One post tagged with "Pulmonary hypertension & cardiopulmonary outcomes"

Automated digest · 99 articles · 15 research areas · March 22, 2026

Overview​

Across this week’s set, a dominant thread is the move from mechanistic insight to scalable clinical impact—especially via biomarkers, decision support, and real-world evidence. AI-enabled tools (e.g., stroke CDSS and AI-assisted patient education) and imaging/biomarker strategies (retinal risk atlases, PET metabolic tumor volume in CAR T, ctDNA for de-escalation decisions, and liquid biopsy approaches for EBV+ Burkitt’s lymphoma) reflect a broader push toward earlier risk stratification and more personalized care. Several studies also emphasize translating biological heterogeneity into clinical decision-making, such as immune-dysregulation–guided immunomodulation in pneumonia/sepsis and immune- or hypoxia-informed prognostic models after cancer therapies.

Mechanistically, immune regulation and immunometabolism recur throughout oncology and inflammatory disease. Multiple papers connect specific immune pathways (TAM-driven signaling axes, macrophage/immune escape programs, necroptosis/necroinflammation, immunothrombosis in NEC, and tumor microenvironment remodeling via targets like WIP1/PPM1D) to therapy resistance or treatment response—often suggesting combination strategies (e.g., checkpoint sensitization, TAM pathway inhibition, or pairing metabolic/immune vulnerabilities). In parallel, metabolism-linked mechanisms—lactylation and mitochondrial quality control in cancer and degenerative disease, microbiome-derived metabolites (serotonin, indole/indoxyl sulfate, microbial lipids) shaping organ outcomes, and nutrient-stress death pathways like mitoxyperilysis and ferroptosis—highlight how upstream metabolic and cellular stress programs can be drugged.

Finally, the digest spans major clinical domains beyond cancer: cardiovascular and cardiopulmonary risk stratification (PVR in group 2 PH, fibrinogen–Bmal1 in aortic dissection, RhoA inhibition in heart failure), neuroimmune framing of syndromes (POTS/ME-CFS/Long COVID), and neurodegeneration links (OSA–astrocyte dysfunction, oxidative stress/inflammasome pathways in Alzheimer’s, and circadian control of pain). Together, these studies reinforce a unifying theme: complex diseases are increasingly being understood as networked systems—where timing, immune state, metabolism, and measurable biomarkers jointly determine outcomes.

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AI-enabled clinical decision support & digital health​

Effect of a clinical decision support system on stroke care quality and outcomes in patients with acute ischaemic stroke (GOLDEN BRIDGE II): cluster randomised clinical trial.​

This multicentre cluster randomised clinical trial evaluated a stroke clinical decision support system (CDSS) using artificial intelligence-assisted imaging analysis, stroke-cause classification, and evidence-based treatment recommendations in 77 Chinese hospitals treating 21,603 adults with acute ischaemic stroke within 7 days of symptom onset. Hospitals receiving the CDSS support improved stroke care quality and clinical outcomes compared with control hospitals. These findings suggest that AI-enabled CDSS integrated into routine hospital workflows can enhance real-world stroke management and patient prognosis at scale.

Zhang X, Ding L, Jing J et al. · BMJ (Clinical research ed.) · (2026) · View on PubMed ↗

Effectiveness of Al-Assisted Patient Health Education Using Voice Cloning and ChatGPT: Prospective Randomized Controlled Trial.​

This prospective randomized controlled trial evaluated AI-assisted patient health education that combined voice cloning and ChatGPT, comparing different voice-cloning strategies and assessing the reliability of automated AI evaluation tools. The study tested whether the AI-delivered, personalized and interactive education improved patient outcomes compared with conventional approaches (details truncated in the provided abstract). If effective, this would support scalable, personalized digital health education workflows using voice cloning plus large language models.

Sun Y, Xu S, Jin H et al. · Journal of medical Internet research · (2026) · View on PubMed ↗

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Targeted protein degradation & drug discovery platforms​

Hijacking ERAD for targeted degradation of transmembrane proteins.​

This study developed ERAD-engaging chimeras (ERADECs), a targeted protein degradation (TPD) platform that hijacks ER-associated degradation (ERAD) to degrade transmembrane proteins, and tested it by designing ERADECs targeting programmed death-ligand 1 (PD-L1). The authors identified desonide as a binder of the ER E3 ligase SYVN1 and showed that ERADECs efficiently degraded PD-L1 with high efficacy. The work provides a mechanistic and design framework for degrading difficult ER-folded transmembrane targets, potentially expanding TPD drug-discovery beyond soluble proteins.

Song H, Wang W, Mei T et al. · Cell · (2026) · View on PubMed ↗

Human DHX29 detects nonoptimal codon usage to regulate mRNA stability.​

This study examined how the human RNA helicase DHX29 regulates mRNA stability in response to nonoptimal codon usage in human cells. Using genome-wide CRISPR screening plus cryogenic electron microscopy and selective ribosome profiling, it found that DHX29 directly interacts with the A-site entrance of the translating 80S ribosome (the eEF1A•GTP•aminoacyl-tRNA ternary complex binding region), supporting a role in monitoring aminoacyl-tRNA sampling and codon-dependent gene expression. These findings reveal a specific molecular mechanism by which codon quality is sensed to control mRNA fate in humans.

Hia F, Wu Y, Yoshinaga M et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Unstructured transcription factor interactions enable emergent specificity.​

This study investigated how intrinsically disordered regions (IDRs) enable emergent specificity in transcription factor interactions with chromatin and each other in live cells. Using proximity-assisted photoactivation (PAPA), it found that the Sp1 DNA-binding domain alone interacts poorly with chromatin, but that fusing an IDR to Sp1 can confer sharp locus specificity, with live imaging in Drosophila polytene chromosomes supporting IDR-driven targeting. This demonstrates how unstructured protein segments can generate functional specificity beyond canonical DNA-binding alone.

Abidi AA, Cattoglio C, Tang NN et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Stage-specific transcriptomics of a leader cell reveals cell machineries driving collective invasion.​

This study generated stage-specific transcriptomic profiles of the Caenorhabditis elegans gonadal leader cell, the distal tip cell (DTC), comparing invasive larval-stage DTCs with noninvasive adult-stage DTCs. The invasive-stage transcriptome revealed molecular programs and cell-machinery signatures that drive collective invasion in vivo. The dataset and identified regulators provide a mechanistic framework for how leader cells coordinate invasion relevant to development, tissue repair, and metastasis.

Agarwal P, Maimon Zielonka I, Gingold H et al. · The Journal of cell biology · (2026) · View on PubMed ↗

Regulation of YAP activity by nuclear G-actin binding.​

This mechanistic study investigated how nuclear G-actin binding regulates the activity of YAP, a TEAD-associated transcriptional co-activator in the Hippo pathway. The key finding is that binding of monomeric actin (G-actin) in the nucleus modulates YAP activity, linking actin cytoskeletal dynamics to transcriptional control of proliferation, differentiation, and mechanotransduction. This advances understanding of how cytoskeletal/biomechanical signals are converted into YAP-driven gene expression programs relevant to development and cancer metastasis.

Wang H, Jayawardana IM, Fleisch JM et al. · Nucleic acids research · (2026) · View on PubMed ↗

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Inflammation, immunomodulation & immune microenvironment​

USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses.​

This mechanistic study investigated how the deubiquitinase USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses, using analyses of human atherosclerotic lesions and ApoE-/- mouse models. USP25 was downregulated in human lesions, and restoring/defining USP25 function reduced atherosclerosis by limiting RIPK1-driven inflammatory signaling, with USP25 substrates identified by mass spectrometry. These results position USP25 as a potential therapeutic target to dampen inflammation-driven progression of atherosclerosis.

Su X, Zhou B, Xu Y et al. · EBioMedicine · (2026) · View on PubMed ↗

CD177⁺ neutrophil-platelet aggregates contribute to thromboinflammation via NETs in necrotizing enterocolitis.​

The study investigated necrotizing enterocolitis (NEC) pathogenesis by focusing on CD177+ neutrophil–platelet aggregates and their contribution to thromboinflammation via neutrophil extracellular traps (NETs) in clinical NEC samples and neonatal mouse models. It found that NEC is characterized by immunothrombosis with infiltrating CD177+ neutrophils and activated platelets, linked to NET-mediated thromboinflammatory injury. This mechanistic evidence highlights CD177+ neutrophil–platelet interactions and NETs as potential targets to prevent or treat NEC in premature infants.

Lan C, Tian B, Shi Y et al. · Nature communications · (2026) · View on PubMed ↗

Quantifying immune dysregulation in pneumonia and sepsis with a parsimonious machine-learning model: a multicohort analysis across care settings and reanalysis of a hydrocortisone randomised controlled trial.​

This multicohort machine-learning analysis quantified immune dysregulation in pneumonia and sepsis and reanalyzed data from a hydrocortisone randomized controlled trial to assess biologically informed immunomodulation. The key finding is that a parsimonious immune-dysregulation model can stratify patients by the extent of dysregulation rather than only clinical severity, potentially explaining heterogeneity in treatment response. Scientifically and clinically, it supports more targeted use of immunomodulators like hydrocortisone by identifying patients most likely to benefit.

Michels EHA, Dequin PF, Butler JM et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

Psoriasis modulates inflammatory bowel disease risk and intestinal epithelium lipid metabolism via IL-1β-producing macrophages.​

This work studied how psoriasis influences inflammatory bowel disease risk and intestinal epithelial lipid metabolism, focusing on IL-1β-producing macrophages, using a clinical cohort, experimental psoriasis mouse models, and intestinal organoids. Psoriasis severity inversely correlated with postprandial apolipoprotein B48 levels, and a recombinant photoconvertible apolipoprotein B reporter enabled real-time quantification of chylomicron production showing psoriasis-driven impairment of intestinal lipid handling. These results mechanistically link psoriasis-associated IL-1β macrophage activity to dysregulated lipid metabolism that may contribute to increased IBD risk.

Wu J, Liu S, Dan W et al. · Cell metabolism · (2026) · View on PubMed ↗

Gsα deficiency in macrophages promotes tumor progression via the MAPK signaling pathway.​

This preclinical study investigated whether Gsα (G protein alpha subunit) deficiency in tumor-associated macrophages (TAMs) affects tumor progression through MAPK signaling using mouse models with B16 and MC38 tumor cells. It reports that Gsα-deficient TAMs accelerate tumor growth and metastasis and that the effect is mediated via activation of the MAPK pathway. These results are clinically relevant because they suggest that restoring or targeting Gsα–MAPK signaling in TAMs could be a strategy to reprogram immunosuppressive macrophages and slow cancer progression.

Yan W, Yang J, Tan S et al. · Journal of molecular medicine (Berlin, Germany) · (2026) · View on PubMed ↗

Albumin-Bound STING Agonist Reprograms HSPCs to Antitumor Neutrophils Enhancing CD8+ T Cell Immunity.​

In preclinical cancer immunology experiments, an albumin-bound STING agonist (Nano ZSA-51D) was tested for its ability to reprogram hematopoietic stem and progenitor cells (HSPCs) into antitumor neutrophils. Nano ZSA-51D enhanced MHC I–mediated CD8+ T cell immunity and sensitized tumors to α-PD1 immunotherapy by shifting neutrophil fate toward antitumor phenotypes. This provides a strategy to improve checkpoint blockade efficacy by targeting innate immune programming at the HSPC stage.

Tao J, Zhao HY, Li C et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

ECM1 produced by hepatic stellate cells serves as gate keeper of liver homeostasis in hepatic fibrosis.​

This study examined hepatic stellate cell (HSC) homeostatic functions during fibrogenesis in Lrat-iDTR inducible HSC ablation mice, comparing two injury contexts: CCl4-driven parenchymal injury and metabolic dysfunction–associated steatohepatitis (MASH) induced by a choline-deficient high-fat diet (CD-HFD). The authors report that ECM1 produced by hepatic stellate cells acts as a “gate keeper” of liver homeostasis and that preserving this HSC homeostatic program is important for limiting maladaptive fibrosis while maintaining regeneration. These findings identify ECM1/HSC homeostasis as a potential therapeutic target to treat liver fibrosis without fully disabling beneficial HSC functions.

Yang A, Yan X, Wang Y et al. · Hepatology (Baltimore, Md.) · (2026) · View on PubMed ↗

A Rare RIPK3 Variant Enhances Necroptosis and Promotes Inflammation in a Still's Disease-like Autoinflammatory Syndrome.​

This study investigated a novel autoinflammatory syndrome resembling Still’s disease in a three-generation family using whole-exome sequencing to identify a RIPK3 p.Q134K variant and then performed functional assays to test its effects on kinase activity, necroptosis, and inflammatory signaling. The key finding is that the RIPK3 p.Q134K variant enhances necroptosis and promotes inflammatory signaling compared with expected wild-type behavior. This provides a mechanistic genetic explanation for a Still’s disease–like phenotype and highlights RIPK3-driven necroptosis as a potential therapeutic pathway in related autoinflammatory conditions.

Chen L, Dai Q, Xiao Y et al. · Arthritis & rheumatology (Hoboken, N.J.) · (2026) · View on PubMed ↗

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Cancer immunotherapy, immune evasion & checkpoint sensitization​

Targeting tumor-associated macrophages-induced IGF1/PI3K/Zic1 axis triggers SHH medulloblastoma regression and chemosensitization.​

The study tested whether targeting the tumor-associated macrophage (TAM)-induced IGF1/PI3K/Zic1 axis can trigger SHH medulloblastoma regression and chemosensitization. In a CD11b-DTR/Ptch1-deficient medulloblastoma mouse model, TAM genetic deletion and pharmacologic inhibition using the CSF1R inhibitor PLX3397 and the PI3K inhibitor buparlisib (alone or with chemotherapy) produced tumor regression and increased chemosensitivity, supported by RNA-seq, Western blotting, flow cytometry, immunohistochemistry, and qPCR analyses. This is significant because it links a specific TAM-driven signaling axis (IGF1/PI3K/Zic1) to SHH pathway control and suggests combination strategies to overcome medulloblastoma chemoresistance.

Pang YC, Wang C, Qiu JF et al. · Neuro-oncology · (2026) · View on PubMed ↗

Targeting WIP1 reprograms immunosuppressive tumor microenvironment to potentiate immunotherapy response in colorectal cancer.​

The study investigated wild-type p53-induced phosphatase 1 (WIP1/PPM1D) as an immunosuppressive driver in colorectal cancer and tested genetic or pharmacological WIP1 inhibition in tumor models. It found that inhibiting WIP1 suppressed tumor growth by remodeling the tumor microenvironment, increasing infiltration of anti-tumor macrophages and cytotoxic T cells and dampening type I interferon (IFN) signaling. This positions WIP1/PPM1D as a therapeutic target to potentiate immune checkpoint inhibitor responses by reversing innate immune suppression in CRC.

Chen L, Chen M, Yuan S et al. · Cell death and differentiation · (2026) · View on PubMed ↗

CAV1-DOT1L axis in TAM-derived EVs orchestrates VM and sensitises PDAC to combined VM and VEGF targeting.​

This mechanistic study investigated how the CAV1–DOT1L axis in tumor-associated macrophage (TAM)-derived extracellular vesicles (EVs) regulates vasculogenic mimicry (VM) and sensitizes pancreatic ductal adenocarcinoma (PDAC) to combined VM and VEGF targeting. The key finding is that TAM-derived EVs carrying signals through the CAV1–DOT1L axis orchestrate VM and increase therapeutic sensitivity to strategies targeting VM together with VEGF. This is significant because it identifies a specific immune–epigenetic EV pathway and a potential combination vulnerability for treating aggressive PDAC.

Liu Z, Zhang Y, Wu H et al. · Gut · (2026) · View on PubMed ↗

Unveiling the multifaceted roles of BCL3: biological functions and disease implications.​

This review article examined the atypical NF-κB inhibitor-of-κB family member BCL3 and its regulation by post-translational modifications, focusing on how BCL3 functions in normal biology and disease. It reports that nuclear BCL3 acts as a bidirectional transcriptional regulator within NF-κB signaling, and that in pathological contexts BCL3 promotes oncogenic phenotypes including abnormal proliferation, apoptosis inhibition, metastasis, and chemotherapy resistance in hematologic malignancies. These mechanistic insights position BCL3 as a potential therapeutic target for NF-κB–driven cancers, where modulating its phosphorylation-dependent activity could alter tumor progression and treatment response.

Guo X, Guo R, Wang W et al. · Apoptosis : an international journal on programmed cell death · (2026) · View on PubMed ↗

HTRA1+ macrophages induce T cells egress through CRIP1/NF-κB/CXCL12 to limit the effects of immunotherapy in triple-negative breast cancer.​

In triple-negative breast cancer (TNBC), this study used single-cell and spatial transcriptomics to define a macrophage subpopulation characterized by high HTRA1 expression that drives T cell egress during immunotherapy. HTRA1+ macrophages induced T cell egress via a CRIP1/NF-κB/CXCL12 signaling axis, which limited the effectiveness of immunotherapy. Mechanistically, this identifies a macrophage-driven immune escape pathway that could be targeted to improve responses to immunotherapy in TNBC.

Weng J, Xu W, Wang F et al. · Cancer immunology research · (2026) · View on PubMed ↗

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Cancer therapeutics & drug development (ADC/bioconjugates/targeted agents)​

SHR-A1811, a novel HER2-targeting antibody-drug conjugate, in advanced solid tumors (HORIZON-X): a global phase 1 trial.​

The study reported long-term follow-up from the global phase 1 HORIZON-X trial evaluating SHR-A1811, a HER2-targeting antibody-drug conjugate, in adults with advanced solid tumors. It found that SHR-A1811 (trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload) showed substantial antitumor activity in heavily treated patients with HER2-expressing or HER2-mutated tumors, with dosing by intravenous administration across multiple cohorts. This is clinically significant because it extends early-phase evidence for a next-generation HER2 ADC with potential activity in refractory HER2-driven cancers.

Yao H, Yan M, Tong Z et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

A bispecific nanobody-drug conjugate targeting TROP2 and c-Met for low-concentration, single-dose treatment of pancreatic cancer.​

This preclinical study developed B6ADC, a nanobody-based bispecific antibody-drug conjugate targeting TROP2 and c-Met, and tested it in TROP2/c-Met-expressing pancreatic cancer cell lines and mouse tumor models. B6ADC showed potent in vitro cytotoxicity across multiple TROP2/c-Met-positive lines and superior in vivo tumor inhibition versus single-target ADCs and their combinations, including sacituzumab govitecan (TROP2 ADC) and Teliso-V (c-Met ADC). These findings suggest that dual TROP2/c-Met targeting with a nanobody-drug conjugate could improve efficacy despite antigen heterogeneity and limited tumor penetration in pancreatic cancer.

Ning W, Liu H, Zeng H et al. · Cell reports. Medicine · (2026) · View on PubMed ↗

Long-term outcomes of eribulin‑based neoadjuvant chemotherapy for triple‑negative breast cancer patients stratified by homologous recombination deficiency status: results of the randomized JBCRG-22 study.​

This randomized JBCRG-22 study investigated long-term outcomes of eribulin-based neoadjuvant chemotherapy in triple-negative breast cancer (TNBC) patients stratified by homologous recombination deficiency (HRD) and germline BRCA mutation (gBRCAm) status. The trial compared paclitaxel+carboplatin vs eribulin+carboplatin (both followed by anthracycline) in HRD-positive/gBRCAm-eligible group A, and eribulin combinations (eribulin+cyclophosphamide vs eribulin+capecitabine) in group B, with outcomes reported by HRD/gBRCA stratification. These results are scientifically and clinically important because they test whether HRD/gBRCA status can inform selection of eribulin-containing neoadjuvant regimens to improve durable outcomes in TNBC.

Masuda N, Yasojima H, Bando H et al. · Breast cancer research and treatment · (2026) · View on PubMed ↗

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Cancer biomarkers & liquid biopsy / imaging prognostication​

Liquid biopsy for the diagnosis of EBV-positive Burkitt's lymphoma in endemic areas.​

The study evaluated a blood-based liquid biopsy approach for diagnosing Epstein–Barr virus (EBV)-positive Burkitt’s lymphoma (BL) in endemic settings. In 377 children and young adults with suspected lymphoma in Tanzania and Uganda, the authors used circulating tumor DNA markers—including MYC mutations, MYC–immunoglobulin translocations, and EBV fragmentomics—alongside pathology capacity building to establish diagnostic accuracy and turnaround time against a gold-standard tissue diagnosis. The significance is that it provides a scalable diagnostic pathway where pathology resources are limited, potentially reducing delays in BL diagnosis.

Chamba C, Christopher H, Josephat E et al. · Nature medicine · (2026) · View on PubMed ↗

Extrachromosomal DNA in urothelial carcinoma: mechanisms and clinical applications.​

The study reviewed how extrachromosomal DNA (ecDNA) drives genomic instability and tumor evolution in urothelial carcinoma and how ecDNA can be detected using sequencing/imaging and liquid biopsy approaches in patients. It found that ecDNA amplifies oncogenes, alters 3D chromatin interactions, reprograms transcription, and promotes APOBEC3-associated mutational evolution, contributing to intratumour heterogeneity and aggressive disease. These insights support ecDNA as a mechanistic driver and as a clinically actionable biomarker detectable in urine/plasma for non-invasive patient stratification.

Li C, Hu Z, Zhang W et al. · Nature reviews. Urology · (2026) · View on PubMed ↗

Prognostic Significance of MSI and EBV Positivity in PD-L1 Positive Gastric Cancer: A Systematic Review and Meta-Analysis.​

The study performed a systematic review and meta-analysis to assess the prognostic significance of microsatellite instability (MSI), Epstein–Barr virus (EBV) positivity, and PD-L1 expression in PD-L1–positive gastric cancer. It synthesized studies (2010–2024) that measured MSI, PD-L1 (immunohistochemistry), and EBV (PCR or in situ hybridization) and evaluated outcomes such as overall survival and progression-free/disease-free survival. The findings are intended to refine prognostic biomarker stratification for gastric cancer patients, particularly to inform immunotherapy-related decision-making.

Petrelli F, Antista M, Ghidini A et al. · Cancer medicine · (2026) · View on PubMed ↗

A predictive atlas of disease onset from retinal fundus photographs: a modelling study using data from population-based cohorts.​

This modelling study used retinal fundus photographs from population-based cohorts to predict incident disease onset across a broad range of conditions in humans. The authors developed a predictive atlas that benchmarks how much retinal imaging adds to baseline risk for future disease. If validated, retinal fundus–based risk stratification could enable scalable, non-invasive early detection to help health systems manage rising disease burden.

Buergel T, Loock L, Steinfeldt J et al. · The Lancet. Digital health · (2026) · View on PubMed ↗

Risk Assessment in Large B-Cell Lymphoma Using Metabolic Tumor Volume: Real-World Data from a Multicenter Cohort of Patients Undergoing CAR T-Cell Therapy.​

This multicenter real-world cohort study evaluated whether PET-derived metabolic tumor volume (MTV) or MTV-based risk scores improve outcome prediction versus the International Prognostic Index (IPI) in 111 patients with relapsed/refractory large B-cell lymphoma undergoing CAR T-cell therapy. The key finding was that quantifying 18F-FDG–avid lymphoma burden/MTV provided more accurate risk assessment for nonresponse and outcomes than IPI alone. Clinically, MTV-based stratification could help identify likely nonresponders before CAR T infusion and support earlier treatment optimization.

Voltin CA, Flossdorf S, Kurch L et al. · Journal of nuclear medicine : official publication, Society of Nuclear Medicine · (2026) · View on PubMed ↗

Hypoxia-related and immune phenotype-related fusion model for non-invasive prognostication of hepatocellular carcinoma treated by TACE: a multicentre study.​

This multicentre study enrolled 1448 hepatocellular carcinoma (HCC) patients receiving transarterial chemoembolisation (TACE) to develop and validate a multimodal fusion prognostic model integrating hypoxia-related and immune phenotype-related features. The key finding is that the model improved survival prognostication and addressed limitations of existing imaging/prognostic scores by adding biological interpretability and generalisability. Scientifically and clinically, it could enable more precise risk stratification to guide post-TACE management and trial enrichment.

Guo Y, Zhang G, Fu X et al. · Gut · (2026) · View on PubMed ↗

Post hoc estimation of a quantitative restriction spectrum imaging biomarker for prostate cancer detection using conventional MRI.​

This study evaluated whether restriction spectrum imaging (RSI) metrics can be estimated post hoc from conventional MRI to detect clinically significant prostate cancer (csPCa). Using conventional diffusion-weighted imaging (DWI) as a surrogate for dedicated multi–b-value RSI acquisition, the authors assessed the accuracy/validity of post hoc estimated RSI biomarkers (RSIrs) for csPCa detection (full quantitative results are truncated in the abstract). If validated, this approach could enable automated csPCa detection without requiring specialized RSI acquisition protocols.

Do DD, Conlin CC, Bagrodia A et al. · Journal of applied clinical medical physics · (2026) · View on PubMed ↗

Machine Learning-Based Sleep Electroencephalographic Brain Age Index and Dementia Risk: An Individual Participant Data Meta-Analysis.​

This individual participant data meta-analysis studied whether a machine learning-based sleep electroencephalography (EEG) brain age index (BAI) predicts incident dementia in community-dwelling populations. Pooling sleep data from five longitudinal cohorts, it evaluates the association between deviation of sleep-EEG brain age from chronological age (the sleep BAI) and future dementia risk. The significance is that a scalable, data-driven sleep EEG biomarker could improve dementia risk stratification and early identification in the general population.

Sun H, Milton S, Fang Y et al. · JAMA network open · (2026) · View on PubMed ↗

Use of ctDNA in Older Women with ER+ Breast Cancer to Facilitate Surgical De-escalation: A Prospective, Hybrid-Decentralized Trial with Correlative Studies.​

In a prospective, hybrid-decentralized trial (NCT05914792) enrolling 43 older women with ER+ breast cancer, ctDNA was used to determine whether ctDNA levels predict tumor progression in patients who chose surgical de-escalation (forgoing breast cancer surgery in favor of primary endocrine therapy). ctDNA status/levels were associated with subsequent tumor progression, supporting ctDNA as a prognostic tool to guide safe de-escalation decisions. This could reduce overtreatment in older patients while maintaining oncologic safety through biomarker-guided management.

Carleton N, Chang AC, Chen F et al. · Clinical cancer research : an official journal of the American Association for Cancer Research · (2026) · View on PubMed ↗

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Tumor metabolism, lactate/lipids & immunometabolism​

Lactylation Converts ABHD6 into a Mitochondrial Regulator that Drives Lenvatinib Resistance in Hepatocellular Carcinoma.​

This cancer biology study examined how lactylation converts ABHD6 into a mitochondrial regulator that drives lenvatinib resistance in hepatocellular carcinoma (HCC). The authors found that ABHD6 promotes resistance by perturbing mitochondrial dynamics through a ligand-binding allosteric switch at the S148 catalytic site, and the pro-resistance effect was independent of ABHD6 catalytic activity but required non-occupied ABHD6. Clinically, targeting the lactylation-dependent ABHD6 mitochondrial regulatory function could help overcome or prevent lenvatinib resistance in HCC.

Sun Y, Luo C, Yang H et al. · Cancer research · (2026) · View on PubMed ↗

Skeletal muscle metabolism in health and disease: Mechanisms, interventions, and clinical perspectives.​

This review focused on skeletal muscle metabolism in health and disease, detailing mechanisms and interventions relevant to clinical outcomes. It emphasizes that metabolic flexibility—coordinated regulation of glucose uptake, fatty acid oxidation, and amino acid metabolism—depends on signaling networks centered on insulin, AMPK, mTOR, and PGC-1α, and that disruptions lead to mitochondrial dysfunction, lipid dysregulation, and muscle wasting. The scientific significance is that it consolidates actionable molecular targets for interventions in metabolic diseases such as obesity, type 2 diabetes, and sarcopenia.

Lin D, Zhang L, Huang C et al. · iScience · (2026) · View on PubMed ↗

Histone lactylation-driven feedback loop modulates pyrimidine metabolism to promote oral carcinogenesis.​

The study examined how lactate-dependent histone lactylation regulates pyrimidine metabolism to promote oral squamous cell carcinoma (OSCC) using human tissue analyses and mechanistic perturbations in vitro and in vivo. It found that histone lactylation levels were increased in oral leukoplakia and OSCC, and that blocking lactylation via glycolysis inhibitors or silencing LDHA reduced OSCC initiation/progression, supported by CUT&Tag, scRNA-seq, and ChIP-qPCR approaches. This identifies a histone lactylation–metabolism feedback mechanism as a potential therapeutic axis for oral carcinogenesis.

Wang Y, Geng Y, Chen Y et al. · Cell death & disease · (2026) · View on PubMed ↗

Resetting of a tandem microRNA156 enables vegetative perennial growth in rice.​

This study investigated the genetic basis of perennial growth habit in rice by analyzing introgression lines between wild and cultivated rice and mapping the Endless Branches and Tillers locus (EBT1). It found that EBT1 contains tandem microRNA156 genes (MIR156BC) and that the wild allele (EBT1W1943) resets MIR156BC expression in tiller buds through higher chromatin accessibility and lower H3K27me3, enabling floral reversion and vegetative propagation. This provides a specific miRNA locus and epigenetic mechanism that can be used to engineer perennial traits in cultivated rice.

Dai B, Lv D, Chen E et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Gut microbe-derived N-acyl serinol lipids shape host postprandial metabolic homeostasis.​

This study examined the role of gut microbe–derived N-acyl serinol lipids (N-acyl amides) in shaping host postprandial metabolic homeostasis. It reported that these bacterial lipids produced after meals act as signaling molecules that influence host metabolic responses during the postprandial period (details truncated in the abstract). The work supports a specific class of microbiome-derived lipids as potential targets for microbiome-inspired therapies to improve human metabolic regulation.

Dutta S, Mahen KK, Massey WJ et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

A CHKA-PML autophagy checkpoint enables tumors to evade glutamine starvation.​

This study examined how glutamine scarcity affects tumor cell survival by focusing on choline kinase alpha (CHKA) and its downstream target promyelocytic leukemia (PML) in cancer models. The authors found that glutamine deprivation upregulates CHKA monomerization and noncanonical kinase activity, leading to CHKA-mediated phosphorylation of PML at tyrosine 339 and a shift to cytoplasmic PML that blocks SUMO-ubiquitin–linked protein degradation. This CHKA–PML autophagy checkpoint helps tumors evade nutrient stress, identifying a potential metabolic vulnerability to target in glutamine-deprived solid tumors.

Wang R, Cao L, He X et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Phospholipid Glutathione Peroxidase Overexpression Mitigates Cancer Cachexia by Protecting Muscle Mass and Lowering Inflammation.​

This study evaluated whether overexpressing phospholipid glutathione peroxidase (GPx) mitigates cancer cachexia in experimental models by protecting skeletal muscle mass and reducing inflammation. The key finding is that phospholipid GPx overexpression attenuates cachexia-associated muscle wasting and lowers inflammatory burden, consistent with improved control of oxidative/lipid-peroxidation stress. Scientifically and clinically, it suggests that enhancing phospholipid antioxidant defenses could be a therapeutic strategy to counteract muscle loss and inflammation in cancer cachexia.

Duggan E, Fuqua JD, Hagy B et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗

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Mitochondrial biology & cell death mechanisms​

FGF21-Mediated Upregulation of SIRT1 Delays Intervertebral Disc Degeneration by Promoting PINK1/Parkin Dependent Mitophagy Through Deacetylation of FOXO3.​

This preclinical study tested whether FGF21-mediated upregulation of SIRT1 delays intervertebral disc degeneration by promoting PINK1/Parkin-dependent mitophagy through deacetylation of FOXO3. In human and rat degenerated intervertebral discs and in vitro models, FGF21 was downregulated and linked to increased senescence markers, while mechanistic experiments supported an FGF21→SIRT1→FOXO3 deacetylation→PINK1/Parkin mitophagy pathway that reduced pathological progression. These findings identify a potentially druggable axis to slow intervertebral disc degeneration by enhancing mitochondrial quality control.

Wu ZL, Ran R, Xie QQ et al. · Aging cell · (2026) · View on PubMed ↗

Apoptotic extracellular vesicles derived from MSCs exposed to hypoxic and inflammatory environments slow intervertebral disc degeneration by enhancing cell activity and regulating immunity microenvironment.​

The study examined whether apoptotic extracellular vesicles (ApoEVs) derived from mesenchymal stem cells (MSCs) exposed to hypoxic and inflammatory conditions can slow intervertebral disc degeneration by modulating nucleus pulposus cell (NPC) activity and the local immune microenvironment. The key finding is that hypoxia/inflammation-conditioned MSC-derived ApoEVs attenuate IVDD progression by enhancing NPC functional activity and regulating the immunity microenvironment. This suggests a cell-free, microenvironment-matched vesicle therapy approach for IVDD where transplanted stem cells are prone to apoptosis.

Zhang W, Ma X, Yin H et al. · Materials today. Bio · (2026) · View on PubMed ↗

Mitoxyperilysis: fasting-induced cell death in immunometabolism and disease.​

This review article describes mitoxyperilysis, a fasting-induced lytic cell death mechanism involving mitochondrial proximity-dependent rupture of the plasma membrane, triggered by immune agonists plus nutrient starvation. The key finding is that mitoxyperilysis links immunometabolism to a distinct, therapeutically targetable death pathway relevant to sepsis and cancer. Scientifically, it reframes how immune activation and metabolic stress cooperate to drive cell death, potentially guiding new interventions.

Al-Zidan R, Gautam M, Man SM · Trends in biochemical sciences · (2026) · View on PubMed ↗

Transplantation of encapsulated mitochondria alleviates dysfunction in mitochondrial and Parkinson's disease models.​

This study investigated mitochondrial transplantation in mice and monkeys by encapsulating mitochondria in vesicles derived from erythrocyte plasma membranes to enhance delivery into somatic tissues. Encapsulated mitochondria complemented loss/deletion/mutations of mitochondrial DNA and rescued bioenergetic and biochemical defects in patient-derived mitochondrial disorder cells. The approach supports a clinically relevant strategy for efficient mitochondrial delivery and functional restoration in mitochondrial disease models.

Du S, Long Q, Zhou Y et al. · Cell · (2026) · View on PubMed ↗

Host-derived nitrate fuels indole production by Escherichia coli to drive chronic kidney disease progression.​

This study examined whether host-derived nitrate supports microbial indole production by Escherichia coli to drive chronic kidney disease (CKD) progression in adenine-induced CKD mice and in fecal samples from CKD patients. It found that impaired clearance of indoxyl sulfate increases mucosal iNOS expression, elevating luminal nitrate that fuels E. coli growth via nitrate respiration, and that CKD patient fecal microbiota generate more indole than healthy controls under anaerobic conditions. These results connect host iNOS–nitrate metabolism to E. coli–indole/indoxyl sulfate pathways, identifying a potential metabolic lever for slowing CKD progression.

Lee JY, Mahan SP, Parente de Carvalho T et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Disruption of iron homeostasis by HERC2-FTL axis leads to chondrocyte loss and exacerbates osteoarthritis.​

This study examined how the HERC2–FTL axis disrupts iron homeostasis to drive ferroptosis and cartilage loss in osteoarthritis using ATDC5 chondrocytes treated with IL-1β or the ferroptosis inducer erastin. It reports that altering HERC2 (knockdown/overexpression) modulates ferroptosis, autophagy, oxidative stress, and expression of cartilage matrix proteins, and that HERC2-driven iron dysregulation exacerbates chondrocyte loss. The findings are significant because they identify an upstream HERC2–iron/FTL regulatory pathway that could be targeted to prevent ferroptosis-mediated OA progression.

Zhong Y, Duan J, Chen Z et al. · Apoptosis : an international journal on programmed cell death · (2026) · View on PubMed ↗

The therapeutic potential of Piezo1 channel-mediated ferroptosis and its inhibitor.​

This review article studied the mechanistic link between Piezo1, mechanically activated Ca2+ influx, and ferroptosis, and evaluated the therapeutic potential of inhibiting this pathway. It reports that Piezo1 activation promotes iron uptake and ferritinophagy (via TfR1, DMT1, and NCOA4), increases ROS and lipid peroxidation, and thereby triggers glutathione-dependent ferroptosis execution. The scientific significance is that Piezo1-mediated ferroptosis provides a druggable mechanotransduction-to-cell-death axis, supporting development of Piezo1 inhibitors as potential ferroptosis-targeted therapies.

Nan K, Zhang L, Zhao Y et al. · Apoptosis : an international journal on programmed cell death · (2026) · View on PubMed ↗

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Cardiovascular disease risk stratification & mechanistic targets​

Fibrinogen-Bmal1 signaling as a therapeutic target to limit aortic dissection by preserving VSMC contractility.​

The study tested fibrinogen–Bmal1 signaling as a therapeutic target to limit aortic dissection progression by preserving vascular smooth muscle cell (VSMC) contractility, using patient-linked analyses and experimental validation. It found that higher fibrinogen levels were associated with improved outcomes in acute aortic dissection and that fibrinogen–Bmal1 signaling can be leveraged to maintain VSMC contractile function to slow disease progression. This provides a translational rationale for targeting the fibrinogen/Bmal1 axis as a pharmacologic strategy for aortic dissection beyond surgery.

Zhong X, Li D, Zhao Y et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

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Heart failure & cytoskeletal remodeling targets​

Inhibiting RhoA Activation Via GDP-State Stabilization to Relieve Heart Failure.​

The study investigated a RhoA activation inhibitor designed to stabilize RhoA in its GDP-bound state to relieve pathological remodeling in heart failure models. Using structural comparisons of RhoA-GTP versus RhoA-GDP conformations and surface plasmon resonance-based screening, the authors identified a druggable RhoA inhibitor that suppresses RhoA activation and improves heart failure phenotypes. This provides a mechanistically targeted strategy to inhibit RhoA-driven cytoskeletal remodeling and fibrosis/hypertrophy, addressing the long-standing “undruggable” nature of RhoA.

Xue M, Liang Y, Yuan Z et al. · Circulation research · (2026) · View on PubMed ↗

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Pulmonary hypertension & cardiopulmonary outcomes​

Prognostic Impact of Elevated Pulmonary Vascular Resistance in Group 2 Pulmonary Hypertension: Insights From a Japanese Multicenter Registry.​

This Japanese multicenter registry analysis assessed the prognostic impact of elevated pulmonary vascular resistance (PVR) in group 2 pulmonary hypertension (PH) due to left heart disease using two prospective registries (2012–2016 and 2018–2024; total n=988). The study evaluated composite outcomes including heart-failure hospitalization, all-cause death, ventricular assist device implantation, and cardiac transplantation, and examined how PVR relates to prognosis and implications for emerging therapies. The results support using PVR for risk stratification in group 2 PH and may guide selection and evaluation of future treatment strategies.

Satoh T, Sugimura K, Fukumoto Y et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗

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Neurology: neurodegeneration, neuroimmune circuits & pain​

Postural Orthostatic Tachycardia Syndrome, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Long COVID as Neuroimmune Disorders.​

This article reviewed the concept that postural orthostatic tachycardia syndrome (POTS), myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and Long COVID represent neuroimmune disorders with overlapping mechanisms. It highlights key mechanistic contributors including autonomic dysfunction, immune dysregulation/autoimmunity, mitochondrial dysfunction, cerebral hypoperfusion, and neuroinflammation. The clinical significance is that grouping these syndromes as neuroimmune conditions may help unify research targets and therapeutic strategies.

Blitshteyn S, Doherty TA, Steinman L · ImmunoTargets and therapy · (2026) · View on PubMed ↗

Cryo-EM structure of TRPM1 reveals a non-canonical architecture with an inverted transmembrane domain.​

The study used cryogenic electron microscopy (cryo-EM) to determine the structure of the vision-related membrane protein TRPM1 in the context of congenital stationary night blindness. It found that TRPM1 forms a non-canonical architecture with an inverted transmembrane domain while maintaining a canonical tetrameric fold in the intracellular domain. This structural resolution clarifies how TRPM1 may function as an ion channel and informs interpretation of TRPM1 mutations underlying retinal disease.

Fabrizio M, Brewer M, Bogdanović N et al. · Nature communications · (2026) · View on PubMed ↗

Commensal-driven serotonin production modulates in vivo delivery of synthetic and viral vectors.​

This study examined how gut microbiota–driven serotonin production affects in vivo delivery efficiency of intestinal epithelial–to–Kupffer cell signaling for synthetic and viral vectors in vivo. It found that disrupting commensal-host interactions or transiently suppressing serotonin signaling (via receptor blockade or dietary intervention) reduces hepatic IDS clearance and increases vector delivery efficiency by more than threefold. These results identify a microbiome–serotonin axis as a tractable target to improve systemic drug and gene delivery outcomes.

Wang Q, Chen Z, Zhang G et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

A sympathetic-eosinophil axis orchestrates psychological stress to exacerbate skin inflammation.​

This study examined in mice how psychological stress alters immune responses in skin by focusing on prodynorphin-positive (Pdyn+) noradrenergic sympathetic neurons and their effects on eosinophils in atopic dermatitis-like models. It found that genetic ablation of Pdyn+ sympathetic neurons or eosinophils mitigated stress-induced worsening of skin inflammation, while optogenetic activation of Pdyn+ neurons precipitated inflammation via eosinophils through a CCL11–CCR3 recruitment axis. These findings define a sympathetic–eosinophil circuit as a mechanistic bridge between stress and exacerbated dermatitis.

Tian J, Cao Y, Li Y et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Hypothalamic clock governs circadian pain.​

This study investigated how the hypothalamic master circadian clock controls circadian variation in pain in a mouse model of neuropathic pain. It found that daily oscillations in nociceptive thresholds are driven by a circuit from suprachiasmatic nucleus VIP neurons (SCNVIP) to paraventricular nucleus (PVN) and ventrolateral periaqueductal gray (vlPAG), where higher daytime VIP activity increases nociceptive sensitivity and reduced nighttime activity decreases pain. This mechanistic framework links specific hypothalamic clock outputs to rhythmic pain processing and suggests timing-aware targets for analgesic strategies.

Wei HR, Lou Q, Li LX et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

From chronic pain to depression: Neurogenesis-driven microglial remodeling in the hippocampal dentate gyrus.​

This study investigated how chronic pain transitions to depression by integrating UK Biobank human neuroimaging with a rodent model to track hippocampal dentate gyrus (DG) remodeling. It found a biphasic pattern where hippocampal volume increases early (with cognitive improvements) but declines with comorbid depression, and in rodents DG lesions prevented affective symptoms while DG hyperactivity drove hyperactive newborn neurons, microglial recruitment, and circuit imbalance. These findings implicate neurogenesis-driven microglial remodeling in the DG as a causal mechanism for pain-associated affective dysfunction.

Ding M, Xiang S, Zhang Y et al. · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Astrocytes at the crossroads of obstructive sleep apnea and Alzheimer's disease: from oxygen sensing to neurodegeneration.​

This review article explored how astrocytes may mechanistically connect obstructive sleep apnea (OSA) to Alzheimer’s disease (AD), emphasizing oxygen sensing and downstream neurodegeneration. The authors synthesized evidence that intermittent hypoxia and sleep fragmentation can drive astrocyte dysfunction and contribute to AD-relevant pathways such as neuroinflammation and neurodegenerative signaling. By framing astrocytes as a mechanistic bridge between OSA and AD, the review highlights potential targets for intervention in sleep-related drivers of neurodegeneration.

Cabot J, Soriano JB, Alonso-Fernández A et al. · Sleep & breathing = Schlaf & Atmung · (2026) · View on PubMed ↗

Interplay of oxidative stress and neuroinflammation in alzheimer's: insights into age-driven pathogenesis.​

This review analyzed the interplay between oxidative stress and neuroinflammation in Alzheimer’s disease (AD) with a focus on age-driven pathogenesis. It highlighted mitochondrial dysfunction and reactive oxygen species (ROS)–mediated redox imbalance that promotes amyloid-β accumulation and cognitive decline, alongside chronic inflammasome activation in microglia and astrocytes involving NLRP3 and NF-κB signaling. The synthesis supports targeting combined oxidative and inflammatory pathways as a strategy to modify AD progression in aging populations.

Firdous SM, Chakrabortty S, Undale VR et al. · Inflammopharmacology · (2026) · View on PubMed ↗

Therapeutic Potential of Somatostatin and Its Analogues in Alzheimer's Disease: From Molecular Mechanisms to Preclinical Studies.​

This review studied the therapeutic potential of somatostatin (SST) and somatostatin analogues (SSAs) in Alzheimer’s disease, integrating molecular mechanisms and preclinical evidence. It reports that SST receptors (SSTR1–5) influence amyloid-β metabolism, tau phosphorylation, neuroinflammation, and synaptic plasticity, and that SSAs may enhance amyloid clearance (e.g., via neprilysin activation) and reduce tau-related pathology in preclinical models. The significance is that SSAs represent multitarget candidates that could modify disease-relevant pathways beyond symptomatic treatments currently approved for AD.

Liu K, Zhang XY, Wang YT et al. · Molecular neurobiology · (2026) · View on PubMed ↗

Transcriptomic Insights Into Alzheimer's Disease: Differentially Expressed Genes and Cholesterol Metabolism.​

This computational study used Mendelian randomization and advanced machine learning on transcriptomic data to investigate differentially expressed genes and cholesterol metabolism pathways in Alzheimer disease (AD). The analysis identified AD-associated gene expression differences linked to cholesterol-related mechanisms, suggesting cholesterol metabolism as a key molecular contributor. These results support cholesterol-centered biomarkers and therapeutic hypotheses for improving AD early detection and mechanistic understanding.

Sun R, Wang X, Wang Z et al. · CNS neuroscience & therapeutics · (2026) · View on PubMed ↗

Early-Life Melatonin Supplementation Reduces the Long-Term Behavioral, Morphological, and Molecular Alterations in a Rat Model of Autism Spectrum Disorder.​

This preclinical study tested whether early-life melatonin supplementation alters long-term outcomes in a rat model of autism spectrum disorder (ASD), assessing behavioral, morphological, and molecular changes after melatonin administration. The key finding is that early melatonin reduces the later behavioral deficits and associated morphological and molecular abnormalities seen in ASD-model rats. These results support melatonin as a potentially disease-modifying early intervention candidate targeting circadian and anti-inflammatory/antioxidant pathways relevant to ASD comorbid sleep and neuroinflammation.

Hernández-Sierra LJ, Salgado-Delgado RC, Ibáñez-Sandoval O et al. · Journal of pineal research · (2026) · View on PubMed ↗

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Neurodevelopmental/psychiatric disorders & microbiome–brain axis​

How gut microbiota contribute to neuropsychiatric disorders: evidence from neuroimaging studies.​

This review summarized how gut microbiota contribute to neuropsychiatric disorders using evidence from neuroimaging studies. It reports that multimodal imaging modalities—such as magnetic resonance imaging, positron emission tomography, and diffusion tensor imaging—can visualize associations between microbiome alterations and brain structure/function changes across neurodevelopmental, neurodegenerative, autoimmune, and psychiatric conditions. The scientific significance is that it frames the microbiota–gut–brain axis as an in vivo, imaging-accessible pathway for generating testable mechanistic hypotheses.

Jia C, Zhu W, Yuan Y et al. · Frontiers in microbiology · (2026) · View on PubMed ↗

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Infectious disease virology & host factors​

LRP8 is a functional receptor for yellow fever virus.​

The study investigated host receptor usage for yellow fever virus (YFV) and identified LRP8 (APOER2) as a functional receptor. Using a barcoded, genome-wide human open-reading frame library screen, the authors found that LRP8 expression increases infection by the live-attenuated 17D vaccine strain and clinical strains (BJ01 and Asibi) by promoting viral entry, and that adeno-associated virus-mediated LRP8 expression in mouse liver worsened infection/pathology of the BJ01 strain. This is clinically significant for understanding YFV tropism and for anticipating how receptor expression may influence vaccine and infection outcomes.

Mei M, Yang Y, Zhang Z et al. · Nature microbiology · (2026) · View on PubMed ↗

ALG6 orchestrates coronavirus replication via the endoplasmic reticulum stress-autophagy axis.​

This study investigated the host factor alpha-1,3-glucosyltransferase ALG6 in coronavirus replication, using transmissible gastroenteritis virus (TGEV) and host-cell genetic perturbations. ALG6 catalytic activity was required for TGEV replication, and ALG6 knockout inhibited viral entry by downregulating the receptor aminopeptidase N (ANPEP) while also triggering endoplasmic reticulum (ER) stress that further suppressed viral replication. These findings position ALG6 as a druggable ER-stress–autophagy axis regulator of coronavirus life cycle and entry.

Fu Y, Gao M, Fu Z et al. · Cell reports · (2026) · View on PubMed ↗

Diagnostic Performance of Anti-Epstein-Barr Virus BNLF2b in Suspected Nasopharyngeal Carcinoma.​

This prospective, multicenter outpatient diagnostic study compared the diagnostic performance of an anti–Epstein-Barr virus (EBV) BNLF2b total antibody assay (P85-Ab) against EBV VCA-IgA, EBV EA-IgA, and EBNA1-IgA in suspected nasopharyngeal carcinoma (NPC). The P85-Ab assay showed superior or more reliable diagnostic accuracy for suspected NPC in the outpatient setting compared with the other EBV serologic markers. Clinically, this supports adopting P85-Ab as a more effective blood-based biomarker to improve early NPC detection and reduce misdiagnosis.

Li SC, Li FG, Wu SJ et al. · JAMA oncology · (2026) · View on PubMed ↗

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Clinical trials, guidelines & real-world evidence (non-oncology)​

Embedded CRISPRi Enhances Gene-Silencing Efficiency in Drosophila.​

This study developed embedded CRISPR interference (emCRISPRi) in Drosophila melanogaster by engineering transcriptional repression domains (Mxi and TRD) into a flexible region of catalytically inactive Cas9 (dCas9). emCRISPRi significantly increased gene-silencing efficiency and repression amplitude, especially for coding genes and cis-regulatory elements near transcription start sites (TSS-proximal regions). The platform improves the reliability of CRISPRi in Drosophila, enabling more effective functional genomics screens.

Fu P, Zhang X, Zhou Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗

Tavapadon as Adjunctive Treatment for Parkinson Disease: The TEMPO-3 Randomized Clinical Trial.​

This randomized clinical trial evaluated tavapadon, an investigational once-daily selective D1/D5 agonist, as adjunctive therapy to oral levodopa in adults with Parkinson disease experiencing motor fluctuations. The study was designed to assess tavapadon’s efficacy, safety, and tolerability, aiming to improve motor control while reducing adverse events associated with preferential D2/D3 receptor activation. If effective, tavapadon could offer a mechanism-targeted adjunct strategy for managing levodopa-induced motor fluctuations with a potentially improved safety profile.

Fernandez HH, Isaacson SH, Hauser RA et al. · JAMA neurology · (2026) · View on PubMed ↗

Trends in 5-year net survival for women diagnosed with breast, cervical or ovarian cancer in Japan, 2000-14 (CONCORD-3).​

Using Japanese population-based cancer registry data from the CONCORD-3 program, this study analyzed 5-year net survival trends for women diagnosed with breast, cervical, or ovarian cancer between 2000 and 2014 (ages 15–99), excluding in situ and death-certificate-only cases. The authors reported long-term survival patterns stratified by cancer type and other factors across the 2000–2014 diagnosis period. These surveillance findings help quantify progress and remaining gaps in cancer outcomes for women in Japan and can inform public health and clinical prioritization.

Watanabe K, Di Carlo V, Sugiyama H et al. · Japanese journal of clinical oncology · (2026) · View on PubMed ↗

Stroke Risk After Bioprosthetic Aortic Valve Replacement in Aortic Stenosis: Systematic Review and Meta-Analysis.​

This systematic review and meta-analysis estimated the proportion of adults (>18 years) who experienced ischaemic stroke after bioprosthetic aortic valve replacement for aortic stenosis, including periprocedural and beyond-periprocedural periods across transcatheter AVR (TAVR), surgical AVR, and valve-in-valve (ViV) replacement. The authors searched MEDLINE, Embase, and Web of Science through March 2024 and synthesized studies reporting post-bioprosthetic AVR stroke incidence. The pooled estimates provide clinically actionable risk benchmarks for counselling, monitoring, and designing strategies to reduce stroke after AVR.

Bou Dargham T, Hassani S, Mac Grory BC et al. · Stroke · (2026) · View on PubMed ↗

Joint TOS/OMA/OAC expert guidance statement on the pharmacological management of United States adults with overweight or obesity using the GRADE approach.​

This article developed an expert guidance statement for pharmacological management of United States adults with overweight or obesity using the GRADE approach. It synthesizes evidence and provides updated recommendations to improve access and appropriate use of FDA-approved anti-obesity medications while addressing barriers such as clinician training, stigma, and reimbursement limitations. The guidance is clinically significant because it standardizes evidence-based obesity treatment decisions at the population level in the US.

Alexander L, Purnell JQ, Burridge K et al. · Obesity pillars · (2026) · View on PubMed ↗

Glucagon-like peptide-1 receptor agonists for major cardiovascular and kidney outcomes in type 1 diabetes.​

This study assessed long-term cardiovascular and kidney outcomes of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in type 1 diabetes using national electronic health record data. In a sequential target trial emulation of 174,678 patients (2013–2024), GLP-1RA initiation was associated with lower risk of major adverse cardiovascular events and end-stage kidney disease after propensity score weighting. The clinical significance is that it provides real-world evidence supporting GLP-1RA benefit for cardiovascular and renal protection in type 1 diabetes, where long-term randomized outcome data have been limited.

Xu Y, Malek ND, Chang AR et al. · Nature medicine · (2026) · View on PubMed ↗

Type 2 diabetes mellitus.​

This Nature Reviews Disease Primer summarized the epidemiology, risk factors, and clinical course of type 2 diabetes mellitus (T2DM) across human populations, emphasizing the roles of genetics, biology, behavior, and social determinants. It highlighted that rising obesity has shifted T2DM epidemiology and that early-onset T2DM (diagnosis over 40 years) is linked to more aggressive progression, higher complication burden, and greater lifetime morbidity than later-onset disease. The review is clinically significant for guiding prevention and risk stratification strategies tailored to modern, younger T2DM populations.

Davies MJ, Lim S, Slater T et al. · Nature reviews. Disease primers · (2026) · View on PubMed ↗

Adherence to the EAT-Lancet Diet and Risk of Sepsis: A Prospective Cohort Study from the UK Biobank.​

The study analyzed whether adherence to the EAT-Lancet diet is associated with sepsis risk in 199,085 participants from the UK Biobank, incorporating genetic susceptibility and proteomic mechanisms. It found that higher EAT-Lancet diet adherence was associated with a reduced risk of sepsis (HR 0.85, 95% CI 0.78, as reported in the abstract). This supports dietary pattern modification as a potential modifiable factor for sepsis prevention and motivates mechanistic work linking diet, host biology, and proteomic pathways.

Nan W, Huang Q, He B et al. · NPJ science of food · (2026) · View on PubMed ↗

Clinical practice guideline for long COVID prevention and treatment.​

This European respiratory society guideline synthesized evidence to provide recommendations for long COVID prevention and treatment in adults with long COVID for use by clinicians and community healthcare providers. The key finding is the establishment of a structured, protocol-driven guideline addressing key clinical questions and translating evidence into practice recommendations. Its significance is to standardize care pathways for long COVID globally and reduce variability in prevention and management.

Cao B, Soriano JB, Wang Q et al. · The European respiratory journal · (2026) · View on PubMed ↗

Anifrolumab in systemic lupus erythematosus: real-world evidence from a Spanish multicentre cohort of 206 patients and literature review.​

This Spanish multicenter real-world study of 206 adults with moderate-to-severe active systemic lupus erythematosus (SLE) assessed anifrolumab effectiveness and safety and compared findings with published observational evidence. The key finding is that anifrolumab showed real-world effectiveness and an acceptable safety profile consistent with prior trial data. Clinically, these data support decision-making for anifrolumab use in routine practice beyond randomized controlled trials.

Calvo-Río V, Secada-Gómez C, Martín Gutiérrez A et al. · RMD open · (2026) · View on PubMed ↗

The efficacy and safety of cannabinoids for the treatment of mental disorders and substance use disorders: a systematic review and meta-analysis.​

This systematic review and meta-analysis evaluated randomized controlled trials of cannabinoids as primary treatment for mental disorders and substance use disorders (SUDs). The key finding is an evidence synthesis of efficacy and safety across included trials, clarifying the overall balance of benefits and harms for cannabinoid-based interventions. Clinically, it informs whether cannabinoids should be used for psychiatric/SUD indications and highlights where evidence remains uncertain.

Wilson J, Dobson O, Langcake A et al. · The lancet. Psychiatry · (2026) · View on PubMed ↗

Epidemiology, ventilation, and outcomes of acute respiratory failure in immunocompromised patients from 103 intensive care units in 26 countries: a retrospective observational study.​

This retrospective observational study analyzed acute respiratory failure (ARF) in immunocompromised adults across 103 intensive care units in 26 countries to characterize epidemiology, ventilation strategies, and outcomes. The key finding is identification of predictors of mortality and intubation in this immunocompromised ARF population, linked to underlying immunosuppression and oxygenation/ventilation approaches. The significance is improved risk prediction and benchmarking of ICU management for immunocompromised patients with ARF.

Azoulay E, McEvoy C, Castro P et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

Integration of Epidemiology and Network Toxicology Revealed the Arrhythmogenic Potential of Neonicotinoid Insecticides.​

This study integrated epidemiology and network toxicology to assess arrhythmogenic potential of neonicotinoid insecticides by measuring urinary neonicotinoids and metabolites in 136 arrhythmia patients and 222 healthy controls. Neonicotinoids were detected in all samples with higher concentrations in patients than controls (except thiamethoxam and clothianidin), and quantile g-computation and Bayesian kernel machine regression suggested that co-exposure to multiple neonicotinoids increased arrhythmia risk. The findings indicate that mixture exposure to neonicotinoids may be a meaningful contributor to human arrhythmia risk and can be prioritized for risk assessment.

Ge Y, Xiao Q, Fu B et al. · Environmental science & technology · (2026) · View on PubMed ↗

Preferences in Cyclin-Dependent Kinase 4/6 Inhibitors for Advanced Breast Cancer Among Medical Oncologists in Latin America.​

This cross-sectional survey studied Latin American medical oncologists’ preferences for cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) in advanced hormone receptor-positive, HER2-negative breast cancer. Among 116 oncologists from 15 countries, ribociclib was the preferred agent (56.8%), with preferences shaped by drug availability and clinical decision-making across scenarios. The results highlight regional prescribing patterns and access-driven differences that may affect real-world CDK4/6i utilization and patient outcomes.

Villarreal-Garza C, Meraz-Brenez A, Reyes Morales A et al. · JCO global oncology · (2026) · View on PubMed ↗

Efficacy and Safety of Remimazolam Tosylate versus Propofol for Sedation of Postoperative Mechanically Ventilated Patients in Intensive Care Units: a Multicenter, Randomized, Single-blind, Non-inferiority, Phase 3 trial.​

This multicenter, randomized, single-blind phase 3 trial compared intravenous remimazolam tosylate versus propofol for sedation in postoperative mechanically ventilated ICU patients. Patients were randomized to remimazolam tosylate (loading 0.08 mg/kg; maintenance 0–2.0 mg/kg/h) or propofol (loading 0.3–0.5 mg/kg; maintenance 0.3–4.0 mg/kg/h) targeting RASS -2 to 1, with non-inferiority as the primary framework (outcomes truncated in the provided abstract). If non-inferiority and safety were confirmed, remimazolam could offer an alternative short-acting benzodiazepine-based sedation strategy for mechanically ventilated ICU patients.

Guan X, Liu N, Lin F et al. · Anesthesiology · (2026) · View on PubMed ↗

Velocity Loss During Resistance Training: Implications for Concurrent Training Adaptations.​

This randomized study examined how different resistance-training velocity loss (VL) thresholds (0%, 15%, 40%) affect adaptations to concurrent training, compared with endurance training alone, in 41 moderately trained men. Over 8 weeks, participants performed squat-based resistance training at 70–85% 1RM followed by running endurance training, and the study assessed strength, endurance, neuromuscular, and hypertrophic outcomes (specific results truncated in the provided abstract). The work informs how manipulating VL during resistance training may optimize or preserve adaptations during concurrent training.

Tundidor-Duque RM, Loturco I, Paéz-Maldondado JA et al. · Scandinavian journal of medicine & science in sports · (2026) · View on PubMed ↗

The relationship between sarcopenia and all-cause and cardiovascular mortality risk among middle-aged and older adults across stages 0-3 of cardiovascular-kidney-metabolic syndrome: evidence from NHANES and CHARLS.​

This study used NHANES (2011–2018) and CHARLS (2011–2020) to investigate whether sarcopenia predicts all-cause and cardiovascular mortality across stages 0–3 of cardiovascular-kidney-metabolic (CKM) syndrome in middle-aged and older adults. Using multivariable Cox regression (details truncated in the provided abstract), it aimed to quantify the mortality risk associated with sarcopenia within CKM strata. The findings could support sarcopenia as a prognostic marker for mortality risk and help refine risk stratification in CKM syndrome.

Chen Y, Liu Y, Liu S et al. · Cardiorenal medicine · (2026) · View on PubMed ↗

A neuroimmune circuit links stress to skin inflammation.​

This Science study investigated a neuroimmune circuit linking stress to skin inflammation, focusing on sympathetic neurons and eosinophils in the context of atopic dermatitis. It reported that sympathetic neurons activate eosinophils during stress, worsening atopic dermatitis flare-ups. The mechanism identifies a stress-to-immunity pathway that could be targeted to prevent or treat inflammatory skin exacerbations.

Gaudenzio N, Basso L · Science (New York, N.Y.) · (2026) · View on PubMed ↗

Association between COVID-19 vaccination and sudden death in apparently healthy younger individuals: A population-based case-control study.​

This population-based case-control study assessed whether COVID-19 vaccination is associated with sudden death in apparently healthy younger individuals aged 12–50 years in Ontario, Canada using linked administrative datasets. The key finding was the presence/absence of an association between vaccination exposure and sudden death risk after accounting for exclusions and study design constraints (details truncated in the abstract). If confirmed, the results would directly inform vaccine safety surveillance and risk communication for rare but serious outcomes in younger adults.

Abdel-Qadir H, Bhatt HA, Swayze S et al. · PLoS medicine · (2026) · View on PubMed ↗

Phase separation of Rht8-derived RNHL1 integrates ethylene and gibberellin signaling to regulate wheat internode elongation.​

This study examined how the wheat semi-dwarfing gene Rht8, which encodes RNHL1 (Ribonuclease H-like 1), regulates internode elongation by integrating ethylene and gibberellin signaling. The authors found that RNHL1 undergoes liquid-liquid phase separation via intrinsically disordered regions to form nuclear condensates and physically interacts with the ethylene signaling transcription factor TaEIL1 to create functional transcriptional hubs. This mechanistic link between RNHL1 phase separation and hormone crosstalk provides a molecular framework for breeding and engineering wheat height control.

Dong C, Cheng X, Yuan M et al. · The Plant cell · (2026) · View on PubMed ↗

Ritlecitinib for Severe Alopecia Areata: A 24-Week, Multicentre, Real-World Study.​

This real-world observational study evaluated ritlecitinib, an oral JAK3 and TEC-family kinase inhibitor, in patients with severe alopecia areata (SALT ≥ 50) aged ≥12 years in an Italian multicenter retrospective cohort with 24-week follow-up. The key finding was the effectiveness and tolerability of ritlecitinib 50 mg/day over 24 weeks in routine clinical practice (specific response rates and adverse-event outcomes are truncated in the abstract). These data extend evidence for ritlecitinib beyond trials by informing clinicians about real-world benefit-risk in severe disease.

Starace M, Rapparini L, Pampaloni F et al. · American journal of clinical dermatology · (2026) · View on PubMed ↗

MASLD as a systemic metabolic disease: expanding the scope of cardiovascular-kidney-metabolic (CKM) syndrome.​

This article reviewed metabolic dysfunction-associated steatotic liver disease (MASLD) as a systemic disease and argued for its inclusion within the cardiovascular–kidney–metabolic (CKM) syndrome framework. The authors highlighted that MASLD increases cardiovascular and renal risk through shared mechanisms including insulin resistance, low-grade inflammation, oxidative stress, atherogenic dyslipidemia, and a procoagulant state. Recognizing MASLD as part of CKM syndrome could improve screening and integrated management across cardiology and nephrology.

Zhou XD, Fan QY, Targher G et al. · Science China. Life sciences · (2026) · View on PubMed ↗

Managing Bone Fragility in Older Adults with Diabetes: Pathophysiology, Assessment, and Therapeutic Considerations.​

This review summarized how diabetes in older adults contributes to bone fragility and fracture risk, contrasting type 1 diabetes (T1D) and type 2 diabetes (T2D) mechanisms. The authors emphasized that T1D typically lowers bone mineral density via insulinopenia, whereas T2D may preserve or increase BMD but impairs bone quality through microarchitectural changes, advanced glycation end products (AGEs), and altered bone turnover. The clinical significance is improved assessment and therapeutic decision-making for fracture prevention tailored to diabetes type and bone phenotype.

Bahat G, Erdogan T, Ozturk S et al. · Drugs & aging · (2026) · View on PubMed ↗

International Expert Opinion on Optimal Switching to Cladribine Tablets from Other High-Efficacy Disease-Modifying Therapies for Relapsing-Remitting Multiple Sclerosis: Opportunities and Challenges.​

This international expert-opinion review studied optimal treatment sequencing for relapsing-remitting multiple sclerosis (RMS) when switching to cladribine tablets (CladT) from other high-efficacy disease-modifying therapies, including S1P modulators, natalizumab, or anti-CD20 agents. It concludes with practical recommendations on how to time and manage switching to CladT to balance efficacy with safety risks such as immune reconstitution–related complications. The guidance is clinically significant because it addresses a major evidence gap in RMS when transitioning between potent DMT classes.

Chan A, Alroughani R, Calabrese M et al. · Neurology and therapy · (2026) · View on PubMed ↗

Proteomic analyses of human islets reveal potential markers of β-cell dysfunction during prediabetes.​

This study investigated proteomic predictors of β-cell dysfunction during prediabetes by analyzing human pancreatic islets from non-diabetic subjects with known glucose tolerance phenotypes. Using laser capture microdissection (LCM) and high-performance liquid chromatography–mass spectrometry (HPLC-MS), it found that impaired glucose tolerance (IGT) is associated with reduced proteins involved in glycolysis (e.g., PGK1, G3P) and lipid/glucose handling (e.g., ACBP, ARF1), alongside broader proteome shifts linked to early β-cell stress. The clinical significance is that these islet proteomic markers could help predict diabetes onset and identify early biological targets for preventing progression from prediabetes to type 2 diabetes.

Cefalo CMA, Mezza T, Quero G et al. · JCI insight · (2026) · View on PubMed ↗

Transradial vs Transfemoral Access for Cerebral Angiography: A Randomized Noninferiority Clinical Trial.​

This randomized noninferiority clinical trial studied whether transradial access (TRA) is as effective and safe as transfemoral access (TFA) for diagnostic cerebral angiography. Conducted at 13 sites in China with blinded outcome assessment, it compared TRA vs TFA in patients undergoing cerebral angiography to test noninferiority on efficacy and safety endpoints. The clinical significance is that it directly informs access-site choice for cerebral angiography, potentially improving patient comfort and procedural safety if TRA performs comparably.

Ni W, Yang H, Su J et al. · JAMA network open · (2026) · View on PubMed ↗

Meat Consumption and Cognitive Health by APOE Genotype.​

This population-based cohort study in the Swedish National Study on Aging and Care-Kungsholmen (SNAC-K) tested whether meat consumption is associated with cognitive health differently by APOE genotype (APOE ε3/ε4 vs ε4/ε4, and other genotypes). Higher meat consumption was associated with cognitive health benefits specifically in individuals carrying APOE ε4 (APOE34/44), with genotype-dependent differences compared with non-ε4 genotypes. These findings support genotype-informed dietary prevention strategies for Alzheimer disease risk in older adults.

Norgren J, Carballo-Casla A, Grande G et al. · JAMA network open · (2026) · View on PubMed ↗

Bireociclib Plus Fulvestrant in Advanced Breast Cancer After Endocrine Progression: The BRIGHT-2 Phase 3 Randomized Clinical Trial.​

In a double-blind, placebo-controlled phase 3 randomized clinical trial conducted at 64 hospitals in China, bireociclib (a CDK4/6 inhibitor) plus fulvestrant was evaluated in patients with hormone receptor–positive, ERBB2 (HER2)-negative advanced breast cancer after endocrine progression. The final analysis (with additional follow-up) confirmed that bireociclib plus fulvestrant improved efficacy and maintained a manageable safety profile versus placebo plus fulvestrant. This provides clinically actionable evidence for using bireociclib-based therapy to extend outcomes after endocrine therapy failure in HR+/ERBB2− advanced breast cancer.

Wang J, Zhang Q, Li H et al. · JAMA oncology · (2026) · View on PubMed ↗

Women with epilepsy: Evidence-based counseling across the lifespan.​

This evidence-based review synthesized current data on women with epilepsy (WWE) across the lifespan, focusing on counseling needs spanning adolescence, transition to adult care, reproductive health, contraception, fertility and pregnancy, lactation, menopause, and bone health. The review highlights persistent gaps in integrating sex- and life-stage–specific epilepsy management into routine clinical care and aligns recommendations with contemporary guidelines. Scientifically and clinically, it provides a structured framework to improve individualized counseling and management beyond seizure control for WWE.

Tettenborn B, Ramantani G, Flügel D et al. · Epilepsia · (2026) · View on PubMed ↗

Identification and Validation of miR-206-3p Targeting WT-1 Promotes Membranous Nephropathy Through a Comprehensive Bioinformatics and Machine Learning Algorithm.​

Using comprehensive bioinformatics and machine-learning analyses followed by validation, this study identified microRNA-206-3p (miR-206-3p) as a regulator targeting WT-1 (Wilms tumor 1) in membranous nephropathy (MN). miR-206-3p promoted MN by modulating the WT-1–linked molecular network, supported by differential expression across datasets and computationally derived pathway relationships. These results nominate the miR-206-3p/WT-1 axis as a potential mechanistic target for future MN diagnostics or therapeutics.

Wang X, Zhou F, Fu C et al. · FASEB journal : official publication of the Federation of American Societies for Experimental Biology · (2026) · View on PubMed ↗

Onasemnogene Abeparvovec in Type I Spinal Muscular Atrophy: 24-Month Follow-Up From the Italian Registry.​

This prospective observational study followed Italian patients with spinal muscular atrophy type I (SMA I) treated with onasemnogene abeparvovec (AAV9 gene therapy) for 24 months, stratifying outcomes by treatment pathway (monotherapy with OA, bridge from nusinersen or risdiplam, or switch after >3 months). The key finding is that real-world clinical outcomes show response variability beyond what is typically reported in earlier trial follow-up, with differences depending on prior/bridging therapy timing. Clinically, these 24-month registry data help refine expectations for OA effectiveness in routine care and inform how sequencing with nusinersen or risdiplam may influence long-term outcomes.

Pane M, Coratti G, Cutrì C et al. · Annals of clinical and translational neurology · (2026) · View on PubMed ↗

The relationship between dietary patterns and neuroinflammation.​

This review synthesized evidence on how dietary patterns modulate neuroinflammation in the central nervous system by shaping immunometabolic balance, immune signaling, and glial (including microglial) activation. The key finding is that persistent neuroinflammation—driven by microglial activation, chronic pro-inflammatory mediator release, and recruitment of peripheral immune cells—emerges as a common mechanistic link between dietary exposures and multiple neurological/psychiatric disorders. Scientifically, it supports targeting diet composition and timing as modifiable upstream regulators of neuroinflammatory pathways relevant to diseases such as Alzheimer’s disease and major depression.

Medoro A, Scapagnini G, Hu FB et al. · Critical reviews in food science and nutrition · (2026) · View on PubMed ↗

Effects of Diactive-1-Supported Progressive Resistance Training on Body Composition in Youth With Type 1 Diabetes.​

This study assessed the effects of Diactive-1–supported progressive resistance training on body composition in youth with type 1 diabetes (n=62, ages 8–18 years) using an mHealth-supported exercise intervention. The key finding is that resistance training delivered with the Diactive-1 platform can improve specific body composition outcomes in this pediatric population at risk for unfavorable changes in fat, lean, and bone compartments. Clinically, it supports using structured, technology-supported resistance exercise as an actionable strategy to mitigate body composition deterioration in children and adolescents with type 1 diabetes.

Muñoz-Pardeza J, López-Gil JF, Hormazábal-Aguayo I et al. · Journal of cachexia, sarcopenia and muscle · (2026) · View on PubMed ↗

International Dermoscopy Society consensus recommendations for the management of lentigo maligna.​

This article presents International Dermoscopy Society consensus recommendations for managing lentigo maligna (LM), a melanoma in situ subtype common on chronically sun-damaged skin in elderly patients. The key finding is the development of practical, evidence-based guidance for LM diagnosis and management that addresses diagnostic uncertainty and subclinical peripheral extension, including how to use dermoscopy in clinical decision-making. Scientifically and clinically, these consensus recommendations aim to standardize care and improve outcomes by translating limited high-quality evidence into actionable management steps for clinicians.

Forsea AM, Pampena R, Akay BN et al. · Journal of the European Academy of Dermatology and Venereology : JEADV · (2026) · View on PubMed ↗

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Other​

Overcoming T cell tolerance to tumor self-antigens through catch-bond engineering.​

This study explored overcoming T cell tolerance to tumor self-antigens by engineering weakly reactive T cell receptors (TCRs) against the nonmutated tumor-associated antigen prostatic acid phosphatase (PAP). It identified a catch-bonding hotspot mutation that increases TCR–pMHC bond lifetime while preserving physiological affinities and antigen fine specificity, leading to markedly improved T cell expansion in tumors, effector differentiation, and tumor elimination. This provides a mechanistically grounded TCR engineering strategy to enhance anti-tumor immunity against self-antigens.

View on PubMed ↗

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Generated automatically on March 22, 2026 from PubMed's trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.