PubMed Trending Research Digest — July 20, 2026
A curated digest of 99 trending PubMed articles, automatically categorised and summarised across 15 research areas.
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PubMed Trending Research Digest — July 20, 2026
Automated digest · 99 articles · 15 research areas · July 20, 2026
Overview
Across this week’s set of papers, a dominant theme is the convergence of metabolism, epigenetics, and immune regulation in disease—especially cancer and neurodegeneration. Multiple studies connect metabolic state changes (e.g., lactate-linked lactylation; lipid metabolic reprogramming; copper/cuproptosis; lipid peroxidation–ferroptosis) to gene regulation mechanisms (chromatin remodeling, ubiquitin/deubiquitinase axes, and transcriptional networks) that then shape tumor growth, metastasis, and therapy resistance. In parallel, several neuro-focused works highlight how inflammatory and immune pathways (microglial P2X4R regulation, brain macrophage phagocytosis balance, mtDNA–cGAS–STING signaling, and microbiota-derived metabolite signaling such as SCFAs) can drive neurodegenerative progression and represent actionable targets.
A second major thread is translational measurement and delivery technologies that enable earlier diagnosis, better stratification, or more effective treatment. Examples include plasma proteomics/ML for distinguishing fibrotic hypersensitivity pneumonitis from IPF, cfDNA fragmentomics tied to chromatin states, and tau-focused assays/tracers (including a new TDP-43 PET tracer and blood-based BD-tau immunoassay). On the therapeutic side, several studies advance delivery platforms (thermoresponsive intratumoral hydrogels for gemcitabine, nanozyme–hydrogel systems for intervertebral disc degeneration, and multiple CAR-T/mRNA programming approaches) aimed at improving efficacy while reducing systemic toxicity or manufacturing barriers.
Finally, the digest also shows strong emphasis on risk prediction and real-world clinical decision support across cardiometabolic, respiratory, and critical care settings. Large cohorts link metabolic/inflammation indices to stroke, cardiometabolic multimorbidity, and mortality; air pollution exposure to glaucoma risk; and COPD to digestive comorbidities. In critical care and infectious disease, pragmatic frameworks and updated evidence on antimicrobial strategies (e.g., H. pylori resistance and first-line regimens) underscore a broader movement toward more personalized, mechanism-informed, and policy-relevant care.
Cancer metabolism & epigenetic regulation
Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.
This mechanistic study investigated how lipid peroxidation and ferroptosis interact to drive osteoarthritis (OA) degeneration, focusing on electrophilic lipid peroxidation aldehydes such as malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE). The key finding is that aldehyde-mediated signaling changes (including effects on NF-κB and MAPK pathways) converge on iron-dependent ferroptosis, linking oxidative stress to cartilage and inflammatory degeneration. Scientifically, it positions the lipid peroxidation–ferroptosis axis as a potential therapeutic target to slow OA progression.
Kulyar MF, Pachaleva J, Brazaite S et al. · Journal of orthopaedic translation · (2026) · View on PubMed ↗ · Free PDF ↗
Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.
This review studied how copper homeostasis and cuproptosis rewire the tumor microenvironment (TME), focusing on mechanisms of immune modulation and therapeutic opportunities. The key finding was a unifying framework describing copper as a “copper ecosystem” that coordinates cellular and extracellular-matrix remodeling, with cuproptosis driven by the FDX1/LIPT1/DLAT/Fe-S regulatory axis. This is significant because it highlights actionable therapeutic avenues that combine copper modulation with immunotherapy by exploiting cuproptosis-sensitive vulnerabilities.
Li G, Wang W · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Protein lactylation in cancer: principles, programmes and therapeutic opportunities.
This review studied lactate metabolism–linked protein lactylation and its regulatory networks in cancer, synthesizing evidence across tumor initiation and progression processes. It found that lactylation mechanistically connects tumor metabolic reprogramming to epigenetic regulation, with roles in malignant proliferation and invasion. The work highlights lactylation as a potential therapeutic target and provides a framework for developing metabolism-epigenetics–informed cancer interventions.
Bu X, Yu X, Wang J et al. · Molecular cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Investigating and validating the molecular mechanisms of lipid metabolism regulation in myasthenia gravis development based on single-cell, bulk transcriptomics, and RT-qPCR.
This study integrated single-cell RNA sequencing and bulk transcriptomics to identify molecular mechanisms of lipid metabolism regulation in myasthenia gravis (MG) development, using GSE85452 (13 MG vs 12 controls) and GSE227835 (10 MG vs 10 controls). Differential expression and weighted gene co-expression network analysis (WGCNA) were used to define disease-related gene modules and regulatory patterns in lipid metabolism pathways. The findings generate candidate lipid-metabolism regulators and networks that could be validated by RT-qPCR and targeted to improve mechanistic understanding of MG.
Chen M, Cai F, Sun Y et al. · Autoimmunity · (2026) · View on PubMed ↗ · Free PDF ↗
Huaier induces lipophagy to promote ferroptosis and chemosensitivity via de-acetylation of PLIN3 in triple-negative breast cancer.
This study tested whether Huaier (a traditional Chinese medicinal mushroom) enhances doxorubicin (DOX) chemosensitivity in triple-negative breast cancer (TNBC) by promoting lipophagy and ferroptosis, and it validated effects in vitro and in xenograft models. It found that Huaier increased lipophagy and ferroptosis and potentiated DOX efficacy through de-acetylation of PLIN3, linking a specific post-translational mechanism to therapy response. These results suggest PLIN3 de-acetylation–driven lipophagy/ferroptosis as a mechanistic basis for combining Huaier with DOX in TNBC.
Ma T, Niu T, Li Y et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
TTYH3 regulates a lysosomal chloride conductance and controls lysosomal fusion, autophagy and senescence.
The study identified TTYH3 as a regulator of lysosomal chloride conductance and examined how it controls lysosomal fusion, autophagy, and senescence. TTYH3 mediated chloride efflux from lysosomes, enhanced TRPML1-dependent lysosomal Ca2+ release, promoted lysosomal fusion via Ca2+/CaM and HSP90 pathways, inhibited AKT/mTOR to enhance autophagy, and activated ERK signaling to alleviate cellular senescence. These findings position TTYH3 as a lysosome-centered ion homeostasis regulator that coordinates multiple cellular stress and aging pathways.
Huang J, Wang Y, Xu Y et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
Immune Repertoire Profiling Reveals Distinct Adaptive Immune Signatures of Dampness ZHENG Across Psoriasis, Rheumatoid Arthritis and Ulcerative Colitis.
This study profiled T cell receptor (TCR) and B cell receptor (BCR) repertoires in 59 participants with psoriasis (Ps), rheumatoid arthritis (RA), ulcerative colitis (UC), and healthy controls, further stratifying patients into “Dampness” vs “non-Dampness” groups using Traditional Chinese Medicine (TCM) diagnostic criteria. It found distinct adaptive immune repertoire signatures across Ps, RA, and UC and also between Dampness and non-Dampness strata. The results are clinically significant because they suggest that TCM-defined phenotypes may map onto measurable immune repertoire differences that could support more refined, targeted stratification.
Tang L, Wang M, Yan Y et al. · Cell proliferation · (2026) · View on PubMed ↗ · Free PDF ↗
The complex lipidome as a driver of tissue-specific pathology in adrenoleukodystrophy.
This molecular study examined how the complex lipidome contributes to tissue-specific pathology in X-linked adrenoleukodystrophy (ALD) caused by pathogenic variants in the ABCD1 gene. ABCD1 deficiency impairs peroxisomal import of very-long-chain fatty acids (VLCFAs), leading to VLCFA accumulation and variable clinical phenotypes such as cerebral demyelination, myelopathy, and adrenal insufficiency (with sex- and X-inactivation–dependent differences). Understanding lipidomic drivers of tissue selectivity in ABCD1-related disease can guide mechanism-based biomarkers and therapeutic targeting for ALD.
Kemp S, Engelen M, Jaspers YRJ · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗
Soulangianolide A targets FAM120A to disrupt SREBP1-driven lipid metabolic reprogramming and suppress clear cell renal cell carcinoma.
This preclinical cancer study tested whether the natural product Soulangianolide A (SA) suppresses clear cell renal cell carcinoma (ccRCC) by targeting FAM120A to disrupt SREBP1-driven lipid metabolic reprogramming. In ccRCC models, stable knockdown of SREBP1 or FAM120A and SA treatment supported a mechanism in which FAM120A is required for SREBP1-dependent lipid metabolic changes that promote tumor phenotypes. Targeting the FAM120A–SREBP1 lipid axis with SA provides a potential therapeutic strategy to counter lipid-driven progression and resistance in ccRCC.
Luo W, Song Z, Liu Z et al. · Journal of experimental & clinical cancer research : CR · (2026) · View on PubMed ↗ · Free PDF ↗
Immune checkpoint therapy & immunotherapy resistance/scheduling
A Dual Response to CD20xCD3 Bispecific Therapy: Remission of Relapsed Diffuse Large B-cell Lymphoma and Improvement in Immune Thrombocytopenia.
This case report described an 81-year-old woman with relapsed diffuse large B-cell lymphoma (DLBCL) arising from marginal zone lymphoma and longstanding immune thrombocytopenia (ITP), treated with CD20xCD3 bispecific therapy. The key finding was complete metabolic remission of relapsed DLBCL alongside improvement in immune thrombocytopenia, suggesting coordinated control of both malignancy and autoimmune cytopenia. The clinical significance is that CD20xCD3 bispecific antibodies may be effective in patients with DLBCL and coexisting ITP, warranting further study beyond isolated lymphoma responses.
Virdi RK, Alrifai T · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗
Hemophagocytic lymphohistiocytosis-like syndrome after CD19-directed CAR T-cells for B-cell lymphoma and B-cell acute lymphoblastic leukemia: A LYSA, SFCE, and GRAALL study from the DESCAR-T registry.
This multicenter retrospective analysis used real-world data from the DESCAR-T registry (NCT04328298) to characterize immune effector cell-associated hemophagocytic lymphohistiocytosis-like syndrome (IEC-HS) after standard-of-care CD19 CAR T-cell therapy in relapsed/refractory B-cell non-Hodgkin lymphoma (B-NHL) and B-cell acute lymphoblastic leukemia (B-ALL). The key finding was the incidence, clinical features, management approaches, and outcomes of IEC-HS in this CD19 CAR T population, distinguishing it from better-characterized toxicities like CRS and ICANS. Scientifically and clinically, it improves recognition and risk management of a serious CAR T complication by defining its real-world behavior and treatment course.
Gower N, Houot R, Pizot C et al. · HemaSphere · (2026) · View on PubMed ↗ · Free PDF ↗
Overall survival according to timing of immune checkpoint inhibitors administration in patients with advanced cancer: results from a large single-centre cohort analysis.
This retrospective single-centre cohort analysis studied overall survival in 2,631 patients with advanced/metastatic cancer treated with immune checkpoint inhibitors (ICIs) between 2018 and 2023, stratifying patients by relative timing of ICI cycles (early vs late based on ≥50% of cycles after the median time). It found that timing of ICI administration was associated with overall survival, with hazard ratios estimated using Cox models with and without time-dependent variables. The results suggest that optimizing ICI scheduling could be a modifiable factor to improve outcomes in advanced cancer care.
Bosetti T, Kennedy OJ, Califano R et al. · British journal of cancer · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Combination of daratumumab, ixazomib, and lenalidomide with or without dexamethasone for initial therapy of newly diagnosed myeloma.
This trial studied fixed-duration initial therapy in newly diagnosed multiple myeloma (MM) patients, testing the quadruplet regimen daratumumab plus ixazomib plus lenalidomide with dexamethasone (Dara-IRd), with or without early steroid discontinuation. The key finding was that the Dara-IRd approach using a fixed schedule achieved high ≥complete response (CR) rates while enabling evaluation of early steroid stopping to reduce steroid exposure. Clinically, this supports steroid-sparing strategies in CD38-targeted quadruplet induction for newly diagnosed MM, potentially improving tolerability without sacrificing depth of response.
Kumar S, Knopf B, Asmus E et al. · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗
Newly diagnosed acute myeloid leukemia in Fit patients: 2026 treatment algorithms.
This article reviewed 2026 treatment algorithms for newly diagnosed acute myeloid leukemia (AML) in fit patients, focusing on how venetoclax (BCL2 inhibitor) and targeted agents (e.g., CD33, FLT3, IDH1/IDH2, menin inhibitors) integrate with risk-adapted strategies. The key finding was that long-term survival is prioritized, with allogeneic stem cell transplant recommended in first complete remission for high-risk genetics (including FLT3-ITD, TP53, and KMT2A rearrangements) and considered for most intermediate-risk patients. Clinically, it consolidates current evidence to guide selection of induction/targeted therapy and transplant timing based on molecular risk and measurable residual disease (MRD).
Gangat N, Ravandi F · Blood cancer journal · (2026) · View on PubMed ↗ · Free PDF ↗
GLP-1 receptor agonists in multiple sclerosis: a systematic review of preclinical and clinical evidence.
This systematic review synthesized preclinical and clinical evidence on glucagon-like peptide-1 receptor agonists (GLP-1RAs) in multiple sclerosis (MS), including studies in confirmed MS patients and experimental autoimmune encephalitis (EAE) models. Across eligible studies, GLP-1RAs were reported to exert anti-inflammatory and neuroprotective effects in EAE and to have emerging clinical evidence in MS, with the review assessing study quality using SYRCLE for preclinical bias. The work clarifies the translational rationale for GLP-1RA repurposing in MS and highlights where stronger comparative and higher-quality evidence is needed.
Sajjad M, Sajjad A, Amer R et al. · Multiple sclerosis and related disorders · (2026) · View on PubMed ↗
Fumarate hydratase-deficient renal cell carcinoma - results of the exploratory analysis in the SUNNIFORECAST trial comparing Ipilimumab plus Nivolumab vs standard of care as first line treatment.
An exploratory analysis of the SUNNIFORECAST trial studied fumarate hydratase (FH)-deficient renal cell carcinoma (RCC) patients to compare first-line ipilimumab plus nivolumab versus standard of care (SOC). Among centrally confirmed FH-deficient RCC cases, the trial reported outcomes including overall survival (OS) at 12 months and other efficacy endpoints (e.g., PFS and ORR), with PD-L1 expression assessed exploratorily. These results are clinically relevant because they inform treatment strategy for a rare molecularly defined nccRCC subtype lacking an established standard therapy.
Ahrens M, Haanen J, Albiges L et al. · Cancer treatment and research communications · (2026) · View on PubMed ↗ · Free PDF ↗
Tumor microenvironment (TME) remodeling & stromal/immune crosstalk
Exosomes in cancer drug resistance: dual roles in therapy failure and emerging precision therapeutics.
This translational review examined how tumor-derived exosomes contribute to cancer drug resistance while also being repurposed for precision therapeutics, focusing on specific exosomal cargo such as P-glycoprotein (P-gp), PD-L1, miR-21, and lncRNA H19. The key finding is the proposed “exosome paradox,” integrating evidence that exosomal signaling remodels the tumor microenvironment (e.g., via PI3K/AKT and MAPK activation) to drive immune evasion and therapy failure while the same platform can be engineered for therapeutic delivery. Scientifically, it frames a unified mechanism-to-application model that can guide rational design of exosome-based precision interventions and strategies to overcome resistance.
Tegegne BA, Belew H, Teffera ZH et al. · Cancer cell international · (2026) · View on PubMed ↗
Hypoxia tumor-associated macrophages facilitate hepatocellular carcinoma metastasis via uPA-uPAR pathway.
The study investigated how hypoxia shapes tumor-associated macrophage (TAM) heterogeneity to promote hepatocellular carcinoma (HCC) metastasis through the uPA–uPAR pathway, integrating multiple single-cell RNA-seq datasets with machine learning and validating with functional assays. The key finding was that hypoxic TAMs (H-TAMs) facilitate HCC metastasis via uPA–uPAR signaling, supported by transcriptomic characterization, pseudotime/regulatory network analyses, in vitro co-culture, and orthotopic mouse experiments. This is significant because it identifies a hypoxia–TAM–uPA/uPAR axis as a mechanistic target for anti-metastatic immunotherapy strategies in HCC.
Wang Y, You X, Luo X et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Chemotherapy-induced senescence promotes stroma stiffness and antioxidant adaptation to promote chemoresistance in pancreatic ductal adenocarcinoma.
This study investigated how chemotherapy-induced senescence drives pancreatic ductal adenocarcinoma (PDAC) chemoresistance by remodeling the tumor stroma and altering tumor cell antioxidant programs. The key finding was that gemcitabine-induced tumor senescence activates cancer-associated fibroblasts via the senescence-associated secretory phenotype, causing fibrotic matrix stiffening that engages Piezo1 to promote metabolic rewiring and increased dependence on BRG1-positive tumor cells for NRF2-mediated antioxidant defenses. Mechanistically, it identifies a senescence–mechanotransduction–NRF2 axis as a potential therapeutic vulnerability to overcome gemcitabine resistance in PDAC.
Liu X, Huang Z, Yang B et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
The CAFs-derived YAP1-periostin axis forms a fibrotic tumor microenvironment to promote metastatic lung tumor growth.
This study investigated how cancer-associated fibroblasts (CAFs) create a fibrotic tumor microenvironment that promotes metastatic lung tumor growth via a YAP1–periostin axis. Using RNA sequencing, immunohistochemistry, co-culture experiments, and genetic mouse models, the authors identified CD248+ CAFs as key regulators of NSCLC metastasis and implicated the CD248–periostin–integrin β1 (ITGB1) signaling axis in driving metastatic behavior. Defining this CAF signaling pathway offers a mechanistic target for therapies aimed at preventing NSCLC metastasis by remodeling the fibrotic TME.
Wu J, Wang X, Yang Z et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
SPP1-positive macrophages drive trastuzumab resistance in HER2-positive breast cancer.
This study explored how SPP1-positive tumor-associated macrophages (SPP1+ TAMs) contribute to trastuzumab resistance in HER2-positive breast cancer using single-cell sequencing of clinical samples and integrative spatial/interaction analyses. Patients with poor radiologic response after trastuzumab-based neoadjuvant therapy showed enrichment of TIGIT+ NK cells, exhausted CD8+ T cells, and immunosuppressive Tregs, and SPP1+ TAMs were implicated in shaping the tumor microenvironment toward resistance. These findings suggest that targeting SPP1+ TAM-driven immune suppression could enhance trastuzumab efficacy in HER2-positive breast cancer.
Wang D, Li G, Lu Y et al. · Cell communication and signaling : CCS · (2026) · View on PubMed ↗ · Free PDF ↗
Targeted protein degradation & signaling axes in cancer
DDRGK1-mediated UFMylation system suppresses STAT3 phosphorylation to alleviate osteoarthritis.
This study investigated whether the DDRGK1-mediated UFMylation system regulates inflammatory signaling by suppressing STAT3 phosphorylation to protect cartilage in osteoarthritis. Using human cartilage analyses and cartilage-specific Ddrgk1 conditional knockout mice plus a DDRGK1 K268R UFMylation-site mutant, the key finding was that DDRGK1 activity reduces STAT3 phosphorylation and alleviates cartilage degeneration. Scientifically, it identifies DDRGK1–UFMylation as a mechanistic brake on STAT3-driven inflammation, suggesting a potential therapeutic target for osteoarthritis.
Zhou T, Yang X, Li Y et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗
TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.
This study investigated how the E3 ubiquitin ligase TRIM24 regulates the p110 CUX1 oncoprotein via USP10 in acute myeloid leukemia (AML) cells, using genetic manipulation and pharmacologic inhibition. TRIM24 stabilized p110 CUX1 by promoting USP10-dependent deubiquitination, thereby increasing CUX1 protein stability and chemoresistance. These findings identify a TRIM24–USP10–CUX1 axis as a potential therapeutic target to overcome chemotherapy resistance in AML.
Ke ZY, Li J, Zhong L et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer drug delivery & biomaterials
Single-cell and longitudinal transcriptomics-guided engineering of FZD1-targeting precision nanotherapy against osteosarcoma cancer stem cells.
Using single-cell and longitudinal RNA-sequencing, the study analyzed osteosarcoma cancer stem cells (OCSCs) to identify transcriptional programs linked to stemness and to engineer FZD1-targeting precision nanotherapy. The key finding was that TCF7L1-associated transcriptional activity correlated with OCSC stemness and that FZD1-associated Wnt/β-catenin signaling acted as a putative upstream driver, supporting FZD1 as a therapeutic target. Scientifically and therapeutically, it provides a transcriptomics-guided rationale for FZD1-targeted nanotherapy aimed at eradicating OCSC-driven osteosarcoma.
Chen Z, Li Z, Yu W et al. · Bioactive materials · (2026) · View on PubMed ↗ · Free PDF ↗
Repurposing Triamterene as Chloride Intracellular Channel 1 Inhibitor via Ligand-Based Approach: A Novel Adjuvant Treatment for Glioblastoma.
The study investigated whether the diuretic triamterene can inhibit chloride intracellular channel 1 (CLIC1) and suppress glioblastoma stem cell (GSC) proliferation, using ligand-based/computational screening followed by whole-cell electrophysiology in GSCs. Triamterene was identified as a previously unrecognized CLIC1 blocker and inhibited CLIC1 activity in GSCs (reported EC50 ~200-fold relative to metformin). This suggests triamterene as a clinically relevant repurposed adjuvant candidate for CLIC1-driven glioblastoma, potentially overcoming metformin’s limited potency and pharmacokinetic constraints.
Barbieri F, Cianci F, Tremonti BF et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗
The closer, the better: intratumoral delivery of a thermoresponsive gemcitabine-loaded hydrogel in preclinical PDAC models.
This preclinical study evaluated intratumoral delivery of a thermoresponsive gemcitabine-loaded hydrogel (ChemoGell) in pancreatic ductal adenocarcinoma (PDAC) models using patient-derived organoids and surgically obtained tumor explants. It found that “closer” intratumoral hydrogel delivery improved preclinical efficacy and tolerability compared with conventional constraints of systemic (neo)adjuvant chemotherapy in the desmoplastic PDAC setting. The findings support hydrogel-based local gemcitabine delivery as a translational strategy to enhance treatment response while reducing systemic side effects.
Vallés-Martí A, Manelkar A, Simpson CR et al. · Drug delivery and translational research · (2026) · View on PubMed ↗ · Free PDF ↗
Developability engineering of scFvs enables robust CAR function under transient mRNA expression.
This engineering study examined how scFv developability affects CAR expression and function under transient mRNA expression delivered by lipid nanoparticles, using scFv variants from three clinically relevant antibody families (FMC63, 14G2a, and MGA271/chBRCA84D). It found that computational developability-guided humanization/optimization produced scFv variants with improved biophysical quality that supported robust CAR function under transient mRNA expression. The results provide a design framework for building more reliable CAR-T constructs for non-viral, mRNA-based manufacturing.
Mangolini M, Ramon A, Li B et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗
Nanozyme-integrated hydrogel orchestrates mitochondrial quality control to counter inflammatory and oxidative milieu during disc degeneration.
This study developed a thermosensitive Pluronic F127-based hydrogel that co-delivers a tannic acid–cerium nanozyme and the FPR1 antagonist HCH6-1 to treat intervertebral disc degeneration (IDD). The nanozyme–hydrogel system reduced oxidative stress and inflammatory signaling while orchestrating mitochondrial quality control, thereby improving nucleus pulposus (NP) cell function under inflammatory/oxidative conditions. The approach suggests a biomaterial platform for sustained, synergistic mitochondrial protection to slow or counteract IDD progression.
Liao Z, Yin G, Liu J et al. · Journal of controlled release : official journal of the Controlled Release Society · (2026) · View on PubMed ↗
Injectable bioinstructive microfoam for rapid bedside/in vivo programming of CAR-T cells.
This study developed an injectable methylcellulose-based microfoam designed to rapidly program T cells with a chimeric antigen receptor (CAR) gene for subcutaneous administration within hours of blood collection. It found that co-localizing T cells and the viral vector within the foam improves CAR gene transfer, and that the newly programmed CAR-T cells can traffic systemically and mediate regression of distal tumors in preclinical models. The approach is significant because it addresses key barriers to CAR-T access by enabling faster, potentially lower-cost bedside/in vivo CAR-T manufacturing.
Stephan SB, Cummings CL, Fitzgerald K et al. · Molecular therapy : the journal of the American Society of Gene Therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Biomarkers & diagnostic technologies (imaging, proteomics, cfDNA, assays)
An Unusual Presentation of Philadelphia Chromosome Positive B-Cell Acute Lymphoblastic Leukemia With Isolated Osteolytic Lesions at Diagnosis: A Case Report.
This case report described a 56-year-old Caucasian woman with Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia (Ph+ B-ALL) presenting with isolated osteolytic lesions at diagnosis despite normal bone marrow evaluation. The key finding is that the disease phenotype was dominated by skeletal involvement rather than typical diffuse marrow disease, making diagnosis diagnostically challenging. Clinically, it highlights the need to consider Ph+ B-ALL with BCR-ABL1 fusion in patients with unexplained lytic bone lesions even when marrow findings are initially normal.
Zhang T, Jamy O, Rangaraju S · Case reports in hematology · (2026) · View on PubMed ↗ · Free PDF ↗
Malignant melanoma identified within a pulmonary sequestration- a case report.
This case report studied a patient undergoing surgery for intralobar pulmonary sequestration to determine the pathology within the congenital lung malformation. The key finding was the identification of malignant melanoma arising within the pulmonary sequestration, described as (to the authors’ knowledge) the first reported such occurrence. Clinically, it highlights that rare malignancies can be present in pulmonary sequestration and supports careful pathological evaluation of resected lesions.
Bečejac T, Penavić M, Vrančić M et al. · Journal of cardiothoracic surgery · (2026) · View on PubMed ↗ · Free PDF ↗
Epigenomic modifications define chromatin states to regulate cell-free DNA fragmentomics.
This study examined how epigenomic modifications regulate plasma cell-free DNA (cfDNA) fragmentation patterns, using cfDNA fragmentomics and epigenetic mark measurements. The key finding was that cfDNA fragmentomic features strongly correlate with histone modification signals and that perturbing histone modifiers supports chromatin organization as a causal regulator of cfDNA fragmentation. Scientifically, it strengthens the molecular basis for using cfDNA fragmentomics as cancer biomarkers by linking fragmentation to specific chromatin states.
Gong F, Pan Y, Lin H et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Integrated Clinicopathological and Multiomic Profiling Reveals MEIS1-rearranged Sarcoma as a Distinct Entity with Two Prognostic Subgroups.
This multi-institutional study integrated clinicopathologic review, genomic profiling, and DNA methylation analysis to characterize MEIS1-rearranged sarcoma as a distinct entity and to define prognostic subgroups. The key finding was that MEIS1-rearranged sarcomas (n=20) showed two prognostic subgroups supported by integrated multiomic data, with tumors occurring predominantly in genitourinary/gynecologic sites. Clinically, it refines diagnosis and risk stratification for this rare sarcoma subtype, supporting more tailored prognostic counseling and future trial design.
Yeung MCF, Ip PPC, Bennett JA et al. · Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · (2026) · View on PubMed ↗
Texture Analysis of Non-contrast Magnetic Resonance Imaging for Liver Fibrosis Staging in Patients with Chronic Hepatitis B.
Non-contrast liver MRI texture analysis was assessed for staging liver fibrosis in 66 patients with chronic hepatitis B using multiple sequences (in-phase T1W, out-of-phase T1W, fat-suppressed T1W, fat-suppressed T2W, and T2W). The study extracted histogram-based texture features from liver parenchyma regions of interest and evaluated which parameters best discriminated fibrosis stages. If validated, this could provide a non-contrast, imaging-based biomarker approach to improve fibrosis staging in chronic hepatitis B patients.
Başaran E, Baykara M, Aktaş S et al. · Journal of gastrointestinal and liver diseases : JGLD · (2026) · View on PubMed ↗ · Free PDF ↗
SYNGR2 as a Multifaceted Biomarker in Hepatocellular Carcinoma Linking Prognosis, Immune Microenvironment and Therapeutic Response.
This bioinformatics-and-cell study investigated SYNGR2 (synaptogyrin-2) as a multifaceted biomarker in hepatocellular carcinoma (HCC) and its links to prognosis, immune microenvironment, and predicted therapeutic response. Using TCGA-LIHC RNA-seq multiomics analyses with Cox regression/Kaplan–Meier, CIBERSORT immune infiltration estimation, and oncoPredict drug-sensitivity prediction, and validating in Hep3B and Huh7 cell lines, it identified SYNGR2 as associated with HCC prognosis and immune regulation and with differential predicted treatment response. Scientifically, it positions SYNGR2 as a candidate integrative biomarker that could help stratify HCC patients by immune context and likely therapeutic sensitivity.
Wang R, Chen D, Du Q et al. · Technology in cancer research & treatment · (2026) · View on PubMed ↗ · Free PDF ↗
UK recommendations for Ki-67 immunohistochemical staining and interpretation in breast cancer.
This review studied the biological rationale and practical laboratory factors affecting Ki-67 immunohistochemical (IHC) staining and interpretation in breast cancer, focusing on hormone receptor-positive (HR-positive), HER2-negative disease where Ki-67 is used for prognosis and prediction. It reports that interobserver and interlaboratory variability can be reduced by standardizing pre-analytical/analytical variables and applying UK-specific recommendations for Ki-67 IHC performance and scoring. These harmonized guidance are clinically significant because they aim to improve reproducibility of Ki-67 results for treatment decisions in routine breast pathology.
Shaaban AM, Dodson A, Rakha E et al. · Histopathology · (2026) · View on PubMed ↗ · Free PDF ↗
Survival Outcomes of Head and Neck Neuroendocrine Carcinoma: A Systematic Review.
This PRISMA-compliant systematic review synthesized pathological features, oncologic outcomes, and survival metrics for head and neck neuroendocrine carcinoma (HNNEC) across published studies. Small-cell carcinoma predominated (n=2334), with common primary sites including the larynx (n=1041) and sinonasal tract (n=917), and treatment patterns varied by site (e.g., laryngeal surgery plus radiotherapy; sinonasal/nasopharyngeal chemoradiotherapy). The review clarifies how tumor stage, location, and therapeutic strategies relate to overall survival and recurrence, informing evidence-based prognostication and treatment planning for HNNEC.
Aïta M, Galofaro I, Maniaci A et al. · Head & neck · (2026) · View on PubMed ↗
Plasma proteomics and machine learning deliver non-invasive distinction between fibrotic hypersensitivity pneumonitis and idiopathic pulmonary fibrosis.
This study developed and validated a non-invasive diagnostic framework using quantitative plasma proteomics combined with machine learning to distinguish fibrotic hypersensitivity pneumonitis (FHP) from idiopathic pulmonary fibrosis (IPF) in an interstitial lung disease cohort. The proteomics–ML model differentiated FHP from IPF more effectively than clinical assessment alone, leveraging plasma protein signatures across healthy controls, non-fibrotic HP (NFHP), FHP, and IPF groups. This approach could improve diagnostic accuracy and guide management where FHP and IPF overlap clinically.
Tian Y, Geng J, Wang M et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Neurodegeneration & tau biology (including imaging/biomarkers)
Distribution of Big Tau Isoforms in the Human Central and Peripheral Nervous System.
The study characterized the composition and anatomic distribution of the longer tau isoform “big tau” (exon 4a inclusion) across human central and peripheral nervous system tissues, including postmortem samples from Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and controls. Using mass spectrometry to sequence big tau and map its regional abundance, the authors report disease-relevant differences in big versus canonical (“small”) tau isoforms across CNS and PNS compartments. These findings refine tau isoform biology beyond canonical brain tau and support big tau as a potential biomarker or mechanistic contributor to neurodegeneration spanning CNS and PNS.
Koppisetti RK, Barthélemy NR, Horie K et al. · Annals of neurology · (2026) · View on PubMed ↗
Differential Proteomic Landscape of Plasma Neuron-Derived Extracellular Vesicles in Parkinson’s Disease with and without RBD: A Pilot Investigation.
In a pilot study of 28 participants stratified into Parkinson’s disease with rapid eye movement sleep behavior disorder (PD-RBD), Parkinson’s disease without RBD (PD-noRBD), and controls, the authors isolated plasma neuron-derived extracellular vesicles (nEVs) using L1CAM immunocapture. Using data-independent acquisition mass spectrometry (DIA-MS), they quantified 1354 proteins and identified differentially expressed proteins between PD subgroups (including PD-RBD versus PD-noRBD and/or controls). The significance is that plasma nEV proteomics may yield subtype-specific biomarkers to distinguish the more aggressive PD-RBD phenotype.
Zhou Y, Zhang W, Lu Y et al. · International journal of nanomedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Development and characterization of a novel TDP-43 positron emission tomography tracer: [18F]JNJ-TDP43-1.
The study developed and characterized a novel TDP-43 PET tracer, [18F]JNJ-TDP43-1, evaluating binding specificity with fluorescent labeling, surface plasmon resonance (SPR), and autoradiography (ARG) and then performing brain PET imaging in rats, nonhuman primates (NHPs), and a disease mouse model. The key finding was that [18F]JNJ-TDP43-1 showed specific binding to TDP-43 pathology targets across these preclinical species/models, supporting its feasibility for imaging TDP-43 aggregates. This is significant because a validated TDP-43-targeting PET tracer could enable earlier diagnosis and pharmacodynamic monitoring in ALS/FTD/LATE and related Alzheimer’s-spectrum TDP-43 disorders.
Xia CA, Salarian M, Gartshore CJ et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗
AQP4-dependent enhancement of glymphatic function attenuates tau pathology and neurodegeneration in PS19 mice.
The study tested whether enhancing aquaporin-4 (AQP4)-dependent glymphatic function attenuates tau pathology and neurodegeneration in PS19 tau transgenic mice, using the MRI-based JJVCPE technique to measure glymphatic water exchange and pharmacologically activating AQP4 with TGN-073. The key finding was that AQP4-dependent enhancement of glymphatic function improved glymphatic transport and reduced tau pathology and neurodegenerative outcomes in PS19 mice. This is significant because it supports a causal role for glymphatic dysfunction in tauopathy and identifies AQP4 activation as a potential therapeutic strategy for tau-driven neurodegeneration.
Yamada K, Ishida K, Sakamoto A et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗
Beyond the brain: Polyglutamine disease pathology outside the nervous system.
This review synthesized clinical, imaging, biochemical, and post-mortem evidence showing that polyglutamine diseases (including Huntington’s disease, SBMA, DRPLA, and multiple spinocerebellar ataxias) involve peripheral organ pathology beyond the nervous system. It found that systemic abnormalities often precede or accompany neurological symptoms and contribute to disability and mortality, only partly explained by deconditioning or medications. The work supports reframing polyglutamine disorders as systemic protein-misfolding diseases, motivating peripheral-targeted research and therapies.
Rausch JP, Bradley B, Demontis F et al. · Neurobiology of disease · (2026) · View on PubMed ↗ · Free PDF ↗
Development of a Novel Blood-Based Assay for Brain-Derived Tau and Its Validation in Traumatic Brain Injury.
This study developed and analytically validated a novel blood-based immunoassay for brain-derived tau (BD-tau) using the ultra-sensitive Quanterix HD-X platform with Single Molecule Array (Simoa) technology for application in traumatic brain injury (TBI). It reported robust analytical performance (including dilution linearity, specificity, precision, detection limits, and spike recovery) meeting expert validation recommendations. The assay is scientifically and clinically significant because it improves access to a validated BD-tau biomarker platform for research and potential clinical monitoring in TBI and related neurodegenerative conditions.
Balogun WG, Zeng X, Nafash MN et al. · Journal of neurochemistry · (2026) · View on PubMed ↗ · Free PDF ↗
Metabolic reprogramming via SIRT2-deficient microglial large extracellular vesicles ameliorates alzheimer’s pathology.
This study tested whether large extracellular vesicles (LEVs) derived from SIRT2-deficient (SIRT2-KD) microglia can ameliorate Alzheimer’s disease pathology in APP/PS1 mice, delivered intranasally. SIRT2-KD microglial LEVs induced metabolic reprogramming in recipient cells and reduced Alzheimer’s pathology compared with control EVs. These results support SIRT2-deficient microglial EVs as a potential disease-modifying, blood-brain-barrier-bypassing therapeutic strategy for AD.
Tang X, Chen R, Xing J et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗
Neuroinflammation & microglia/macrophage mechanisms
Delayed astrocyte development impairs Sema6a-Plxna2/4-mediated astrocyte-neuron crosstalk and causes depressive-like behavior.
This study used an Egfr knockout mouse model during the neuronal maturation critical period to examine how delayed astrocyte development disrupts Sema6a–Plxna2/4-mediated astrocyte–neuron crosstalk and affects behavior. The key finding was that Egfr loss caused a transient absence of astrocytes with impaired Sema6a-Plxna2/4 signaling and resulting depressive-like behavior, with astrocyte recovery in adulthood. Scientifically, it provides a tractable in vivo model linking delayed neuron–astrocyte interactions to neuropsychiatric-like phenotypes.
Jiang X, Qi Y, Yang L et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Single-cell analysis identifies monocyte signatures of disease activity and clinical subtypes in Behçet’s disease.
This study used single-cell RNA sequencing on peripheral blood mononuclear cells from 34 patients with Behçet’s disease (BD) and 12 healthy controls to identify monocyte signatures associated with disease activity and clinical subtypes. The key finding was that monocyte transcriptomic programs differed between active and remission states and mapped to distinct clinical phenotypes through differential expression and pathway enrichment analyses. Clinically, it suggests that monocyte-based molecular signatures could improve immune stratification and monitoring in BD.
Carmona E, Deniz R, Bes C et al. · Annals of the rheumatic diseases · (2026) · View on PubMed ↗ · Free PDF ↗
Phagocytosis by Brain Macrophages in Central Nervous System Diseases: Dual Effects, Cellular Heterogeneity, and Targeted Therapeutic Strategies.
This review article synthesized evidence on phagocytosis by brain macrophages in central nervous system (CNS) diseases, focusing on microglia, border-associated macrophages (BAMs), and recruited blood-derived macrophages. The key finding was that brain macrophage phagocytosis can have dual effects—neuroprotective when moderate but damaging when excessive—driven by complex regulatory mechanisms involving phagocytic receptors. Scientifically and therapeutically, it highlights targeted strategies aimed at modulating phagocytosis to rebalance beneficial versus harmful immune clearance in CNS disorders.
Su B, Dong W, Su L et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗
Dual-regulation of mitophagy and cytosolic mtDNA-induced inflammation for the treatment of inflammatory bone loss.
This study examined how the mtDNA–cGAS–STING axis and defective mitophagy contribute to lipopolysaccharide (LPS)-induced inflammatory bone loss in human bone marrow mesenchymal stem cells (BMSCs). It found that LPS-driven mtDNA release activates cGAS–STING–mediated inflammation while impaired mitophagy sustains mitochondrial damage, worsening BMSC dysfunction and inflammatory osteogenic failure. These findings support dual targeting of mitophagy and cytosolic mtDNA–cGAS–STING signaling as a therapeutic strategy for immunoporosis/inflammatory osteoporosis.
Zheng K, Che B, Cui Y et al. · Free radical biology & medicine · (2026) · View on PubMed ↗
Advances in Traditional Chinese Medicine for Diabetic Glaucoma: A Systematic Review From Holistic Pathogenesis to Multi-Target Interventions.
This systematic review studied Traditional Chinese Medicine (TCM) approaches for diabetic glaucoma, focusing on multi-target interventions aimed at oxidative stress, inflammation, microcirculatory dysfunction, and retinal ganglion cell (RGC) apoptosis. It found that TCM strategies—framed by holistic syndrome differentiation—are proposed to provide longer-term neuroprotection beyond conventional intraocular pressure (IOP) control, via multi-component, multi-pathway mechanisms. The review’s significance is that it consolidates mechanistic and therapeutic rationales for TCM as potential adjuncts to slow progression in diabetic glaucoma.
Liu J, Yu Y, Hu C et al. · Medicinal research reviews · (2026) · View on PubMed ↗
RNA-Guided Engineering of the Chloroplast Genome Enabled by Plastid-Expressed Guide RNAs.
This work studied RNA-guided genome engineering of tobacco chloroplast DNA using CRISPR/Cas9 with plastid-expressed guide RNAs (sgRNAs) generated from an rRNA operon promoter and processed by downstream trnG or an HDV ribozyme. It demonstrated that nuclear Cas9 targeted to chloroplasts via a transit peptide can introduce double-strand breaks in plastid genes such as ndhA and rpoC1, with repair occurring via microhomology-mediated end joining. This is scientifically significant because it establishes a practical platform for programmable chloroplast genome editing using RNA-guided, plastid-localized guide RNA expression.
Mirzaee M, Best C, Wachowski EV et al. · Plant biotechnology journal · (2026) · View on PubMed ↗ · Free PDF ↗
Autoreactive B cells in systemic lupus erythematosus: insights from integrative multi-omics analyses.
This integrative multi-omics analysis study investigated autoreactive B-cell biology in systemic lupus erythematosus (SLE) using approaches designed to overcome limitations of bulk RNA-seq/ATAC-seq that depend on predefined cell subsets and markers. The key finding was that multi-omics strategies can more effectively resolve cellular heterogeneity and generate mechanistic insights into how autoreactive B-cell programs contribute to SLE pathogenesis. These insights could improve patient stratification and support more targeted therapeutic selection in SLE.
Ushijima TS, Okamura T, Fujio K · Inflammation and regeneration · (2026) · View on PubMed ↗ · Free PDF ↗
Diabetic retinopathy: shaped by the “hidden hand” of post-translational modifications.
This review summarized how post-translational modifications (PTMs) act as a “hidden hand” shaping diabetic retinopathy (DR), a neurovascular retinal disease. The key finding is that PTMs such as phosphorylation and glycosylation dynamically regulate core retinal cell functions (retinal endothelial cells, Müller cells, and pericytes) and related signaling pathways involved in neovascularization, nerve damage, oxidative stress, and chronic inflammation. By linking PTM dysregulation to DR mechanisms, the article supports PTM-focused biomarkers and therapeutic development for preventing vision loss.
Xiao R, Zhang M · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗
A BRD4/p300/SP1 epigenetic cascade drives microglial P2X4R transcription and promotes neuropathic pain.
This study examined an epigenetic mechanism controlling microglial P2X4R transcription in neuropathic pain, focusing on a BRD4/p300/SP1 cascade in a mouse spared nerve injury (SNI) model. After nerve injury, microglia showed increased p300 and histone acetylation (including H3K9ac/H3K27ac/H4K5ac/H4K8ac) with enhanced chromatin accessibility at the P2rx4 promoter, and microglia-specific deletion of p300 reduced P2X4R-driven neuropathic pain behaviors. The work links chromatin remodeling to P2X4R upregulation and suggests BRD4/p300/SP1–P2rx4 as a mechanistic therapeutic target for neuropathic pain.
Wang D, Wang T, Li Y et al. · Journal of neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗
CNS vascular repair & neurotrauma therapeutics
Semaglutide promotes angiogenesis and blood-brain barrier repair after traumatic brain injury via PDGF-BB/PDGFRβ/Ang1/Tie2/VEGF signaling pathway.
This mouse controlled cortical impact (CCI) study tested whether semaglutide (SEMA) promotes angiogenesis and blood–brain barrier (BBB) repair after traumatic brain injury through the PDGF-BB/PDGFRβ/Ang1/Tie2/VEGF signaling axis. It found that SEMA improved BBB integrity and angiogenesis and modulated endothelial cell–pericyte signaling markers consistent with activation of the specified pathway. The findings support semaglutide as a mechanistically grounded candidate therapy to reduce TBI-associated edema and neuronal loss via vascular repair signaling.
Shi Y, Dong X, Zhu C et al. · Scientific reports · (2026) · View on PubMed ↗ · Free PDF ↗
Ciliogenesis, fertility & developmental cell biology
Basal body docking failure triggers centriole clustering and elimination in mammalian spermatogenesis.
This mechanistic mouse study investigated how basal body docking failure affects centriole behavior during mammalian spermatogenesis by conditionally ablating the distal appendage protein CEP164 in male germ cells. It found that CEP164 loss prevents basal body docking/ciliogenesis, eliminates zygotene primary cilia and sperm flagella, triggers centriole clustering, and leads to male infertility. The work links a specific ciliogenesis failure step (CEP164-dependent docking) to downstream centriole elimination, advancing understanding of infertility mechanisms tied to ciliary dysfunction.
Chen JJ, Gong X, Mak M et al. · EMBO reports · (2026) · View on PubMed ↗ · Free PDF ↗
Psychiatric neuroimaging & computational brain modeling
Remote programming versus standard in-person programming following deep brain stimulation in patients with Parkinson’s disease: a randomised controlled trial.
In a single-center, open-label, non-inferiority randomized controlled trial in China, Parkinson’s disease patients who underwent bilateral subthalamic nucleus deep brain stimulation (DBS) were assigned to remote programming (RP) versus standard in-person programming (SP). The study found that RP produced motor-symptom improvement rates that were comparable to SP, supporting non-inferiority for clinical efficacy. Clinically, this supports remote DBS programming as a practical alternative that may improve access and continuity of care for PD patients after DBS.
Wan X, Zhou Y, Huang P et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Breaking the norm: population-scale deviations of brain structure in depression and anxiety.
This population-scale neuroimaging study used autoencoder-based normative modeling on structural MRI from two cohorts (German National Cohort ~29,000 and UK Biobank ~25,000) to quantify brain-structure deviations across depression and anxiety symptom dimensions. It found that deviation magnitude increased with symptom severity and that individuals with high alcohol use showed the most pronounced deviations, with shared deviation patterns across depressive dimensions. Scientifically, it demonstrates a scalable way to characterize heterogeneous brain alterations in mood/anxiety disorders beyond group-averaged approaches.
Wiegert J, Marty-Lombardi S, Oweda J et al. · Molecular psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗
Latent profile analysis of compassion fatigue among hemodialysis nurses and subtype-specific differentiated effects of core competencies and work engagement.
Compassion fatigue subtypes were identified in 3128 Chinese hemodialysis nurses using latent profile analysis, and the study tested how nurse core competencies and work engagement differentially relate to compassion satisfaction, burnout, and secondary traumatic stress across subtypes. The key finding was that distinct compassion fatigue latent classes existed and that the associations of competencies and work engagement with ProQOL-5 outcomes varied by subtype. This supports targeted workforce interventions in dialysis settings by matching competency/work-engagement strategies to specific compassion fatigue profiles.
Wanning J, Jiayao L, Haitao L et al. · International journal of nursing studies · (2026) · View on PubMed ↗
Enhanced multimodal MRI classification of schizophrenia through cross-attention graph neural networks.
A tri-branch cross-attention graph neural network (TB-GCAN) was developed and evaluated for schizophrenia classification using multimodal MRI (sMRI, fMRI, DTI) across a multi-site dataset of 1191 samples from seven scanning sites. TB-GCAN achieved 84.63% accuracy in a 7-site leave-one-site-out evaluation and outperformed baseline models (e.g., GAT/GCN/CNN/SVM/MMGNN), with attention-based region ranking highlighting schizophrenia-relevant brain regions. This demonstrates that cross-attention graph learning can improve robust, interpretable multimodal MRI classification for schizophrenia across sites.
Gao J, Wu J, Qian M et al. · Medical image analysis · (2026) · View on PubMed ↗
Mixed Methods Trajectory Analysis of Daily Educational and Social Experiences of Youth With Cancer From Diagnosis to Early Survivorship.
This longitudinal mixed-methods trajectory analysis studied academic and social experiences from diagnosis through early survivorship in youth with cancer, using perspectives from youth, caregivers, and educators. Across three timepoints (diagnosis, mid-treatment, and one-year post-treatment) in 75 triads, it characterized how challenges evolve over time rather than relying on single-informant or cross-sectional snapshots. The findings are significant for designing age-appropriate, time-sensitive educational and psychosocial interventions for pediatric oncology survivorship.
Moscato EL, Duan Q, Hammad S et al. · Psycho-oncology · (2026) · View on PubMed ↗
Multi-threshold polygenic risk improves hippocampal-based cognitive decline prediction.
This study developed and tested hippocampal-volume–based cognitive decline prediction models that integrate multi-threshold polygenic scores (PGS) using Gaussian Process Regression (GPR) in UK Biobank participants. Multi-threshold PGS improved cognitive decline prediction over hippocampal volume–only normative models across multiple experimental setups, with training on 23,997 UK Biobank participants and validation on 3,000 out-of-sample participants. The results support using genetically informed, multi-threshold PGS within MRI normative modeling to better forecast cognitive trajectories relevant to neurodegenerative disease risk.
Janahi M, Lorenzini L, Oxtoby NP et al. · Genome medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Comparative efficacy of pharmacological, adjunctive, and non-pharmacological interventions across behavioral domains in children and adolescents with autism spectrum disorder: a network meta-analysis.
This network meta-analysis compared the comparative efficacy of pharmacological, adjunctive, and non-pharmacological interventions across behavioral domains in children and adolescents with autism spectrum disorder (ASD) using randomized controlled trials. Across 67 RCTs (total N reported as 4, [truncated] in the abstract), the authors used a frequentist network meta-analysis to estimate relative effects and ranking probabilities for outcomes such as irritability, hyperactivity, social withdrawal, stereotypic behavior, and inappropriate speech. The findings help clinicians and researchers prioritize interventions by behavioral domain, supporting more tailored ASD treatment selection.
Liu L, Xin X, Ying Z · Child and adolescent psychiatry and mental health · (2026) · View on PubMed ↗ · Free PDF ↗
Microbiome–gut–brain/immune axis & natural products
Decoding dry eye disease based on bioinformatics and in vitro experimental: the role of immune responses and natural product intervention.
This bioinformatics-and-experimental study examined immune-response mechanisms underlying dry eye disease (DED) and assessed the potential of a natural product intervention to modulate those pathways. The key finding was the identification of DED-associated genes/pathways from public datasets followed by experimental support for immune-related dysregulation and therapeutic effects of the natural product (details truncated in the abstract). The significance is that it provides candidate immune targets and a rationale for natural-product-based adjunct therapy in DED beyond monotherapy.
Long X, Liu G, Liu P et al. · Human genomics · (2026) · View on PubMed ↗ · Free PDF ↗
Multi-omics analysis reveals the effects of Jinfeng pills on the outcomes of IVF-ET in patients with poor ovarian response: a randomized controlled trial.
This randomized controlled trial studied whether Jinfeng pills (JFP), a 9-herb traditional Chinese medicine, improve IVF-ET outcomes in patients with poor ovarian response (POR) and explored potential mechanisms. The key finding was the comparative effect of JFP versus standard POR management on IVF-ET outcomes in Bologna-criteria POR patients (with mechanistic details truncated in the abstract). Clinically, it suggests JFP may be a beneficial adjunct for improving reproductive outcomes in POR, warranting further mechanistic clarification and larger trials.
Kong X, Luo Q, Huang T et al. · Journal of ovarian research · (2026) · View on PubMed ↗ · Free PDF ↗
Sustainable next-generation prebiotics for brain health: microbiota-gut-brain axis in neurodegenerative and demyelinating diseases.
This review evaluated evidence linking microbiota-gut-brain axis disruption to neurodegenerative and demyelinating diseases and summarized dietary next-generation prebiotics for brain health. It found common mechanistic themes—reduced beneficial taxa, impaired short-chain fatty acid production, barrier dysfunction, and sustained inflammation—and highlighted polyphenols, bioactive peptides, and pectin-derived oligosaccharides (POS) as candidate prebiotic or prebiotic-like compounds. The review supports microbiota-targeted dietary interventions as a potentially scalable adjunct strategy for neuroinflammation and neurodegeneration.
Barrera-Chamorro L, Gonzalez-de la Rosa T, Arzalluz-Luque J et al. · Critical reviews in food science and nutrition · (2026) · View on PubMed ↗
Jiao-tai-wan suppresses ferroptosis induced by heart-kidney disharmony insomnia by regulating the PDE4D/BDNF signaling pathway.
Jiao-tai-wan (JTW) was studied in a mouse model of Heart-Kidney Disharmony insomnia and in hippocampal HT22 cells to determine whether it suppresses insomnia-associated ferroptosis via PDE4D/BDNF signaling. JTW (and JTWS) inhibited ferroptosis markers and improved behavioral/pathological outcomes, with network pharmacology and docking implicating PDE4D/BDNF as a key pathway regulating this effect. These findings suggest JTW may protect hippocampal neurons by targeting PDE4D/BDNF-linked ferroptotic mechanisms, supporting a mechanistic basis for a traditional insomnia therapy.
Ye W, Lin Z, You Z et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
Biochanin A alleviates HFD-induced MAFLD by inhibiting IRE1α-SPT-ceramide axis and improving intestinal homeostasis.
Biochanin A (BCA) was evaluated in sodium palmitate (PA)-induced AML-12 hepatocytes and in high-fat diet (HFD) mice with MAFLD to test whether it modulates the IRE1α–SPT–ceramide axis and intestinal homeostasis. BCA reduced hepatocyte death and MAFLD phenotypes, and IRE1α agonist IXA4 rescue experiments supported that BCA’s protection depends on inhibiting the IRE1α–SPT–ceramide signaling cascade. This positions BCA as a candidate natural compound for MAFLD therapy by linking ER stress/ceramide biology to ferroptosis-related inflammatory-oxidative pathways and gut-liver homeostasis.
Liu N, Wang R, Gao Y et al. · Phytomedicine : international journal of phytotherapy and phytopharmacology · (2026) · View on PubMed ↗
A catalase-mediated redox-epigenetic switch governs rice immunity hijacked by a fungal effector.
A catalase-mediated redox-epigenetic mechanism was investigated in rice (Oryza sativa) to explain how immunity is hijacked by a fungal effector, focusing on the histone deacetylase OsHDA705 and oxidative post-translational control. Pathogen-induced ROS oxidized OsHDA705 at cysteine 256 (C256) to block deacetylase activity, promoting hyperacylation of OsIPA1 and histones and thereby activating defense gene expression, while the catalase OsCATB reduced oxidized OsHDA705 to restore deacetylation. This reveals a specific redox-to-epigenetic switch governing rice defense, identifying OsHDA705 C256 and OsCATB as mechanistic control points relevant to plant-pathogen interactions.
Fang Y, Wang R, Duan Y et al. · The Plant cell · (2026) · View on PubMed ↗
Short-Chain Fatty Acid-Dependent Neuroimmune Regulation in Autism Spectrum Disorder Pathogenesis.
This mechanistic review studied how short-chain fatty acids (SCFAs) regulate neuroimmune processes in autism spectrum disorder (ASD) via the microbiota-gut-brain-immune axis. It found that SCFA insufficiency—linked to depletion of SCFA-producing taxa (e.g., Bifidobacterium, Faecalibacterium, Roseburia) and increased endotoxin-producing taxa (e.g., Desulfovibrio, Bacteroides)—can impair neuroimmune homeostasis through GPR43/GPR109A-dependent histone deacetylase inhibition, astrocytic tryptophan–aryl hydrocarbon receptor signaling, and maintenance of blood-brain/blood-CSF barrier tight junctions. The significance is that SCFA-dependent pathways provide testable targets for microbiome-based or metabolic interventions to modulate ASD neuroimmune dysfunction.
Dhungel A, Bora R · The European journal of neuroscience · (2026) · View on PubMed ↗ · Free PDF ↗
Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα-SCD1 axis.
This study investigated how Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis (UC) and concomitant liver injury, focusing on hepatic lipid metabolism remodeling via the LXRα–SCD1 axis. It found that colitis-associated corticosterone (CORT) downregulates hepatic LXRα–SCD1 signaling, leading to reduced monounsaturated fatty acids and altered unsaturated lysophospholipids, and that L. johnsonii helps restore protection through this pathway. The work is significant because it links a specific gut microbe–drug effect to a defined hepatic lipid regulatory axis that may be therapeutically targetable in UC with liver involvement.
Cheng Y, Wu ZE, Huang R et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗
Coffee as a polypharmacological modulator of mitochondrial health: from molecular mechanisms to translational implications.
This narrative review synthesized evidence that coffee’s multiple bioactive constituents (beyond caffeine, including chlorogenic acids, trigonelline, diterpenes, and melanoidins) modulate mitochondrial health. The authors propose a polypharmacological framework in which coffee acts as a systemic “mitochondrial network optimizer,” linking molecular mechanisms to translational implications for chronic disease prevention. The review highlights mechanistic targets for future experimental and clinical studies evaluating coffee-derived compounds in mitochondrial dysfunction–driven conditions.
Jiang Z, Ding Y · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Metabolic syndrome, cardiometabolic risk & inflammation markers
Efficacy and safety of HRS-7535, an oral small-molecule GLP-1 receptor agonist, in patients with diabetic kidney disease (SOLID-DKD): a randomised, double-blind, placebo-controlled, phase 2 trial.
This multicentre, randomized, double-blind, placebo-controlled phase 2 trial evaluated HRS-7535, an oral small-molecule GLP-1 receptor agonist, as add-on therapy in adults with diabetic kidney disease (UACR 300 to <3000 mg/g and eGFR ≥30 mL/min/1.73 m²) in China. The key finding was the efficacy and safety profile of HRS-7535 versus placebo (with dose arms) on kidney-related outcomes, indicating whether the drug improves disease measures under contemporary high-intensity care. If beneficial, HRS-7535 could expand non-peptide GLP-1–based options for diabetic kidney disease management.
Lv R, Peng L, Xu Y et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Device-measured movement behaviours and cancer incidence in a population sample of UK adults: Dual 24-hour analyses of postural and intensity compositions.
This observational study examined associations between device-measured movement behaviors and cancer incidence in a UK adult population sample using a dual 24-hour compositional analysis of postures, intensities, and sleep. The key finding was that differences in the 24-hour composition of movement behaviors (posture/intensity patterns) were differentially associated with cancer incidence across 13 physical-inactivity–linked cancer sites. This is significant because it supports more personalized, behavior-pattern-based guidance rather than one-size-fits-all physical activity recommendations for cancer prevention.
Mitchell JJ, Biswas RK, Koemel NA et al. · BMC medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Association between the cholesterol-high-density lipoprotein-glucose index and new-onset stroke in middle-aged and older adults with depressive symptoms: a longitudinal cohort analysis.
This longitudinal cohort study examined whether the cholesterol–high-density lipoprotein–glucose (CHG) index predicts new-onset stroke in 5,138 Chinese adults aged ≥45 with depressive symptoms (CES-D ≥10) from CHARLS (2011–2018). It found an association between higher CHG index values and increased risk of incident stroke using sequential Cox proportional hazards models. Clinically, CHG index could serve as a practical metabolic risk marker to stratify stroke prevention efforts in people with depression.
Wen Y, Zhang W, Wu L et al. · Lipids in health and disease · (2026) · View on PubMed ↗ · Free PDF ↗
Evidence from two large prospective cohorts: variations in remnant cholesterol inflammation index and the risk of cardiometabolic multimorbidity in middle-aged and elderly populations.
This study evaluated whether the remnant cholesterol inflammation index (RCII = remnant cholesterol × hs-CRP / 10) predicts cardiometabolic multimorbidity (CMM) using two large prospective cohorts: CHARLS (n=5,870) and ELSA (n=2,295), with additional longitudinal analyses in a subcohort (n=5,966). The key finding was that variations in RCII were associated with the risk of developing CMM over time, supporting RCII as a combined marker of residual cholesterol and systemic inflammation. Clinically, it suggests RCII could improve cardiometabolic risk prediction in middle-aged and elderly populations beyond using residual cholesterol or hs-CRP alone.
Wen S, Sun Z, Song Y et al. · Diabetes research and clinical practice · (2026) · View on PubMed ↗
Molecular basis of insulin resistance and its impact on the brain: the role of physical exercise.
The review studied insulin resistance (IR) in peripheral tissues and the brain and how physical exercise modulates the molecular pathways in men and women. It found that exercise improves insulin signaling, glucose uptake, and mitochondrial function in skeletal muscle, liver, and adipose tissue and that brain-relevant mediators such as PGC-1α and irisin help counter central IR. These mechanistic links support exercise as a dual peripheral-and-central strategy to reduce metabolic disorder risk and cognitive decline associated with IR.
De Sousa RAL · Molecular biology reports · (2026) · View on PubMed ↗
Combination cardiometabolic therapy in type 2 diabetes: optimizing SGLT2 inhibitor and GLP‑1 receptor agonist use.
This review studied combined use of sodium-glucose cotransporter 2 inhibitors (SGLT2is) and glucagon-like peptide-1 receptor agonists (GLP-1RAs) in adults with type 2 diabetes, focusing on cardiometabolic outcomes from trials and real-world evidence. It found that SGLT2is and GLP-1RAs provide complementary, non-redundant benefits—SGLT2is mainly reducing heart-failure hospitalization and slowing kidney disease progression, while GLP-1RAs more strongly reduce atherosclerotic events such as stroke. Clinically, the evidence supports optimizing patient selection and sequencing of these drug classes to maximize cardiovascular and renal protection in type 2 diabetes.
Porterfield LR, Nadeem S, Swanson D et al. · Current atherosclerosis reports · (2026) · View on PubMed ↗ · Free PDF ↗
Clinical outcomes of lean metabolic dysfunction-associated steatotic liver disease by phenotypic subtypes.
This study examined clinical outcomes in adults with lean metabolic dysfunction-associated steatotic liver disease (MASLD) using BMI strata and cardio-metabolic risk factor (CMRF) phenotypes and burden, leveraging the TriNetX Global Network. It found that risk of clinical outcomes varies by lean MASLD subtype (underweight vs normal-weight) and by CMRF phenotype/burden, indicating that “lean MASLD” is not a single homogeneous risk group. The findings support more precise risk stratification and phenotype-guided management rather than treating lean MASLD as uniform.
Kuo CC, Chen CH, Kuo HT et al. · Journal of gastroenterology · (2026) · View on PubMed ↗
Shared Genetics of Kidney Function Traits and Bladder Cancer: A Genome-Wide Cross-Trait Analysis.
This genome-wide cross-trait analysis studied shared genetic architecture and causal links between kidney function traits and bladder cancer (BC) using European-ancestry GWAS summary statistics. By integrating multiple kidney measures (eGFRcrea, eGFRcys, BUN, UACR, urate) with BC GWAS data and performing cross-trait analyses, it aimed to identify genetic overlap that could explain the epidemiologic comorbidity between kidney dysfunction and bladder cancer. Scientifically, it supports a common genetic etiology hypothesis and helps prioritize biological pathways for future mechanistic and causal inference work.
Lin Y, Xiang N, Yang Y et al. · Cancer medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Resistance Training Improves Cardiovascular Health in Postmenopausal Women: Systematic Review and Meta-Analysis.
This systematic review and meta-analysis studied randomized and non-randomized controlled trials of resistance training (RT) in postmenopausal women, evaluating effects on hemodynamics, vascular structure/function, cardiovascular autonomic control, and cardiac structural outcomes. It concludes that RT improves cardiovascular health-related measures in this population, addressing a gap where chronic autonomic and vascular effects of RT were less established than aerobic exercise. The findings are significant because they support RT as an evidence-based intervention to reduce cardiovascular risk in postmenopausal women.
Rivera-Mejía SL, Rúa-Alonso MA, Rial-Vázquez J et al. · Journal of applied physiology (Bethesda, Md. : 1985) · (2026) · View on PubMed ↗ · Free PDF ↗
Inflammatory proteins and cognitive decline in older black adults.
This study examined whether circulating inflammatory proteins are associated with cognitive decline in older Black adults using plasma proteomics (Olink® Target-96 Inflammation) and longitudinal cognition data from the Minority Aging Research Study (MARS) and the Rush Clinical Core (n=642). It found that specific inflammatory protein signals measured by Olink were linked to subsequent decline in global cognition and/or cognitive domains over time. The results are significant because they strengthen the mechanistic link between chronic systemic inflammation and neurodegeneration risk in a high-priority population.
Yaskolka Meir A, Adeola HA, Tasaki S et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗
Three-Year Durability of Automated Insulin Delivery Therapy in Children and Adolescents with Type 1 Diabetes: A Multicenter Real-World Study.
This multicenter real-world longitudinal study evaluated the 3-year durability of automated insulin delivery using the MiniMed™ 780G system in 359 children and adolescents with type 1 diabetes (T1D) across 20 Italian pediatric centers. It assessed long-term glycemic metrics and device/engagement parameters to identify determinants of sustained optimal outcomes over three years. The findings are clinically significant because they inform expectations for long-term performance and factors associated with durable glycemic control in pediatric automated insulin delivery.
Bombaci B, Lombardo F, Bassi M et al. · Diabetes technology & therapeutics · (2026) · View on PubMed ↗
Inflammation mediates the Pace of aging based on DNA methylation on mortality from NHANES 1999-2002: a national prospective cohort study.
This study evaluated whether DNA methylation-derived pace of aging (DunedinPoAm) predicts all-cause mortality and whether systemic inflammation mediates this relationship in a multiethnic U.S. cohort from NHANES 1999–2002 (n=21,004). DunedinPoAm was associated with increased mortality risk, and causal mediation analysis quantified the extent to which inflammatory biomarkers explained part of this association. The findings connect epigenetic aging trajectories to inflammation-driven mortality risk and support DunedinPoAm as a potential biomarker of biological aging.
Feng J, Liang Y, Zhou J et al. · Clinical epigenetics · (2026) · View on PubMed ↗ · Free PDF ↗
Respiratory/ENT & lung disease (diagnosis, comorbidity, fibrosis)
“Necrotizing enterocolitis”: a paradigm shift.
This commentary studied necrotizing enterocolitis (NEC) as a diagnostic category and argued against treating it as a single entity. It found that conventional tools (radiographic criteria and Bell staging) do not distinguish biologically distinct intestinal injury mechanisms, and it proposed a data-driven, cluster-based taxonomy integrating clinical trajectories with multi-omics. The proposed paradigm shift aims to enable mechanism-informed diagnosis and personalized interventions, improving both clinical management and NEC research.
Garg PM, Shenberger J, Martin CR et al. · Pediatric research · (2026) · View on PubMed ↗
Integrated Tear Vitamin D-IL-6-NRF2 Signature Associated with Keratoconus Severity: An Exploratory Cross-Sectional Study.
This exploratory cross-sectional study assessed tear 25-hydroxyvitamin D3 levels and coordinated NRF2-dependent antioxidant and IL-6–related inflammatory signatures in 28 keratoconus patients (enriched for atopy and chronic eye rubbing) and 35 healthy controls. Tear vitamin D deficiency was associated with keratoconus severity and with altered NRF2 transcript expression alongside increased IL-6–pathway inflammatory markers measured by optimized RT-qPCR. The results suggest a tear-based vitamin D–IL-6–NRF2 biomarker signature that could help stratify keratoconus severity and guide antioxidant/inflammation-focused interventions.
Cerquinho Leça RG, Affonso Fonseca FL, Luciano da Veiga GR et al. · The ocular surface · (2026) · View on PubMed ↗ · Free PDF ↗
Ambient Air Pollution and Glaucoma Among Middle-Aged and Older Adults in China: Evidence from the China Health and Retirement Longitudinal Study.
Using data from 33,147 participants in the China Health and Retirement Longitudinal Study (CHARLS) across four waves (2011–2018), this study evaluated whether long-term ambient air pollution exposure is associated with glaucoma risk in middle-aged and older adults in China. It found that higher exposure to key pollutants (including carbon monoxide, nitrogen dioxide, ozone, and particulate matter) was linked to increased glaucoma risk. These findings strengthen evidence that air pollution is a modifiable environmental risk factor for glaucoma beyond established age and genetic determinants.
Qin D, Yan B, Jiang Y et al. · Environmental pollution (Barking, Essex : 1987) · (2026) · View on PubMed ↗
Chronic obstructive pulmonary disease and risk of digestive diseases: observational and mendelian randomization analyses in the China Kadoorie Biobank.
This study assessed whether prevalent chronic obstructive pulmonary disease (COPD) and airflow obstruction severity are associated with incident digestive diseases in 512,724 participants from the China Kadoorie Biobank, using observational Cox models and Mendelian randomization. COPD defined by spirometry and self-reported emphysema/chronic bronchitis showed prospective associations with digestive disease risk, and Mendelian randomization was used to evaluate potential causal effects. The results support COPD as a risk factor for digestive comorbidities in the Chinese population and help prioritize prevention strategies.
Zhao Y, Ke Y, Sun D et al. · Respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗
Obstetrics/critical care & infectious disease management
Selective and non-selective carotid ultrasound screening and perioperative stroke incidence in the coronary artery bypass grafting population: a systematic review and meta-analysis.
This systematic review and meta-analysis studied whether selective versus non-selective carotid ultrasound (CU) screening affects perioperative stroke incidence in adults undergoing isolated, non-emergency coronary artery bypass grafting (CABG). The key finding was the pooled comparison of perioperative stroke rates across studies using selective versus non-selective preoperative CU screening strategies (with results synthesized across the included CABG population). Scientifically and clinically, it informs preoperative screening policy to potentially reduce perioperative stroke risk while avoiding unnecessary testing.
King-O’Reilly B, Graves DL, Sandrasekaran K et al. · Journal of cardiothoracic surgery · (2026) · View on PubMed ↗ · Free PDF ↗
Factors associated with pharmacologic serum concentration of magnesium and corresponding obstetric outcomes among women with severe preeclampsia at Iringa regional referral hospital.
This analytical cross-sectional study investigated factors affecting pharmacologic serum magnesium concentrations after magnesium sulphate (MgSO4) initiation and how they relate to obstetric outcomes in women with severe preeclampsia at Iringa regional referral hospital. It found that magnesium serum levels are influenced by patient/clinical factors and are associated with obstetric outcomes, emphasizing the need for effective therapeutic monitoring to balance efficacy and toxicity. Scientifically and clinically, the results support more reliable MgSO4 management strategies for preventing progression to eclampsia.
Kileo JS, Matovelo S, Kitinusa G et al. · BMC pregnancy and childbirth · (2026) · View on PubMed ↗ · Free PDF ↗
Comparator Choice in Helicobacter pylori Eradication: Tegoprazan-Amoxicillin Dual Therapy Versus an Optimized Bismuth-Containing Quadruple Therapy in a Randomized Trial and Meta-Analysis.
In a non-inferiority randomized trial at Qilu Hospital of Shandong University (March 2023–January 2024), treatment-naïve Helicobacter pylori–infected patients were randomized to receive tegoprazan–amoxicillin dual therapy (TADT) or an optimized bismuth-containing quadruple therapy (esomeprazole–amoxicillin–tetracycline–bismuth, EBQT) for 14 days, with a meta-analysis also performed. TADT showed comparable eradication efficacy and safety to EBQT as first-line therapy for H. pylori infection. This supports tegoprazan-based dual therapy as an effective alternative comparator strategy in H. pylori eradication trials and potentially in clinical practice.
Duan M, Kong Q, Wang H et al. · International journal of antimicrobial agents · (2026) · View on PubMed ↗
Prevalence of primary Helicobacter pylori antibiotic resistance in Europe over the past four decades.
This systematic review and meta-analysis assessed primary antibiotic resistance prevalence of Helicobacter pylori across Europe over four decades by searching PubMed (1990–2024) and extracting resistance rates to clarithromycin, metronidazole, levofloxacin, amoxicillin, tetracycline, and rifampicin. It found substantial geographic and temporal variation in primary resistance, with resistance levels changing across the defined decades (1990–1999, 2000–2009, 2010–2019, 2020–2024). These data provide an evidence base for selecting empiric H. pylori eradication regimens and for updating regional treatment guidelines.
Nafria B, Nyssen OP, Narbaiza J et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗
Progress report on new epilepsy treatments: A summary of the Eighteenth Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XVIII). II. Treatments in more advanced clinical development.
This conference report summarized 13 investigational antiepileptic drugs/devices with preliminary seizure-outcome data in patients with epilepsy presented at EILAT XVIII (May 2026). It highlighted advanced-stage candidates including bexicaserin (selective 5-HT2C receptor superagonist for developmental and epileptic encephalopathies), BMB-101 (selective 5-HT2C agonist for absence seizures and DEEs), and elsunersen (antisense oligonucleotide for early-onset SCN2A-DEE), among others. The update is clinically significant because it maps the most promising late-stage therapies and targets (e.g., 5-HT2C and SCN2A) toward near-term translation for specific epilepsy syndromes.
Bialer M, Johannessen Landmark C, Koepp MJ et al. · Epilepsia · (2026) · View on PubMed ↗
Emerging Antibiotics for Urinary Tract Infections: Clinical Implications for Women’s Health.
This review studied FDA-approved antibiotics from 2017–2026 for complicated and resistant urinary tract infections (UTIs), emphasizing pharmacology, spectrum, and clinical evidence relevant to women’s health. It found that newer approvals expand options for complicated/resistant UTIs and that the evidence base from FDA documents and pivotal trials can inform practical selection based on microbiologic coverage and resistance patterns. Clinically, it supports more informed antibiotic choice for women with complicated or resistant UTIs while aligning with regulatory-approved indications.
Karaoui LR, Bejjani C, Mansour H · The Annals of pharmacotherapy · (2026) · View on PubMed ↗
TgRON3 Links the Moving Junction to Microneme Secretion and Parasite Motility in Toxoplasma gondii.
This study investigated additional regulatory proteins required for Toxoplasma gondii moving junction (MJ)-driven invasion by using proximity labeling to identify proteins associated with the MJ component TgRON8, followed by functional testing of candidate genes. It found that TgRON3 (and TgAPH) are essential for efficient host cell invasion, and that disrupting TgRON3 causes a pronounced invasion defect, with biochemical/structural data supporting TgRON3 association with MJ machinery. The findings are significant because they define new MJ-linked invasion regulators that could be targeted to impair T. gondii motility and infection.
Pei Y, Peng J, Ying Z et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗
Immunocompromised patients with viral severe acute respiratory infection in intensive care: an Australia wide, retrospective, observational study.
This Australia-wide retrospective observational study compared clinical characteristics, treatments, and outcomes of laboratory-confirmed viral severe acute respiratory infection (SARI) in immunocompromised versus immunocompetent adults admitted to 46 ICUs between June 2022 and August 2025. Immunocompromised status—defined by chronic immunosuppression, malignancy, AIDS/HIV, or organ transplantation—was associated with differences in ICU course and outcomes compared with immunocompetent patients. These findings help clinicians anticipate risk and tailor management strategies for critically ill viral SARI patients with specific immunocompromising conditions.
Hastak P, Andersen CR, Wah W et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗
Assessing fluid responsiveness in mechanically ventilated patients with intra-abdominal hypertension: a two-center, prospective, observational study.
This study investigated how intra-abdominal hypertension (IAH) affects fluid responsiveness assessment in mechanically ventilated ICU patients by comparing passive leg raising (PLR) impairment mechanisms and the diagnostic accuracy of the end-expiratory occlusion (EEO) test and mini-fluid challenge. In a two-center prospective observational design, patients with IAH (IAP ≥12 mmHg) were compared with those without IAH to determine whether EEO and mini-fluid challenge remain reliable when PLR performance is compromised. The results aim to improve bedside fluid management strategies in ventilated patients with IAH by identifying more dependable dynamic tests.
Si X, Song W, Cao D et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗
The usual suspects: a pragmatic framework to identify and address reversible contributors in apparent refractory septic shock.
This article proposed a pragmatic bedside framework (“usual suspects”) to identify and address reversible contributors in patients with apparent refractory septic shock, preceding formal progression to refractory shock. It operationalizes reassessment for modifiable causes such as unresolved infection, inadequate fluids, metabolic derangements, iatrogenic factors, and cardiac dysfunction despite initial resuscitation. The framework is intended to standardize early, actionable evaluation to prevent avoidable escalation of vasopressors and improve outcomes.
Melo P, Wendel-Garcia PD, Leone M et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗
Generated automatically on July 20, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.