PubMed Trending Research Digest — August 10, 2026

Automated digest · 95 articles · 15 research areas · August 10, 2026

Overview

This week’s digest is dominated by two cross-cutting trends: (1) using large-scale data and mechanistic biomarkers to refine risk and treatment decisions, and (2) translating targeted biology into more precise therapies across oncology, cardiometabolic disease, and inflammatory disorders. Multiple studies focus on prognostic stratification—ranging from ATTR cardiomyopathy staging in the treatment era, to PSA nadir in metastatic hormone-sensitive prostate cancer, to ctDNA and pathology-based recurrence models in GI and renal cancers. In parallel, several cardiometabolic papers emphasize practical risk markers (e.g., TyG-VLR trajectories, post-STEMI vascular ultrasound changes, and proteomic signatures for PAD) and highlight how modern therapies (incretin-based drugs, SGLT2 inhibitors) are increasingly evaluated for benefits beyond their original indications.

On the mechanistic/therapeutic front, immunology and targeted delivery appear repeatedly. In oncology, the pipeline spans next-generation KRAS pathway inhibition, ADC targeting (e.g., NPTXR), and fusion-peptide vaccination, alongside mechanistic work on ferroptosis control and dendritic-cell states that govern T-cell priming. In inflammatory disease, airway epithelial–immune circuits (alarmins), IBD biology and dysplasia “field cancerization,” and perioperative management of biologics in chronic rhinosinusitis with nasal polyps all underscore a move toward pathway-guided interventions. Across neurology and aging, studies connect cell-state remodeling (blood-brain barrier endothelial subtypes, astrocyte APOE isoforms) and metabolic/inflammatory licensing mechanisms to disease progression, while stroke-related work explores exosome-based microglial reprogramming for post-stroke depression.

Finally, several papers reinforce the importance of context in real-world evidence and safety: registry comparisons in heart failure management, pharmacovigilance for combination urothelial regimens, and observational vaccine effectiveness analyses that explicitly address bias (healthy vaccinee effect). Together, the set suggests a field increasingly integrating rigorous risk modeling, mechanistic biology, and real-world implementation considerations to improve both outcomes and clinical decision-making.

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Cardiovascular risk, biomarkers, and imaging

Empagliflozin’s Effects on Carotid Ultrasound Parameters in Type 2 Diabetes Patients Post-ST-Elevation Myocardial Infarction: A Randomized Controlled Trial.

This randomized controlled trial studied the 3-month effects of the SGLT2 inhibitor empagliflozin on carotid ultrasound measures—carotid intima-media thickness (CIMT) and Doppler hemodynamic indices (resistive index [RI], pulsatility index [PI])—in 80 patients with type 2 diabetes (T2D) after ST-elevation myocardial infarction (STEMI). It reports changes in these carotid ultrasound parameters following empagliflozin treatment compared with control (as assessed over the trial period). The significance is that empagliflozin may provide measurable vascular benefits in post-STEMI T2D patients, supporting its cardioprotective role beyond glycemic control.

Sabat Sani H, Aghaei S, Kalantari S et al. · Iranian journal of medical sciences · (2026) · View on PubMed ↗

Antihypertensive Efficacy and Safety of Angiotensin Receptor Blockers (ARBs) with and without Inverse Agonism: A Systematic Review and Network Meta-analysis.

This systematic review and network meta-analysis compared antihypertensive efficacy and safety of angiotensin receptor blockers (ARBs) with inverse agonism versus ARBs without inverse agonism in randomized clinical trials of first-line monotherapy for mild-to-moderate hypertension. It found differential blood pressure–lowering potential depending on whether the ARB exhibits inverse agonism, while also synthesizing comparative safety across included agents. The results are clinically significant because they may inform ARB selection for hypertension based on pharmacologic mechanism (inverse agonism) rather than drug class alone.

Liu J, Geng J, Liu J et al. · American journal of cardiovascular drugs : drugs, devices, and other interventions · (2026) · View on PubMed ↗

The Renaissance of Bronchiectasis.

This narrative review summarized the evolving research landscape of bronchiectasis, focusing on major shifts in domains of study and highlighting gaps in prevention, equity, and translation to care. It found that bronchiectasis research growth has accelerated rapidly (faster than asthma and COPD) and identified priority areas where evidence and access remain limited, including medication and RCT participation for underserved populations. The review is clinically significant because it frames future research directions aimed at improving outcomes for both children and adults with bronchiectasis.

Martinez-Garcia MA, Chang AB, Chotirmall SH et al. · American journal of respiratory and critical care medicine · (2026) · View on PubMed ↗ · Free PDF ↗

Keratin 17 Methyltransferasean14 Methylation Axis: A Novel Mechanism in Pulmonary Vascular Remodeling.

This study investigated the Keratin 17 methyltransferase–associated methylation axis in pulmonary vascular remodeling using transcriptome sequencing of lung artery tissues from control and Sugen5416 plus hypoxia-induced rat models, followed by in vitro and in vivo functional assays. The authors identified a mechanistic link between K17 methylation regulation and pathological remodeling driven by aberrant proliferation of pulmonary arterial smooth muscle cells (PASMCs). Defining this methylation axis may reveal new molecular targets to prevent or treat pulmonary hypertension.

Liu Y, Kong M, Xia Y et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

The impact of an intensive care telemedicine program on weaning from invasive ventilation: a secondary analysis of the ERIC trial.

This secondary analysis of the stepped-wedge cluster-randomized ERIC trial studied whether a complex ICU telemedicine program (daily telemedicine rounding by an intensivist and ICU nurse) improves weaning from invasive mechanical ventilation in ICU patients across 10 ICU clusters in metropolitan Berlin, Germany. The intervention was assessed for effects on guideline adherence for weaning and related clinical outcomes compared with usual care. If effective, this telemedicine strategy could improve ventilator liberation processes and patient outcomes at the system level.

Adam MF, Grunow JJ, Edel A et al. · Critical care (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

Utility of Prognostic Staging Systems in Transthyretin Amyloidosis Cardiomyopathy in the Era of Available Disease-Modifying Treatment.

This study evaluated how contemporary prognostic staging systems (National Amyloidosis Centre [NAC] and modified Mayo staging using high-sensitivity troponin T [hsTnT] cutoff >65) stratify risk in patients with newly diagnosed transthyretin (ATTR) amyloid cardiomyopathy at Mayo Clinic, Rochester, Minnesota, using baseline biomarker data from 2019–2023. Across staging approaches, risk stratification and predicted outcomes were assessed with Kaplan–Meier analyses to determine whether older staging frameworks remain useful in the era of available disease-modifying therapy for ATTR cardiomyopathy. The findings support clinicians in selecting and interpreting ATTR cardiomyopathy prognostic stages for modern treatment decision-making and trial/registry risk adjustment.

Skov JK, Clemmensen TS, Scott CG et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

Endometriosis and long-term risk of venous thromboembolism: a Danish nationwide study.

This Danish nationwide registry cohort study examined whether endometriosis is associated with long-term venous thromboembolism (VTE) risk in women diagnosed with endometriosis from 1977–2024, matched 1:4 to women without endometriosis by birth and index year. The key finding was the magnitude and direction of the association between endometriosis and incident VTE (deep venous thrombosis and pulmonary embolism composite) over long-term follow-up. Clinically, the results help quantify whether endometriosis confers increased thrombotic risk and can inform VTE risk assessment and prevention strategies in affected women.

Ryde HV, Reinert MS, Hartwell D et al. · European heart journal · (2026) · View on PubMed ↗

Temporal comparison of clinical practice and outcomes in heart failure: the JROADHF and JROADHF-NEXT studies.

The JROADHF (2013) and JROADHF-NEXT (2019–2021) Japanese heart failure registries were compared to assess temporal changes in real-world HF management and how these changes affected outcomes, using propensity score matching (1:1). After matching, the study identified whether guideline-recommended therapies and care processes improved over time and which factors were associated with improved patient outcomes. Scientifically and clinically, this provides evidence on how evolving HF treatment patterns translate into survival and morbidity benefits in routine practice.

Tohyama T, Ikeda M, Watanabe T et al. · European heart journal · (2026) · View on PubMed ↗

Bruton’s tyrosine kinase inhibitors and cardiovascular risk: a meta-analysis.

This systematic review and meta-analysis of Phase 3 randomized controlled trials assessed cardiovascular safety of Bruton’s tyrosine kinase inhibitors (ibrutinib, acalabrutinib, zanubrutinib) by estimating risk of incident non-fatal ischaemic major adverse cardiovascular events (MACE) in trial populations. The key finding was the pooled effect of BTK inhibitor exposure on non-fatal ischaemic MACE risk across eligible RCTs up to 19 December 2024. This informs clinicians and guideline developers about the magnitude of ischaemic cardiovascular risk when selecting BTK inhibitors for patients requiring these therapies.

Alexandre J, Font J, Haddad S et al. · European heart journal · (2026) · View on PubMed ↗

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Diabetes, metabolic syndrome, and cardiovascular complications

Baseline, repeated-measure burden, and two-time-point patterns of the triglyceride-glucose index-visceral lipid ratio (TyG-VLR) and incident cardiovascular disease in cardiovascular-kidney-metabolic (CKM) syndrome stages 0-3: a longitudinal China Health and Retirement Longitudinal Study (CHARLS) analysis.

This longitudinal CHARLS analysis studied whether baseline, repeated-measure burden, and two-time-point patterns of the triglyceride-glucose index–visceral lipid ratio (TyG-VLR) predict incident cardiovascular disease (CVD) across cardiovascular-kidney-metabolic (CKM) syndrome stages 0–3. It reports associations between TyG-VLR metrics (including burden and pattern-based trajectories) and future CVD outcomes and subtypes during follow-up through 2020. The significance is that TyG-VLR can serve as a practical risk marker for early CVD prediction in CKM populations before overt cardiovascular disease.

Lu AM, Han HJ, Xu Q et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

An epigenetic switch in β-cells links mitochondrial stress to inflammatory fate via HMGB1 acetylation.

This mechanistic study investigated how sublethal oxidative stress in pancreatic β-cells triggers an epigenetic switch that links mitochondrial metabolic stress to inflammatory fate, focusing on NAD+/acetyl-CoA flux and the SIRT1–p300/CBP balance. Oxidative stress disrupted mitochondrial NAD+/acetyl-CoA flux, shifted nuclear acetylation control toward p300/CBP, and drove site-specific hyperacetylation of the alarmin HMGB1 at K96/K128 in β-cells. These findings identify HMGB1 acetylation as a β-cell–specific inflammatory licensing mechanism, suggesting potential targets to prevent β-cell failure in diabetes driven by chronic inflammation.

Cheng Y, Wang L, Bai X et al. · Cell death and differentiation · (2026) · View on PubMed ↗

Association Between Dietary Magnesium Intake and All-Cause Mortality in Patients with Chronic Kidney Disease: Insights from NHANES 1999-2018.

This NHANES 1999–2018 analysis studied whether food-derived dietary magnesium intake is associated with all-cause mortality in adults with chronic kidney disease (CKD) aged ≥20 years. Using multivariable Cox proportional hazards models with restricted cubic splines, Kaplan–Meier analyses, and sensitivity/subgroup testing, the study estimated the mortality risk across magnesium intake levels. The results are important for CKD dietary guidance because they link a modifiable nutrient exposure to long-term survival risk.

Xu ZY, Zou J, Xie LJ et al. · Clinical medicine (London, England) · (2026) · View on PubMed ↗ · Free PDF ↗

GLP-1 Receptor Agonist Therapy for Obesity Under Japan’s Optimal Use Guideline: A Prospective Real-World Study of Lifestyle Pre-Treatment, Time-Limited Treatment Cap, and Post-Cessation Regain.

This prospective real-world study evaluated Japan’s optimal use guideline for GLP-1 receptor agonists in 104 patients with obesity without type 2 diabetes, comparing semaglutide and tirzepatide under a mandated 6-month lifestyle phase, time-limited treatment cap (68 or 72 weeks), and post-cessation washout. It assessed how pre-treatment weight change during lifestyle intervention influenced on-treatment response and post-cessation weight regain. The study is significant for clinical implementation because it quantifies the real-world effectiveness and rebound risk under guideline-constrained GLP-1 RA regimens.

Inamine S, Uesato Y · Diabetes, obesity & metabolism · (2026) · View on PubMed ↗

Proteomic insights of peripheral artery disease across the glycemic spectrum: a prospective cohort study.

This prospective cohort study used 43,875 UK Biobank participants stratified by glycemic status (normoglycemia, prediabetes, and type 2 diabetes) to identify plasma protein signatures associated with incident peripheral artery disease (PAD). Using Cox regression across 2,920 proteins, followed by pathway enrichment, protein–protein interaction analyses, and LASSO-based protein predictor selection, it characterized glycemia-specific proteomic correlates of PAD risk. The results are important because they suggest candidate protein biomarkers and pathways that may explain why PAD risk differs across glycemic states.

Yu H, Zhang J, Qian F et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

Weight-loss-independent actions of GLP-1 medicines.

This article reviewed evidence that GLP-1 medicines exert clinically relevant effects beyond weight loss, focusing on GLP-1 receptor (GLP-1R)–mediated neural and immune circuit recruitment and inter-organ communication. It concluded that defining dose–response relationships for these weight-loss-independent mechanisms is important for optimizing therapeutic benefit across cardiovascular, renal, hepatic, musculoskeletal, and other health outcomes. The review provides a framework for translating GLP-1R biology into improved, mechanism-based clinical dosing strategies.

Gonzalez-Rellan MJ, Drucker DJ · Cell metabolism · (2026) · View on PubMed ↗

When HbA1c Lies: Recognizing and Managing HbA1c-Glucose Discordance in Clinical Practice.

This clinical review examined why hemoglobin A1c (HbA1c) can be discordant with measured glucose in diabetes care and how to manage HbA1c–glucose discordance. It identified common contributors such as iron deficiency, chronic kidney disease, altered red blood cell turnover, hemoglobin variants, and rapid glycemic change, warning that unrecognized discordance can cause inappropriate treatment escalation and increased hypoglycemia risk. The article’s practical stepwise approach supports safer interpretation of glycemic status and more accurate treatment decisions.

Burroughs B · Southern medical journal · (2026) · View on PubMed ↗

Early-life sugar restriction causally reduces adult cancer incidence and slows biological aging.

The study used a natural experiment from the abrupt end of UK sugar rationing in September 1953 to test whether early-life sugar restriction causally affects adult cancer incidence and biological aging in 64,761 UK Biobank participants born 1951–1956. It found dose-dependent reductions in adult cancer incidence for multiple sites (including liver/intrahepatic bile duct, rectum, lung, prostate, and breast) among those whose first 1,000 days fell under rationing. These findings support a causal role for early-life dietary sugar exposure in long-term cancer risk and aging biology.

Zhu C, Zhang W · Proceedings of the National Academy of Sciences of the United States of America · (2026) · View on PubMed ↗

Incretin analogues as cardiovascular agents: a state-of-the-art review.

This state-of-the-art review synthesized evidence that incretin analogues—GLP-1 receptor agonists and the dual GIP/GLP-1 receptor agonist tirzepatide—have evolved into cardiovascular agents with proven outcome benefits across multiple clinical scenarios. It organized cardiovascular evidence by clinical scenario and discussed proposed mechanisms such as direct vascular endothelium effects, while also addressing deployment challenges in low- and middle-income countries. The review frames how incretin-based therapies may be leveraged for cardiovascular risk reduction and guides future implementation considerations.

Araiza-Garaygordobil D, Rico-Fontalvo J, Hernández-Balbuena B et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

A three-metabolite microbiota-associated signature for early risk stratification of gestational diabetes mellitus.

This multicenter nested case-control and prospective study developed an early gestational diabetes mellitus (GDM) risk stratification model using a three-metabolite microbiota-associated signature in 2,693 pregnant women. By integrating untargeted metabolomics with metagenomics, the authors identified three consistently dysregulated metabolites and associated gut microbial alterations that improved early prediction of GDM compared with relying on later oral glucose tolerance testing. Such a biomarker panel could enable earlier identification and intervention to reduce adverse pregnancy and long-term cardiometabolic outcomes.

Ma S, Zhang C, Yao Y et al. · Cardiovascular diabetology · (2026) · View on PubMed ↗ · Free PDF ↗

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Oncology: targeted therapy and precision medicine

Randomized phase 2 trial of a PARP inhibitor TSL-1502 in germline BRCA-mutated, HER2-negative locally advanced/metastatic breast cancer.

This randomized phase 2 trial studied the PARP inhibitor glucuronide prodrug TSL-1502 in women (18–75 years) with germline BRCA-mutated, HER2-negative locally advanced or metastatic breast cancer. Patients received TSL-1502 (350 mg or 500 mg once daily) versus investigator’s-choice chemotherapy (eribulin, capecitabine, or vinorelbine), and the study evaluated clinical outcomes and safety (details truncated in the abstract). If effective and tolerable, TSL-1502’s glucuronide prodrug strategy could improve PARP targeting and reduce toxicity for BRCA-mutated breast cancer patients.

Lan B, Xu F, Sun T et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

The KRAS targeting revolution in metastatic pancreatic cancer: insights from the landmark RASolute-302 trial and emerging allele-specific strategies at ASCO 2026.

This correspondence reviewed the KRAS targeting shift in metastatic pancreatic ductal adenocarcinoma (mPDAC), focusing on the phase III RASolute-302 trial and emerging allele-specific strategies discussed around ASCO 2026. It reports that the pan-RAS (ON) inhibitor daraxonrasib (RMC-6236) nearly doubled median overall survival (13.2 vs 6.6 months) and improved progression-free survival versus chemotherapy in second-line mPDAC. The significance is that targeted KRAS pathway inhibition is establishing a new standard of care and motivating next-generation allele-specific approaches.

Pillozzi S, Giommoni E, Petroni G et al. · Journal of hematology & oncology · (2026) · View on PubMed ↗ · Free PDF ↗

Exploring PDLIM2 as a prognostic biomarker and therapeutic target in lung adenocarcinoma.

This study analyzed lung adenocarcinoma (LUAD) tissues from 15,765 patients using next-generation sequencing and immunohistochemistry for PDLIM2 and PD-L1, and tested PDLIM2 gene therapy in syngeneic LUAD mouse models delivered as intravenous nano-complexed plasmid DNA alone or with chemoimmunotherapy. PDLIM2-high tumors were more frequent in primary/local biopsies than metastatic samples, and high PDLIM2 expression was associated with lower mutation rates in several cancer genes (including RB1, TP53, SMARCA4, STK11, and others). These results position PDLIM2 as a prognostic biomarker and potential therapeutic target, with preclinical support for plasmid-based PDLIM2 delivery combined with chemoimmunotherapy.

Ashouri K, Sun F, Krause H et al. · British journal of cancer · (2026) · View on PubMed ↗ · Free PDF ↗

Comparative Treatment Outcomes Across Actionable Genomic Alterations in NSCLC: A Large Multicenter Real-World Study.

This retrospective multicenter real-world study evaluated treatment outcomes and safety in 810 Japanese patients with advanced or recurrent NSCLC receiving molecular targeted therapy, stratified by actionable genomic alterations: EGFR mutations, ALK/ROS1/RET fusions, and other alterations (including MET exon 14 skipping, BRAF V600E, and KRAS G12C). Across these genomic groups, efficacy and adverse-event profiles differed, demonstrating that outcomes are not interchangeable even within “actionable” categories. The findings support more granular, alteration-specific expectations for targeted therapy selection and toxicity management in routine clinical practice.

Kato Y, Nishijima N, Takahashi S et al. · JTO clinical and research reports · (2026) · View on PubMed ↗ · Free PDF ↗

NPTXR as a novel therapeutic target: efficacy of antibody-drug conjugates in preclinical tumor models.

This preclinical study evaluated NPTXR as a therapeutic target by testing antibody-drug conjugates (ADCs) based on the fully humanized monoclonal antibody YB-800 (YB-800ADCs) in tumor models. The authors assessed NPTXR expression in human cancer and healthy tissues and then measured ADC efficacy across preclinical settings to determine whether NPTXR targeting improves anti-tumor activity. If translatable, NPTXR-directed ADCs could provide a new targeted therapy approach for cancers with elevated NPTXR expression.

Lyndin M, Janicot M, Müller J et al. · Cancer cell international · (2026) · View on PubMed ↗ · Free PDF ↗

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Oncology: immunotherapy, vaccines, and cancer immunobiology

Lysosome-Targeted Self-Adjuvanting Ammonia Nanogenerator Potentiates Hepatocellular Carcinoma Immunotherapy via Ammonia Death.

This preclinical study developed a lysosome-targeted ammonia nanogenerator (AlN@HA) to induce ammonia death in hepatocellular carcinoma (HCC) cells and enhance HCC immunotherapy. After CD44 receptor-mediated endocytosis, AlN@HA accumulated in lysosomes and released excessive ammonia plus nanoscopic aluminum hydroxide (Al(OH)3), promoting ammonia-death–linked immunogenic effects (mechanistic and efficacy details truncated). The approach suggests a targeted nanomedicine strategy to overcome limitations of ammonia death therapy by coupling tumor targeting with immunostimulatory cell death.

Zhao H, Qian J, Wang Y et al. · Advanced materials (Deerfield Beach, Fla.) · (2026) · View on PubMed ↗

Durable clinical and immunologic response to an off-the-shelf EWSR1-FLI1 peptide vaccine in metastatic Ewing sarcoma.

The study evaluated an off-the-shelf multi-peptide vaccine targeting the type 1 EWSR1-FLI1 fusion breakpoint in a patient with high-burden metastatic Ewing sarcoma after multimodal therapy, with GM-CSF and topical imiquimod as adjuvants. Longitudinal immune monitoring using in vitro peptide stimulation and intracellular cytokine staining showed durable de novo polyfunctional CD4+ T-cell responses against all tested EWSR1-FLI1 peptides. This provides clinical proof-of-concept that an EWSR1-FLI1 breakpoint–directed peptide vaccine can generate sustained, multi-functional T-cell immunity in metastatic Ewing sarcoma, supporting fusion-peptide immunotherapy strategies.

Calukovic B, Benzler K, Zelba H et al. · NPJ precision oncology · (2026) · View on PubMed ↗ · Free PDF ↗

CCR7+ activated dendritic cells are essential for spontaneous and immunotherapy-driven anti-tumor immunity.

This mouse study investigated how CCR7+ activated dendritic cells (actDCs) contribute to spontaneous and immunotherapy-driven anti-tumor immunity. Using CCR7-based conditional labeling/ablation models and single-cell transcriptomic-defined actDC states, it showed that tumor-specific cytotoxic T lymphocyte (CTL) priming depended on the actDC state, with cDC1-derived actDCs supporting cross-presentation and cDC2-derived actDCs supporting cross-dressing. The findings are clinically relevant because they identify CCR7+ actDCs as essential functional intermediates that could be leveraged to improve dendritic-cell–targeted or immunotherapy responses.

Koufaki MA, Richardson E, Bonavita E et al. · Immunity · (2026) · View on PubMed ↗

Targeting peripheral 5-HT2AR enhances antitumor immunity in colorectal cancer.

The study tested whether targeting the peripheral serotonin receptor 5-HT2AR with lysergic acid diethylamide (LSD) and a non-brain-penetrant 5-HT2AR agonist (IHCH-8110) could enhance antitumor immunity in colorectal cancer (CRC). It found that 5-HT2AR activation increased CD8+ T cell-mediated antitumor immunity and suppressed CRC growth, with IHCH-8110 acting on enteric glial cells to induce CXCL10. This supports a druggable peripheral immune-activation pathway for CRC that aims to avoid psychedelic CNS effects.

Wen Y, Tang L, Duan W et al. · Cell · (2026) · View on PubMed ↗

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Oncology: prognostic models, staging, and treatment response

Circulating tumor DNA in gastrointestinal cancers: promise, pitfalls, and the path forward.

This narrative review evaluated the clinical utility of circulating tumor DNA (ctDNA) in gastrointestinal cancers, emphasizing evidence from colorectal cancer and discussing how ctDNA can guide prognosis and potentially treatment selection. It summarizes that postoperative ctDNA positivity predicts recurrence risk and that serial clearance patterns refine risk, while randomized evidence such as DYNAMIC and DYNAMIC-III suggests limited or context-dependent benefit for chemotherapy de-escalation/escalation based on ctDNA status (details truncated). The review frames ctDNA as promising but highlights pitfalls that must be addressed before ctDNA can reliably determine therapy choices across GI cancer types.

Mukherjee S, Sarfraz A, Aung KL et al. · EClinicalMedicine · (2026) · View on PubMed ↗ · Free PDF ↗

A Pathology-Based Model for Postoperative Recurrence or Metastasis Prediction and Adjuvant Immunotherapy Implications of Clear-Cell Renal Cell Carcinoma: A Multicenter, Retrospective Study.

This multicenter retrospective study investigated a pathology-based model to predict postoperative recurrence or metastasis in 2154 patients with clear-cell renal cell carcinoma (ccRCC) who did not receive postoperative adjuvant therapy. It found that a multivariable model stratified patients by risk of disease-free survival (DFS) and was intended to inform which patients might benefit from adjuvant immune checkpoint inhibitors (ICIs). The clinical significance is improved postoperative risk stratification to guide adjuvant immunotherapy decisions in nonmetastatic ccRCC.

Zhu Y, Ge L, Liu Z et al. · Annals of surgical oncology · (2026) · View on PubMed ↗

Molecular evaluation of residual disease following neoadjuvant chemotherapy in triple negative breast cancer CALGB40603 (Alliance).

The study performed comprehensive transcriptomic profiling of 340 pre-treatment and 70 matched residual disease (RD) samples from stage II/III triple-negative breast cancer (TNBC) patients in the CALGB 40603 (Alliance) neoadjuvant chemotherapy trial. It aimed to identify survival-associated molecular features of RD and tested RD-mimicking strategies using antibody-drug conjugate (ADC) treatments in patient-derived xenograft (PDX) mouse models. This work seeks to improve prognostication and guide targeted therapy for patients with residual disease after neoadjuvant treatment.

Rädler PD, Felsheim BM, Fernandez-Martinez A et al. · The Journal of clinical investigation · (2026) · View on PubMed ↗

Sentinel node biopsy and survival in cutaneous melanoma: a nationwide population-based cohort study.

This nationwide retrospective cohort study evaluated whether sentinel node biopsy (SNB) is associated with survival and recurrence outcomes in Danish patients with cutaneous melanoma diagnosed between 2010 and 2017 who met contemporary SNB eligibility criteria. Using augmented inverse probability of treatment weighting (AIPTW) to estimate standardized 5-year overall survival, melanoma-specific mortality, other-cause mortality, and recurrence under hypothetical SNB vs no-SNB scenarios, the study found an association between SNB and survival/recurrence outcomes (direction and magnitude reported in the full text). These findings help clarify the real-world clinical value of SNB for melanoma staging and prognosis in a population-based setting, informing guideline and decision-making about SNB use.

Weitemeyer MB, Helvind NM, Gjorup CA et al. · European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology · (2026) · View on PubMed ↗ · Free PDF ↗

A Chemotherapy Progression Decision Score for Treatment Selection After Initial Assessment in Pancreatic Ductal Adenocarcinoma.

This multicenter retrospective study developed and externally validated a chemotherapy Progression Decision (cPD) score to guide treatment selection after the first RECIST assessment in 616 patients with pancreatic ductal adenocarcinoma (PDAC). The cPD score incorporated biological markers and imaging metrics to better predict progression risk than RECIST alone, addressing RECIST limitations from stromal fibrosis–related radiographic pseudoprogression. Clinically, the model aims to reduce inappropriate early treatment changes and improve decision-making in PDAC patients after initial imaging response assessment.

Zhang Y, Sun Z, Ding H et al. · MedComm · (2026) · View on PubMed ↗ · Free PDF ↗

JAVEMACS: a real-world study of avelumab maintenance therapy for advanced urothelial carcinoma in Japan.

This real-world chart review study (JAVEMACS) evaluated outcomes of avelumab maintenance therapy in Japan for 350 patients with unresectable locally advanced or metastatic urothelial carcinoma who had not progressed after first-line platinum-based chemotherapy. The analysis characterized patient demographics and treatment context in routine practice, providing the primary real-world effectiveness/safety dataset for Japanese patients receiving avelumab maintenance after 1L PBC. The study supports evidence for how approved maintenance therapy performs outside clinical trials and informs expectations for clinicians managing la/mUC in Japan.

Kitamura H, Kobayashi T, Endo Y et al. · ESMO real world data and digital oncology · (2025) · 1 citations · View on PubMed ↗ · Free PDF ↗

The real-world safety profile of enfortumab vedotin with or without pembrolizumab: insights from a comparative analysis of FAERS.

This pharmacovigilance study used FAERS data (2020 Q4–2025 Q3) to compare the real-world adverse event (AE) profiles of enfortumab vedotin plus pembrolizumab (EV+P) versus enfortumab vedotin monotherapy (EV) in advanced urothelial carcinoma. Disproportionality analyses across System Organ Class, HLGT, and Preferred Term levels, along with time-to-onset (Kaplan–Meier) and narrative validation, identified differences in AE landscapes between combination and monotherapy, including signals consistent with pneumonitis. The results help clinicians anticipate and monitor toxicity patterns when choosing EV+P versus EV in real-world care.

Chen H, Huang J, He G · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of PSA Nadir on Outcomes in Metastatic Hormone-Sensitive Prostate Cancer: A Systematic Review and Reconstructed Individual Patient Data Meta-analysis.

This systematic review and reconstructed individual patient data meta-analysis evaluated whether prostate-specific antigen (PSA) nadir during treatment predicts outcomes in metastatic hormone-sensitive prostate cancer (mHSPC) treated with androgen deprivation therapy intensification strategies, including docetaxel and androgen receptor pathway inhibitors (abiraterone, enzalutamide, apalutamide, darolutamide). The key finding was the prognostic value of PSA nadir as an early surrogate for subsequent outcomes such as progression and survival endpoints across included trials. Clinically, PSA nadir could be used to risk-stratify mHSPC patients earlier and potentially guide treatment escalation or closer monitoring.

Di Civita MA, Pappalardo L, De Angelis D et al. · Targeted oncology · (2026) · View on PubMed ↗ · Free PDF ↗

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Oncology: radiotherapy/chemotherapy/combination regimens

LZTFL1 rewires NADPH-glutathione metabolism to amplify ferroptosis.

This mechanistic cancer biology study identified leucine zipper transcription factor-like 1 (LZTFL1) as a regulator that amplifies ferroptosis by rewiring NADPH–glutathione metabolism. LZTFL1 promoted oxidation of glucose-6-phosphate dehydrogenase (G6PD) to limit NADPH production and impair GSH regeneration, and GSH depletion enhanced LZTFL1 translation via an AKT–mTOR–eIF4E feedforward loop. The work is significant because it reveals a targetable metabolic control point that could be exploited to trigger ferroptosis in apoptosis-resistant tumors.

Xue X, Zhang X, Zhou Q et al. · Molecular cell · (2026) · View on PubMed ↗

Boosting anti-leukemia cytotoxicity of CD4 and CD8 T cells through combined inhibition of MEK and HDAC.

The study evaluated whether combined MEK and HDAC inhibition—trametinib plus quisinostat (TQ)—could boost cytotoxicity of CD4 and CD8 T cells and improve outcomes in acute myeloid leukemia (AML), including NRAS;ASXL1- and MLLr/NPM1-mutant models. It found that TQ potently inhibited growth of multiple AML genotypes in vitro and drastically slowed AML progression in NA-AML mice, prolonging survival. This provides a rationale for combination epigenetic–signaling therapy to overcome AML’s poor responsiveness to T-cell–based immunotherapies.

Gayatri MB, Jia B, Veltri AJ et al. · Blood · (2026) · View on PubMed ↗

DRP1-mediated mitochondrial fragmentation is a druggable vulnerability in multiple myeloma.

The study investigated mitochondrial dynamics in multiple myeloma (MM) using ultrastructural analyses, transcriptomic profiling across patient-derived datasets, and functional testing in drug-resistant MM models. It found that MM cells exhibit a highly fragmented mitochondrial network that worsens with proteasome inhibitor resistance, alongside upregulation of the mitochondrial fission gene DNM1L (encoding DRP1) in relapsed/refractory disease. This identifies DRP1-mediated mitochondrial fragmentation as a druggable vulnerability that may be exploitable to counter treatment resistance.

Gallo Cantafio ME, Puccio N, Torcasio R et al. · Blood · (2026) · View on PubMed ↗

Depletion of CARM1 slows in vivo tumorigenicity and rewires developmental programming in glioma stem-like cells.

This mechanistic study investigated how depletion of the arginine methyltransferase CARM1 affects glioma stem-like cells (GSCs) in vivo and in vitro. CARM1 depletion slowed in vivo tumorigenicity, increased apoptosis, rewired histone post-translational modifications and global transcriptomic/proteomic programs toward a radial glial-like state, and increased NGFR/NTRK signaling, thereby sensitizing GSCs to NTRK and AKT inhibition. The work is clinically relevant because it identifies CARM1 as a potential therapeutic target and suggests combination strategies using NTRK/AKT pathway inhibition for CARM1-low or CARM1-targeted GSC states.

Young DL, Stransky S, Molero MG et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurology: neurodegeneration, brain aging, and neuroinflammation

Single-cell transcriptomic analysis reveals age-related remodeling of brain endothelial cells.

This single-cell transcriptomic study profiled brain endothelial cells (68,316 cells; 15,564 genes) from young and old mice to define age-related remodeling of blood-brain barrier (BBB) endothelial subtypes. Unsupervised clustering identified five endothelial subtypes (including capillary EC1/EC2 and venous EC1/EC2) and showed aging shifted subtype distributions, including reduced Capillary EC1 and increased other subtypes (downstream mechanistic details truncated). The findings provide molecular targets for preserving BBB integrity during aging by clarifying how endothelial cell states change over time.

Nguyen HD, Siddiqui S, Bohannon DG et al. · Aging brain · (2026) · View on PubMed ↗ · Free PDF ↗

Lactate Signaling and Lactylation in Retina: From Physiological Warburg Effect to Pathological Metabolic Reprogramming.

This review synthesized current evidence on lactate signaling and lactylation in the retina, connecting physiological lactate-mediated “Warburg effect” concepts to pathological metabolic reprogramming. It emphasizes how lactate coordinates energy redistribution, receptor-mediated signaling, and epigenetic regulation across retinal cell types (photoreceptors, Müller glia, retinal pigment epithelium, vascular cells, and retinal ganglion cells). The review is significant for framing lactate/lactylation pathways as potential mechanistic drivers and therapeutic targets in retinal disease.

Gu X, Zhuang A, Fan J et al. · Progress in retinal and eye research · (2026) · View on PubMed ↗

Metabolic Reprogramming-Driven Neuroimmunoregulation: Key Mechanisms and Therapeutic Opportunities and Challenges in Central Nervous System Disorders.

This narrative review synthesized evidence on metabolic reprogramming-driven neuroimmunoregulation in CNS disorders, focusing on immunometabolic changes in microglia, immunomodulatory astrocytes, and infiltrating immune cells across Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and ischemic stroke. It highlights how dysregulated glucose, lipid, amino acid metabolism and oxidative phosphorylation shape immune cell function, while proposing an evidence-transparency framework to distinguish well-established from less certain metabolic alterations. The work is significant because it frames metabolic pathways as therapeutic opportunities and challenges for CNS immunotherapies.

Li N, Wu Y, Feng H et al. · Ageing research reviews · (2026) · View on PubMed ↗

Distinct cellular phenotypes of language and executive decline in amyotrophic lateral sclerosis.

The study mapped prefrontal cortex regions in cognitively stratified amyotrophic lateral sclerosis (ALS) patients using integrated spatial transcriptomics and single-nucleus transcriptomics. It found that language and executive decline correspond to distinct, region-specific neuronal dysfunction and glial–vascular dysregulation patterns, with executive dysfunction linked to reduced mitochondrial and synaptic activity in deep-layer dorsolateral prefrontal cortex neurons. These findings provide mechanistic, subtype-resolved molecular targets for cognitive impairment in ALS and support precision approaches to therapy and biomarker development.

Petrescu J, Gouveia Roque C, Jackson CA et al. · Cell · (2026) · View on PubMed ↗

Metabolic atlas of early human cortex reveals glycolytic remodeling and pentose phosphate pathway control of cell fate transitions.

The study generated a metabolic atlas of early human cortex using primary tissue and stem cell–derived cortical organoids to define how glycolysis and the pentose phosphate pathway (PPP) regulate cell fate transitions. It found that late neurogenesis showed increased glycolysis and PPP activity, and that manipulating glucose availability shifted cortical organoid cell-type composition by increasing outer radial glia (oRG) and inhibitory neurons. These results link specific metabolic programs to human cortical developmental trajectories and suggest metabolic control points for influencing cell fate.

Mil J, Soto JA, Krall AS et al. · Cell · (2026) · View on PubMed ↗

APOE3 and APOE4 human astrocytes differentially modulate Alzheimer’s disease pathology and microglial responses in chimeric mice.

This study used a chimeric mouse model of Alzheimer’s disease by transplanting isogenic APOE3- or APOE4-carrying human induced pluripotent stem cell-derived astrocyte progenitors into neonatal AD mice. APOE3 and APOE4 astrocytes differentially associated with AD hallmarks, with APOE3 astrocytes linked to reduced Aβ burden and Tau pathology and altered microglial responses compared with APOE4 astrocytes. These findings are significant because they provide causal, variant-specific evidence that astrocyte APOE isoforms modulate amyloid and neuroinflammatory processes, informing APOE-targeted therapeutic strategies.

Cruz-Sese J, Mirón-Alcala M, Alfonso-Triguero M et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Interactive Effects of Plasma Alzheimer Disease Biomarkers and White Matter Hyperintensities on Cognitive Decline and Clinical Progression in Nondemented Adults.

This study analyzed how plasma Alzheimer disease biomarkers interact with white matter hyperintensities (WMHs) to influence cognitive decline and progression to cognitive impairment/dementia in 463 nondemented adults from ADNI. Using linear mixed-effects models and Cox models, the authors tested interaction effects between plasma biomarkers and WMH burden on cognitive trajectories and clinical progression risk. Understanding this combined risk mechanism could improve early identification of individuals likely to deteriorate before dementia onset.

Yang J, Zhao X, Liu Y et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

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Neurology: stroke/brain injury and neuroprotection

Biomimetic exosomal delivery of Ginsenoside Rd reduces post-stroke depression via microglial reprogramming in a pathway involving EGFR/JAK2/STAT3.

This study developed biomimetic microglia-derived exosomes encapsulating ginsenoside Rd (Exos@Rd) to treat post-stroke depression (PSD) by reprogramming microglia through an EGFR/JAK2/STAT3 pathway. In a multidimensional screening approach, Rd was identified as a key blood-absorbed constituent linked to EGFR signaling, and the exosomal delivery system was engineered to overcome bioavailability limitations and promote lesion-homing. The findings suggest a BBB-relevant, target-pathway–based strategy for PSD that leverages microglial reprogramming via EGFR/JAK2/STAT3.

Chen J, Yin X, Yan D et al. · Pharmacological research · (2026) · View on PubMed ↗ · Free PDF ↗

Neuroprotection and Enhanced Hemoglobin Excretion by Intrathecal Clazosentan in Mice With Subarachnoid Hemorrhage.

This mouse study tested whether intrathecal clazosentan, a selective endothelin receptor subtype A antagonist, provides neuroprotection and enhances hemoglobin excretion in acute subarachnoid hemorrhage (SAH). In male C57BL/6 mice subjected to prechiasmatic cisternal SAH, continuous intracerebroventricular infusion of clazosentan (dose-ranging) was compared with saline to evaluate neuroinflammation and lymphatic clearance of hemoglobin. If confirmed, intrathecal clazosentan could represent a route-optimized strategy to reduce secondary brain injury and improve clearance of blood products after SAH.

Kawakita F, Hakozaki K, Aoki K et al. · Journal of the American Heart Association · (2026) · View on PubMed ↗ · Free PDF ↗

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Genetics, genomics, and multi-omics for disease risk

Whole genome sequencing in cerebral palsy: a UK paediatric pilot study.

This UK prospective pilot study evaluated the diagnostic utility of gene-agnostic trio whole genome sequencing (WGS) with AI-based variant prioritisation in 86 children with cerebral palsy (CP) recruited from NHS specialist clinics. It reports that candidate pathogenic/likely pathogenic variants were reviewed in multidisciplinary meetings using a CP gene list, aiming to quantify monogenic diagnostic yield in routine UK care. The clinical significance is that WGS could improve CP diagnosis and enable more precise genetic counselling and management for a subset of patients.

Ratnaike TE, Pierce HH, Coffey AJ et al. · The Lancet regional health. Europe · (2026) · View on PubMed ↗ · Free PDF ↗

A SNP altering the MUC5AC mucin structure is increased in idiopathic pulmonary fibrosis together with the MUC5B SNP.

This genetic association study examined whether the MUC5AC SNP rs878913005 (Arg1201Trp) is associated with idiopathic pulmonary fibrosis (IPF) and whether it co-occurs with the known MUC5B risk SNP rs35705950. Using whole genome sequence data from UK Biobank and analyses of IPF diagnostic honeycomb cysts, it found that the MUC5AC structural-altering variant is increased in IPF alongside the MUC5B SNP. The significance is that combined mucin genetic risk may help explain mucus-net biology in IPF and refine genetic susceptibility models.

Trillo-Muyo S, Ermund A, Dolan B et al. · Respiratory research · (2026) · View on PubMed ↗ · Free PDF ↗

Towards a molecular understanding of the role of helix 8 in GPCR trafficking.

This study examined the role of helix 8 in G protein-coupled receptor (GPCR) trafficking by testing whether helix 8 acts as a surface-active amphipathic element that promotes membrane binding and senses membrane curvature. Using molecular dynamics simulations and circular dichroism spectroscopy on six amphipathic peptides (including helix 8 segments from five GPCRs spanning a range of internalization rates), the authors found the strongest relationship between helix 8 secondary structure in membrane-mimicking conditions and internalization behavior. The results provide a molecular biophysical framework for how helix 8 can regulate GPCR internalization, informing rational design of interventions targeting receptor trafficking.

Ehler Nielsen TT, Schmidt JH, Mustafa S et al. · Journal of molecular biology · (2026) · View on PubMed ↗ · Free PDF ↗

NUDT2 and A proteome-wide causal map of plasma proteins in osteoporosis.

This study used proteome-wide Mendelian randomization (PW-MR) to map causal plasma protein signals for osteoporosis and to prioritize therapeutic targets supported by genetic evidence. By integrating large-scale GWAS meta-analysis data, it constructed a causal plasma proteome “map” and identified high-confidence proteins/targets with translational potential. The approach is significant because it can accelerate biomarker discovery and target selection for osteoporosis by leveraging causal inference rather than correlation.

Wang Z, Chen S, Luo J et al. · Journal of advanced research · (2026) · View on PubMed ↗ · Free PDF ↗

Identification of Glycolysis-Related Diagnostic Biomarkers for Amyotrophic Lateral Sclerosis Using Machine Learning.

This study aimed to identify glycolysis-related diagnostic biomarkers for amyotrophic lateral sclerosis (ALS) by combining two-sample Mendelian randomization with differential expression and multiple machine-learning methods. It investigated causal relationships between blood glucose traits and ALS and then used machine learning plus correlation analyses to derive candidate diagnostic biomarkers. The scientific significance is that it provides a data-driven pipeline to generate potentially actionable, glycolysis-linked biomarkers for earlier ALS diagnosis.

Ye P, Guo B · Clinical laboratory · (2026) · View on PubMed ↗

Mosaic Loss of Y Chromosome and Risks of Peripheral Arterial and Aortic Diseases.

This UK Biobank cohort study examined whether mosaic loss of the Y chromosome (mLOY) in males is associated with incident peripheral arterial disease (PAD) and aortic aneurysm and dissection (AAD). Using the Mosaic Chromosomal Alterations pipeline to detect mLOY and Cox proportional hazards models to estimate risk, it tested interactions with smoking status for PAD and AAD outcomes. The findings are clinically relevant because they connect a common age-related somatic alteration to vascular disease risk and may inform risk stratification in men.

Zeng Z, Li Y, Li Z et al. · JACC. Advances · (2026) · View on PubMed ↗ · Free PDF ↗

Integrative single-cell eQTL and GWAS analyses identify cell-type-specific regulatory mechanisms underlying ESCC susceptibility.

This study integrated single-cell RNA sequencing with genotype data to build a cell-type-resolved expression quantitative trait loci (sc-eQTL) map and then intersected it with genome-wide association study (GWAS) signals to identify regulatory mechanisms underlying esophageal squamous cell carcinoma (ESCC) susceptibility. Most regulatory effects were highly cell-type-specific and were largely missed by bulk analyses, and ESCC risk variants were significantly enriched in specific cellular populations, especially invasive epithelial compartments. These findings are scientifically significant because they pinpoint which ESCC-relevant cell types mediate genetic risk, guiding functional follow-up of noncoding variants and improving interpretation of GWAS loci.

Song L, Pan M, Li Y et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Genetic Predisposition and Pharmacological Effects Shape the Divergent Effects of Type 2 Diabetes on Atherosclerosis.

This genomics/proteomics/bioinformatics study investigated how genetic predisposition and pharmacological effects shape the “diabetes-atherosclerosis paradox” by analyzing type 2 diabetes (T2D) associations with coronary artery disease (CAD) versus abdominal aortic aneurysm (AAA). It found a robust positive genome-wide correlation between T2D and CAD, while the weak genetic correlation between T2D and AAA was counterbalanced by a majority of positive and a minority of negative correlations, supported by single-nucleotide variant colocalization, gene/pathway enrichment, and cell-type associations. The work is scientifically significant because it links specific genetic architecture and mechanistic pathways to divergent atherosclerotic outcomes in T2D.

Zheng S, Wu Y, Li A et al. · Genomics, proteomics & bioinformatics · (2026) · View on PubMed ↗ · Free PDF ↗

Expanded ATXN3 CAG Repeat is Stable in Human Purkinje Cells.

This study investigated somatic stability of the mutant ATXN3 (mATXN3) CAG repeat in human cerebellar Purkinje cells in individuals with spinocerebellar ataxia type 3 (SCA3). Using nuclei sorting from post-mortem brain tissue, transcriptome-based sample purity confirmation, and high-depth sequencing of ATXN3 exon 10 amplicons, the authors found that the expanded ATXN3 CAG repeat is stable in Purkinje cells. These findings constrain models of disease progression by suggesting limited somatic repeat expansion in the output cerebellar neurons most affected in SCA3.

Chetia H, Kus L, Sipos E et al. · Movement disorders : official journal of the Movement Disorder Society · (2026) · View on PubMed ↗ · Free PDF ↗

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Autoimmune and inflammatory disease mechanisms and therapies

Gastrointestinal dysfunction associated with autoimmune glial fibrillary acidic protein astrocytopathy.

This clinical study investigated gastrointestinal (GI) dysfunction in patients with autoimmune GFAP astrocytopathy (GFAP-A), enrolling individuals diagnosed at a single center based on CSF GFAP-IgG positivity. Using I-FEED scoring and collected clinical parameters, it characterized GI dysfunction features and explored potential pathogenic mechanisms via pathological examination in a subset of patients (specific results truncated). Defining GI involvement in GFAP-A could improve recognition, risk stratification, and mechanistic understanding of this autoimmune neurologic disease.

Xiao L, Qin B, Guo Y et al. · Journal of neurology · (2026) · View on PubMed ↗

Progress in the Application of Exosomes in Androgenetic Alopecia: Focusing on Molecular Mechanisms.

The review examined the role of exosomes—nano-sized extracellular vesicles carrying proteins, lipids, and nucleic acids—in the molecular pathogenesis of androgenetic alopecia (AGA) and how they might be used therapeutically. It reports that exosome-based approaches could address key dysregulated hair-follicle signaling pathways that underlie follicle miniaturization and shortened anagen, potentially overcoming limitations of FDA-approved minoxidil and finasteride. This supports exosome engineering and mechanistic targeting as a promising route to safer, more effective AGA treatments beyond current standard drugs.

Chen Y, Chen S, Ding W et al. · International journal of nanomedicine · (2026) · View on PubMed ↗ · Free PDF ↗

Suspected levetiracetam drug-induced lupus in a child: A case report.

This case report studied suspected levetiracetam-induced lupus erythematosus in a previously healthy 6-year-old girl treated for absence seizures. It found that several months after starting levetiracetam she developed cytopenias (thrombocytopenia, neutropenia, anemia), generalized lymphadenopathy, and a petechial rash, consistent with drug-induced lupus after extensive infectious and oncologic evaluation. The significance is heightened clinician awareness that levetiracetam can rarely trigger lupus-like syndromes in pediatric patients.

Landells F, McColl J · SAGE open medical case reports · (2026) · View on PubMed ↗ · Free PDF ↗

Perioperative Use of Biologics in Patients with Chronic Rhinosinusitis with Nasal Polyps: What Is the Evidence?

This Clinical Perspective reviewed evidence on perioperative biologic therapy management in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) who undergo endoscopic sinus surgery (ESS) despite standard-of-care medical therapy. It addresses whether biologics should be initiated, continued, interrupted, or resumed around surgery, focusing on safety, sequencing, postoperative disease control, and evidence specific to healing. The article’s significance is to guide clinicians in perioperative decision-making for biologics in CRSwNP, where direct trial evidence is limited and practical protocols are needed.

Konstantinou GN, Desrosiers M · The journal of allergy and clinical immunology. In practice · (2026) · View on PubMed ↗

Simultaneous Dual Type 2 Biologic Therapy Improves Sinonasal Outcomes in Selected Patients With Chronic Rhinosinusitis With Nasal Polyps.

This retrospective multicenter study assessed real-world outcomes of simultaneous dual type-2 biologic therapy in adults with severe uncontrolled chronic rhinosinusitis with nasal polyps (CRSwNP). It reported improved sinonasal outcomes in selected patients treated with two biologics concurrently when disease control was inadequate with standard approaches. The findings inform clinical decision-making for complex CRSwNP cases where dual biologic therapy may be considered.

Bärhold F, Hagemann J, de Corso E et al. · Allergy · (2026) · View on PubMed ↗

An iguratimod prodrug reduces RA-FLS invasiveness by disrupting STAT1-C3-TNFα-mediated crosstalk between fibroblast-like synoviocytes and macrophages.

This study investigated how the iguratimod (IGU) prodrug affects rheumatoid arthritis pathology by testing its impact on fibroblast-like synoviocyte (RA-FLS) invasiveness and inflammatory signaling in MH7A cells and rat RA-FLS, using RNA sequencing and conditioned-medium fast-astral DIA proteomics. The prodrug reduced RA-FLS invasiveness by disrupting STAT1-C3-TNFα-mediated crosstalk between RA-FLS and macrophages, identifying STAT1-pathway signaling as an upstream regulatory node. These findings suggest a targeted mechanism for improving IGU pharmacokinetics while preserving disease-modifying activity in RA.

Tao L, Jiang W, Huang Y et al. · Journal of orthopaedic translation · (2026) · View on PubMed ↗ · Free PDF ↗

Estetrol/drospirenone for combined oral contraception: a systematic review of efficacy, cycle control, and safety.

This systematic review evaluated contraceptive efficacy, cycle control, safety, and selected noncontraceptive effects of estetrol 15 mg/drospirenone 3 mg (E4/DRSP) in women of reproductive age, using PRISMA 2020 and GRADE certainty assessments. Across included clinical trials and comparative studies, E4/DRSP showed evidence supporting contraceptive performance and acceptable bleeding/cycle control with a safety profile summarized by hemostatic and endocrine-metabolic outcomes. These findings help clinicians and guideline developers judge the overall benefit–risk and evidence certainty for E4/DRSP as a combined oral contraceptive option.

Sánchez-Prieto M, Coll S, Romero-Domínguez M et al. · Frontiers in endocrinology · (2026) · View on PubMed ↗ · Free PDF ↗

Effect of apremilast on entheseal bone damage in psoriasis patients at risk of developing psoriatic arthritis - data from the prospective, interventional EPOS study.

The prospective, interventional EPOS study evaluated whether apremilast 30 mg (in psoriasis patients at risk of psoriatic arthritis) can reduce entheseal bone damage using hand MRI and/or HR-pQCT measures. In this single-arm, open-label trial, apremilast was tested to modulate subclinical entheseal inflammation and structural remodeling that precede psoriatic arthritis. These data support early pharmacologic risk modification in psoriasis patients before overt PsA develops.

Simon D, Minopoulou I, Bayat S et al. · Arthritis research & therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Targeting the IL-17C-M2 macrophage axis ameliorates fibrosis in endometriosis through MAPK/ERK signaling.

This study examined whether targeting the IL-17C–M2 macrophage axis ameliorates fibrosis in endometriosis via MAPK/ERK signaling using spatial transcriptomics and cellular interaction analyses of human endometriotic lesions plus an endometriosis mouse model treated with the IL-17C neutralizing antibody MOR106. The authors found that IL-17C neutralization reduced ectopic lesion growth and fibrosis and altered macrophage polarization and extracellular matrix (ECM) pro-fibrotic programs through MAPK/ERK signaling. These results identify IL-17C–driven M2 macrophage activation as a mechanistic therapeutic pathway for endometriosis-associated fibrosis.

Li J, Yao B, Chu L et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗

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Gastrointestinal diseases (including IBD, GI autoimmunity, and GI cancers)

How Biologics Are Changing the Global Burden of Inflammatory Bowel Disease: A Review.

This narrative review studied how biologic therapies for inflammatory bowel disease (IBD)—including anti-TNF antibodies, vedolizumab (anti-integrin), ustekinumab (IL-12/23), and IL-23 p19 inhibitors such as risankizumab and mirikizumab—have changed the global burden and treatment landscape of Crohn’s disease and ulcerative colitis. It finds that biologics have expanded effective options and, more recently, oral small-molecule advanced therapies (JAK inhibitors and S1P receptor modulators) further broaden treatment beyond biologics alone. The clinical significance is that these therapies likely contribute to improved disease control worldwide as IBD has become more globally prevalent.

Abu Osba Y, Elshebli S, Abureesh A et al. · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

HBV RNA, HBcrAg, and HBsAg levels at year 6 do not predict HCC risk in patients with cirrhosis on long-term entecavir therapy.

This prospective multicenter study assessed whether on-treatment serum HBV RNA, hepatitis B core-related antigen (HBcrAg), and quantitative hepatitis B surface antigen (HBsAg) measured at enrollment predict hepatocellular carcinoma (HCC) risk in patients with HBV-related cirrhosis receiving long-term entecavir therapy. At year 6, these viral biomarkers did not predict HCC risk, despite ongoing entecavir treatment and HCC surveillance. The findings suggest that, in entecavir-treated cirrhosis, routine monitoring of HBV RNA/HBcrAg/HBsAg may have limited value for HCC risk stratification, informing future biomarker selection.

Pan HH, Su TH, Hu TH et al. · Hepatology international · (2026) · View on PubMed ↗

Comparative risk of postoperative complications in ulcerative colitis patients following preoperative advanced therapies: a network meta-analysis with meta-regression.

This network meta-analysis with meta-regression compared short-term postoperative complication risks in adults with ulcerative colitis (UC) undergoing colorectal surgery after preoperative exposure to biologic therapy, small-molecule therapy, or no biologic/small-molecule therapy within 12 weeks. Across included cohort studies, the analysis estimated relative complication risks among treatment classes and assessed how effects varied with study and patient factors via meta-regression. The results are clinically significant for perioperative risk stratification and selection of UC advanced therapies when surgery is planned.

Hayek MA, Estevinho MM, Kayal M et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗

Autoimmune diseases involving the gastrointestinal tract: clinical patterns, imaging spectrum, and complications.

This review examined autoimmune diseases that involve the gastrointestinal (GI) tract and summarized their clinical patterns, cross-sectional imaging spectrum, and complications across affected patients. It found that GI autoimmune/vasculitic disease can range from subtle motility disturbances to mural, mesenteric, and vascular imaging signatures that correlate with underlying pathophysiology and help narrow differential diagnoses. The pattern-based imaging framework is clinically significant because it supports earlier recognition and management of potentially life-threatening complications such as ischemia, perforation, or obstruction.

Diab M, Chaudhry H, Wang MX et al. · Abdominal radiology (New York) · (2026) · View on PubMed ↗ · Free PDF ↗

Impact of GLP-1 Analogue Therapy on Gastrointestinal Outcomes in Patients with Irritable Bowel Syndrome: A Real-World TriNetX Analysis.

This real-world retrospective cohort study used the TriNetX federated electronic health records network to evaluate IBS patients (ICD-10 K58) who initiated GLP-1 receptor agonist therapy. It found an association between GLP-1 receptor agonist initiation and subsequent gastrointestinal outcomes in IBS, leveraging large-scale observational data to address limited prior evidence. The findings are significant for clinicians considering GLP-1 analogues in patients with comorbid diabetes/obesity and IBS, where effects on motility and visceral sensitivity may matter.

Khan SA, Marasini A, Shrestha A et al. · Digestive diseases and sciences · (2026) · View on PubMed ↗

Colitis-Associated Dysplasia in Inflammatory Bowel Diseases: From Pathogenesis to Treatment.

This review focused on colitis-associated dysplasia in inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn’s disease with colonic involvement, linking pathogenesis to treatment. It found that IBD-associated dysplasia follows an inflammation-driven “field cancerization” pathway characterized by multifocal lesions and early genetic/epigenetic alterations that connect chronic inflammation to colorectal carcinogenesis. The review is clinically significant because it frames mechanistic targets and informs strategies for prevention and management of premalignant dysplasia in high-risk IBD patients.

Fousekis F, Vieth M, Rath T et al. · Visceral medicine · (2026) · View on PubMed ↗

Diagnostic and management guidelines for biliary atresia in 2025.

This 2025 clinical guideline article synthesized expert recommendations for screening, diagnosis, treatment, and follow-up of biliary atresia (BA) in pediatric patients. It found that, despite progress, BA remains challenging and requires structured, evidence-informed pathways to prevent rapid progression to fibrosis in untreated children. The guideline is clinically significant because it standardizes care decisions across the BA diagnostic and management continuum using a formal GRADE-based development process.

Ge L, Yang J, Li T et al. · Hepatobiliary surgery and nutrition · (2026) · View on PubMed ↗ · Free PDF ↗

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Respiratory diseases (asthma, bronchiectasis, airway immunity)

Mechanisms and therapeutic strategies of asthma: from bench to bedside.

This review examined asthma pathobiology and therapeutic strategies in the context of genetic susceptibility and environmental exposures, focusing on immune and airway structural pathways in patients with asthma. It highlights that epithelial “alarmin” cytokines (TSLP, IL-33, IL-25) drive downstream type 2/type 17 networks involving Th2/Th17 cells, ILC2s, eosinophils, and mast cells, converging on bronchial hyperresponsiveness and mucus-driven airflow obstruction. The synthesis supports mechanism-guided development of targeted asthma therapies beyond inhaled corticosteroids and bronchodilators by mapping upstream epithelial signals to actionable immune circuits.

Xie C, Wei Y, Su C et al. · Signal transduction and targeted therapy · (2026) · View on PubMed ↗

APOE and genetic risk variants influence Alzheimer’s disease onset in carriers of an extra copy of APP, with and without Down syndrome.

This study analyzed clinical and genetic data from 100 APP duplication (APPdup) carriers and 957 individuals with Down syndrome (DS) to test whether sporadic Alzheimer’s disease (AD) risk variants modify age at onset (AAO). It found that AAO differed between APPdup and DS and that APOE ε2 delayed onset, with Cox models also evaluating an AD genetic risk score (AD-GRS excluding APOE and chromosome 21 variants). The findings are significant because they clarify how APOE and additional AD risk variants influence AD timing in populations with an extra APP copy, including those with DS.

Groeneveld J, Perlaza D, Olivé C et al. · Alzheimer’s & dementia : the journal of the Alzheimer’s Association · (2026) · View on PubMed ↗ · Free PDF ↗

The airway epithelial-immune axis: mechanisms and therapeutic implications.

This narrative review summarized the airway epithelial–immune axis, focusing on how airway epithelial cells actively regulate mucosal immunity in chronic respiratory diseases. It highlighted that environmental allergens, pollutants, and pathogens disrupt epithelial tight junctions and trigger alarmin release (TSLP, IL-33, IL-25), which drives epithelial–immune crosstalk with innate lymphoid cells (ILC2s) and Th2 cells. The review provides therapeutic implications by framing epithelial alarmins and epithelial-immune circuits as actionable targets for chronic airway inflammation.

Zhu Z, Li Q, Hua B · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗

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Renal and urologic disease (including AKI/CKD and kidney transplant)

Early identification of acute kidney injury progression in critically ill patients with sepsis: interpretable machine learning approach.

This study developed an interpretable machine-learning prediction model for early identification of acute kidney injury (AKI) progression in critically ill patients with sepsis-associated AKI (SA-AKI). It used multicenter ICU datasets (MIMIC-IV for training/internal validation, plus MIMIC-III, eICU-CRD, and SICdb for external validation) to predict progression from AKI stage 1–2 to stage 3 within 7 days after sepsis-associated AKI diagnosis (model performance details truncated). A clinically usable, interpretable tool could enable earlier intervention to reduce morbidity and mortality in septic patients at risk of rapid AKI worsening.

You X, Chen Y, Chen J et al. · Clinical kidney journal · (2026) · View on PubMed ↗ · Free PDF ↗

The AKI-CKD Continuum: Mechanisms and Therapeutic Interventions.

This narrative review synthesized evidence on the acute kidney injury (AKI) to chronic kidney disease (CKD) continuum and the mechanisms and therapeutic interventions across distinct phases. It proposes that AKI-to-CKD progression unfolds through four mechanistically distinct stages, including hyperacute injury with mitochondrial and oxidative stress features and later phases involving coordinated cell death programs such as PANoptosis and ferroptosis. The review is clinically significant because it frames timing- and mechanism-specific intervention opportunities to prevent CKD after AKI.

Kulkarni HV, Mulay SR, Gaikwad AB · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗

Individualizing pharmacologic and non-pharmacologic therapy for CKD associated with diabetes.

This review focused on individualizing pharmacologic and non-pharmacologic therapy for chronic kidney disease associated with diabetes (diabetic kidney disease, DKD). It summarizes kidney-protective evidence for renin-angiotensin system inhibitors (RASi), SGLT2 inhibitors, GLP-1 receptor agonists, and the nonsteroidal mineralocorticoid receptor antagonist finerenone, while highlighting gaps such as the lack of head-to-head RCTs across drug classes and limited long-term safety data for sustained multi-class combinations. The review is significant for guiding personalized DKD treatment selection and sequencing to maximize hard kidney outcomes while managing tolerability and safety.

Zhang Z, Li L, Yang M et al. · Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · (2026) · View on PubMed ↗

Differing effects of Nefecon and Sparsentan in a patient with recurrent IgA nephropathy post-kidney transplantation.

This case report studied targeted-release budesonide (Nefecon) versus subsequent combined therapy with sparsentan plus empagliflozin in a young male kidney transplant recipient with biopsy-proven recurrent IgA nephropathy 7 years after living-donor transplantation. Nefecon was associated with a delayed and incomplete antiproteinuric response, systemic glucocorticoid-related adverse effects, and progressive graft function decline, whereas sparsentan plus empagliflozin after Nefecon discontinuation produced sustained albuminuria reduction and graft function stabilization. The report highlights the need for careful selection and monitoring of IgA nephropathy–specific therapies in the post-transplant setting where response may be incomplete and steroid toxicity clinically relevant.

Mühlfeld AS, Floege J, von Stillfried S et al. · Clinical kidney journal · (2026) · View on PubMed ↗ · Free PDF ↗

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Musculoskeletal, bone, and osteometabolic disorders

Y-RBCEVs accelerate fracture repair through osteogenesis and VCAN-mediated CD44/PI3K/AKT-dependent macrophage polarization.

This study investigated whether young human red blood cell–derived extracellular vesicles (Y-RBCEVs) accelerate fracture repair and defined a mechanism involving VCAN-mediated CD44/PI3K/AKT-dependent macrophage polarization. It combined NHANES analyses with a murine femoral fracture model, in vitro osteogenic differentiation and bone marrow macrophage polarization assays, and proteomic comparisons between Y-RBCEVs and old RBC EVs (O-RBCEVs) (key results truncated). If validated, Y-RBCEVs could represent an EV-based therapeutic strategy to enhance osteogenesis and modulate macrophage phenotype via VCAN–CD44–PI3K/AKT signaling.

Wang J, Zhang X, Zhang Q et al. · Bioactive materials · (2027) · View on PubMed ↗ · Free PDF ↗

Dual-modal antioxidant and epigenetic synergy attenuates the self-perpetuating senescence cycle in osteoarthritis.

This study investigated whether a dual-modal antioxidant and epigenetic strategy could break the self-perpetuating senescence cycle in osteoarthritis (OA) chondrocytes by targeting oxidative stress and m6A methylation. It found that cartilage-targeted HPcLW nanoparticles co-loaded with lycopene and WTAP (Wilms tumor 1-associating protein) siRNA reduced chondrocyte senescence by combining antioxidant effects with inhibition of the m6A methyltransferase WTAP. The significance is a preclinical therapeutic concept that simultaneously targets oxidative stress and m6A regulation to attenuate OA progression.

An X, Cai H, Wu W et al. · Bioactive materials · (2027) · View on PubMed ↗ · Free PDF ↗

Effects of exercise and nutritional interventions on muscle-specific strength in older adults: A systematic review and meta-analysis.

This systematic review and meta-analysis evaluated randomized controlled trials in adults aged ≥60 years examining how exercise, nutrition, and other interventions affect muscle-specific strength normalized by muscle mass. Across eligible RCTs of at least 8 weeks, interventions were synthesized to determine their effects on muscle-specific strength, with standardized mean differences used for pooling. These findings are clinically relevant for sarcopenia prevention strategies because they clarify which intervention types most improve muscle strength relative to muscle mass in older adults.

Ohta T, Hatanaka S, Li J et al. · Ageing research reviews · (2026) · View on PubMed ↗

Postoperative Delirium After Dexmedetomidine versus Propofol Sedation in Older Adults Undergoing Hip Fracture Surgery with Spinal Anesthesia: A Randomized Controlled Trial.

This multicenter, randomized, double-blind, parallel-group trial compared dexmedetomidine versus propofol sedation for postoperative delirium in older adults undergoing hip fracture surgery with spinal anesthesia. It found a difference in the incidence of postoperative delirium between the two sedation strategies, supporting the hypothesis that dexmedetomidine’s α2-adrenergic agonist properties may reduce delirium risk. The results are clinically significant because they can guide anesthetic/sedation choice to lower delirium-related morbidity in elderly hip-fracture patients.

Zhang L, Su Z, Zhang X · Drug design, development and therapy · (2026) · View on PubMed ↗ · Free PDF ↗

Therapeutic Soreness in Manual Therapy for Chronic Neck Pain: A Triphasic Model of Descending Pain Modulation.

This article proposed a triphasic model for how “therapeutic soreness” during manual therapy (MT) for chronic neck pain may reflect neurophysiological modulation of descending pain inhibitory pathways. It synthesized evidence to support the working hypothesis that MT effects are mediated not only by peripheral biomechanical factors but also by central nociplastic changes and endogenous pain modulation. The model is significant because it offers a mechanistic framework that could improve interpretation of patient responses and guide optimization of MT for chronic neck pain.

Zhang X, Zhang L, Fang M · Journal of pain research · (2026) · View on PubMed ↗ · Free PDF ↗

Timing matters: Exon skipping therapy is most effective when initiated early in a mouse model of Duchenne muscular dystrophy.

This preclinical study tested how treatment timing affects exon skipping efficacy in dystrophin-deficient mdx mice by initiating peptide-conjugated phosphorodiamidate morpholino oligonucleotide (PPMO) exon skipping conjugates at adult (12-week-old) versus aged (75-week-old) stages, with biochemical and transcriptomic analyses in tibialis anterior muscle. Exon 23 skipping was higher when therapy started in adults (mean 79%) than in aged mice (mean 44%), indicating reduced effectiveness with later initiation. The results provide mechanistic and translational support for earlier intervention in DMD exon-skipping strategies to maximize dystrophin restoration.

Stenler S, Huang J, van Westering TLE et al. · Molecular therapy. Nucleic acids · (2026) · View on PubMed ↗ · Free PDF ↗

Mechanisms and management strategies for exacerbated bone loss following denosumab discontinuation.

This review examined mechanisms underlying exacerbated bone loss after denosumab discontinuation and summarized management strategies to mitigate rebound fracture risk. It synthesized hypotheses including increased osteoclast precursors and osteomorph accumulation, RANKL/OPG imbalance, uncoupled remodeling, and osteocyte-mediated aberrant microdamage repair. The review supports sequential treatment approaches after stopping denosumab to prevent rapid bone turnover rebound and subsequent fractures.

Yang J, Yang M, Zeng Y · Frontiers in aging · (2026) · View on PubMed ↗ · Free PDF ↗

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Infectious diseases and antimicrobial resistance

The Association Between COVID-19 and Herpes Zoster in Adult Populations: A Systematic Review.

This systematic review assessed the temporal relationship between COVID-19 infection and herpes zoster (shingles) in adult populations. It synthesizes evidence that SARS‑CoV‑2–associated immune dysregulation—especially lymphopenia and impaired T-cell immunity—may facilitate varicella-zoster virus reactivation, and it evaluates onset timing, outcomes, and prognostic implications (specific pooled estimates truncated). Clarifying COVID-19–HZ risk can inform surveillance and vaccination/management strategies for adults after SARS‑CoV‑2 infection.

Khawaja I, Khan N, Kannangara L et al. · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗

ZBP1 activated by mitochondrial damage binds to STAT3 to suppress Legumain production and exacerbate macrophage inflammation in Klebsiella pneumoniae-induced sepsis.

This mechanistic study examined how Z-DNA binding protein 1 (ZBP1) activated by mitochondrial damage regulates inflammation in Klebsiella pneumoniae–induced sepsis. Using transcriptomic datasets from human sepsis cohorts plus murine KP infection models and single-cell RNA sequencing, it reported that ZBP1 binds STAT3 to suppress Legumain production and thereby modulate macrophage inflammation (specific experimental outcomes truncated). Identifying the ZBP1–STAT3–Legumain axis could provide a translational target to dampen dysregulated macrophage-driven inflammation in KP sepsis.

Deng LT, Yang H, Zhang XF et al. · Military Medical Research · (2026) · View on PubMed ↗ · Free PDF ↗

Healthy vaccinee effect in the evaluation of updated COVID-19 vaccines in elderly populations.

This population-based Swedish study evaluated the “healthy vaccinee effect” when estimating vaccine effectiveness of the 2024–2025 COVID-19 vaccine adapted to the Omicron JN.1 lineage in adults aged ≥65 years (N=245,696). Vaccine effectiveness against COVID-19-related hospitalization was 75% overall, but estimates differed by prior vaccination status (84% in those vaccinated in 2023–2024 vs 65% in those not), and negative control outcome (all-cause mortality) was used to probe bias. The work highlights how baseline health differences among vaccine recipients can influence real-world VE estimates in elderly populations, improving interpretation of observational vaccine effectiveness studies.

Lyth J, Spreco A, Hinkula J et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗

Glutamine synthetase deficiency triggers mitochondrial oxidative stress and a ribotoxic stress response during acute hepatic metabolic crisis.

This study investigated how glutamine synthetase (GLUL) deficiency contributes to mitochondrial oxidative stress and a ribotoxic stress response during acute hepatic metabolic crisis, using transcriptomic, proteomic, and metabolomic profiling in cultured hepatocytes. Mechanistically, GLUL loss was linked to downstream stress signaling involving ZAKα and JNK, and rescue experiments using MitoTEMPO, glutamine, and GSH plus GLUL overexpression/CRISPR knockout supported causality. The work is significant because it clarifies hepatotoxic mechanisms relevant to chlorfenapyr (CHL) lethality and identifies potential intervention points in mitochondrial oxidative and ribotoxic stress pathways.

Jin G, Lin C, Wei Y et al. · Metabolism: clinical and experimental · (2026) · View on PubMed ↗

PKR engages viral RNA and intron-retained host transcripts during poxvirus infection.

This mechanistic study examined how the double-stranded RNA sensor PKR is activated during poxvirus infection, focusing on vaccinia virus (VacV) infection. PKR binding was enriched on viral RNAs and host intron-retained transcripts, and defective pre-mRNA splicing (including cytoplasmic intron-retaining transcripts driven by RNase L activation) generated PKR ligands; small-molecule splicing inhibition activated PKR independently of RNase L. The results are scientifically important because they define splicing defects and intron-retained host RNAs as a source of PKR ligands during infection, expanding understanding of antiviral RNA-sensing pathways.

Zhang R, Ye X, Dixson AC et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗

Infectious Diseases Society of America 2026 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections.

This IDSA 2026 guidance document reviewed and updated treatment recommendations for antimicrobial-resistant (AMR) Gram-negative infections, including ESBL-producing Enterobacterales (ESBL-E), AmpC-producing Enterobacterales (AmpC-E), carbapenem-resistant Enterobacterales (CRE), difficult-to-treat resistant Pseudomonas aeruginosa (DTR P. aeruginosa), carbapenem-resistant Acinetobacter baumannii (CRAB), and Stenotrophomonas maltophilia. The key output is an evidence-informed set of antimicrobial treatment suggestions tailored to resistance phenotype and organism group, replacing earlier versions of the guidance. This is clinically significant because it standardizes management of high-risk AMR infections and supports more appropriate antibiotic selection to improve outcomes and stewardship.

Tamma PD, Bonomo RA, Heil EL et al. · Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · (2026) · View on PubMed ↗

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Generated automatically on August 10, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.