PubMed Trending Research Digest — June 25, 2026

Automated digest · 98 articles · 15 research areas · June 25, 2026

Overview

The dominant thread across this digest is that biology is increasingly understood as context-dependent: immune programs are shaped not only by genes and cytokines, but also by physical forces, spatial microenvironments, and metabolic cues. Mechanistic work on mechanotransduction-driven “mechano-inflammation,” STING activation rules, and immune niche dynamics in tuberculosis all point to the same lesson—signals integrate across trafficking, cell state, and tissue architecture to determine whether inflammation resolves or persists.

A second major theme is the push toward better prediction and stratification using richer data streams. Studies and analyses leverage longitudinal AI risk trajectories in breast cancer, MRI-augmented heart-failure risk models, ctDNA MRD in stage III NSCLC, and broad metabolite atlases to refine who is at risk and when. Several efforts also highlight limitations of “bulk” biomarkers when spatial heterogeneity matters, as seen in the bladder cancer tumor inflammation signature trial.

Finally, translational advances span both therapies and tools: continued progress in cancer immunotherapy (including long-term CAR T durability and KRAS-mutant vaccination feasibility), targeted immunomodulation (e.g., B-cell–tolerogenic antigen delivery), and next-generation drug modalities such as molecular glues and targeted protein degraders. In parallel, microbiome-derived metabolites and host metabolic pathways (including GLP-1 biology, frailty–diabetes–kidney links, and gut–immune signaling via AHR/NLRP6/IL-18) reinforce that metabolic state is tightly coupled to immune function and disease trajectory.

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Mechanobiology & Innate Immune Mechanotransduction

Nivolumab plus Ipilimumab versus Lenvatinib or Sorafenib as First-Line Treatment for Unresectable Hepatocellular Carcinoma: CheckMate 9DW Japanese Subgroup Analysis.

This preplanned interim Japanese subgroup analysis of the phase 3 CheckMate 9DW trial studied first-line nivolumab plus ipilimumab versus lenvatinib or sorafenib in Japanese patients with unresectable hepatocellular carcinoma (HCC) without prior systemic therapy. Nivolumab plus ipilimumab improved overall survival versus lenvatinib/sorafenib (HR 0.79, 95% CI 0.65–0.96; p=0.018). These results support nivolumab+ipilimumab as a clinically significant first-line option for unresectable HCC in the Japanese population.

Kudo M, Hiraoka A, Numata K et al. · Liver cancer · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Hepatic Safety of Orforglipron in Adults With Obesity or Overweight and/or Type 2 Diabetes: A Pooled Analysis of the Orforglipron Phase 3 Clinical Trials.

This pooled analysis of seven phase 3 trials assessed hepatic safety of the oral GLP-1 receptor agonist orforglipron in 11,220 adults with obesity/overweight and/or type 2 diabetes, compared with placebo and active comparators (including oral semaglutide, dapagliflozin, and insulin glargine). Across up to 104 weeks, participants were selected with baseline ALT/AST limits (e.g., <3×ULN in weight management and ≤5×ULN in T2D), and the study evaluated liver-related safety outcomes across treatment arms. The findings are important for determining whether orforglipron has an acceptable hepatic safety profile for long-term use in metabolic disease populations.

Wharton S, Stefanski A, Chen J et al. · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Emerging Paediatric Uses of Dupilumab Beyond Approvals.

This review article surveyed emerging pediatric off-label and beyond-approval uses of dupilumab, a fully human IgG4 monoclonal antibody targeting IL4Rα to block IL-4 and IL-13 signaling. It summarizes how dupilumab’s type-2 inflammation mechanism is being explored across pediatric conditions beyond its current FDA/EMA-approved indications (e.g., atopic dermatitis, asthma, eosinophilic esophagitis, chronic rhinosinusitis with nasal polyps, and chronic spontaneous urticaria). The clinical significance is that it helps clinicians and researchers identify evidence gaps and potential pediatric therapeutic expansions for IL-4/IL-13–driven diseases.

Foti Randazzese S, Calamita A, D’Angelo D et al. · Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of the orexin receptor antagonist, suvorexant, on sleep architecture in the early postoperative period following cardiac surgery: a randomized controlled trial.

This multicenter, double-blind randomized controlled trial studied whether the orexin receptor antagonist suvorexant improves sleep architecture and reduces delirium in 100 adult patients in the ICU during the early postoperative period after cardiac surgery. The trial was designed to test effects on sleep onset/duration while addressing concerns that conventional sedative-hypnotics can disrupt sleep architecture and increase delirium risk. If positive, the results would support suvorexant as a targeted perioperative strategy to improve sleep quality and potentially lower delirium incidence after cardiac surgery.

Wongtangman K, Reddy Janga S, Azimaraghi O et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Association between glycolipid metabolism 7 factors (GLM7) and sarcopenia: insights from NHANES and CHARLS.

This cross-sectional study analyzed NHANES 2011–2018 data (n=1,563) to evaluate the association between the glycolipid metabolism 7-factor index (GLM7) and sarcopenia risk in middle-aged and older adults. Using survey-weighted multivariable logistic regression and restricted cubic spline dose-response modeling, it tested whether higher GLM7 correlates with greater sarcopenia risk and whether GLM7 improves prediction. The scientific significance is that GLM7 could serve as a composite metabolic biomarker to identify older adults at higher sarcopenia risk.

Chen Y, Zhang Y, Fan W et al. · Lipids in health and disease · (2026) · View on PubMed ↗ · Free PDF ↗

Association between insulin resistance surrogate markers and cardiovascular disease risk in individuals with subclinical metabolic disorders: a prospective cohort study based on baseline levels, cumulative exposure, and longitudinal trajectories.

This prospective cohort study evaluated how insulin resistance surrogate markers relate to cardiovascular disease (CVD) risk in people with subclinical metabolic disorders, considering baseline levels, cumulative exposure, and longitudinal trajectories. It aimed to clarify how early metabolic states such as prediabetes, prehypertension, and predyslipidemia contribute to CVD risk and how dynamic changes in insulin resistance markers track with incident CVD. The clinical significance is improved risk stratification for CVD using IR-related surrogate indices in large populations where direct insulin resistance measurement is impractical.

Zhao W, Tang R, Tian J et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

Astrocytes viewed through the lens of their proteomes and subproteomes.

This Nature Reviews Neuroscience article synthesized evidence on astrocyte biology using proteomics and subproteomics approaches, focusing on how protein abundance and subcellular localization relate to astrocyte function. It highlights advances enabled by genetically encoded proximity-dependent biotinylation to map astrocyte proteomes and subproteomes, addressing the gap between transcriptomic signals and protein-level molecular mechanisms. The scientific significance is that proteome-resolved astrocyte maps can better explain cell-state function in health and disease beyond gene-expression alone.

Casha VH, Wu L, Wohlschlegel JA et al. · Nature reviews. Neuroscience · (2026) · View on PubMed ↗

Mapping and engineering the human cell-cell interactome.

This Nature Biotechnology Perspective proposed a large-scale initiative to map and engineer the human cell-cell interactome, aiming for a functional atlas of how major human cell types communicate. It argues that while single-cell transcriptomics and spatial profiling measure cellular states and locations, they do not fully capture context-dependent cell-cell influence, motivating new experimental and computational innovations. The significance is that a systematic interactome atlas could accelerate mechanistic discovery and therapeutic engineering across human tissues.

Di Carlo D, Morsut L, McCain ML et al. · Nature biotechnology · (2026) · View on PubMed ↗

The metabolic vulnerability index predicts outcomes in patients with metabolic dysfunction associated steatotic liver disease.

This cohort study evaluated the prognostic performance of the metabolic vulnerability index (MVX), reflecting inflammation and amino acid dysmetabolism, in 1,613 patients spanning the full histological spectrum of metabolic dysfunction–associated steatotic liver disease (MASLD). Over a median follow-up of 4 years, higher MVX predicted increased all-cause mortality and liver outcomes, including liver-related mortality, hepatic decompensation, progression to MELD ≥15, and decline in eGFR ≥40%. The clinical significance is that MVX can stratify risk in MASLD and may improve prognostication when combined with fibrosis stage.

Siddiqui MS, Van Natta ML, Connelly MA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Biophysical modeling for accurate T cell specificity prediction of viral and tumor antigens.

This study developed a dual experimental and computational framework to predict T cell specificity from T cell receptor (TCR) sequences by integrating TCR primary sequences with TCR–pMHC structural data, and applied it to serial clinical samples. In the setting of hematopoietic stem cell transplant with HLA-A*02-restricted epitopes—including Melan-A (ELAGIGILTV), influenza A M1 (GILGFVFTL), and CMV pp65 (NLVPMVATV)—the model accurately predicted specificity for previously uncharacterized donor- and patient-derived TCRs. The scientific significance is that improved TCR specificity prediction can accelerate identification of relevant antiviral and tumor-reactive T cells for immunotherapy and transplant monitoring.

Ghoreyshi ZS, Tubo N, Zammataro L et al. · Nature communications · (2026) · View on PubMed ↗

Rapid boosting increases germinal center responses to sequential vaccines.

In a mouse model using human immunodeficiency virus (HIV) envelope surface protein immunogens, the study examined how rapid sequential homologous or heterologous boosts affect germinal center (GC) responses. Rapid boosting expanded on-target GC B cell populations that largely emerged from existing GC B cells, with early homologous boosting avoiding prohibitive antibody titers and leveraging off-target antibodies to maximize the GC response. This supports vaccine design strategies that use timing and boost composition to dynamically tune GC evolution for improved humoral immunity.

Haupt S, Cottrell CA, Zhou X et al. · Nature immunology · (2026) · 1 citations · View on PubMed ↗

Mutant KRAS peptide vaccine with dual checkpoint blockade in metastatic colorectal cancer: a phase I trial.

This phase I single-arm trial studied the pooled mutant KRAS peptide vaccine mKRAS-VAX (targeting six KRAS mutations) combined with nivolumab and ipilimumab in 13 patients with pretreated metastatic mismatch repair proficient/microsatellite stable (MMRp/MSS) colorectal cancer. The study met primary safety and immunogenicity endpoints within 17 weeks post-vaccination. These results support KRAS-mutant neoantigen vaccination plus dual checkpoint blockade as a feasible immunotherapy strategy for MMRp/MSS metastatic CRC, a group with historically limited ICI activity.

Wang HH, Huff AL, Haldar SD et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial transcriptomics reveals coordinated ventricular patterning and maturation in the developing human heart.

This study generated a spatiotemporal transcriptomic atlas of developing human hearts by profiling 30 sections from 8–15 post-conception weeks using spatial transcriptomics. Trajectory inference in the ventricle revealed continuous maturation patterns and anatomically coherent compartments with specialized subpopulations such as papillary muscle and the atrioventricular plane. The atlas provides a mechanistic framework for how regional gene programs coordinate human cardiac structure formation during development.

Yao Z, Bai L, Xie Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

YIF1A activates mTORC1 signaling to promote cellular senescence.

This work investigated how the Golgi-localized protein YIF1A regulates growth factor-mediated mTORC1 signaling to promote cellular senescence. YIF1A was identified as a regulator that interacts with the E3 ubiquitin ligase RNF126 to facilitate K48-linked polyubiquitination of G3BP1/2, thereby promoting Golgi-associated mTORC1 activation. These findings define a specific YIF1A–RNF126–G3BP axis controlling mTORC1-driven senescence, offering a potential targetable pathway for senescence-related biology.

Zhang X, Liu L, Shang M et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

A Type VII-secreted toxin enables inter-mycobacterial competition.

This study examined whether mycobacteria can use secreted protein toxins for inter-mycobacterial competition and identified the responsible effector and secretion route. It showed that endo-D-arabinanases of the GH183 family are secreted via the type VII secretion system (T7SS) to cleave the arabinogalactan layer of the mycobacterial cell envelope. This reveals a previously unrecognized mechanism of bacterial competition in mycobacteria and links T7SS effector activity to cell-wall vulnerability.

Benedict ST, Bowran K, Lee EKE et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.

This study tested how the microbial metabolite urolithin A (UroA) affects intestinal epithelial immune signaling by activating the aryl hydrocarbon receptor (AHR) in mouse intestinal epithelial cells. UroA-triggered AHR activation induced the NLRP6 inflammasome to release IL-18 but not IL-1β, and IL-18 was required for downstream IL-22 and mucin 2 responses that strengthen gut barrier integrity. These results connect a specific diet/microbiome-derived AHR ligand to an AHR–NLRP6–IL-18 axis that may be therapeutically relevant for inflammatory bowel disease.

Ghosh S, Vanwinkle ZM, Bodduluri SR et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Stromal and endothelial transcriptional changes during progression from MGUS to myeloma and after treatment response.

This study used two-sample Mendelian randomization plus a retrospective hemodialysis cohort to evaluate whether genetically predicted frailty is associated with type 2 diabetes–related renal complications. The analysis assessed pleiotropy and robustness via exclusion of potentially pleiotropic variants and multivariable MR, and then compared frailty burden between DKD-related versus non-DKD end-stage renal disease patients (n=100). The combined genetic and clinical evidence aims to clarify whether frailty is a causal risk marker or contributor to diabetic kidney disease complications.

Cenzano I, Cócera M, Larrayoz M et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Structural basis for selective and potent degradation of IRAK4 by KT-474.

This paper determined the structural basis for selective and potent degradation of IRAK4 by the heterobifunctional degrader KT-474. Using cryo-EM and biophysical/computational methods, the authors resolved an IRAK4:KT-474:CRBN/DDB1 complex with a non-native protein–protein interaction surface, including a key hydrophobic contact mediated by CRBN Phe150. The structure explains how KT-474 achieves IRAK4 selectivity through CRBN recruitment, informing rational design of next-generation targeted protein degraders.

Fei X, Ramanathan A, Daigle CA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

EFHD2 drives lactate-mediated DNA damage repair and immunosuppression via HMGB1 and HIF-1α to confer radioresistance in colorectal cancer.

This study investigated how EFHD2 drives lactate-mediated DNA damage repair, immunosuppression, and radioresistance in colorectal cancer using multi-omics and functional immune assays. It implicated EFHD2 lysine 9 (K9) lactylation and linked EFHD2-dependent pathways to HMGB1 and HIF-1α, integrating lactyl-proteomics, spatial transcriptomics, and single-cell RNA sequencing with co-culture experiments and multiplex immunofluorescence. These findings identify an EFHD2–lactylation–HMGB1/HIF-1α axis as a mechanistic driver of CRC radioresistance and immune evasion.

Yu Y, Wu H, Xiao Y et al. · Cell death & disease · (2026) · View on PubMed ↗ · Free PDF ↗

Frailty index and type 2 diabetes with renal complications: insights from Mendelian randomization and retrospective observational study.

This study used Mendelian randomization and retrospective observational data to assess the relationship between frailty and type 2 diabetes with renal complications. It applied two-sample MR using GWAS summary statistics, performed sensitivity analyses to address pleiotropy (including exclusion of pleiotropic variants and multivariable MR), and then analyzed a hemodialysis cohort (n=100) comparing frailty burden in DKD-related versus non-DKD end-stage renal disease. The work aims to clarify whether frailty is causally linked to diabetic kidney disease complications and could inform risk stratification.

Wu H, Lin J, Wu X et al. · Renal failure · (2026) · View on PubMed ↗ · Free PDF ↗

Molecular Glues Recruiting RNF213 As an E3 Ligase for Targeted Protein Degradation: A Minimal Dibromoacetamide Warhead As a Recruitment Ligand.

This chemistry study identified RNF213 as a recruitable E3 ligase for targeted protein degradation by molecular glue degraders. The authors designed CYB-5067 by attaching a minimal dibromoacetamide covalent warhead to the pan-FGFR inhibitor infigratinib, enabling RNF213 recruitment to degrade FGFR1–4 with strongest potency for FGFR2 (DC50 27 nM; Dmax 96%). These results expand the E3 ligase repertoire beyond CRBN/VHL and provide a lead molecular glue strategy for FGFR-targeted cancer therapy.

Jiang J, Chen Y, Wan R et al. · Journal of the American Chemical Society · (2026) · View on PubMed ↗

Context-Dependent Short-Chain Fatty Acids in Inflammatory Skin Diseases: Immunometabolic Mechanisms, Evidence Boundaries, and Translational Perspectives.

This narrative review synthesizes mechanistic, preclinical, and clinical evidence on how short-chain fatty acids (acetate, propionate, and butyrate) regulate cutaneous immunity and barrier function in inflammatory skin diseases. It highlights that SCFA effects are context-dependent and mediated through free fatty acid receptors (FFARs), with translational uncertainties that challenge the assumption of uniform benefit. Scientifically, it clarifies evidence boundaries and translational considerations for targeting SCFA–FFAR immunometabolic pathways in skin inflammation.

Su Z, Huang Z, Huang Y et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Spatial architecture contributes to failure of bulk biomarker-guided neoadjuvant immunotherapy selection in bladder cancer: The DUTRENEO study.

The DUTRENEO prospective randomized phase 2 trial tested whether an 18-gene bulk tumor inflammation signature (TIS) could prospectively select patients for neoadjuvant immune checkpoint inhibitor therapy in muscle-invasive bladder cancer. The trial failed to meet its primary endpoint, showing that bulk gene-expression stratification did not sufficiently enrich for responders, and spatial single-cell transcriptomics across large tissue regions was used to explain the failure. Scientifically, the results argue that spatial heterogeneity and microenvironmental context limit the predictive value of bulk biomarkers for neoadjuvant immunotherapy response.

Grande E, Sibai M, Grases D et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Immuno-Proteomic Features Associated to Relapse Risk in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.

The study aimed to define immuno-proteomic and cellular signatures that distinguish relapse risk and subphenotypes in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) versus multiple sclerosis (MS) and Alzheimer disease (AD) as a neurodegeneration comparator. It reported molecular and cellular features associated with relapse risk in MOGAD and used these to separate MOGAD from MS and AD. These biomarkers could improve risk stratification and guide therapy selection in MOGAD, where reliable relapse predictors are currently limited.

Gallaccio G, Müller A, Wang M et al. · Neurology(R) neuroimmunology & neuroinflammation · (2026) · View on PubMed ↗ · Free PDF ↗

Addressing Biases in Analysis of Time of Infusion: NCI/SWOG Trial S1404 Among Participants With High-Risk Resectable Melanoma Who Received Adjuvant Anti-PD-1 Therapy.

Using data from NCI/SWOG trial S1404 in participants with high-risk resectable melanoma receiving adjuvant pembrolizumab (anti–PD-1), the study re-analyzed whether time of infusion (earlier vs later in the day) is associated with outcomes while addressing confounding, survivor bias, and multiple testing. The key finding was that prior claims about “earlier infusion” benefits were sensitive to analytic choices and bias control, and the study emphasized that results can change when confounding and multiplicity are properly handled. Methodologically, it provides a more rigorous framework for evaluating infusion-time effects on immunotherapy outcomes.

Othus M, Truong TG, Sharon E et al. · JCO oncology practice · (2026) · View on PubMed ↗

Association between albumin-bilirubin score, model for end-stage liver disease score, platelet-albumin-bilirubin score, and acute-on-chronic liver failure complications: a cross-sectional study in a Chinese population.

This retrospective cross-sectional study enrolled 2104 Chinese patients with acute-on-chronic liver failure (ACLF) and assessed whether albumin-bilirubin (ALBI), model for end-stage liver disease (MELD), and platelet-albumin-bilirubin (PALBI) scores measured within 48 hours of admission predict major ACLF complications. The key finding was that these scores were independently associated with major ACLF complications, with predictive performance evaluated using multivariable logistic regression, restricted cubic splines, and ROC analyses. This supports using readily calculated liver scores for early risk stratification of ACLF complications in a real-world Chinese population.

Xie J, Pei X, Wang L et al. · European journal of gastroenterology & hepatology · (2026) · View on PubMed ↗

Yield of Fecal Immunochemical Test Screening for Colorectal Cancer in Adults Aged 45-49 vs 50-54 years.

Within a provincial colorectal cancer (CRC) screening program in China, the study compared FIT-based CRC screening yield between adults aged 45–49 and 50–54 using two-sample FIT followed by colonoscopy for FIT-positive results. The key finding was the relative FIT positivity and detection rates (including adenoma and advanced colorectal neoplasia detection) between the two age groups, informing whether lowering the screening start age improves yield. These real-world effectiveness data help guide policy decisions on initiating FIT screening at 45–49 versus 50–54 years.

Wang L, Zhu C, Qiu Y et al. · The American journal of gastroenterology · (2026) · View on PubMed ↗

Optimal Use of Targeted Therapy and Immunotherapy in Early-Stage, Resectable Non-Small Cell Lung Cancer.

This educational review assessed how to optimally use targeted therapy and immunotherapy to improve long-term surgical outcomes in early-stage, resectable non-small cell lung cancer (NSCLC), focusing on patients with resected pathologic stage II/III EGFR-mutated or ALK-rearranged disease and on trial evidence for neoadjuvant strategies. It highlights FDA-approved adjuvant osimertinib for resected stage II/III EGFR-mutated NSCLC and adjuvant alectinib for resected stage II/III ALK-mutated NSCLC, while noting that neoadjuvant use remains an active area of clinical trials. Clinically, it frames how biomarker-defined targeted therapy and emerging immunotherapy trial data may be integrated around surgery to reduce recurrence risk in resectable NSCLC.

Osarogiagbon RU, Cetnar JP, Aljumaily R · American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting · (2026) · View on PubMed ↗ · Free PDF ↗

DHODH Drives Sunitinib Resistance Via a Non-Enzymatic Mechanism by Inhibiting TRIM28 Ubiquitination and Consequent VEGFA Activation in RCC.

This study investigated the molecular driver of sunitinib resistance in renal cell carcinoma (RCC) using patient-derived xenograft (PDX) models generated from surgically resected RCC tissues and proteomic profiling to identify resistance regulators. It found that DHODH promotes sunitinib resistance through a non-enzymatic mechanism by inhibiting TRIM28 ubiquitination, leading to increased VEGFA activation. Scientifically, it implicates the DHODH–TRIM28–VEGFA axis as a potential therapeutic target to overcome anti-angiogenic resistance to sunitinib in RCC.

Qian S, Pu S, Xu Z et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗

Dupilumab for Eosinophilic Esophagitis in Adolescents and Adults: Real-World Outcomes Across Different Dosing Regimens from the EoE CONNECT Registry.

This real-world cross-sectional analysis evaluated dupilumab effectiveness and safety for eosinophilic esophagitis (EoE) in adolescents and adults using the EoE CONNECT registry, comparing dosing regimens of 300 mg weekly versus semi-weekly. Across 161 patients (145 adults, 16 adolescents), it assessed clinico-histological response (CHR), dose adjustments, and tolerability to determine whether flexible dosing and fibrostenotic phenotypes influence outcomes. Clinically, the findings support evidence-based dosing decisions for dupilumab in routine practice for EoE patients with different disease characteristics.

Laserna-Mendieta EJ, Úbeda-Vargas V, Amorena E et al. · The American journal of gastroenterology · (2026) · View on PubMed ↗

A guardian role of TagA in protecting Mycobacterium tuberculosis from nitrosative killing.

This study examined how Mycobacterium tuberculosis survives nitrosative killing inside macrophages by identifying bacterial genes required for survival in distinct macrophage subsets using transposon insertion sequencing. It showed that tagA (TagA) has a specialized protective role for Mtb survival in M1-polarized macrophages and in mice at 4 weeks post-infection, when macrophages are biased toward an M1 state. The work is significant because it defines TagA as a macrophage-state–dependent DNA-damage resistance factor that could inform host-directed or bacterial-targeted strategies against tuberculosis.

Zhang Y, Wang H, Liu Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

MDM2 suppresses c-Myc synthesis by binding to the 5’ mRNA translation regulatory sequence.

This mechanistic cancer biology study investigated how MDM2 regulates c-Myc expression by using the small MDM2-binding drug milademetan to test effects on c-Myc mRNA translation. It found that milademetan promotes MDM2 binding to the 5’ untranslated region of c-Myc mRNA, suppressing c-Myc protein synthesis without changing c-Myc RNA levels. Scientifically, it reveals a translation-level control mechanism linking the p53/MDM2 axis to c-Myc and supports milademetan as a potential strategy to downregulate c-Myc in tumors.

Habault J, Salomao N, Wang L et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Fasting primes small intestinal regeneration after damage via a microbiome-metabolite-chromatin axis.

This study tested how fasting primes small intestinal regeneration after radiation damage by integrating microbiome, metabolite, and chromatin analyses in mice and intestinal stem cell cultures. It identified Akkermansia muciniphila as a key mediator: antibiotic depletion removed radioprotection, while reintroduction restored survival and intestinal integrity, with fasting increasing propionic acid and inducing histone H3 acetylation (including H3K27ac and H3K9ac) and promoter–enhancer remodeling in crypt epithelial cells. The findings are significant because they define a microbiome–metabolite–chromatin axis (AKK/propionate → histone acetylation) that could be leveraged to enhance radioprotection and tissue repair.

Barrodia P, Saw AK, Jeter-Jones SL et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Immune cell-intrinsic STING activation drives tumor ferroptosis via AA-mediated suppression of ACSL4 lactylation in colorectal cancer.

This study investigated how immune cell-intrinsic STING signaling drives tumor ferroptosis in colorectal cancer (CRC) by linking STING to lipid metabolism and post-translational modifications in the tumor microenvironment. It showed that STING activation in immune cells triggers TBK1-dependent phosphorylation of cPLA2 (Ser505), releasing arachidonic acid (AA) into the tumor microenvironment, which then suppresses ACSL4 lactylation and promotes ferroptosis in tumor cells. The work is significant because it identifies a STING–TBK1–cPLA2–AA–ACSL4 lactylation pathway that could be targeted to increase ferroptotic sensitivity in CRC.

Ding L, Du W, Zhu J et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Natural variation of CTS1 confers cold tolerance and blast resistance in rice.

This plant genetics study analyzed natural variation in rice to determine how CTS1 (Cold Tolerance at the Seedling stage1), encoding the transcription factor OsWRKY74, affects abiotic and biotic stress tolerance. Using a genome-wide association study, it found that the CTS1Hap1 allele confers greater cold tolerance than CTS1Hap2 by mildly repressing CTB2 expression, thereby maintaining sterol glycoside homeostasis and membrane stability and also improving blast resistance. The significance is agricultural: CTS1/OsWRKY74 provides a pleiotropic genetic lever to breed rice with improved cold tolerance and blast resistance.

Ye W, Ma W, Li Y et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

A broadly conserved gram-positive lipoprotein regulates cell elongation.

This bacterial cell biology study searched for previously unrecognized components of the gram-positive Rod complex/elongasome by combining high-throughput genetics with AlphaFold-Multimer structural predictions. It converged on the broadly conserved lipoprotein ClcR (formerly YerH/CamS) as a required factor for cell elongation across gram-positive bacteria. The findings are significant because they expand the known elongasome machinery and identify ClcR as a potential target for antibacterial strategies that disrupt cell shape and growth.

Brogan AP, Schmid EW, Rudner DZ · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Intracellular delivery of full-length antibodies via organ-targeted lipid nanoparticles.

This study developed and tested organ-targeted lipid nanoparticles (LNPs) for intracellular delivery of full-length therapeutic antibodies into the cytosol of cells. It reported that the LNP platform can efficiently deliver multiple antibodies into various cancer cell lines, enabling inhibition of key cytosolic transcription factors involved in inflammatory and cancer signaling. The scientific and clinical significance is that it provides a delivery technology to overcome the long-standing barrier of getting antibodies into the cytosol to target intracellular disease proteins.

Alamgir A, Yaneva M, Sela M et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanobiology of inflammation: Pulling the strings of innate immunity.

This article reviews how mechanical forces (stretch, tissue stiffness, and shear stress) regulate innate immune responses across barrier epithelia, stromal niches, and vascular endothelium. It highlights that conserved mechanotransduction pathways can both initiate and reprogram “mechano-inflammatory” programs, thereby remodeling immune synapses, tissue architecture, and leukocyte trafficking, with chronic mechanical perturbation driving pathological inflammation in diseases such as asthma and arthritis. The mechanistic synthesis is clinically significant because it frames tissue mechanics as a potential therapeutic target for controlling innate immune–driven inflammation.

Maniak MK, Jenkins SJ, Hansen CG · The Journal of experimental medicine · (2026) · View on PubMed ↗

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Cancer Immunotherapy (CAR T, Vaccines, Checkpoint Inhibitors)

Ten-Year Outcomes after CAR T-Cell Therapy for B-Cell Lymphomas.

The study evaluated 10-year outcomes of CAR T-cell therapy in patients with relapsed or refractory B-cell non-Hodgkin lymphomas treated with CTL019/tisagenlecleucel (CD19-directed, 4-1BB-costimulated CAR T cells). Among 38 patients (24 with large B-cell lymphoma and 14 with follicular lymphoma), it assessed long-term lymphoma-free survival and related relapse and death endpoints from infusion onward. These data clarify durability and potential curative benefit of tisagenlecleucel over a decade, informing long-term risk counseling and future CAR T trial design.

Ruella M, Paruzzo L, Chong ER et al. · The New England journal of medicine · (2026) · View on PubMed ↗

Autoantigen-loaded Polymeric Microparticles associate with B cells and promote tolerogenic antigen presentation in a mouse model of experimental autoimmune encephalomyelitis.

The authors tested whether antigen-loaded acetalated dextran polymeric microparticles (AMP) can target B cells and induce tolerogenic antigen presentation in a mouse model of experimental autoimmune encephalomyelitis (EAE). AMP surface-association with B cells increased IL-10 secretion and MHCII expression, promoting tolerogenic antigen presentation and supporting antigen-specific suppression of autoreactive responses. This suggests a B-cell–targeted, antigen-specific tolerance strategy that could improve on current multiple sclerosis therapies that broadly suppress protective immunity.

Lukesh NR, Barbery BG, Clark KA et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Optimized L1CAM-CAR T cells enhance activity against moderate-antigen-density rhabdomyosarcoma models.

This preclinical study optimized L1CAM-targeted CAR T cells to improve activity against rhabdomyosarcoma (RMS) models with moderate antigen density. It profiled L1CAM expression across cell lines, patient-derived xenografts, and healthy tissues, then engineered CAR T cells using the CE7-derived single-chain variable fragment and compared their anti-tumor performance. The significance is translational for solid-tumor CAR T therapy: it addresses antigen heterogeneity and aims to enhance efficacy while managing on-target/off-tumor risk in RMS.

Piccand C, Gauthier C, Klöckner P et al. · Cancer letters · (2026) · View on PubMed ↗ · Free PDF ↗

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Cancer Biomarkers, Risk Prediction & Imaging/Omics Modeling

Alternate RNA decoding results in stable and abundant proteins in mammals.

The study analyzed deep proteomic, transcriptomic, and genomic data from over 1,000 human samples to determine how alternate RNA decoding (deviations from the genetic code) affects protein output. It identified 60,803 fragmentation spectra corresponding to 8,746 unique amino-acid substitutions from 1,767 genes (1,955 confidently localized sites), with substitution patterns that were shared across samples or specific to tissue types and cancers. This demonstrates that alternate decoding can generate stable, abundant proteins in mammals, reshaping how genetic variation and proteome diversity may contribute to physiology and cancer.

Tsour S, Machné R, Leduc A et al. · Nature · (2026) · View on PubMed ↗

Spatial multi-omics implicate the interaction between Tpex and B cells in tertiary lymphoid structures after neoadjuvant therapy.

This study used spatial multi-omics (whole-transcriptome spatial transcriptomics with single-cell resolution plus high-throughput spatial proteomics and TCR-seq) to analyze tertiary lymphoid structures (TLSs) in clinical breast cancer samples after neoadjuvant therapy. It found that precursors of exhausted T cells (Tpex cells) preferentially reside within TLSs and that tumor-specific Tpex cells are present inside TLSs, with spatial TLS pharmacodynamics linked to therapy response. These results implicate Tpex–TLS interactions as a spatially defined immune mechanism that may help explain variability in treatment efficacy.

Huang J, Chen Y, Deng P et al. · Cancer discovery · (2026) · View on PubMed ↗

GABA signaling activation drives glioblastoma progression in female mice through myeloid-derived suppressor cells.

The study used large-scale human plasma metabolomics to build a comprehensive NMR-derived metabolite atlas from 251 metabolites measured in 212,751 UK Biobank participants, with independent validation in 177,013 individuals. Across 884 health-related traits, 722 prevalent diseases, and 1,137 incident diseases, the authors performed multivariable regression with stringent Bonferroni correction to systematically map metabolite–phenotype associations. This resource improves the ability to connect circulating metabolites to disease risk and comorbidity patterns, supporting future causal and predictive analyses in population health.

Pathak A, Sravya P, Colon B et al. · Nature cancer · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

Refining the Correa Cascade: Gastric Stem Cell Plasticity, Niche Remodelling, and Parallel Pathways to Neoplasia.

This review examines gastric cancer progression along the Correa cascade, focusing on gastric stem cell plasticity, niche remodeling, and parallel routes to neoplasia using lineage tracing, single-cell multi-omics, and organoid models. It proposes that gastric homeostasis involves cycling LGR5+ antral basal and IQGAP3+ isthmus progenitors plus quiescent MIST1+/TROY+ chief-cell reserves, coordinated by Wnt/R-spondin, Notch, BMP, Hedgehog, and EGFR signaling, with non-sequential trajectories to neoplasia. The work is significant because it reframes precancerous progression as heterogeneous and plastic, informing future strategies to intercept gastric adenocarcinoma development.

Zhang T, Wang Z, Zhang B et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

ctDNA based MRD detection in stage III NSCLC treated with chemoradiotherapy and durvalumab.

This prospective multicenter study evaluated ctDNA-based minimal residual disease (MRD) detection in unresectable stage III non-small cell lung cancer (NSCLC) patients treated with chemoradiotherapy (CRT) followed by durvalumab. Using a tumor-agnostic, hybrid-capture ctDNA MRD assay personalized to each patient, it assessed ctDNA detection at multiple timepoints to identify patients at high risk of early treatment failure during and after durvalumab. Clinically, it tests whether ctDNA MRD can refine prognosis and potentially guide escalation or de-escalation strategies in stage III NSCLC immunotherapy.

Horndalsveen H, Haakensen VD, Madebo T et al. · Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Epithelial FOXP3 orchestrates O-glycosylated IL-6 secretion to drive pancreatic fibrocarcinogenesis.

This study investigated how the epithelial transcription factor FOXP3 drives pancreatic fibrocarcinogenesis by orchestrating O-glycosylated IL-6 secretion in pancreatic ductal adenocarcinoma (PDAC) models. Using human tissues and genetically engineered mouse models with epithelial-specific FOXP3 knockout and knock-in strategies, it linked FOXP3-dependent epithelial programs to fibrogenesis and neoplasia progression. The significance is mechanistic and therapeutic: it identifies an epithelial FOXP3–O-glycosylated IL-6 axis as a potential early driver of pancreatic fibrosis that promotes PDAC.

Gong R, Wang J, Ren M et al. · Gastroenterology · (2026) · View on PubMed ↗

Methionine-supplemented longevity diet increases growth hormone, GLP-1, and FGF21; reduces frailty; and promotes healthspan.

In mice, the study compared longevity diet formulations and tested whether a methionine-supplemented low-protein longevity diet (LDMM) alters endocrine and metabolic pathways relevant to aging and frailty. LDMM reduced fat mass and frailty while increasing growth hormone, GLP-1, and fibroblast growth factor 21 (FGF21), with reduced IGF-1, and these benefits required FGF21. Clinically and translationally, the work supports methionine-supplemented low-protein dietary strategies as a potential healthspan intervention mediated by the GH/GLP-1/FGF21 axis.

Fanti M, Brandhorst S, Navarrete G et al. · Cell metabolism · (2026) · View on PubMed ↗

Targeting GLP1R and IL17A suppresses obesity-induced leukemia in an oncogenic PTPN11 mutation-driven model.

This study combined UK Biobank human association analyses with an obesity-driven oncogenic PTPN11 (Shp2E76K/+) mutant hematopoietic stem/progenitor mouse model to test whether targeting GLP1R and IL17A suppresses obesity-induced leukemia. The key finding was that obesity-associated metabolic inflammation promoted leukemogenesis via IL-17A–linked pathways and reduced GLP1R signaling, and that pharmacologic targeting of GLP1R and IL17A suppressed obesity-induced leukemia in the PTPN11-mutant model. This is significant because it links obesity-driven inflammation to a defined oncogenic signaling context (PTPN11) and identifies GLP1R/IL17A as actionable therapeutic targets.

Kapur R, Li L, Kanumuri R et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗ · Free PDF ↗

Longitudinal Analysis of Changes in Deep Learning Image-based Breast Cancer Risk Scores over Time.

This multisite retrospective cohort study examined whether image-only deep learning (DL) breast cancer risk scores derived from screening mammograms change over time and whether their trajectories differ between women who later develop invasive cancer or ductal carcinoma in situ versus those who remain cancer-free. The key finding is the characterization of longitudinal changes in DL risk score trajectories across follow-up rather than assuming static risk estimates. The significance is that it may improve how AI-based mammography risk models are used for ongoing surveillance and risk-adapted prevention.

Lehman CD, Mercaldo SF, Azam S et al. · Radiology · (2026) · 1 citations · View on PubMed ↗

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Clinical Trials & Comparative Effectiveness (Oncology & Other)

Efficacy and safety of tirofiban after successful endovascular reperfusion in acute ischaemic stroke (ATTRACTION) in China: a multicentre, double-blind, randomised controlled trial.

The trial studied whether intra-arterial tirofiban, a glycoprotein IIb/IIIa receptor antagonist, improves outcomes in patients with acute ischemic stroke who achieved successful endovascular reperfusion after thrombectomy. In a multicentre, double-blind, randomized controlled design across 82 hospitals in China, patients with anterior-circulation large-vessel occlusion were assigned to tirofiban versus control after successful reperfusion. If effective, this would support adding targeted antiplatelet therapy post-thrombectomy to improve functional recovery and safety in a high-risk stroke subgroup.

Huang H, Xu S, Qin T et al. · Lancet (London, England) · (2026) · View on PubMed ↗

Increasing incidence and changing trends in etiology & survival rates in HCC in a European cohort.

This population-based study analyzed consecutive patients with newly diagnosed hepatocellular carcinoma (HCC) in the Netherlands Cancer Registry from 2014–2022 to assess changing incidence trends, etiologies, tumor characteristics, and survival. It reports increasing incidence and shifts in etiology and survival patterns over time in a European cohort, with statistical trend testing using average annual percentage change (AAPC) and Cox regression for mortality risk factors. The significance is public-health and clinical: it highlights evolving HCC drivers and outcomes in the Netherlands, informing prevention and risk-stratified management.

van Son KC, van Eekhout KMA, de Vos-Geelen J et al. · JHEP reports : innovation in hepatology · (2026) · View on PubMed ↗ · Free PDF ↗

Proactive Fecal Calprotectin Home Monitoring in Ulcerative Colitis: Results of a Prospective Randomized Control Trial.

This prospective randomized controlled trial tested proactive home monitoring of fecal calprotectin (FC) in adults with ulcerative colitis (UC) in remission. Participants were randomized to standard care versus FC testing every 2 months for 18 months, with therapy changes triggered by confirmatory FC ≥250 μg/g, and the primary endpoint was time to symptomatic flare. Clinically, it evaluates whether FC-guided early intervention can prevent symptomatic UC flares compared with usual care.

Rosenfeld G, Narula N, Leung Y et al. · Gastroenterology · (2026) · View on PubMed ↗

Predicting elevated transcranial doppler velocity among patients with sickle cell anemia in Uganda: A cross-sectional study.

This cross-sectional study evaluated predictors of elevated transcranial Doppler (TCD) velocities in children with sickle cell anemia (SCA) in Uganda, using routinely collected clinical data to model stroke-risk screening. The key finding was that a predictive model could identify children at higher likelihood of elevated TCD velocity, potentially enabling targeted screening where universal TCD is not feasible. Clinically, this supports resource-sparing strategies to prevent SCA stroke by directing TCD testing and subsequent interventions to children most likely to benefit.

Nayiga D, Mukunya D, Odoch S et al. · PloS one · (2026) · View on PubMed ↗ · Free PDF ↗

Interim Estimated Effectiveness of 2025-2026 COVID-19 Vaccines in Adults Using a Test-Negative Design.

This US test-negative case-control study assessed interim effectiveness of the 2025–2026 COVID-19 vaccine (targeting JN.1 and JN.1-derived sublineages) against medically attended COVID-19 in immunocompetent adults aged ≥18 years using electronic health record encounters from the Virtual SARS-CoV-2, Influenza, and Other Respiratory Viruses Network. The key finding was an estimate of vaccine effectiveness during the 2025–2026 season against medically attended disease in this population. Scientifically and clinically, it provides timely real-world effectiveness evidence to guide ongoing vaccine policy and risk communication for adults.

Wiegand RE, Chickery S, Yang DH et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Palliative Care Coaching for Family Caregivers of Patients With Advanced Cancer: A Randomized Clinical Trial.

This single-blind randomized clinical trial tested whether lay coach-led early palliative care telehealth coaching (ENABLE Cornerstone) improves outcomes for African American and rural family caregivers of patients with advanced cancer at 24 weeks. The key finding was the intervention’s effect on caregiver and patient outcomes compared with usual care (as evaluated in the trial). The clinical significance is that it evaluates a scalable, culturally and geographically targeted palliative support model that could improve quality of life and care delivery for underserved populations.

Odom JN, Azuero A, Taylor RA et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗

Current issues in clinical staging of perihilar cholangiocarcinoma-a European snapshot survey.

This pan-European snapshot survey studied current issues in clinical staging of perihilar cholangiocarcinoma (pCCA) by surveying clinicians across Europe from two centers (Karolinska University Hospital, Stockholm, and Amsterdam UMC). The key finding was that multiple staging-related domains—such as centralization, multidisciplinary team review, imaging approaches, biliary drainage, cholangioscopy, and staging laparoscopy—have practical gaps and inconsistencies affecting staging quality. The significance is that it identifies actionable areas to standardize pCCA staging pathways and improve diagnostic accuracy and treatment selection.

Jansson H, Nebbia M, Zonderhuis BM et al. · Updates in surgery · (2026) · View on PubMed ↗ · Free PDF ↗

Darolutamide versus abiraterone acetate-based triplets in patients with hormone-sensitive prostate cancer: real-world, head-to-head comparison from the ARON-3 study.

This retrospective real-world head-to-head study compared darolutamide-based versus abiraterone acetate-based triplet therapy in 247 patients with metastatic hormone-sensitive prostate cancer (mHSPC) treated with DARO+DOCE+ADT or ABI+DOCE+ADT across 37 institutions in 14 countries. The key findings (reported as progression-free survival, overall survival, PSA kinetics, and safety with propensity-score adjustment) address comparative efficacy and tolerability of these triplets in routine practice. The clinical significance is that it informs selection of androgen-receptor–targeted triplet regimens for mHSPC outside clinical trials.

Rescigno P, Taha T, Fita MJ et al. · Minerva urology and nephrology · (2026) · View on PubMed ↗

A phase 3, randomized study to evaluate the safety, tolerability, and immunogenicity of V116 in children and adolescents with increased risk of pneumococcal disease (STRIDE-13).

This phase 3 randomized study evaluated the safety and immunogenicity of V116, a 21-valent pneumococcal conjugate vaccine, versus PPSV23 in children and adolescents (age 2 to <18 years) with increased risk of pneumococcal disease due to chronic medical conditions (e.g., diabetes, chronic heart/lung/kidney, and other listed conditions). The study’s central finding is that V116 was assessed for immunogenic responses and tolerability in this high-risk pediatric population after prior completion of a primary pneumococcal vaccination series. The scientific/clinical significance is that it supports evidence for vaccine choice and booster strategies in children with comorbidities that increase pneumococcal disease risk.

Jagannath V, Pathirana J, Perez Yepes CA et al. · Human vaccines & immunotherapeutics · (2026) · View on PubMed ↗ · Free PDF ↗

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Cardiovascular Risk, Heart Failure & Vascular Outcomes

Lipoprotein(a), Inflammation, and Risk of Coronary Artery Disease and Aortic Valve Stenosis.

This cohort study tested whether inflammatory biomarkers modify lipoprotein(a) [Lp(a)]-associated risk for coronary artery disease (CAD) and aortic valve stenosis (AS) in UK Biobank participants without prevalent CAD or AS, using plasma proteomic profiling. The key finding was that inflammatory markers can differentially influence the relationship between elevated Lp(a) and incident CAD/AS risk in a primary prevention population (exact biomarkers and interaction results are truncated). This supports an inflammation-modified model of Lp(a) pathogenicity, with potential implications for risk stratification and targeted anti-inflammatory or Lp(a)-lowering strategies.

Mohammadnia N, Li L, Ezzat D et al. · JAMA cardiology · (2026) · View on PubMed ↗

Investigating the relationship between ATP synthase and the TCA cycle by crosslinking mass spectrometry.

The study used in-solution crosslinking mass spectrometry (XL-MS) together with quantitative proteomics, complexome profiling, and blue native PAGE (BN-PAGE) to map how mitochondrial ATP synthase (complex V) is structurally positioned relative to the tricarboxylic acid (TCA) cycle in murine wild-type hearts under physiological and pathological conditions. The authors report that the F1 catalytic head of ATP synthase forms a direct, previously underappreciated structural relationship with components of the TCA-associated metabolic network beyond the canonical complex II link. This provides mechanistic evidence that ATP synthase participates in physical coupling with TCA-cycle metabolism, informing how mitochondrial OXPHOS–TCA coordination is remodeled in disease.

Pérez Pañeda L, Misic J, Kadavá T et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Semaglutide for Primary Prevention of Major Adverse Cardiac and Cerebrovascular Events in Patients with Type 2 Diabetes and Comorbid Rheumatoid Arthritis: A Target-Trial Emulation.

This target-trial emulation study used TriNetX US data to assess primary prevention of major adverse cardiovascular and cerebrovascular events (MACCE) with semaglutide in obese adults with type 2 diabetes mellitus (T2DM) and comorbid rheumatoid arthritis (RA). The key finding was an estimated effect of semaglutide on incident MACCE risk in this high-risk, primary-prevention population. Clinically, it informs whether GLP-1 receptor agonist therapy may reduce cardiovascular events in patients where RA-related inflammation and activity limitations increase baseline risk.

Malik F, Shah M, Chang Y et al. · European heart journal. Cardiovascular pharmacotherapy · (2026) · View on PubMed ↗ · Free PDF ↗

Extending the PREVENT Equations with Cardiac MRI: Prediction of 10-year Heart Failure Risk.

This secondary analysis used UK Biobank participants who underwent cardiac MRI to test whether adding multidimensional cardiac MRI variables to the PREVENT (Predicting Risk of Cardiovascular Disease EVENTs) equations improves prediction of 10-year heart failure risk. The key finding is the evaluation of incremental predictive performance of the MRI-augmented PREVENT model using a 70% training and 30% internal test split. The clinical significance is that it could enable more accurate long-term heart failure risk stratification by combining standard risk equations with cardiac MRI biomarkers.

Zhu M, Dai Y, Pan Y et al. · Radiology · (2026) · 1 citations · View on PubMed ↗

Early effects of SGLT2 inhibitors in acute heart failure: an individual patient-level meta-analysis.

This individual patient-level meta-analysis pooled randomized controlled trials of SGLT2 inhibitors versus placebo/control in acute heart failure to determine whether early SGLT2 inhibitor treatment improves decongestion and outcomes. The primary endpoint was 24-hour diuresis, with secondary outcomes including diuresis measures and in-hospital and post-discharge outcomes, thereby quantifying early effects on fluid removal. The clinical significance is that it clarifies whether early SGLT2 inhibitor therapy in acute HF translates into measurable decongestive benefit and downstream clinical improvements.

Zonneveld LEEC, Ter Maaten JM, Voors AA et al. · European journal of heart failure · (2026) · View on PubMed ↗ · Free PDF ↗

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Metabolic Disease & GLP-1/Insulin Resistance/Obesity

Dietary cholesterol activates a Ral-dependent pathway driving LDLR turnover.

The study examined how chronic dietary cholesterol regulates hepatic low-density lipoprotein receptor (LDLR) trafficking and turnover in relation to Ral GTPases and RAS activity. It found that dietary cholesterol increases RAS activity to activate Ral proteins, driving LDLR routing to lysosomal degradation and inhibiting recycling independently of transcriptional regulation and PCSK9. This identifies a Ral-dependent post-translational control pathway that could be therapeutically targeted to modulate LDLR levels and cholesterol homeostasis beyond PCSK9.

Feng X, Zhang S, Wang Y et al. · Nature · (2026) · View on PubMed ↗

Long-Term Safety and Renal Outcomes of Semaglutide in Non-Diabetic Obesity with Chronic Kidney Disease or Hypertension: A Systematic Review and Meta-Analysis.

This systematic review and meta-analysis studied semaglutide, a GLP-1 receptor agonist, in non-diabetic adults with obesity plus chronic kidney disease (CKD) or hypertension, evaluating outcomes including BMI, blood pressure, eGFR, and albuminuria. The key finding was the overall pooled assessment of semaglutide’s renal and cardiometabolic effects and safety in this under-studied non-diabetic CKD/obesity population (details truncated in the provided abstract). Clinically, the results inform whether semaglutide can extend the renal benefit profile seen in diabetic populations to higher-risk non-diabetic patients.

Elganyny MKE, Elganyni AKE, Maskji HA et al. · La Clinica terapeutica · (2026) · View on PubMed ↗

An emergent disease-associated motor neuron state precedes cell death in ALS.

The study used longitudinal single-nucleus RNA sequencing and chromatin accessibility profiling plus spatial transcriptomics in spinal motor neurons from the SOD1-G93A ALS mouse model to define molecular events preceding degeneration. Vulnerable alpha motor neurons transitioned into a distinct “disease-associated motor neuron” (DM) state with thousands of molecular changes, and transcription factor networks governing healthy-to-DM transitions and subtype-selective vulnerability were identified, with DM-associated transcription factor upregulation also observed in human motor neurons. This provides a mechanistic, pre-death cellular state in ALS that could be targeted to halt or slow neurodegeneration.

Gautier O, Blum JA, Nguyen TP et al. · Cell · (2026) · View on PubMed ↗ · Free PDF ↗

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Microbiome, Microbial Metabolites & Gut-Immune Signaling

Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3.

The study examined whether gut microbiota-derived lysine phenylacetylation (Kpaa) affects host mitochondrial function and insulin signaling, and whether the deacetylase SIRT3 can alleviate these effects. In mice with high-fat-diet-induced obesity, hepatic Kpaa levels were elevated and reduced by SIRT3, and PAA (phenylacetic acid)-linked phenylacetylation disrupted mitochondrial function and impaired insulin signaling. This links a specific microbiota metabolite-driven post-translational modification to mitochondrial dysfunction and suggests SIRT3 as a potential therapeutic node in metabolic disease.

Du W, Xu JY, Li Y et al. · Cell metabolism · (2026) · View on PubMed ↗

Bidirectional Communication of the Gut-Brain Axis in Pain Regulation: From Microbial Metabolites to Neuroinflammation.

This review examined the bidirectional gut-brain axis (GBA) mechanisms in pain regulation, linking microbial metabolites to neuroinflammation and central nervous system (CNS) changes. The key finding is a mechanistic framework in which gut microbiota and intestinal epithelial/enteric nervous system signaling influence pain through neural, endocrine, immune, and metabolic pathways, and that dysbiosis is implicated in conditions such as IBS, migraine, and fibromyalgia. Clinically, it motivates microbiome- and metabolite-targeted strategies as potential interventions to modulate neuroinflammation and chronic pain.

Song Z, Zhou K, Liang G et al. · Journal of inflammation research · (2026) · View on PubMed ↗ · Free PDF ↗

Host metabolism can produce many indoles and phenols independently of the microbiome.

Using stable isotope tracing in cell culture, mice, and rats, the study quantified host (mammalian) production of indole and phenol metabolites that are often attributed to gut microbiota. Mammalian cells were shown to generate aryl-pyruvate–derived indoles and phenols independently of the microbiome, demonstrating a substantial host contribution to circulating pools. These findings reshape interpretation of indole/phenol biomarker biology and indicate that therapeutic modulation of these metabolites must consider host metabolic pathways, not only microbial enzymes.

AbuSalim JE, Olszewski K, Youssef S et al. · Nature metabolism · (2026) · View on PubMed ↗ · Free PDF ↗

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Immunology of Inflammation (Innate/T2/Immune Niches)

The mutational landscape of STING-induced immunity.

The study investigated how sequence elements govern STING (stimulator of interferon genes) activation and downstream type I interferon/inflammatory signaling in cells. Using a massively parallel sequence-function assay, it mapped a mutational landscape that links ligand-induced structural transitions, protein-protein interactions, and intracellular trafficking to STING (in)activation. These findings provide a framework for predicting STING gain- or loss-of-function variants and for improving STING-targeted immunotherapies.

Zhang B, Xu P, Meng Y et al. · Nature · (2026) · View on PubMed ↗

Small-molecule modulation of β-arrestins.

The study developed and characterized small-molecule inhibitors that modulate β-arrestin function in the context of GPCR signaling. It found that the inhibitors selectively target β-arrestins and disrupt β-arrestin engagement with downstream partners (including components of the arrestin-mediated signaling interface) based on integrated pharmacological, biochemical, biophysical, and structural analyses. This provides chemical tools to directly control β-arrestin pathways, enabling more precise GPCR pharmacology than approaches limited to orthosteric/allosteric sites or G-protein/kinase targets.

Kahsai AW, Pakharukova N, Kwon HY et al. · Nature · (2026) · View on PubMed ↗

The 2026 British Society for Rheumatology guideline for the management of children, young people and adults with systemic lupus erythematosus.

This article presents the 2026 British Society for Rheumatology life-course guideline for managing systemic lupus erythematosus (SLE) in children, young people, and adults. It emphasizes empowering patients to suppress systemic disease activity and prevent organ damage, building on the 2017 adult SLE guideline and expanding recommendations across the lifespan. Clinically, it standardizes evidence-based care pathways for pediatric-to-adult SLE management in the UK, aiming to improve outcomes and reduce morbidity and mortality.

Md Yusof MY, Smith EMD, Lythgoe H et al. · Rheumatology (Oxford, England) · (2026) · View on PubMed ↗

Innate immunity in allergic diseases: Novel concepts.

This review summarizes novel concepts in innate immunity as drivers of type 2 (T2) immune dysregulation in allergic diseases, including allergic rhinitis and chronic rhinosinusitis. It argues that innate immune cells initiate and sustain T2-mediated disease and can serve as biomarkers and therapeutic targets through mechanisms that link innate and adaptive immunity. The significance is translational: it supports developing innate-immune–directed interventions to prevent chronification of T2 allergic disorders.

Maldonado A, Angelina A, Cuervo N et al. · The Journal of allergy and clinical immunology · (2026) · View on PubMed ↗

BIRC3 (Encoding Cellular Inhibitor of Apoptosis Protein 2) Variants Result in Dysregulated Receptor-Interacting Protein Kinase 1 Signaling Leading to Increased Epithelial Cell Death and Are Associated With Monogenic Crohn’s Disease.

The study screened exomes from patients with monogenic Crohn’s disease for BIRC3 variants and then used cellular assays, intestinal organoids (including iPSC-derived organoids), and knock-in/knockout mouse and zebrafish models to test effects on TNF signaling and RIPK1-dependent epithelial death. BIRC3 variants disrupted cIAP2 regulation of receptor-interacting protein kinase 1 (RIPK1) signaling, leading to increased epithelial cell death and were associated with monogenic Crohn’s disease. These findings identify BIRC3–cIAP2–RIPK1 pathway dysregulation as a causal mechanism and a potential precision-therapy target for a genetically defined Crohn’s subgroup.

Li Q, Nambu R, Yaqiang H et al. · Gastroenterology · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmune & Rheumatology (SLE, Asthma, RA, Demyelinating Disease)

Severe asthma and remission prospects in Europe (SHARP): insights from a multicentre observational study based on the European Severe Asthma Registry.

The study assessed severe asthma remission prospects and real-world disease burden in Europe using observational data from the European Severe Asthma Registry (SHARP). It analyzed 13,455 adults with severe asthma to estimate remission potential and characterize factors associated with remission and ongoing morbidity despite modern care including biological treatments. These findings help clinicians and researchers benchmark remission likelihood in routine practice and identify targets to reduce corticosteroid harm and improve outcomes.

Fouka E, Bansal AT, Håkansson KEJ et al. · The Lancet. Respiratory medicine · (2026) · View on PubMed ↗

Anti-CD20 Therapies in Pediatric Acquired Demyelinating Syndromes: Evidence Across MS, AQP4-IgG-Positive NMOSD and MOGAD.

This review synthesized evidence on anti-CD20 therapies in pediatric acquired demyelinating syndromes, focusing on multiple sclerosis (MS), aquaporin-4 IgG-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). The key finding was that B-cell–targeted anti-CD20 treatment is increasingly supported across these pediatric conditions, with rationale extending beyond antibody production to antigen presentation and T-cell modulation. Clinically, it supports the growing use of anti-CD20 strategies to improve early disease control and reduce long-term disability in neurodevelopmental-age patients.

Margoni M, Preziosa P, Rocca MA et al. · CNS drugs · (2026) · View on PubMed ↗

Real-world evidence on JAK inhibitors in rheumatology practice: comparative safety, efficacy, and outcomes between JAK inhibitors.

This retrospective three-arm comparative cohort study evaluated real-world drug survival, adverse events, and discontinuation for three Janus kinase inhibitors (JAK inhibitors) in rheumatology practice. The key finding was comparative retention and safety/discontinuation patterns among patients with rheumatic diseases (including seropositive and seronegative rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis) treated with tofacitinib, baricitinib, and another JAK inhibitor. The significance is that it provides practical effectiveness and tolerability signals to support shared decision-making and treatment sequencing in routine care.

Deniz R, Yılmaz A, Boncukcuoğlu AE et al. · Clinical rheumatology · (2026) · View on PubMed ↗

Relative frequencies of muscle specific kinase antibody myasthenia in 46 centres worldwide.

This global multicenter analysis assessed the relative frequency of muscle-specific kinase (MuSK) antibody–positive myasthenia gravis among 465 previously untested acetylcholine receptor (AChR) antibody–seronegative myasthenia gravis (SNMG) sera collected from 35 centers across 6 continents since 2002. MuSK antibodies were detected in 143/465 (30.8%) SNMG samples, and were not found in 147 adult AChR-antibody–positive patients or in 63 adult ocular myasthenia patients. The significance is that it provides population-level estimates of MuSK antibody prevalence and supports more accurate serologic stratification and treatment planning in SNMG.

Vincent A, Badi R, Barisic N et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurology & Neurodegeneration (ALS/FTD, GBM, Brain Aging, Pain)

IRE1 regulates the proteostasis of TDP-43/TARDBP in ALS/FTD through ribosome-associated quality control.

This study examined the role of endoplasmic reticulum stress signaling in TAR DNA-binding protein 43 (TDP-43/TARDBP) proteostasis in ALS/FTD, using genetic screening to identify regulators in relevant models. The authors found that inositol-requiring enzyme 1 (IRE1) potently suppresses TDP-43 protein levels via ribosome-associated quality control, thereby reducing TDP-43 accumulation. The work suggests IRE1 as a mechanistic target to modulate TDP-43 proteostasis in ALS/FTD.

Liu D, Li Y, Huang S et al. · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Neurometabolites and Antipsychotic Response in Psychosis: A Mega-Analysis.

This mega-analysis investigated whether neurometabolites measured in psychosis differ between individuals who are antipsychotic nonresponsive versus responsive, using individual participant data meta-analysis across 18 contributing studies. The key finding was identification of neurometabolite differences associated with antipsychotic nonresponse in psychosis (specific metabolites/effect directions are not visible in the truncated abstract). Scientifically, these neurochemical markers could improve prediction of treatment outcome and point to new biological targets for refractory psychosis.

King B, Bojesen KB, Crisp C et al. · JAMA psychiatry · (2026) · View on PubMed ↗

Engineering drug-responsive replication machinery for precise control of self-amplifying RNA.

The study investigated how γ-aminobutyric acid (GABA) signaling drives glioblastoma (GBM) progression in female mice by focusing on myeloid-derived suppressor cells (gMDSCs) and the GABA receptor B (GABBR) pathway. GABBR signaling enhanced the T cell suppressive function of gMDSCs via upregulation of the cationic amino acid transporter 2 (CAT2)–NOS2 pathway, and GABBR agonism promoted GBM growth while GABBR antagonism extended survival in preclinical models. This identifies a female-specific immune-cancer mechanism that could be therapeutically targeted to modulate suppressive myeloid immunity in GBM.

Yousefpour P, Gregory JR, Si K et al. · Nature biomedical engineering · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗

A large-scale human plasma metabolite atlas from over 380,000 participants.

The authors integrated multimodal neuroimaging (MRI), plasma metabolomics, and genomic data from UK Biobank to identify metabolic markers of brain aging and test their causal relevance. They trained and validated machine learning models for brain age prediction using 1079 imaging-derived phenotypes from 4,333 healthy participants, with a LASSO model achieving mean absolute error of 3.26 years and R² of 0.68. This provides metabolite-linked, genetically informed biomarkers of accelerated brain aging that may help stratify neuropsychiatric and neurodegenerative risk.

Li Z, Miao Y, Jin L et al. · Communications biology · (2026) · View on PubMed ↗ · Free PDF ↗

Metabolomic signatures of brain aging: A multimodal and genetic study.

In the prospective multicenter BALTAZAR cohort of individuals diagnosed with mild cognitive impairment (MCI) at baseline and followed for 3 years, the study assessed whether synaptic and neurodegenerative biomarkers improve prediction of progression to dementia beyond amyloid and tau. Paired cerebrospinal fluid (CSF) and plasma samples were analyzed using the NULISA ultrasensitive multiplex platform quantifying >120 CNS biomarkers, and prognostic performance was evaluated using AUC and hazard ratios for individual markers and elastic-net models. This is clinically significant because it targets the unmet need for better, progression-relevant biomarkers in MCI by leveraging broader CNS biomarker panels.

Li Z, Miao Y, Zhang X et al. · Molecular psychiatry · (2026) · View on PubMed ↗

Use of Sedative-Hypnotic Drugs and the Risk of Developing Alzheimer’s Disease: A Systematic Review, Meta-Analysis and Meta-Regression.

This systematic review, meta-analysis, and meta-regression examined whether sedative-hypnotic use—specifically benzodiazepines (BZDs) and non-benzodiazepine hypnotics (Z-drugs)—is associated with incident Alzheimer’s disease (AD), using observational evidence. The key finding was an overall assessment of the relationship between BZD/Z-drug exposure and future AD risk, including differences by drug class and methodological factors. Scientifically, it clarifies long-term cognitive safety signals for commonly prescribed sleep/anxiety medications and informs risk-benefit decisions in older adults.

da Silva AMP, Tudella GCN, Gonçalves OR et al. · Drugs · (2026) · View on PubMed ↗

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Neuroimaging, Brain-on-a-Chip & Translational Modeling

Brain-on-a-Chip and Blood-Brain Barrier-on-a-Chip Modeling for Neurodegenerative Disorders: Recent Progress.

This 2026 review summarized advances in brain-on-a-chip and blood-brain barrier-on-a-chip microphysiologic modeling platforms for neurodegenerative disorders. The key finding was that microfluidic BBB-on-a-chip systems are increasingly enabling mechanistic study of BBB dysfunction and improving evaluation of neurotherapeutics intended to cross the BBB. Scientifically, it highlights how these engineered models can accelerate discovery and testing of treatments for neurodegenerative diseases by addressing a major translational barrier.

Kempuraj D, Shi H, Truong TD et al. · The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · (2026) · View on PubMed ↗

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Hematologic Malignancies & Blood Disorders (MDS, Lymphoma, Leukemia)

Spatial and multi-omic profiling reveals pericyte-derived CCL19 as a key prognostic factor in CNS lymphoma.

This study performed genetic and transcriptomic profiling of 82 central nervous system lymphoma (CNSL) specimens and used spatial/multi-omic approaches to determine the role of pericyte-derived CCL19 in human disease. It found that CCL19 expression varied widely across patients and that high CCL19 expression was associated with immunosuppressive and anti-apoptotic tumor signatures and was independently linked to worse progression outcomes. These findings position pericyte-derived CCL19 as a prognostic factor and potential therapeutic axis in CNS lymphoma.

Kuehn JC, Miarka L, Sankowski R et al. · HemaSphere · (2026) · View on PubMed ↗ · Free PDF ↗

Real-world, multi-omics validation of the clinical relevance of molecular taxonomy for myelodysplastic syndromes (MDS).

This study validated the International Working Group for Prognostication of MDS (IWG_PM) molecular taxonomy in myelodysplastic syndromes (MDS) using a large retrospective cohort (n=5136) and transcriptomic data from a prospective cohort (n=477). The key finding was that the 16 taxonomy subgroups—defined by 21 gene mutations, 6 cytogenetic abnormalities, and LOH at TP53 and TET2—successfully stratified patients into clinically meaningful risk groups in real-world datasets. Scientifically, it supports the clinical utility of the MDS taxonomy for more precise prognostication and potentially more personalized treatment selection.

Maggioni G, Todisco G, Sauta E et al. · HemaSphere · (2026) · View on PubMed ↗ · Free PDF ↗

Disorders of Telomere Length.

This NEJM Evidence review summarizes how telomere length extremes contribute to inherited disease risk, focusing on short telomere length (degenerative phenotypes such as immunodeficiency, bone marrow failure, and pulmonary disease) and ultra-long telomere length (predisposition to neoplasia including lympho- and myeloproliferative disease). It emphasizes that genetics affecting telomere length have clarified natural history and treatment approaches for conditions such as idiopathic pulmonary fibrosis and inform clinical decision-making. The clinical significance is that it frames telomere biology as actionable for diagnosis, prognosis, and management across multiple inherited and acquired disease contexts.

Schratz KE, Armanios M · NEJM evidence · (2026) · View on PubMed ↗

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Infectious Disease (TB, HIV, Bacterial/Fungal/Host-Pathogen)

Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.

After aerosol infection with Mycobacterium tuberculosis (Mtb), the study analyzed myeloid and CD4+ T cell dynamics in lung-draining mediastinal lymph nodes (medLNs) to determine how immune niches enable persistence. It found that early dissemination involved monocytes and IL-12-producing conventional dendritic cells that prime Th1 responses, but later the medLNs became dominated by heavily infected monocyte-derived aggregates as cDC migration and T cell activation declined, allowing persistence. These results identify monocyte-dominated niches as a mechanism of immune escape in lymph nodes, informing strategies to prevent long-term Mtb persistence.

Shamskhou EA, Duffy FJ, Cross LM et al. · Immunity · (2026) · View on PubMed ↗ · Free PDF ↗

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Organ Injury, Repair & Tissue Homeostasis (Liver, Intestine, Radiation)

FUBL-3/FUBP1 mediates mitochondrial stress-induced chromatin remodeling and longevity.

This study investigated how mitochondrial stress regulates nuclear chromatin remodeling and longevity in Caenorhabditis elegans, focusing on the FUBL-3 homolog of human FUBP1. FUBL-3 translocated to intestinal nuclei during stress and drove nucleosome remodeling and deacetylase-dependent chromatin condensation, activating the mitochondrial unfolded protein response (UPRmt), while loss of fubl-3 disrupted chromatin compaction and abolished stress-linked longevity effects. These findings identify FUBL-3/FUBP1 as a conserved mitochondrial-stress-to-chromatin effector that links epigenetic remodeling to organismal lifespan and stress adaptation.

Zhang Q, Dong H, Jiang Y et al. · Science advances · (2026) · View on PubMed ↗

Pediatric Penetrating Foot Injury Complicated by Soft-Tissue Infection.

This case report described a 4-year-old child with a pediatric penetrating foot injury complicated by deep soft-tissue infection after a puncture wound. The key clinical finding was that delayed presentation led to purulent infection requiring aggressive debridement, removal of retained foreign material, irrigation, and negative pressure wound therapy (NPWT/VAC). The report highlights the need for prompt recognition and surgical management of puncture wounds in children to prevent complications such as abscess, septic arthritis, and osteomyelitis.

Marku V, Andrikopoulou C, Fragkakis I et al. · Chirurgia (Bucharest, Romania : 1990) · (2026) · View on PubMed ↗ · Free PDF ↗

Macrophage-enriched GPR91 aggravates acute liver injury by inhibiting efferocytosis via the AC/cAMP/PPARγ pathway.

This study investigated the role of the macrophage-enriched GPCR GPR91 (encoded by Sucnr1) in acute liver injury using Sucnr1-knockout mice and carbon tetrachloride (CCl4)–based injury models. It found that loss of Sucnr1/GPR91 aggravation is mediated by inhibition of efferocytosis through the AC/cAMP/PPARγ pathway. Scientifically and clinically, it identifies the Sucnr1–GPR91 axis and the AC/cAMP/PPARγ signaling cascade as potential therapeutic targets to improve resolution of acute liver injury.

Qiu S, Hu J, Guo K et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

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Developmental Biology & Regenerative Engineering (Embryogenesis, Devices)

Epiblast diversification and blood formation in a human pregastrula.

The study profiled early human gastrulation by generating high-resolution spatial transcriptomic maps of a Carnegie stage 6 embryo (~13–14 days post-conception) during epiblast diversification and the onset of blood formation. It identified an anterior visceral endoderm-like hypoblast population and a trifurcated epiblast trajectory toward amnion, primitive streak, and node/prechordal plate/notochord (axial mesoderm), while noting that gastrulation-derived mesoderm/endoderm progenitors were not yet transcriptomically detected at this stage. This provides a spatially resolved reference for when and how human embryonic lineages begin to diversify before primitive streak visibility.

Xiao Z, Gong Y, Yang X et al. · Nature · (2026) · View on PubMed ↗

Reconstituting human primitive streak formation through extra-embryonic cell coordination.

The study aimed to recreate human primitive streak formation by coordinating embryonic stem cells (ESCs) with defined extra-embryonic cell types in a co-culture system. It showed that different extra-embryonic lineages (mimicking amniotic ectoderm, trophoblast, and extra-embryonic mesoderm) differentially regulate embryonic organization and primitive streak-like development, using microengineering to spatially and molecularly control the system. This provides an experimental platform to dissect how extra-embryonic tissues instruct early human body-axis patterning.

Shen Q, Zhang X, Chen N et al. · Cell · (2026) · View on PubMed ↗

EasyGrid: a versatile platform for automated cryo-EM sample preparation and quality control.

The paper describes EasyGrid, an automated cryo-EM/cryo-ET sample preparation and quality-control platform integrating in-line plasma treatment, microfluidic dispensing, blot-less spreading, jet-based vitrification, and light-interferometry grid QC. The authors demonstrate that EasyGrid can reproducibly prepare grids for multiple purified macromolecular complexes and enable cryo-EM structure determination. This is significant for scaling high-throughput, standardized cryo-EM workflows and improving consistency of sample quality across experiments.

Gemin O, Armijo V, Lecomte L et al. · Nature methods · (2026) · 13 citations · View on PubMed ↗ · Free PDF ↗

Non-invasive removal of the Smart tracheal occlusion device for fetal congenital diaphragmatic hernia: a single-arm, open-label, phase 1 study.

This first-in-human, single-arm phase 1 study evaluated the Smart tracheal occlusion device (Smart-TO) for fetoscopic endoluminal tracheal occlusion (FETO) in adults with singleton pregnancies complicated by left-sided congenital diaphragmatic hernia (CDH) with moderate-to-severe pulmonary hypoplasia. The key finding was that the Smart-TO device could be non-invasively removed because it spontaneously deflates when near a strong magnetic field, addressing the need for a second intervention to restore airway patency. If confirmed in larger trials, this device could simplify FETO workflows and reduce procedural burden and risk in severe CDH.

Russo FM, Sananès N, Letourneau A et al. · Lancet (London, England) · (2026) · View on PubMed ↗

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Generated automatically on June 25, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.