress disorder). It highlights that microbiota alterations change systemic metabolite profiles that can modulate host physiology and thereby influence stress-disorder pathophysiology. The significance is that metabolite-mediated gut–brain mechanisms may offer actionable biomarkers and therapeutic targets for stress-related psychiatric conditions.

Yuan M, Qin F, Wu L et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗

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RNA biology & epitranscriptomics

RNA exonuclease REXO4 resolves m6A-marked R-loops and suppresses anti-tumor immunity.

This study examined how the RNA exonuclease REXO4 resolves N6-methyladenosine (m6A)-marked R-loops and how this affects anti-tumor immunity. It found that REXO4 resolves RNA–DNA hybrids via 3’-to-5’ exonucleolytic cleavage of the RNA strand, with m6A promoting REXO4 localization to R-loops; REXO4 loss increased DNA damage, triggered interferon responses, and enhanced tumor immune infiltration in mouse models. These results are significant because they link m6A-regulated R-loop homeostasis to innate immune activation, suggesting REXO4 as a potential immunomodulatory target in cancer.

Zhang J, Bao K, Hou Y et al. · Molecular cell · (2026) · View on PubMed ↗ · Free PDF ↗

RNA modifications in cancer: regulators of tumor evolution and therapeutic response.

This review examined how RNA modifications (including m6A, m1A, m5C, m7G, pseudouridine, and A-to-I editing) regulate tumor evolution and therapeutic response by acting through epitranscriptomic “writers,” “readers,” and “erasers.” The key finding is that dysregulated RNA modification networks can control transcript stability and translation efficiency, thereby shaping tumor progression and treatment sensitivity/resistance. Scientifically, it consolidates mechanistic links between epitranscriptomic regulation and actionable therapeutic strategies across cancer contexts.

Gu X, He Y, Xu Z et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗

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Cell stress, autophagy/lysosomes & innate immune signaling

Mitochondrial-derived vesicles drive budding-type fission of damaged lysosomes.

Researchers studied lysosomal renewal under hypoxia–reoxygenation stress and identified a budding-type fission (B-fission) pathway that restores lysosomal function by generating small, functional lysosomes. The key finding is that damaged lysosomes undergo membrane budding and scission independently of autophagic lysosome reformation, and that mitochondrial-derived vesicles (MDVs) deliver the fission adaptor MFF to lysosomes to recruit DRP1. This mechanistic insight links mitochondrial signaling to lysosome integrity, informing how cells maintain degradative capacity during stress.

Luo Y, Yu J, Li Z et al. · Nature cell biology · (2026) · 2 citations · View on PubMed ↗

Structures of dynamic interactors at native proteasomes by PhIX-MS and cryo-electron microscopy.

This structural proteomics study developed PhIX-MS (photo-induced in situ crosslinking-mass spectrometry) and combined it with cryo-electron microscopy to map dynamic interactors at native proteasomes. Using proteasome regulatory particle (RP) preparations, it localized the redox sensor TXNL1 and its dynamic thioredoxin-like domain near RPN2/PSMD1 and RPN13/ADRM1, including structural resolution of RPs without the core particle when bound to TXNL1. The findings are significant because they provide a method to capture transient protein–protein interactions and clarify how TXNL1 positions redox activity at the proteasome.

Lee K, Negi H, Chen X et al. · Molecular cell · (2026) · View on PubMed ↗

The orchestration of ciliary opus: Interplay of signalling molecules, GTPases, and trafficking machinery.

This review studied how primary cilia signaling is orchestrated by the interplay of intraflagellar transport (IFT) machinery, the BBSome coat complex, small GTPases, and trafficking components. It found that kinesin-2 and dynein-2 motors coordinate bidirectional receptor and signaling trafficking, while ciliary lipid composition and secondary messengers such as cAMP and Ca2+ regulate ciliary composition and signaling output. The synthesis is clinically significant because it frames how defects in these trafficking/signaling networks can drive ciliopathies and tissue homeostasis disorders.

Piyush R, Giri P, Shinde SR · Current opinion in cell biology · (2026) · View on PubMed ↗

Mitochondria-targeted MXene-based nanozymes promote mitophagy and inhibit mtDNA-triggered cGAS/STING inflammation in osteoarthritis.

This preclinical study developed a mitochondria-targeted MXene-based nanozyme (MS@PMXene-TK) incorporating a mitochondria-targeting peptide (MTP-131) and a ROS-responsive thioketal-linked PEG shell to treat osteoarthritis by promoting mitophagy and suppressing mtDNA-triggered cGAS/STING inflammation. The key finding was that the nanozyme promoted mitophagy and inhibited mtDNA–cGAS/STING inflammatory signaling, thereby supporting cartilage repair-related effects. These results suggest a subcellularly targeted nanotherapeutic strategy for OA that directly addresses mitochondrial dysfunction and innate immune activation.

Li T, Zheng A, Zhu C et al. · Bioactive materials · (2026) · View on PubMed ↗ · Free PDF ↗

Divergent Autophagy Pathways in Plasmodium: Mechanisms, Functions, and Therapeutic Potential.

This review studied autophagy mechanisms in the malaria parasite Plasmodium, focusing on the reduced but functional autophagy-related (ATG) protein repertoire and the ubiquitin-like marker ATG8. It found that Plasmodial autophagy shows divergent, branched localization of ATG8 with association to the apicoplast membrane, implying roles beyond canonical bulk autophagy. These parasite-specific autophagy features suggest new therapeutic targets for malaria by exploiting differences in ATG8/ATG8-dependent pathways versus yeast and mammalian systems.

Rajput S, Mehra P, Nandi R et al. · Molecular microbiology · (2026) · View on PubMed ↗

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Gene regulation & genome architecture

Mechanism of actin thin filament pointed-end elongation by leiomodin.

This mechanistic study investigated how leiomodin (Lmod), particularly leiomodin-2 (Lmod2), promotes actin thin filament pointed-end elongation in striated muscle systems where actin exchange is normally biased to the pointed end. The key finding (from the provided context) is that Lmod2 acts as an additional regulator of pointed-end actin filament growth alongside capping proteins such as tropomodulin (Tmod) and CapZ, helping explain how uniform thin-filament length is maintained. This advances understanding of sarcomere assembly and turnover, with implications for muscle physiology and potential myopathy mechanisms.

Brotzman SB, Palmer NJ, Boczkowska M et al. · Nature communications · (2026) · 2 citations · View on PubMed ↗ · Free PDF ↗

Promoter strength and position govern promoter competition through transcript-dependent insulation.

This study examined how promoter strength and genomic position govern promoter competition within the Sox2 regulatory landscape by inserting diverse promoters into defined genomic sites at the Sox2 locus. It found that the reduction in endogenous Sox2 transcription correlated with inserted promoter strength, that competition required transcription from the inserted promoter, and that longer transcripts increased competition via transcript-dependent insulation. Scientifically, these results define rules for how promoter transcriptional units insulate and compete, informing models of gene regulation in development and disease.

Koska M, Nagano M, Swigut T et al. · Nature genetics · (2026) · View on PubMed ↗

Ligand regulation and function of preformed EGFR dimers.

This study used cryo-electron microscopy to determine the structural basis of ligand regulation and function of preformed epidermal growth factor receptor (EGFR) dimers. The key finding was a detailed structural view showing how preformed EGFR dimers are regulated by ligands, refining the classic ligand-induced dimerization model for EGFR activation. Scientifically, this provides a mechanistic framework that can inform rational design of EGFR-targeted therapeutics and improve understanding of receptor tyrosine kinase signaling in disease.

Zuo Y, Schwartz HT, Walker K et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

A genome-wide functional analysis of conserved intronic regions reveals essential roles for speckle-associated retained introns.

This genome-wide functional study used a dual CRISPR-Cas editing strategy to delete 2,600 conserved human intronic regions enriched for intron retention, focusing on speckle-associated retained introns in human cells. The key finding was that a subset of these conserved “fitness” intronic sequences affects cell growth by altering intron retention and host gene expression, with deletions in nuclear speckle-associated retained introns in FNBP4 and DDX5 producing downstream effects on gene regulation. Scientifically, it establishes an essential role for speckle-associated retained introns in regulating gene expression and cellular fitness.

Farhangmehr S, Braunschweig U, Wu M et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious disease & antiviral strategies

Viral syncytia evolve to resist interferon.

This study examined how SARS-CoV-2–mediated syncytia formation affects viral evolution toward interferon resistance using SARS-CoV-2 and Spike (S) replacement vesicular stomatitis virus (VSV) in cultured cells, human lung cell cultures, and hACE2 transgenic mice. It found that S-mediated syncytia impair interferon antiviral effects and that Spike amino-acid substitutions modulating syncytia formation in Delta and Omicron similarly modulate interferon resistance, also reducing antibody-mediated neutralization. These results suggest syncytia can be a selectable viral trait that helps SARS-CoV-2 evade innate immunity and humoral responses.

Li T, Kang I, Ye J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Mapping in-cell protein contact sites reveals hijacking of paraspeckles during influenza A virus infection.

This work applied in-cell cross-linking mass spectrometry combined with structural modeling and functional assays to map native protein contact sites during influenza A virus infection in human cells. It revealed previously unrecognized virus–host interactions, including hijacking of paraspeckles, and identified host factors linked to maturation of distinct haemagglutinin glycoforms via the membrane-bound endoplasmic reticulum–Golgi system. The approach and interaction map provide mechanistic targets for antiviral strategies by defining spatially organized host processes exploited by influenza.

Kotova I, Mühlberg L, Gilep K et al. · Nature microbiology · (2026) · View on PubMed ↗ · Free PDF ↗

Viral protease-initiated lytic cell death as a universal antiviral mRNA therapy.

This preclinical study developed viral protease-initiated lytic cell death (VID), a universal antiviral mRNA platform, by engineering gasdermin-D (GSDMD) with viral protease-specific cleavage motifs to create VID activators (VIDAs). In a hepatitis A virus (HAV) mouse model, lipid nanoparticle (LNP)-encapsulated VIDA mRNA selectively triggered lytic death in infected cells, abolished viral replication and shedding, and mitigated liver injury. The work is significant because it proposes a broadly applicable mRNA antiviral strategy that uses viral protease activity to drive targeted cell killing.

Li L, Yan XL, Wang HY et al. · Cell · (2026) · View on PubMed ↗

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Host-directed anti-inflammatory therapies

All-trans retinoic acid suppresses systemic inflammation induced by severe fever with thrombocytopenia syndrome virus in mice.

This study examined all-trans retinoic acid (ATRA) in the context of severe fever with thrombocytopenia syndrome virus (SFTSV) infection, first correlating patient serum vitamin A/ATRA depletion with clinical severity and then testing ATRA in an SFTSV mouse model. ATRA administration suppressed virus-induced systemic hyperinflammation through a PPARγ-dependent mechanism that downregulated macrophage AP-1 transcriptional activity. These results support ATRA as a potential host-directed anti-inflammatory therapy to reduce mortality risk during SFTSV infection.

Yu X, Wu J, Yin X et al. · Nature microbiology · (2026) · View on PubMed ↗

Endothelial cell-intrinsic NOD2 signaling regulates the intestinal immune response through the generation of effector and memory T cells.

This study investigated how endothelial cell-intrinsic NOD2 signaling regulates intestinal immunity by driving effector and memory T cell generation, focusing on Crohn’s disease-relevant NOD2 biology. It showed that NOD2 engagement by muramyl dipeptide coordinates innate–adaptive immune cross-talk to promote T cell homing and differentiation programs that maintain intestinal homeostasis. The findings clarify how NOD2 variants can paradoxically increase Crohn’s disease risk despite NOD2 ligands being immunostimulatory, informing therapeutic strategies targeting NOD2 pathways.

Tsankov BK, Denney M, Ahn JSY et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗

NOD1/2 signaling in macrophages drives adaptive immune resistance in cancer.

This study tested whether NOD1/2 signaling in macrophages controls adaptive immune resistance to cancer therapies, using murine tumor models and mechanistic perturbations. It found that genetic ablation of NOD1/2 or RIPK2 and pharmacologic inhibition of NOD1/2 enhanced responses across multiple antitumor modalities, including immune checkpoint blockade, adoptive T-cell therapy, and cytotoxic chemotherapy. These results identify macrophage NOD1/2 signaling as a druggable resistance pathway that could be targeted to improve the efficacy of diverse cancer treatments.

Wei X, Yang L, Wang Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials in immunology/hematology

The 2026 British Society for Rheumatology guideline for pain management in people with inflammatory arthritis.

This work presents the 2026 British Society for Rheumatology guideline for pain management in people with inflammatory arthritis, synthesizing evidence on pharmacologic and non-pharmacologic approaches. It highlights that UK practice often relies on long-term opioids and gabapentinoids despite limited trial evidence for efficacy, and it emphasizes underused supportive non-pharmacological pain care. The guideline provides an evidence-based, UK-specific framework to improve pain outcomes and reduce reliance on interventions with weak efficacy evidence in inflammatory arthritis.

Scott IC, Smith TM, Babatunde O et al. · Rheumatology (Oxford, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Immune-Enhancing Nutrition and Outcomes After Radical Cystectomy: A Randomized Clinical Trial.

This multicenter, randomized, double-blind phase 3 clinical trial (SWOG S1600) studied whether perioperative specialized immunonutrition reduces 30-day complications compared with standard oral nutrition support in adults undergoing radical cystectomy for bladder cancer. The key finding was that immune-enhancing nutrition improved perioperative outcomes by reducing complications within 30 days relative to standard nutrition support. Clinically, it supports using targeted immunonutrition as an adjunct to surgery to lower morbidity in patients undergoing radical cystectomy.

Hamilton-Reeves JM, Unger JM, Holzbeierlein JM et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Abemaciclib rechallenge after progression on abemaciclib plus endocrine therapy in patients with hormone receptor-positive HER2-negative metastatic breast cancer: results from the phase II again study (WJOG14220B).

This phase II again study evaluated abemaciclib rechallenge in hormone receptor-positive, HER2-negative metastatic breast cancer patients who progressed after prior abemaciclib plus endocrine therapy, using a single-arm design. Patients were switched between aromatase inhibitor/tamoxifen and fulvestrant while continuing abemaciclib, with progression-free survival as the primary endpoint. Clinically, the study tests whether continuing abemaciclib after progression can recapture benefit, informing treatment sequencing after CDK4/6 inhibitor exposure.

Nishimura M, Kogawa T, Sugiyama K et al. · Breast cancer research and treatment · (2026) · View on PubMed ↗ · Free PDF ↗

Caffeine and Cardiovascular Disease: A Scientific Statement From the American Heart Association.

This American Heart Association scientific statement reviewed evidence on caffeine intake and cardiovascular disease outcomes across human observational studies and differing patterns of acute versus chronic consumption. Overall, the relationship between caffeine and cardiovascular risk appears complex and heterogeneous, with many studies suggesting an inverse J-shaped association for naturally occurring caffeinated beverages and effects that vary by individual propensity and caffeine source. Clinically, the statement emphasizes that cardiovascular guidance should consider dose/timing, beverage type, and patient-level factors rather than assuming a uniform cardiovascular effect of caffeine.

Marcus GM, Hu FB, van Dam RM et al. · Circulation · (2026) · View on PubMed ↗

Deucravacitinib in Active Psoriatic Arthritis: Efficacy and Safety up to 52 Weeks From the Randomized, Double-Blind, Phase 3 POETYK PsA-2 Trial.

The POETYK PsA-2 phase 3 randomized, double-blind trial evaluated the efficacy and safety of deucravacitinib, an oral selective TYK2 inhibitor, in patients with active psoriatic arthritis (PsA) who were biologic-naïve or previously treated with TNF inhibitors. Up to 52 weeks, patients were randomized to deucravacitinib 6 mg daily, placebo, or apremilast 30 mg twice daily (safety reference), with the primary endpoint based on ACR20 improvement (details truncated). If efficacy and safety are confirmed through week 52, deucravacitinib would strengthen evidence for TYK2 inhibition as a longer-term oral treatment option in PsA across different prior treatment backgrounds.

Mease PJ, Chandran V, Armstrong AW et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

Ruxolitinib cream in adults with moderate atopic dermatitis after failure of other topicals: A randomized trial.

This randomized trial studied ruxolitinib cream in adults (≥18 years) with moderate atopic dermatitis (IGA 3, EASI >7, itch NRS ≥4) who had inadequate response, intolerance, or contraindications to topical corticosteroids (TCS) and topical calcineurin inhibitors (TCI) in the prior 12 months (TRuE-AD4, NCT06238817). The 8-week results reported improved atopic dermatitis signs/symptoms versus baseline after escalation to ruxolitinib cream following TCS/TCI failure. These findings support ruxolitinib cream as a targeted topical JAK inhibitor option for adults needing non-steroid/non-calcineurin-inhibitor therapy in moderate disease.

Carrascosa JM, Prajapati VH, Hong HC et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting BLyS and APRIL with Telitacicept versus Conventional Immunotherapy in Generalized Myasthenia Gravis: A Comparative Study.

This retrospective real-world comparative study evaluated telitacicept versus conventional immunotherapy in patients with acetylcholine receptor antibody–positive generalized myasthenia gravis (AChR-Ab+ gMG), including 215 total patients with propensity score matching (35 per group). The key finding was that telitacicept showed treatment responses and safety outcomes that could be compared with conventional immunotherapy in a broader AChR-Ab+ population than typical randomized trials. Clinically, it provides real-world evidence supporting telitacicept’s effectiveness and tolerability for AChR-Ab+ gMG in routine practice.

Yang Y, Kang N, Zhu Y et al. · ImmunoTargets and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Temporal variability in outcomes of identical regimens across newly diagnosed myeloma trials: a systematic review.

This systematic review analyzed temporal variability in progression-free survival (PFS) outcomes for identical myeloma regimens across newly diagnosed myeloma trials, focusing on bortezomib/lenalidomide/dexamethasone (VRd) and lenalidomide/dexamethasone (Rd) without transplant. The key finding was that PFS for the same regimen varied across trials over time, consistent with changes in patient populations and trial conduct (including informative censoring and diagnostic reclassification affecting prior smoldering myeloma). Scientifically and clinically, it cautions against naive cross-trial comparisons and highlights factors that can bias apparent regimen efficacy trends.

Mohyuddin GR, Vaquera-Alfaro HA, Godara A et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Redefining functional high-risk multiple myeloma in the context of upfront quadruplet therapy and autologous stem cell transplantation.

This analysis studied how to redefine functional high-risk (FHR) multiple myeloma in the era of upfront quadruplet therapy plus autologous stem cell transplantation (QUAD + ASCT) using 310 newly diagnosed MM patients. The key finding was that the historical FHR definition based on progression within 18 months and expected overall survival <2 years may not optimally capture risk under modern QUAD + ASCT treatment, prompting an updated FHR cutoff and associated outcome factors. This helps clinicians stratify patients more accurately for prognosis and treatment planning in contemporary MM care.

Ravi G, Dhakal B, Callander NS et al. · Cancer · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

γδ T cells show distinct responses to CMV after stem cell transplantation.

This study examined how γδ T cells respond to cytomegalovirus (CMV) after allogeneic hematopoietic stem cell transplantation (aHSCT) by tracking clonal dynamics over time. Using longitudinal single-cell RNA sequencing combined with paired T cell receptor sequencing across five post-transplant time points, it found patient-specific expansion of non-Vγ9Vδ2 γδ T cell clones, particularly within Vδ1+ and Vδ3+ subsets, associated with differences in CMV reactivation status. The work is significant because it defines clonal, subset-specific γδ T cell response patterns to CMV that could inform immune monitoring and risk stratification after aHSCT.

Sibbertsen F, Song Z, Ly C et al. · Journal of molecular medicine (Berlin, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Efficacy of magnesium-calcium ionic oral rinse for primary burning mouth syndrome: a randomized, double-blind, placebo-controlled trial.

This randomized, double-blind, placebo-controlled trial tested a magnesium–calcium ionic oral rinse for efficacy and safety in patients with primary burning mouth syndrome (BMS). The magnesium–calcium rinse improved outcomes compared with placebo (with effects attributed to modulation of the oral mucosal ionic microenvironment). A locally delivered ionic rinse could offer a safer, non-systemic treatment strategy for chronic orofacial neuropathic pain in primary BMS.

Carrió N, Garawani BE, Alahmad A et al. · BMC oral health · (2026) · View on PubMed ↗ · Free PDF ↗

Eltrombopag Added to Standard Immunosuppressive Treatment as Front-Line Therapy for Severe Aplastic Anemia: Long-Term Outcomes of the Phase-3 Randomized Superiority EBMT-SAAWP RACE Study.

This phase 3 randomized superiority trial (EBMT-SAAWP RACE; NCT02009747) evaluated whether adding eltrombopag to front-line immunosuppressive therapy improves long-term outcomes in 197 treatment-naïve patients with severe aplastic anemia, comparing horse ATG plus cyclosporine A (hATG/CsA) versus hATG/CsA plus eltrombopag 150 mg/day. The 2-year analysis showed a significantly higher cumulative incidence of complete response with eltrombopag added to standard IST. The long-term benefit supports eltrombopag as an effective intensification strategy for severe aplastic anemia induction therapy.

Risitano AM, Iacobelli S, Kulasekararaj A et al. · American journal of hematology · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials in cardiometabolic disease

EndoBridge 2025: pearls and highlights.

EndoBridge 2025 was studied as a scientific meeting (not a biomedical experiment) covering endocrinology and metabolism topics across disorders of the pituitary, thyroid, adrenal glands, bone metabolism, neuroendocrine tumors, diabetes, obesity, clinical nutrition, and lipid abnormalities. The key finding is that the congress delivered state-of-the-art lectures and interactive case discussions with a broad expert audience. Scientifically and clinically, it provides an updated synthesis of current endocrinology research and practice themes for clinicians and researchers.

Yildiz BO, Armenti M, Brandi ML et al. · Hormones (Athens, Greece) · (2026) · View on PubMed ↗

Patient-reported Outcomes After Prostate Stereotactic Body Radiotherapy at 5 yr: Results from the PACE-B Trial.

This analysis reported patient-reported outcomes at 5 years from the phase 3 PACE-B trial in men with localized prostate cancer randomized to stereotactic body radiotherapy (SBRT) versus conventionally fractionated radiotherapy (CRT). At 5 years, urinary incontinence outcomes were favourable and comparable between SBRT and CRT, with leak-free rates reported as 64% (164/…). The PROMs complement oncologic endpoints and help patients and clinicians weigh long-term functional outcomes when choosing between SBRT and CRT.

Cooper S, Patel J, Moore C et al. · European urology · (2026) · View on PubMed ↗ · Free PDF ↗

Multidomain Lifestyle Intervention in Mild Cognitive Impairment: Subgroup Analysis of the SUPERBRAIN-MEET Randomized Trial.

This prespecified subgroup analysis of the 24-week SUPERBRAIN-MEET randomized controlled trial studied whether the cognitive benefits of a multidomain lifestyle intervention (MLI) delivered via face-to-face sessions plus digital platforms differed by sociodemographic factors, digital readiness, baseline cognitive status, and vascular risk profiles in people with mild cognitive impairment (MCI). The key finding was that the intervention’s cognitive effects varied across these baseline subgroup characteristics rather than being uniform across all participants. Clinically, this supports tailoring multidomain lifestyle programs for MCI based on patient digital readiness, baseline cognition, and vascular risk to maximize dementia-prevention benefit.

Kim DA, Lee SM, Sun K et al. · Neurology · (2026) · View on PubMed ↗

Does Characterization of Phenotypic Heterogeneity Provide Mechanistic Insights or Influence the Response to Treatment? Experience in Positive and Neutral Trials in Patients With Heart Failure and a Preserved Ejection Fraction.

This article reviewed and analyzed whether characterizing phenotypic heterogeneity in heart failure with preserved ejection fraction (HFpEF) improves mechanistic understanding or treatment response, drawing on experience from positive and neutral HFpEF trials. The key finding was that despite extensive subgrouping efforts, phenotypic heterogeneity characterization has not reliably identified consistent responders to therapy in neutral trials. Clinically, it argues for more rigorous, mechanism-driven approaches (rather than purely descriptive phenotyping) to develop effective HFpEF treatments.

Packer M, Schiattarella GG, Petrie MC et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗

Accelerated Epigenetic and Inflammatory Aging and Intrinsic Capacity.

This population-based cohort study examined cross-sectional and longitudinal associations between accelerated epigenetic and inflammatory aging and intrinsic capacity (IC), including domain-specific IC and sex differences, in older adults. The key finding was that faster epigenetic and inflammatory aging was associated with lower global intrinsic capacity over time, with evidence for interactions between epigenetic and inflammatory aging in relation to IC decline. Scientifically and clinically, it links molecular aging signatures to functional capacity, supporting preventive, function-oriented strategies for healthy longevity.

Rouch L, De Souto Barreto P, Rolland Y et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Implications of the 2026 Dyslipidemia Guideline for Primary Prevention Statin Therapy.

This study modeled the population health impact of the 2026 American Heart Association/American College of Cardiology/multisociety dyslipidemia guideline on primary prevention statin eligibility among nonpregnant adults aged 30–79 years without known ASCVD using NHANES 2017–2023 data. The guideline’s updated ASCVD risk estimation and expanded statin-eligible populations were projected to change the proportion of adults recommended for statin therapy. These findings are significant for anticipating downstream effects on cardiovascular prevention at a national scale and for planning implementation of the 2026 guideline in routine primary care.

Anderson TS, Wilson LM, Sussman JB · JAMA · (2026) · View on PubMed ↗ · Free PDF ↗

Effects of Lifestyle Modification on Intrapancreatic Fat Deposition: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis evaluated whether lifestyle modification interventions reduce intrapancreatic fat deposition (IPFD) in humans by synthesizing PubMed/Embase studies. Across included trials, lifestyle changes showed beneficial effects on IPFD, supporting IPFD as a modifiable ectopic fat depot linked to pancreatic disease risk. Clinically, the results strengthen the rationale for lifestyle-based metabolic interventions to target pancreatic fat accumulation, potentially lowering future endocrine and exocrine pancreatic complications.

Ahmad S, Sul HH, Danpanichkul P et al. · Current obesity reports · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonists and All-Cause Overdose Risk in Veterans With Type 2 Diabetes and Opioid Use Disorder.

This target trial emulation study used Veterans Health Administration data to compare overdose risk among Veterans with type 2 diabetes and opioid use disorder who initiated semaglutide or tirzepatide versus other diabetes medications. The analysis found that GLP-1 receptor agonist initiation was associated with a lower all-cause overdose risk compared with the comparator diabetes therapies. Clinically, these findings—if confirmed—support GLP-1RA consideration as a potential adjunct strategy to reduce overdose risk in high-risk OUD populations.

Kennedy KP, Bremseth-Vining R, Lynch KG et al. · The Journal of clinical psychiatry · (2026) · View on PubMed ↗

Gut Metabolism Links Precision Nutrition, Exercise, and Healthspan in Drosophila melanogaster.

This Drosophila melanogaster study tested whether gut metabolism can link precision nutrition, exercise, and healthspan by combining methionine restriction (MR), taurine supplementation (Tau), and moderate exercise on a chemically defined diet (CDD). The multimodal intervention additively extended lifespan while preserving reproductive capacity and improving locomotor function, and stable isotope tracing with targeted metabolomics indicated increased mitochondrial TCA cycle flux and improved gut redox homeostasis. Scientifically, it links specific gut metabolic shifts to concurrent longevity and performance benefits, informing how dietary and activity interventions may be optimized to avoid trade-offs.

Wei F, Liu S, Sun Y et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗

Durability and Safety of Imeglimin as an Add-On to DPP-4 Inhibitors in Japanese Type 2 Diabetes: The 104-Week FAMILIAR Trial.

This multicenter randomized placebo-controlled trial (FAMILIAR) evaluated imeglimin as an add-on to DPP-4 inhibitors in Japanese adults with type 2 diabetes inadequately controlled on DPP-4 monotherapy, including a 24-week double-blind phase followed by an 80-week open-label extension (104 weeks total). The key finding was that imeglimin maintained glycemic efficacy over 104 weeks with an acceptable long-term safety profile, with particular attention to elderly patients. Clinically, it supports imeglimin as a durable, well-tolerated intensification strategy for Japanese patients already on DPP-4 inhibitors.

Shimoda M, Osonoi T, Iwamoto M et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Electroacupuncture Treatment on Sarcopenia in Patients Undergoing Maintenance Haemodialysis: An Effective Therapy.

This randomized controlled clinical study evaluated electroacupuncture (EA) as a treatment for sarcopenia in patients undergoing maintenance haemodialysis (MHD), comparing an EA group to a control group. It found that EA delivered over 24 sessions (30 minutes, three times per week) improved outcomes related to sarcopenia versus usual care/lifestyle continuation. Clinically, the results support EA as a potentially effective adjunct therapy to improve muscle health in MHD patients with sarcopenia.

Chen R, Qian Q, Wang B et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗ · Free PDF ↗

Frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity in Chinese middle-aged and older adults.

This study analyzed whether frailty mediates the association between sleep duration and physical, psychological, and cognitive multimorbidity (PPC-MM) in Chinese middle-aged and older adults using CHARLS data. Using multivariate logistic regression and Cox proportional hazards models (with nonlinear dose-response assessed by restricted cubic spline analysis), it found that frailty partially explains how sleep duration relates to PPC-MM risk over cross-sectional and longitudinal follow-up. The findings are clinically relevant because they suggest that targeting frailty may reduce multimorbidity risk associated with abnormal sleep duration.

Ding H, Li L, Luo G et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗

Sodium bicarbonate therapy in severe metabolic acidemia: an individual patient data meta-analysis of the BICAR-ICU and BICAR-ICU2 trials.

This individual patient data meta-analysis pooled the BICAR-ICU and BICAR-ICU2 randomized trials to test intravenous sodium bicarbonate therapy in adults with severe metabolic acidemia (pH ≤ 7.20), comparing bicarbonate titrated to pH ≥ 7.30 versus no bicarbonate. The key finding is the trial-level, patient-level estimate of effects on 90-day mortality and renal replacement therapy (RRT) use, including exploration of heterogeneity across prespecified subgroups. The significance is that it provides higher-resolution evidence to guide bicarbonate use in severe metabolic acidemia and identify which patient subgroups may benefit.

Fosset M, Pensier J, Jabaudon M et al. · Critical care (London, England) · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Work-to-sleep ratio as a novel marker of NAFLD risk: evidence from U.S. and Korean national cohorts.

This cohort study evaluated whether the work-to-sleep ratio (WSR)—a combined behavioral metric of occupational time relative to sleep recovery—predicts risk of NAFLD/MASLD using U.S. and Korean national cohorts. The key finding is that WSR functions as a novel risk marker for NAFLD risk beyond what work hours or sleep duration alone capture. Clinically, it suggests that WSR could be used for risk stratification and prevention strategies targeting lifestyle balance in metabolic liver disease.

Zhong Y, Kou Y, Lu Z et al. · Nutrition & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Clinical trials in respiratory/ENT & pulmonary care

Phase III LUNA clinical programme: design of four randomised, double-blind, placebo-controlled studies assessing the efficacy and safety of tozorakimab in patients with symptomatic COPD and a high risk of exacerbations.

This article describes the design of the phase III LUNA clinical programme, consisting of four randomized, double-blind, placebo-controlled studies of tozorakimab in symptomatic COPD patients with a high risk of exacerbations. It targets IL-33 dysregulation by using an anti-IL-33 monoclonal antibody that inhibits both IL-33 reduced (IL-33red) and oxidised (IL-33ox) forms, enrolling participants on optimized inhaled therapy. The programme aims to establish efficacy and safety of IL-33 blockade to reduce exacerbations in a clinically high-risk COPD population.

Watz H, Sciurba FC, Bonini M et al. · BMJ open respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

COVID-19 and Global Perinatal Health: Lessons Learned on Maternal-Neonatal Outcomes, Infant Feeding Practices, and Health Care Economics across Income Settings.

This narrative review synthesized evidence on how the COVID-19 pandemic affected maternal–neonatal outcomes, infant feeding practices, and health care economics across high-income countries (HICs) and low- and middle-income countries (LMICs). It found that SARS-CoV-2 infection and health-system disruption together worsened perinatal outcomes and altered breastfeeding practices, with substantial financial burden on maternal–newborn care systems that differed by income setting. These cross-setting findings highlight where pandemic preparedness and maternal–newborn service continuity (including breastfeeding support) should be prioritized to reduce inequities.

Gunasekaran V, Woo S, Shetty AK et al. · American journal of perinatology · (2026) · View on PubMed ↗

Use of tezepelumab for chronic rhinosinusitis with nasal polyps by eosinophilic endotype: WAYPOINT post-hoc analysis.

This post-hoc analysis evaluated tezepelumab 210 mg versus placebo every 4 weeks in Japanese adults with severe chronic rhinosinusitis with nasal polyps (CRSwNP), stratified by eosinophilic chronic rhinosinusitis endotypes defined using the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis (ECRS). Tezepelumab improved nasal polyp outcomes and related clinical measures across eosinophilic subgroups while maintaining an acceptable safety profile. The results support using tezepelumab for CRSwNP patients enriched for eosinophilic disease biology, informing more targeted biologic selection in Japan.

Fujieda S, Otori N, Han JK et al. · Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of high-dose versus standard-dose influenza vaccines on hospitalisation outcomes and mortality in older adults: a systematic review and meta-analysis.

This systematic review and meta-analysis studied randomized controlled trials comparing high-dose inactivated influenza vaccine (HD-IIV; 60 μg haemagglutinin per strain) versus standard-dose inactivated influenza vaccine (SD-IIV) in adults aged 65 years or older. It found differences in hospitalization and mortality outcomes favoring one dosing strategy (HD-IIV) across the pooled evidence base, with safety considerations assessed alongside efficacy. The findings are important for immunization policy in older adults where maximizing protection against severe influenza is a priority.

Zhao W, Lian R, Zhao Y et al. · The lancet. Healthy longevity · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Global, regional, and national burden of road injuries 1990-2023: a systematic analysis for the Global Burden of Disease Study 2023.

This Global Burden of Disease Study 2023 analysis estimated the global, regional, and national burden of road injuries (incidence, mortality, and morbidity) for 204 countries and territories from 1990 to 2023. It found substantial and persistent road-injury burdens with marked geographic variation, enabling identification of intervention gaps relative to road-safety targets. These estimates are scientifically and policy significant for tracking progress toward the UN Decade of Action for Road Safety and targeting prevention resources.

The Lancet. Public health · (2026) · View on PubMed ↗ · Free PDF ↗

Clesrovimab in Infants at Increased Risk For Severe Disease During 2 RSV Seasons: A Randomized Clinical Trial.

This randomized clinical trial evaluated clesrovimab, a long-acting monoclonal antibody, in infants at increased risk for severe respiratory syncytial virus (RSV) disease across two RSV seasons, comparing clesrovimab (105 mg) versus palivizumab in season 1 and assessing safety of 210 mg clesrovimab in season 2. The key finding was that clesrovimab was safe and tolerable in this high-risk infant population across the subsequent RSV seasons. Clinically, it provides evidence to support extended prophylaxis strategies with clesrovimab for infants who remain at risk for severe RSV after an initial season.

Zar HJ, Bont LJ, Manzoni P et al. · JAMA pediatrics · (2026) · View on PubMed ↗ · Free PDF ↗

Prone positioning in ARDS.

This article reviewed the evidence and clinical role of prone positioning in acute respiratory distress syndrome (ARDS), including early use in intubated patients with PaO2/FiO2 <150 mmHg and the awake prone position (APP) approach in non-intubated patients. It reports that prone positioning consistently improves oxygenation and has evolved from rescue therapy to an integral lung-protective ventilation strategy, with APP requiring further confirmation outside COVID-19 settings. The significance is practical: it supports prone positioning as a core ARDS intervention while highlighting where additional routine ICU evidence is still needed.

Ehrmann S, Li J, Liu L et al. · Intensive care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.

This study analyzed airway transcriptomic profiles to identify molecular pathways distinguishing type 2 (T2) cytokine biomarker-high versus biomarker-low severe asthma. Using bronchial biopsies and brushes from the UK Refractory Asthma Stratification Programme cohort (18 T2-high, 23 T2-intermediate, 11 T2-low) plus 20 healthy controls, and comparing pre- and post-treatment with high-dose inhaled corticosteroids, it reported widespread gene dysregulation across T2 strata (truncated). Scientifically, it helps explain persistent airway pathology when T2 activity is suppressed and may support biomarker-driven endotyping and targeted therapy development.

Shen J, Chaudhuri R, Bicknell S et al. · Allergy · (2026) · View on PubMed ↗ · Free PDF ↗

PROSPECT guideline for total hip arthroplasty: updated systematic review and procedure-specific postoperative pain management recommendations.

This updated PROSPECT guideline systematic review evaluated evidence from randomized controlled trials and systematic reviews (Jan 2020–Jun 2024) to update procedure-specific postoperative pain management recommendations for elective primary total hip arthroplasty. It specifically incorporates new evidence on motor-sparing regional techniques and peri-operative analgesic strategies to improve pain control and functional recovery (details truncated). Clinically, the guideline aims to standardize safer, more effective postoperative analgesia after total hip arthroplasty based on the most recent comparative evidence.

Carella M, Bugada D, Van de Velde M et al. · Anaesthesia · (2026) · View on PubMed ↗ · Free PDF ↗

Hemoperfusion during extracorporeal membrane oxygenation: an updated systematic review and meta-analysis of 8,151 patients.

This systematic review and meta-analysis evaluated clinical efficacy and safety of hemoperfusion in adults receiving extracorporeal membrane oxygenation (ECMO), comparing ECMO plus hemoperfusion (ECMO+HP) versus ECMO alone across 8,151 patients. The key finding is the pooled assessment of all-cause mortality (primary outcome) and safety outcomes, with subgroup analyses by study design (RCT vs non-RCT), ECMO type (VA vs VV), and etiology (cardiogenic shock vs cardiac arrest). Clinically, it aims to clarify whether adding hemoperfusion to ECMO improves survival and outcomes in critically ill adult populations.

Xie T, Yang C, Tao H et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

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Generated automatically on July 28, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.