PubMed Trending Research Digest — May 24, 2026
A curated digest of 97 trending PubMed articles, automatically categorised and summarised across 21 research areas.
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PubMed Trending Research Digest — May 24, 2026
Automated digest · 97 articles · 21 research areas · May 24, 2026
Overview
Across this week’s set of papers, a dominant theme is the push toward more precise, mechanism-informed care—whether by standardizing diagnostic criteria (e.g., Delphi consensus for neurogenic thoracic outlet syndrome and harmonized laparoscopic liver biopsy practice) or by improving risk stratification using data-driven phenotypes and biomarkers (e.g., CMR remodeling phenotypes after STEMI, inflammatory-cell ratios in biliary tract cancer, and genetically supported protein biomarkers for multiple sclerosis). In oncology and immunology, several studies converge on immune evasion and how to overcome it: PTEN loss driving immune exclusion in MSS colorectal cancer, mitochondrial/ROS and iron/ferroptosis mechanisms that impair immune responses, and multiple strategies to “re-inflame” tumors (STING agonist + osimertinib, irradiation-assisted CAR T, and tumor-irradiation-enhanced antigen dressing onto dendritic cells).
A second major thread is metabolic and inflammatory modulation as therapy or adjunct: GLP-1-based approaches appear repeatedly (from vaccine-adjunct geroprotection and post-bariatric weight rescue to mechanistic signaling in GLP1R neurons and potential effects on cancer progression), while cardiovascular and cardiorenal protection reviews and mechanistic studies highlight targeted receptor/pathway modulation (e.g., finerenone’s MR selectivity, SREBP1–NHE3 and Sam68-driven metabolic remodeling in heart failure). In parallel, neuroimmune and neurodegenerative work spans from mitochondrial DNA–cGAS–STING signaling in neuropathic pain to sleep and orexin receptor modulation in Alzheimer’s models, and from micro/nanoplastics transport to CNS neurotoxicity pathways.
Finally, the digest reflects a translational pipeline mindset: multiple papers emphasize how to make interventions more durable, safer, and broadly applicable—through improved trial design (external-control reanalysis), next-generation delivery platforms (lentiviral vector targeting), and governance of AI in medical education. Together, these studies illustrate a field moving toward tighter coupling between mechanistic insight, biomarker-driven patient selection, and standardized clinical implementation.
Clinical Diagnostic Criteria & Consensus Algorithms
An international multidisciplinary consensus statement on laparoscopic liver biopsy.
This international multidisciplinary consensus statement studied and standardized laparoscopic liver biopsy (LLB) practice by convening 45 experts across 6 continents and using a modified Delphi process. The key output was an evidence-informed set of recommendations to improve procedural quality and diagnostic efficiency for LLB, addressing variability across centers. Clinically, the consensus aims to harmonize LLB indications, technique, and workflow so that LLB can better complement percutaneous liver biopsy in complex or high-risk cases.
Lei SY, Han Y, Rockey DC et al. · Cell reports. Medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Glucosamine links hyperglycemia to mTORC1 activation and glucose toxicity in diabetes.
This study investigated how glucosamine links hyperglycemia to mTORC1 activation and glucose toxicity in pancreatic islets and kidney in diabetic rodent models, using 13C6-glucose metabolic labeling with targeted metabolomics and interventions including the SGLT2 inhibitor dapagliflozin and insulin. It identified glucosamine as a key metabolite that connects elevated glucose to mTORC1 signaling, promoting downstream ER stress, oxidative stress, and inflammation. Scientifically, it pinpoints a specific metabolic mediator of glucose-driven mTORC1 activation, potentially informing more targeted strategies to prevent β-cell failure and diabetic organ complications.
Riahi Y, Kogot-Levin A, Teselpapa Z et al. · JCI insight · (2026) · View on PubMed ↗ · Free PDF ↗
International Consensus on Severe Lung Cancer-The Second Edition.
This article is an international multidisciplinary consensus update (second edition) on the management of severe lung cancer, focusing on patients with performance status (PS) 2–4 and incorporating new evidence. It synthesizes guidance on emerging systemic therapies, interventional procedures, supportive care, and real-world data to standardize care pathways for this higher-need population. The consensus is significant for harmonizing clinical decision-making and improving outcomes and quality of care in severe lung cancer patients.
Lin X, Chu Q, Dong Y et al. · Translational lung cancer research · (2026) · View on PubMed ↗ · Free PDF ↗
Defining Diagnostic Criteria for Neurogenic Thoracic Outlet Syndrome: An Expert Consensus.
This expert consensus used a Delphi method with a panel of 20 upper-extremity experts to define diagnostic criteria for neurogenic thoracic outlet syndrome (nTOS) and build a clinical diagnostic algorithm. The study’s key finding was the ranking and consensus prioritization of 54 clinical items (via mean/SD scoring and Cronbach alpha reliability) to distinguish nTOS from other causes of thoracic outlet symptoms. Clinically, the resulting criteria framework is intended to reduce diagnostic ambiguity and standardize nTOS diagnosis in practice.
Wagner ER, Sullivan CM, Cuneo KR et al. · Orthopaedic journal of sports medicine · (2026) · View on PubMed ↗ · Free PDF ↗
HIV Treatment Strategies & Viral Rebound Risk
Risk of Developing Low-Level Viral Rebound Among People With HIV Receiving 2- or 3-Drug Regimens: A Case-Control Study Nested in the ICONA Cohort.
This matched 1:3 case-control study nested in the ICONA HIV cohort evaluated people with HIV (PWH) who achieved HIV-1 RNA suppression on 2-drug regimens (2DR) versus 3-drug regimens (3DR) and then developed low-level viral rebound (LLVR). The key finding was the estimated risk of a single HIV-RNA measurement of 51–199 copies/mL after suppression in the 2DR group compared with those maintaining ≤50 copies/mL (controls), matched on history of care gaps. Scientifically and clinically, the results address whether 2DR strategies increase LLVR risk, informing regimen selection and monitoring intensity after suppression.
Vergori A, Cervo A, Roen A et al. · Open forum infectious diseases · (2026) · View on PubMed ↗ · Free PDF ↗
Immunosenescence & Vaccine Adjuvants/Boosters
Immune development in early life.
This review integrated current evidence on immune development in early life, describing how prenatal, maternal, and postnatal cues shape durable immune trajectories. It emphasizes that fetal and infant immunity follow distinct ontogeny-specific programs for tissue protection, tolerance, and rapid effector function, influenced by blood/tissue seeding and microbial/environmental exposures. The synthesis provides a framework for understanding when and how interventions (e.g., vaccines or microbiome modulation) might most effectively steer immune outcomes.
Palma P, Farber DL, Konnikova L et al. · Nature immunology · (2026) · View on PubMed ↗
A glycan-based adjuvant expands the breadth and duration of protection of mRNA-based vaccines.
This preclinical-to-NHP study tested whether a glycan-based PRR-targeting adjuvant (mannadjuvant: fungal mannan plus aluminum hydroxide targeting dectin-2) can broaden and extend immunity elicited by an mRNA vaccine encoding the ancestral SARS-CoV-2 spike protein. Mannadjuvant increased the magnitude and durability of vaccine responses in mice and non-human primates and induced neutralizing antibodies against high-escape variants, addressing antigenic imprinting limitations. These results support a rational adjuvant approach to improve mRNA vaccine breadth and longevity by tuning innate PRR-driven inflammation.
Jena KK, Qu P, Baracco L et al. · Nature immunology · (2026) · View on PubMed ↗ · Free PDF ↗
Mitochondrial complex I activity promotes antigen cross-presentation in dendritic cells.
The study investigated how mitochondrial electron transport chain complex I controls antigen cross-presentation by dendritic cells in mice, focusing on the complex I subunit NDUFS4. DC-specific NDUFS4 deficiency disrupted complex I subcomplex formation, limited endosomal escape of internalized antigens, and impaired antigen cross-presentation while largely preserving direct presentation. This mechanistic link between complex I activity and cross-presentation highlights mitochondrial complex I as a metabolic checkpoint that could be leveraged to enhance vaccine and anti-tumor immunity.
Khouili SC, Priego E, Heras-Murillo I et al. · Science immunology · (2026) · View on PubMed ↗
Spermidine Mitigates Immune Cell Senescence and Boosts Vaccine Responses in Healthy Older Adults-A Pilot Study.
This double-blind, randomized, placebo-controlled pilot study tested whether daily oral spermidine supplementation (6 mg for 13 weeks) improves vaccine-induced immunity in 40 healthy adults over 65 years following their third SARS-CoV-2 vaccine dose. The key finding was that spermidine was well tolerated and enhanced vaccine responses while mitigating immune cell senescence-related changes associated with immunosenescence. This supports spermidine as a potential geroprotective adjunct to improve COVID-19 vaccine effectiveness in older adults.
Alsaleh G, Ali M, Kayvanjoo AH et al. · Aging cell · (2026) · View on PubMed ↗ · Free PDF ↗
GLP-1/GIP-Based Metabolic Therapies & Obesity/Cancer Outcomes
GLP-1 RAs May Prevent Metastatic Progression.
This study examined whether initiating a glucagon-like-peptide-1 receptor agonist (GLP-1 RA) after diagnosis of stage I–III obesity-related cancers (lung, breast, colorectal, or liver) could reduce progression to stage IV. The key finding was that post-diagnosis GLP-1 RA use was associated with prevention of metastatic/progression advancement to stage IV in these earlier-stage populations. If confirmed in prospective trials, GLP-1 RAs could become a repurposed adjunct strategy to improve outcomes in obesity-associated early-stage cancers.
Cancer discovery · (2026) · View on PubMed ↗
Novel Amylin-Based Therapies for Weight Management in Adults With Overweight or Obesity Without Diabetes: A Network Meta-Analysis.
This frequentist random-effects network meta-analysis compared novel long-acting amylin-based therapies (ABTs) versus placebo or active comparators in randomized trials of adults with overweight or obesity without diabetes, focusing on percent body-weight change and gastrointestinal adverse events. ABTs were ranked for weight and anthropometric improvements while also assessing overall and specific GI safety outcomes across doses. Clinically, the analysis helps prioritize which amylin-based agent and dose may provide the best balance of efficacy and tolerability for non-diabetic obesity.
Kamrul-Hasan ABM, Khalil I, Mahajan K et al. · Endocrinology, diabetes & metabolism · (2026) · View on PubMed ↗ · Free PDF ↗
Semaglutide versus placebo in individuals with poor weight loss after bariatric surgery: a double-blinded, randomized, placebo-controlled trial.
This double-blind, randomized, placebo-controlled trial studied semaglutide 2.4 mg weekly versus placebo as an adjunct to lifestyle intervention in adults at least 1 year after bariatric surgery (gastric bypass or sleeve gastrectomy) with poor weight loss (<20% from surgery), in the BARI-STEP population. The key finding is that semaglutide was tested to determine whether it improves percentage weight loss over 68 weeks compared with placebo in this post-bariatric subgroup (primary outcome defined as intention-to-treat weight loss). Clinically, the trial addresses whether GLP-1 receptor agonist therapy can rescue suboptimal metabolic/bariatric surgery responses and improve long-term weight outcomes.
Stanley C, Mallik R, Hamid N et al. · Nature medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Semaglutide drives weight loss through cAMP-dependent mechanisms in GLP1R-expressing hindbrain neurons.
This work examined how semaglutide signals in GLP1R-expressing hindbrain neurons in the area postrema (APGlp1r), using neuronal signaling readouts to define intracellular pathways. It found that semaglutide activates both Gs- and Gq-dependent signaling in Glp1r-expressing neurons and produces graded increases in the secondary messenger cAMP across neuronal clusters, with differential neuronal activation patterns. Scientifically, it clarifies intracellular mechanisms downstream of GLP1R that likely underlie semaglutide-driven appetite/weight effects.
Gao C, Geneve IC, Rodriguez-Gonzalez S et al. · Nature metabolism · (2026) · View on PubMed ↗ · Free PDF ↗
Cardiovascular Pharmacology & Cardiorenal Protection
Rethinking Post-Infarction Remodeling: Identification and Validation of Data-Driven Cardiac MRI Phenotypes for Risk Stratification.
This prospective longitudinal study used unsupervised clustering of cardiac MRI (CMR) measurements to identify prognostic adverse left ventricular remodeling (ALVR) phenotypes in reperfused ST-elevation myocardial infarction (STEMI) patients, with derivation (n=337) and independent validation (n=190) cohorts. The key finding was that data-driven CMR remodeling phenotypes provided better risk stratification than conventional ALVR definitions based on changes in left ventricular end-diastolic volume index and ejection fraction. Clinically, this phenotype-based CMR approach could improve post-STEMI prognosis prediction and guide individualized follow-up and therapy.
Xiang JY, Wu J, Zhao Y et al. · European heart journal. Cardiovascular Imaging · (2026) · View on PubMed ↗
Endothelial soluble APP/APLP2 promote heart repair through KIT-mediated angiogenesis.
This work studied the physiological role of endothelial amyloid precursor protein (APP) and amyloid precursor-like protein 2 (APLP2) in postischemia angiogenesis after myocardial infarction (MI) using mouse models with endothelial APP/APLP2 loss. Endothelial hypoxia induced α-secretase activity to generate soluble APPsα and APLP2sα, and loss of endothelial APP/APLP2 reduced neovascularization while increasing heart failure and mortality after MI. The results identify endothelial APP/APLP2 as pro-repair regulators via KIT-mediated angiogenesis, suggesting potential therapeutic targets to improve cardiac recovery after ischemic injury.
Kawase H, Liu S, Kurz S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Finerenone in Cardiorenal Disease: A Narrative Review of Molecular Mechanisms, Clinical Evidence, and Emerging Therapeutic Roles.
This narrative review analyzed finerenone, a non-steroidal selective mineralocorticoid receptor (MR) antagonist, focusing on molecular mechanisms and clinical evidence in cardiorenal disease. The review highlights that MR overactivation drives cardiac and renal injury beyond blood-pressure effects and that finerenone’s receptor selectivity and tissue distribution translate into anti-inflammatory and antifibrotic benefits compared with steroidal MR antagonists. Scientifically and clinically, the synthesis supports finerenone’s emerging therapeutic role as a targeted MR-modulating strategy for cardiorenal protection.
Geraci G, Sinatra N, Paternò V et al. · Cardiovascular drugs and therapy · (2026) · View on PubMed ↗ · Free PDF ↗
SREBP1 Transactivation of NHE3 Impairs Cardiac Contraction and Aggravates Heart Failure.
This study investigated how the metabolic transcription factor SREBP1 (sterol regulatory element-binding protein 1) transactivates NHE3 (Na+/H+ exchanger 3) to impair cardiac contraction and worsen heart failure in human HFrEF tissue and mouse models of transverse aortic constriction (TAC). The key finding was that SREBP1-driven NHE3 dysregulation disrupts cardiomyocyte ion handling (Na+/H+ and Ca2+ cycling) and contributes to reduced contractility in HFrEF. Scientifically, it links SREBP1 signaling to specific ion-transport mechanisms, suggesting NHE3/SREBP1 pathways as potential therapeutic targets for HFrEF.
Gu H, Wen J, Liu Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗
Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation.
This study examined the role of the RNA-binding protein Sam68 (KHDRBS1) in pathologic cardiac hypertrophy by testing its effects on cardiomyocyte glucose oxidation in failing human hearts and in cardiomyocyte-specific Sam68 knockout mice (Sam68cKO), including models of cardiac stress. The key finding was that Sam68 exacerbates pathological hypertrophy by suppressing cardiomyocyte glucose oxidation, thereby promoting maladaptive metabolic remodeling. Clinically, targeting Sam68-mediated metabolic control could represent a strategy to mitigate progression of heart failure–associated hypertrophy.
An J, Han C, Jiang Y et al. · Circulation · (2026) · View on PubMed ↗ · Free PDF ↗
[Glucagon-like peptide-1 agonists and heart failure].
This narrative review summarized evidence on glucagon-like peptide-1 receptor agonists (GLP-1 RAs), focusing on cardiovascular outcomes in heart failure populations. The key finding was that semaglutide and tirzepatide have shown benefits in obesity-associated heart failure with preserved or mildly reduced ejection fraction (e.g., fewer hospitalizations and improved symptoms/functional capacity), while evidence remains limited for heart failure with reduced ejection fraction. Clinically, it provides practical guidance on where GLP-1 RAs may fit in current heart failure care and highlights gaps for HFrEF.
Soborun N, Favre L, Lu H et al. · Revue medicale suisse · (2026) · View on PubMed ↗
Lipid-Lowering Therapies (PCSK9 & Beyond)
Efficacy and Safety of Oral PCSK9 Inhibitors: Insights from a Meta-analysis of RCTS.
This meta-analysis of randomized controlled trials evaluated oral PCSK9 inhibitors for lipid lowering, comparing oral agents versus placebo and pooling LDL-C and other lipid changes. The key finding was the magnitude of LDL-C reduction and associated lipid effects across RCTs of oral PCSK9 inhibitors (including siRNA inclisiran and other oral approaches) relative to placebo. Scientifically, it clarifies efficacy and safety signals for oral PCSK9 strategies that could improve adherence compared with injectable monoclonal antibodies (evolocumab, alirocumab).
Olmastroni E, Xie S, Galimberti F et al. · European journal of preventive cardiology · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer Immunotherapy: Checkpoint Resistance & Immune Evasion
Outcomes of Patients With Hepatocellular Carcinoma Treated With Durvalumab Plus Tremelimumab in Real-World Clinical Practice Who Met or Did Not Meet the Inclusion Criteria for the Phase 3 HIMALAYA Trial.
This real-world cohort study evaluated outcomes of unresectable hepatocellular carcinoma patients treated with durvalumab plus tremelimumab (Dur/Tre) at 30 Japanese institutions, stratifying 92 patients who met versus 320 who did not meet the phase 3 HIMALAYA trial eligibility criteria. Progression-free survival was longer in the HIMALAYA-eligible group (median 5.4 vs 3.0 months; p=0.012). These findings suggest that HIMALAYA trial eligibility criteria may identify a subgroup with better Dur/Tre benefit in routine practice, supporting more tailored patient selection for immunotherapy in HCC.
Matono T, Tada T, Hiraoka A et al. · Journal of gastroenterology and hepatology · (2026) · View on PubMed ↗
PTEN deficiency impairs MHC-I-mediated tumour immunity via NRF2-dependent autophagy in microsatellite stable colorectal cancer.
This study examined how PTEN deficiency affects immune checkpoint blockade (ICB) resistance in microsatellite stable (MSS) colorectal cancer (CRC), using integrative clinical/TCGA analyses plus single-cell RNA sequencing and flow cytometry. PTEN loss promoted impaired MHC-I-mediated tumor immunity through NRF2-dependent autophagy, contributing to immune exclusion and reduced ICB responsiveness. These findings identify a PTEN–NRF2–autophagy axis as a mechanistic driver of MSS CRC immune evasion and a potential therapeutic target to improve ICB outcomes.
Cai R, Zhan W, Lyu X et al. · Gut · (2026) · View on PubMed ↗ · Free PDF ↗
Overcoming Primary and Acquired Resistance to Immunotherapy in Non-Small Cell Lung Cancer: Mechanisms, Challenges, and Emerging Strategies.
This review synthesized current evidence on mechanisms of primary and acquired resistance to immune checkpoint inhibitors (ICIs) in non-small cell lung cancer (NSCLC), emphasizing tumor evolution, immune escape, and metabolic reprogramming. Key resistance pathways include impaired antigen presentation (e.g., β2-microglobulin and HLA alterations), T-cell exhaustion, and tumor microenvironment remodeling, with emerging strategies targeting checkpoints such as TIGIT and LAG-3 and using epigenetic modulators (e.g., HDAC and DNMT inhibitors). Understanding these mechanisms is clinically important to guide combination therapies that restore durable anti-tumor immunity in NSCLC.
Hidalgo-Filho CM, Santo V, Gariazzo E et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗
Ablation of the adhesion G protein-coupled receptor ADGRL1 activates anti-tumor immune response via cDC1-T cell hub formation.
This study examined whether ablation of the adhesion G protein-coupled receptor ADGRL1 can trigger anti-tumor immune responses by promoting cDC1–CD8+ T cell hub formation, using a Drosophila tumor model with RNAi screening and single-cell transcriptomics. ADGRL1 ablation activated type I interferon signaling and promoted JAK/STAT1-dependent Decorin secretion through disruption of the GSK3β/β-catenin pathway, enabling cDC1–CD8+ T cell hub formation and anti-tumor immunity. The findings position ADGRL1 as a promising immunotherapy target by defining a specific immune-activation axis that could be translated to mammalian cancer contexts.
Cheng G, Wu J, Wang Y et al. · Cell reports · (2026) · View on PubMed ↗ · Free PDF ↗
Efficacy and safety of first-line osimertinib in Chinese patients with EGFR-mutated advanced non-small cell lung cancer: a prospective, multicenter, non-interventional study (FLOURISH).
This prospective, multicenter, non-interventional real-world study evaluated first-line osimertinib in treatment-naïve adults (≥18 years) with locally advanced or metastatic EGFR-mutated non-small cell lung cancer (NSCLC) in China (FLOURISH). The key finding was that osimertinib delivered in routine practice provided real-world efficacy and safety outcomes consistent with its established benefit in EGFR-mutated NSCLC, with time to treatment discontinuation (TTD) as the primary endpoint. This supports the clinical effectiveness and tolerability of first-line osimertinib for EGFR-mutated advanced NSCLC in Chinese patients outside randomized trials.
Shen L, Lv D, Tang KJ et al. · Cancer biology & medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Reprogramming the immune suppressive tumor microenvironment in glioma enhances the efficacy of immune-mediated gene therapy.
This study examined how mutant IDH1 (IDH1 R132H; mIDH1) reprograms the glioma tumor microenvironment (TME) to enhance immune-mediated gene therapy efficacy, focusing on adenosine production via the ectoenzyme CD73. It found that mIDH1 glioma cells show reduced CD73 expression driven by DNA hypermethylation, leading to lower adenosine levels and a more immune-permissive TME. Scientifically, this identifies the mIDH1–CD73/adenosine axis as a mechanism to improve immunotherapy responsiveness in glioma.
McClellan BL, Peña Agudelo JA, Mujeeb AA et al. · Molecular therapy. Oncology · (2026) · View on PubMed ↗
Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr-mutated lung cancer.
This preclinical study tested whether a stimulator of interferon genes (STING) agonist augments antitumor immunity when combined with osimertinib in EGFR-mutated non-small-cell lung cancer using a syngeneic genetically engineered mouse model. The key finding was that combining STING agonist ADU-S100 with osimertinib produced stronger systemic antitumor immune activation than either treatment alone, assessed using immunohistochemistry and flow cytometry of the tumor microenvironment. This supports a rational combination strategy to convert a noninflamed EGFR-mutant tumor microenvironment into one more responsive to immunotherapy.
Nishimura J, Kuribayashi T, Brägelmann J et al. · Molecular oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer Immunotherapy: Cell Therapy (CAR T) & Combination Strategies
Chlorella Polysaccharide Extract Attenuates Skin Aging via MAPK Pathway Suppression: Implications for Cosmetic Dermatology.
This study evaluated whether chlorella polysaccharide extract (CPE) attenuates skin aging in an oxidative-stress-induced zebrafish model and explored mechanism via suppression of the MAPK pathway. The key finding was that CPE reduced oxidative stress and senescence markers (including ROS, MDA, SA-β-gal activity, and inflammatory/neutrophil infiltration) while improving antioxidant enzyme activities (SOD, CAT) and increasing IL-10, alongside MAPK pathway inhibition. In cosmetic dermatology, these results support CPE as a candidate anti-aging ingredient with a defined MAPK-targeted mechanism.
Zhang M, Guo Y, Jiang X et al. · Journal of cosmetic dermatology · (2026) · View on PubMed ↗ · Free PDF ↗
Tumor irradiation promotes antigen dressing of dendritic cells to enhance CAR T cell persistence and efficacy in lung metastases.
This study used syngeneic mouse models of extensive metastatic lung adenocarcinoma and melanoma to test whether tumor irradiation improves CAR T cell persistence and efficacy, focusing on dendritic cell (DC) dependence. Delivering 8 Gy tumor irradiation enhanced CAR T cell persistence in a DC-dependent manner by promoting trogocytic antigen dressing of tumor antigens onto DCs, which then supported CAR T expansion. These findings suggest a practical combination strategy—local irradiation plus CAR T therapy—to widen the therapeutic window by boosting tumor-site antigen presentation while limiting off-tumor toxicity.
Navarre S, Ishibashi MN, Nair A et al. · Nature cancer · (2026) · View on PubMed ↗ · Free PDF ↗
Prolonged Cytokine Release Syndrome Is Associated With Hypofibrinogenemia After CD19-Directed CAR T-Cell Therapy in Adult Patients With Relapsed/Refractory Lymphoma.
This retrospective real-world cohort study assessed the incidence, risk factors, and clinical impact of hypofibrinogenemia after CD19-directed CAR T-cell therapy in adult patients with relapsed/refractory B-cell lymphoma. Prolonged cytokine release syndrome (CRS) was associated with hypofibrinogenemia, linking severe inflammatory toxicity to coagulation abnormalities after CAR T. The results support closer coagulation monitoring and CRS management to reduce bleeding risk and improve safety in CD19 CAR T recipients.
Bamba S, Jo T, Kitawaki T et al. · Transplantation and cellular therapy · (2026) · View on PubMed ↗ · Free PDF ↗
Tumor Microenvironment, Metastasis & Intratumoral Microbiota
Reprogramming the Immune Landscape of Inflammatory Breast Cancer.
This article reviewed how inflammatory breast cancer (IBC) remodels the tumor microenvironment to promote immune evasion and therapeutic resistance, emphasizing cytokine signaling loops, immune checkpoint overexpression, and tumor emboli that shield cancer cells from immune surveillance. The key finding was that multi-omics and spatial transcriptomic studies reveal extensive, spatially organized immune alterations that drive IBC aggressiveness. The scientific significance is that mapping the IBC immune landscape can identify actionable biomarkers and guide development of more effective immunotherapy or combination strategies.
Martinez-Rodriguez V, Ogata S, Wang X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Intratumoral microbiota in cancer: molecular mechanism and therapeutic strategies.
This review summarized emerging evidence on intratumoral microbiota (ITM), focusing on how microbial localization and host interactions shape cancer phenotypes and therapeutic outcomes. The key finding is that ITM can directly influence tumor genomic stability, signaling, metabolism, and cellular plasticity while indirectly modulating tumor evolution through effects on immune responses. These mechanistic insights support new therapeutic strategies that target ITM spatial organization and host–microbe interactions to improve cancer treatment responses.
Yu Y, Guo Z, Luo Z et al. · Molecular biomedicine · (2026) · View on PubMed ↗ · Free PDF ↗
Bioinformatics Combined With Biological Experiments to Explore the Promotion of Lung Metastasis by CCL18 in the Immune Microenvironment of Colorectal Cancer.
This study used GEO/TCGA bioinformatics and downstream biological experiments to identify genes and mechanisms by which CCL18 promotes lung metastasis in the immune microenvironment of colorectal cancer (CRC). It found CCL18-associated molecular programs linked to prognostic DEGs and immune microenvironment features that support lung metastatic progression. These findings suggest CCL18 and its immune-metastasis network as potential biomarkers and therapeutic targets to improve outcomes in CRC patients at risk for pulmonary metastasis.
Xia Q, Yin S, Chen J et al. · Human mutation · (2026) · View on PubMed ↗ · Free PDF ↗
Cancer Signaling, Metabolism & Targetable Molecular Pathways
FARP1 Mediates cMET-Driven Motility in Androgen-Independent Prostate Cancer Cells.
This study investigated how FARP1 regulates cMET-driven motility in androgen-independent prostate cancer cells, focusing on Rac1 signaling and actin-rich protrusion formation. The key finding was that FARP1 mediates cMET-dependent motility by functioning within the Rac1 activation pathway that drives invasive cytoskeletal dynamics. Scientifically, identifying FARP1 as a cMET motility mediator highlights a potential therapeutic target to limit metastatic behavior in advanced, androgen-independent prostate cancer.
Robayo P, Kazanietz MG, Baker MJ et al. · Endocrinology · (2026) · View on PubMed ↗
Stress granules restrain ferroptosis by sequestering ferritin.
This study investigated how stress granules (SGs) affect ferroptosis in glioblastoma stem cells (GSCs) exposed to irradiation (IR) and temozolomide (TMZ). It found that disrupting SGs sensitizes GSCs to IR/TMZ-induced ferroptosis, with SG protein profiling showing recruitment of ferritin and mechanistic dependence on G3BP1 interacting with ferritin light chain via G3BP1 methionine-333 oxidation to sequester ferritin in SGs and limit Fe2+ and ferritinophagy. The significance is that SG–ferritin coupling via G3BP1 can be targeted to enhance ferroptosis-based vulnerability in treatment-resistant GSCs.
Ge Z, Wang Z, Zhao E et al. · Nature cell biology · (2026) · 1 citations · View on PubMed ↗
Iron overload in the tumor microenvironment induces CD8+ T cell ferroptosis and dysfunction.
This study examined how iron overload in the tumor microenvironment (TME) affects CD8+ T cells, focusing on iron levels in tissues populated by CD8+ T cells and downstream cell fate. It found that the TME is iron-enriched (unlike systemic iron deficiency) and that this iron overload triggers CD8+ T cell ferroptosis and dysfunction, mechanistically linked to tumor necrosis and tumor-derived hepcidin alongside TCR hyperactivation. The significance is that it identifies iron-driven ferroptosis as a mechanism of CD8+ T cell impairment in cancer, suggesting iron/hepcidin/ferroptosis pathways as immunotherapy-relevant targets.
Lin Z, Chen H, Ke Y et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
MARCHF6 orchestrates hepatic lipid homeostasis by targeting SREBP1 for ER-associated degradation.
This study investigated the role of the ER-associated degradation (ERAD) E3 ubiquitin ligase MARCHF6 in hepatic lipid homeostasis and MASLD pathogenesis, using liver-specific Marchf6 knockout models. MARCHF6 promoted SREBP1 turnover via ER-associated degradation, thereby regulating de novo lipogenesis and protecting against lipid accumulation. Clinically, targeting the MARCHF6–SREBP1 degradation pathway could represent a strategy to treat MASLD by modulating post-translational control of lipogenesis.
Xu Y, Yue T, Batbold U et al. · Journal of hepatology · (2026) · View on PubMed ↗
Emerging roles of combined curcumin and berberine in disease modulation: a comprehensive review of mechanisms and therapeutic relevance.
This narrative review evaluated combined curcumin and berberine as disease-modulating agents by synthesizing mechanistic evidence across multiple conditions. The key finding is that curcumin and berberine share multifaceted bioactivities (e.g., antioxidant, anti-inflammatory, antimicrobial, and anticancer effects) and may act through overlapping and complementary molecular pathways relevant to diseases such as NAFLD, malignancies, and neurodegeneration. Therapeutically, the review supports continued preclinical and clinical investigation of curcumin–berberine combinations as multi-target interventions.
Ghoflchi S, Vatanparast RG, Jalili-Nik M et al. · Molecular biology reports · (2026) · View on PubMed ↗
Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.
This study examined the role of renal insulin-like growth factor binding protein 6 (IGFBP6) and its interaction with thrombospondin-1 (THBS1) in driving renal cellular senescence and fibrosis in chronic kidney disease models. It found that global or tubule-specific IGFBP6 knockout attenuated senescence and fibrosis in mice, preserved epithelial phenotype, inhibited fibroblast activation, and that anti-IGFBP6 treatment showed therapeutic promise. These results support IGFBP6–THBS1 signaling as a mechanistic target for anti-fibrotic interventions in CKD.
Yu JT, Xu CG, Hu XW et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Master Regulator SMC1A, Stabilized by N6-Methyladenosine Reader IGF2BP1, Promotes HCC Progression Through Facilitating Enhancer-Promoter Interaction of Nestin.
This study investigated how the cohesin subunit SMC1A acts as a master regulator in hepatocellular carcinoma (HCC) progression, focusing on its stabilization by the m6A reader IGF2BP1 and its downstream control of enhancer–promoter interactions involving the stemness marker nestin. Using ICGC and single-cell datasets plus validation in tissue microarrays and clinical specimens, and mechanistic assays combining transcriptomics, chromatin analyses, and post-transcriptional/m6A-dependent experiments (including patient-derived organoids), it found that IGF2BP1-stabilized SMC1A promotes HCC progression via nestin enhancer–promoter facilitation. Scientifically and therapeutically, the work positions the IGF2BP1–SMC1A–nestin axis as a potential target, with siRNA-based delivery explored for intervention.
Peng Z, Wen D, Zeng L et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
DNA hypomethylation-activated PRAME drives early-stage lung adenocarcinoma recurrence via ZNF740 and PI3K/AKT/mTOR signaling.
This study investigated how DNA hypomethylation activates PRAME to drive early-stage lung adenocarcinoma (LUAD) recurrence, using molecular pathway analyses and functional experiments to connect PRAME with ZNF740 and PI3K/AKT/mTOR signaling. It showed that hypomethylation-induced PRAME promotes recurrence via ZNF740-dependent activation of the PI3K/AKT/mTOR pathway. Scientifically and clinically, targeting the PRAME–ZNF740–PI3K/AKT/mTOR axis could represent a strategy to prevent or treat early LUAD relapse.
Zhu GN, Zheng Q, Yang P et al. · Translational lung cancer research · (2026) · View on PubMed ↗ · Free PDF ↗
Gastroenterology: Ulcerative Colitis & IBD Therapeutics
Lonely minds, inflamed guts: metabolic and circulating protein pathways linking social isolation and loneliness to inflammatory bowel disease.
This UK Biobank analysis studied associations between social isolation/loneliness and inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, using metabolomic and circulating protein data. It analyzed 275,157 adults with metabolomics in 68,362 and proteomics in 29,339 to identify metabolic and protein pathway alterations related to loneliness/social isolation that associate with IBD risk. The significance is that it connects psychosocial stress exposures to measurable circulating molecular pathways that may help explain gut-brain links and identify biomarkers for IBD susceptibility.
Zhao J, Ye J, Zhang M et al. · Translational psychiatry · (2026) · View on PubMed ↗ · Free PDF ↗
Does inflammatory bowel disease play a role in cognitive decline? A systematic review.
This systematic review evaluated observational and preclinical studies on whether inflammatory bowel disease (IBD) is associated with cognitive impairment and dementia in human populations and experimental models. Across the literature, the relationship appears influenced by proposed mechanisms including chronic inflammation, gut–brain axis dysfunction, and psychological comorbidities, but findings remain heterogeneous and mechanistically unresolved. Clarifying these pathways is clinically important for identifying IBD patients at risk of cognitive decline and for targeting modifiable contributors to preserve cognitive health.
Motisi Bertulli A, Bezzio C, Marsano S et al. · Journal of Crohn’s & colitis · (2026) · View on PubMed ↗
Anti-TNF Drug-Induced Sarcoidosis in Inflammatory Bowel Diseases: Multicentric Case Series and Literature Review.
This retrospective international multicentric case series and literature review studied anti-TNF drug-induced sarcoidosis reaction (DISR) in patients with inflammatory bowel diseases (IBD) receiving anti-TNF therapy. The key finding was identification of nine new long-follow-up DISR cases (median follow-up ~45 months) plus 26 total cases after literature review, highlighting the clinical overlap between sarcoidosis and IBD and the association with anti-TNF exposure. Clinically, recognizing anti-TNF-related DISR is important for timely diagnosis and management in IBD patients who develop granulomatous symptoms during biologic therapy.
Bez P, Chkolnaia Z, Aratari A et al. · BioMed research international · (2026) · View on PubMed ↗ · Free PDF ↗
Comparative effectiveness and safety of biologics and targeted small-molecule therapies plus stable background therapy in systemic lupus erythematosus: a systematic review and network meta-analysis.
This systematic review and network meta-analysis compared biologics and targeted small-molecule therapies added to stable background therapy for systemic lupus erythematosus (SLE) using randomized controlled trials. Across efficacy endpoints such as SRI-4 and BICLA responses, the analysis synthesized relative benefits and safety profiles among treatment classes. The findings are significant for evidence-based selection of advanced SLE therapies by balancing response rates and adverse-event risk.
Li W, Zhao Y, Shu S et al. · Frontiers in immunology · (2026) · View on PubMed ↗ · Free PDF ↗
Biomarkers & Risk Stratification in Oncology
First-Line Systemic Treatments for Metastatic Hormone-Sensitive Prostate Cancer: Updated Systematic Review and Network Meta-analysis.
This updated systematic review and frequentist random-effects network meta-analysis studied first-line systemic combination therapies for metastatic hormone-sensitive prostate cancer (mHSPC), comparing progression-free survival/overall survival and severe adverse events across randomized controlled trials. It synthesized comparative efficacy and safety evidence for intensified combination regimens used in the modern treatment landscape. The findings are significant for clinicians selecting optimal first-line combinations to improve survival while balancing severe toxicity in mHSPC.
Miyajima K, Miszczyk M, Matsukawa A et al. · The Journal of urology · (2026) · View on PubMed ↗ · Free PDF ↗
A Mitoxyperilysis-Related Single-Cell and Machine-Learning Framework Defines an Immune-Cold Melanoma Phenotype and a Robust Prognostic Signature.
This work analyzed melanoma single-cell RNA-seq data (GSE215120) to build a mitoxyperilysis-related score (MRS) and used machine-learning and cell-cell communication inference to define an immune-cold melanoma phenotype. MRS-high tumors showed stronger predicted intercellular communication and distinct malignant and immune cell-state heterogeneity compared with MRS-low tumors, yielding a robust prognostic signature. Clinically, the MRS may help stratify melanoma patients by immune phenotype and prognosis and guide selection of immunotherapy-responsive subgroups.
Zhou Y, Fang J, Fei L et al. · Human mutation · (2026) · View on PubMed ↗ · Free PDF ↗
Baseline neutrophil-to-eosinophil ratio and neutrophil-to-lymphocyte ratio as prognostic markers in patients with unresectable biliary tract cancer treated with gemcitabine-cisplatin-durvalumab: an international, multicentre, retrospective cohort study.
This retrospective multicentre cohort study assessed whether baseline neutrophil-to-eosinophil ratio (NER) and neutrophil-to-lymphocyte ratio (NLR) predict outcomes in unresectable biliary tract cancer treated with gemcitabine-cisplatin-durvalumab (anti–PD-L1). It found that pretreatment NER and/or NLR were associated with prognosis and could stratify patients likely to have different survival outcomes under this immunochemotherapy regimen. These biomarkers may help personalize treatment intensity and follow-up planning for advanced BTC patients receiving durvalumab-based therapy.
Vandeputte H, Casadei-Gardini A, Peeters F et al. · ESMO gastrointestinal oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Pulmonary Disease: Fibrosis, PAH, Lung Cancer Risk & Management
Combined Upadacitinib and Vedolizumab as 8-Week Induction Therapy for Moderate-to-Severe Ulcerative Colitis: A Multicenter, Randomized Controlled Trial.
This multicenter, randomized, open-label superiority trial studied whether 8-week induction with upadacitinib plus vedolizumab, followed by vedolizumab maintenance, improves outcomes versus vedolizumab monotherapy in adults with moderate-to-severe ulcerative colitis. The key finding reported in the abstract is that the combination induction regimen was evaluated for superiority on clinical and endoscopic endpoints compared with standard vedolizumab alone. If effective, this regimen could raise induction efficacy beyond the current “ceiling” for endoscopic remission in UC by combining a JAK inhibitor (upadacitinib) with an anti-integrin biologic (vedolizumab).
Yao J, Wu H, Wu L et al. · Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · (2026) · View on PubMed ↗
Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.
This study investigated early mechanisms of inflammation-driven pulmonary fibrosis by integrating multi-omics analyses with animal models. It found that acute inflammation triggered stronger immune amplification alongside mitochondrial dysfunction and reactive oxygen species (ROS) accumulation in the lung, which then initiated fibrotic signaling. The work highlights mitochondrial/ROS pathways as early drivers of fibrotic remodeling in sepsis and suggests potential targets for preventing progression to irreversible lung fibrosis.
Zhong Z, Wu K, Wang J et al. · Redox biology · (2026) · View on PubMed ↗ · Free PDF ↗
Hemodynamic and metabolomic responses to infusion of GLP-1 agonist exenatide in pulmonary arterial hypertension.
This first-in-disease clinical study evaluated acute hemodynamic and metabolomic responses to intravenous exenatide, a GLP-1 agonist, in patients with idiopathic pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) during right heart catheterization, and in a monocrotaline (MCT) PAH rat model using cardiac magnetic resonance imaging. Exenatide was well tolerated and acutely reduced mean pulmonary artery pressure while producing measurable circulating metabolite changes across multisite sampling. The results suggest GLP-1 receptor agonism may rapidly modulate pulmonary vascular physiology in PAH/CTEPH and provide metabolomic signals for mechanism and future therapeutic trials.
Samaranayake CB, Niglas M, Baxan N et al. · JCI insight · (2026) · View on PubMed ↗ · Free PDF ↗
Refining the Definition for “Low Risk” in Pulmonary Arterial Hypertension: Time to Reduce Morbidity and Mortality.
This analysis studied how to refine the definition of “low risk” in pulmonary arterial hypertension (PAH) by using patient-level data from a harmonized dataset of 8 PAH randomized controlled trials and leveraging REVEAL 2.0 risk score concepts. It proposed extending the <5% 1-year mortality threshold to a 3-year horizon and adding a morbidity criterion at 1 year to better reflect treatment-era outcomes. Clinically, a more stringent low-risk definition could reduce morbidity and mortality by improving risk stratification and guiding treatment intensity.
Fauvel C, Jaque PC, Liu Y et al. · JACC. Heart failure · (2026) · View on PubMed ↗
Occupational physical workload and risk of lung cancer and chronic respiratory diseases: a prospective cohort study of the UK Biobank.
This prospective cohort study in 221,845 UK Biobank participants evaluated whether occupational physical workload predicts incident lung cancer and chronic respiratory diseases (COPD, asthma, and idiopathic pulmonary fibrosis). It found that baseline occupational physical workload was associated with subsequent risks of lung cancer and specific chronic respiratory outcomes after accounting for available confounders. The results support occupational workload as a potentially modifiable risk factor and motivate further mechanistic and risk-stratification research.
Ma S, Liu Y, Wang Z et al. · Translational lung cancer research · (2026) · View on PubMed ↗ · Free PDF ↗
Neurology: Neurodegeneration, Pain & Neuroimmune Interfaces
Electroacupuncture Improves the Learning and Memory by Modulating Hippocampal Glucose Metabolism through IGF1/IGF1R Signaling in Alzheimer’s Disease.
This study tested whether electroacupuncture (EA) improves learning and memory in a 5×FAD mouse model of Alzheimer’s disease by modulating hippocampal glucose metabolism via IGF1/IGF1R signaling. The key finding was that EA reduced β-amyloid deposition and attenuated learning/memory deficits while enhancing hippocampal glucose metabolism and information processing in brain metabolic networks. These results suggest EA could be a non-pharmacologic strategy that targets IGF1/IGF1R-linked metabolic dysfunction in AD.
Liang S, Zhang Q, Wang X et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) · (2026) · View on PubMed ↗ · Free PDF ↗
Comparison of blood dopamine in Parkinson’s patients treated with levodopa carbidopa entacapone vs levodopa benserazide: A randomized controlled trial.
This prospective, single-center randomized controlled trial compared short-term plasma dopamine effects in early-stage, unilateral Parkinson’s disease patients treated with levodopa/carbidopa/entacapone (LCE) versus levodopa/benserazide (LB). The study found differential biochemical dopamine responses between the two levodopa combination regimens. Scientifically, it clarifies how adjunct components (entacapone vs benserazide) influence dopamine bioavailability, which may inform optimization of early Parkinson’s pharmacotherapy.
Korucu O, Özdemir S, Türkeş GF et al. · Medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Mitochondrial DNA release contributes to neuropathic pain via a cGAS-STING-IRF3-CMPK2-associated immunometabolic feedback mechanism.
This mouse study investigated whether mitochondrial DNA (mtDNA) release drives neuropathic pain through a cGAS–STING–IRF3–CMPK2 immunometabolic feedback mechanism after peripheral nerve injury. mtDNA release in the spinal cord activated the cGAS–STING–IRF3 pathway and was linked to CMPK2-associated immunometabolic signaling, with genetic silencing of CMPK2 implicating this axis in pain-related neuroinflammation. These mechanistic findings identify the mtDNA–cGAS–STING–IRF3–CMPK2 pathway as a potential therapeutic target to reduce neuropathic pain.
Wang B, Zeng H, Zhan H et al. · Journal of translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Dual orexin receptor antagonism with lemborexant enhances microglial clearance of β-amyloid in mice.
This preclinical study tested whether dual orexin receptor antagonism with lemborexant improves amyloid-beta pathology and microglial clearance in PSAPP transgenic mice compared with doxepin or vehicle. Lemborexant enhanced microglial clearance of β-amyloid and reduced amyloid pathology, with effects depending on treatment timing relative to plaque onset. The results support repurposing the FDA-approved DORA lemborexant as a strategy to modulate sleep-related risk and amyloid-driven neuroinflammation in Alzheimer’s disease models.
Sharma A, Segawa E, Chen X et al. · Molecular neurodegeneration · (2026) · View on PubMed ↗ · Free PDF ↗
Tryptophan Metabolism at the Crossroads of Immunity, Barrier Function, and the Microbiome in Atopic Dermatitis.
This narrative review synthesized evidence on how tryptophan (TRP) metabolism—via the kynurenine pathway, microbial indole production, and the serotonin–melatonin axis—links immune dysregulation, barrier dysfunction, and microbiome changes in atopic dermatitis. It summarizes how TRP-derived metabolites can modulate cutaneous inflammation, immune responses, and barrier integrity across preclinical and clinical studies. Scientifically, it highlights TRP metabolic pathways as actionable mechanistic nodes that may guide future AD biomarkers and therapies.
Tan Y, Peng G, Abudouwanli A et al. · Clinical reviews in allergy & immunology · (2026) · View on PubMed ↗
Micro- and nanoplastics in the central nervous system: Transport pathways, neurotoxicity, and implications for brain disorders.
This review summarized current evidence on how micro- and nanoplastics (MNPs) enter and exit the central nervous system (CNS), their transport pathways, and their neurotoxicity and links to brain disorders. It highlights that small MNPs are difficult to clear from the brain and may accumulate, potentially contributing to neurotoxic effects through mechanisms such as blood–brain barrier crossing, nasal-to-brain routes, and glymphatic transport. Scientifically, the review consolidates transport-and-toxicity pathways to guide future risk assessment and mechanistic studies of MNP exposure in brain disease.
Jing W, Zheng M, Yang X et al. · Ecotoxicology and environmental safety · (2026) · View on PubMed ↗ · Free PDF ↗
The posteroventral part of the medial amygdala nucleus glutamatergic neurons encodes conspecifics’ individual identity in rodents.
This rodent neuroscience study examined how glutamatergic neurons in the posteroventral medial amygdala (MeApv; VGluT2-positive) encode conspecific identity in mice. Calcium activity and c-Fos expression increased in MeApv VGluT2 neurons during exposure to conspecifics/odors, and optogenetic silencing of MeApv VGluT2 neurons (or activation of Gad2-positive neurons) disrupted odor-driven social behaviors including identity recognition and odor discrimination. These findings are significant because they define a circuit mechanism for individual social identity processing that could inform broader models of social cognition.
Zheng L, Pan L, Fu X et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
TDP-43 Acetylation at the Neuroimmune Interface: A Hypothesis-Driven Framework for Peripheral Inflammatory Stratotypes in ALS.
This hypothesis-driven narrative review proposed a framework linking TDP-43 acetylation at the neuroimmune interface to peripheral inflammatory stratotypes in amyotrophic lateral sclerosis (ALS). It argues that acetylated, mislocalized TDP-43 species in the periphery may shape immunogenicity and monocyte/cytokine signatures, integrating evidence from single-cell transcriptomics, proteomic immunoprofiling, and clinical inflammatory phenotyping. The proposed stratification approach could enable more precise immune-targeted biomarker development and patient stratification in ALS.
Condorelli GA, Iozzia A, Bonifacio D et al. · Neurochemical research · (2026) · View on PubMed ↗
Soluble epoxide hydrolase drives neurovascular dysfunction in a model of amyloidosis.
This preclinical study investigated whether soluble epoxide hydrolase (sEH) drives neurovascular dysfunction in amyloidosis using APPPS1 mice crossed with an inducible soluble epoxide hydrolase (EPHX2) knock-out line induced before amyloid deposition. It found that loss of sEH activity altered histological and molecular measures of neurovascular dysfunction, with analyses including RNA sequencing to characterize downstream pathways. The results support sEH as a potential therapeutic target to mitigate vascular complications associated with amyloid pathology.
DeMeglio M, De Biasi ES, Breunig P et al. · Brain : a journal of neurology · (2026) · View on PubMed ↗
Co- and Multi-Pathologies in Parkinson’s Disease: An International Parkinson and Movement Disorder Society Scientific Issues Committee Review.
This review studied the concept of co- and multi-pathologies in Parkinson’s disease (PD), emphasizing that beyond α-synuclein Lewy pathology, many patients exhibit additional neuropathological processes linked to clinical heterogeneity. It synthesized evidence on the spectrum and frequency of these co-pathologies and how they may relate to specific clinical features and outcomes. The review is significant because it reframes PD as a multi-pathology disorder, informing biomarker development and more personalized therapeutic approaches.
Matarazzo M, Borghammer P, Elsayed I et al. · Movement disorders : official journal of the Movement Disorder Society · (2026) · View on PubMed ↗ · Free PDF ↗
Integrative Analysis of Pharmacological and Non-pharmacological Interventions in Alzheimer’s Dementia.
This integrative analysis reviewed pharmacological and non-pharmacological intervention strategies across the Alzheimer’s dementia disease course, emphasizing disease-modifying anti-amyloid monoclonal antibodies for early symptomatic stages. It synthesized evidence on when to use anti-amyloid therapy versus symptomatic drugs and how to incorporate non-pharmacological approaches to improve quality of life and caregiver outcomes. The review is significant for guiding practical, stage-specific care decisions in Alzheimer’s dementia.
Patel D, Patel T, Patel PN · Cureus · (2026) · View on PubMed ↗ · Free PDF ↗
Lithium as a disease-modifying therapy for Parkinson’s disease: mechanisms, preclinical evidence, and clinical prospects.
This review evaluated lithium as a potential disease-modifying therapy for Parkinson’s disease by summarizing mechanisms and preclinical/early clinical evidence. It highlighted lithium’s neuroprotective actions through inhibition of GSK-3β, enhancement of autophagy, suppression of neuroinflammation, and reduction of oxidative stress, with data suggesting preservation of dopaminergic neurons and improved motor function. The clinical significance is that lithium—an established drug—may be repurposed for PD neuroprotection, warranting further rigorous trials.
Boonstra JT · Clinical parkinsonism & related disorders · (2026) · View on PubMed ↗ · Free PDF ↗
Musculoskeletal/Bone/Orthopedic & Rehabilitation Interventions
Post-competition recovery in natural physique athletes: body composition, metabolic adaptation, and refeeding responses.
This study characterized body composition, resting metabolic rate, thyroid hormones (FSH, FT3, FT4), strength (IMTP peak force), and psychological responses across contest preparation and 2–12 weeks post-competition in 19 natural physique athletes, and assessed how different post-competition refeeding strategies influenced recovery. The key finding was that measurable physiological and psychological adaptations occurred over the recovery period and differed according to the refeeding approach. Clinically, these data can help optimize refeeding timing and composition to support safer, more effective recovery after bodybuilding-style contest dieting.
Buechel C, Pumpa K, Etxebarria N et al. · Journal of the International Society of Sports Nutrition · (2026) · View on PubMed ↗ · Free PDF ↗
The interplay between vitamin D status and exerkine signaling: implications for exercise adaptation in athletes: narrative review.
This narrative review synthesized mechanistic and clinical evidence on whether vitamin D status and supplementation modulate exercise-responsive “exerkines” relevant to training adaptation and recovery in athletes. The key finding was the proposed “vitamin D–exerkine axis,” linking vitamin D’s immunomodulatory/myotropic roles to potential regulation of exerkine signaling after exercise. Scientifically, this framework supports targeted research to determine which vitamin D–exerkine pathways meaningfully affect athletic performance and recovery.
Kim DH · Journal of the International Society of Sports Nutrition · (2026) · View on PubMed ↗ · Free PDF ↗
Macrophage piezo1 senses mechanical force to drive osteoclastogenesis via ZBP1: Implications for bone remodelling therapy.
This study examined how macrophage mechanosensing via Piezo1 converts mechanical force into osteoclastogenic signaling through ZBP1 (Z-DNA binding protein 1) during alveolar bone remodeling relevant to orthodontic tooth movement (OTM). The key finding was that macrophage Piezo1 senses mechanical force and drives osteoclastogenesis via a Piezo1–ZBP1 pathway, supported by human periodontal ligament tissue analyses, murine OTM/fracture models with macrophage-specific Piezo1 and Zbp1 knockouts, and in vitro mechanistic RNA-seq. Therapeutically, targeting the Piezo1–ZBP1 axis could improve bone remodeling outcomes and reduce risks like root resorption during orthodontic treatment.
Zhu L, Zhang K, Song A et al. · Clinical and translational medicine · (2026) · View on PubMed ↗ · Free PDF ↗
Research into Resistance Training Response Heterogeneity: a Summary of the 2025 Conference at the University of Jyväskylä.
This conference summary synthesized themes from the 2025 Inter-Individual Variation in Resistance Training Response meeting at the University of Jyväskylä, focusing on heterogeneity in resistance-training adaptations. It highlights that resistance training drives multi-dimensional changes across tissue, muscle fiber, and ultrastructural levels (e.g., radial hypertrophy via increased myofibril number and longitudinal growth via sarcomere addition) and that program variables such as weekly sets, volume-load, and rest intervals likely contribute to response variability. The synthesis is important for designing more personalized resistance-training prescriptions and for improving mechanistic understanding of why individuals adapt differently.
Roberts MD, Bamman MM, Hornberger TA et al. · Journal of applied physiology (Bethesda, Md. : 1985) · (2026) · View on PubMed ↗ · Free PDF ↗
The gut-bone axis: microbial metabolism and nutritional interventions for bone health.
This review studied how gut microbiota and their metabolites influence osteoporosis development and how nutritional interventions (postbiotics like butyrate, probiotics such as Bifidobacterium animalis and Lacticaseibacillus rhamnosus LGG, prebiotics like fructo-oligosaccharides, synbiotics, and dietary patterns including Mediterranean/vegetarian diets) may improve bone health. It found that microbial effects on gut permeability, nutrient digestion/absorption, pH balance, and immune regulation can shift bone remodeling toward less bone loss. These findings support targeting the gut-bone axis as a scientific rationale for adjunct nutritional strategies to reduce osteoporosis risk and progression.
Rodriguez-Bryant A, Papageorgiou M, Horcajada MN et al. · Gut microbes · (2026) · View on PubMed ↗ · Free PDF ↗
Nutrition and rehabilitation after anterior cruciate ligament reconstruction: A systematic review.
This systematic review studied the evidence for nutrition and rehabilitation strategies after anterior cruciate ligament reconstruction (ACLR), focusing on outcomes relevant to rehabilitation and return to sport (RTS) across patients of any age. It summarized findings from randomized and non-randomized trials as well as observational studies examining nutritional interventions and diet patterns in the post-ACLR period. The review is clinically important because it evaluates whether nutrition can improve RTS safety and success, guiding future rehabilitation protocols.
Raghoebar S, Roozenboom-van Vliet C, Wal WV et al. · Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · (2026) · View on PubMed ↗ · Free PDF ↗
Impact of Resistance Training on Body Composition, Physical Fitness, and Cardiometabolic Health in Children and Adolescents With Overweight/Obesity: An Umbrella Review With Meta-Analyses.
This umbrella review with meta-analyses synthesized evidence from systematic reviews to evaluate resistance training (RT) effects on body composition, physical fitness, and cardiometabolic health in children and adolescents with overweight/obesity. The key finding was that RT improves multiple health domains (e.g., body composition and fitness-related outcomes) but effects vary across outcomes and study designs, leading to overall inconsistent evidence in some cardiometabolic endpoints. Clinically, the findings support RT as a promising intervention for youth with overweight/obesity while emphasizing the need to tailor programs and further clarify cardiometabolic benefits.
Poon ET, Iu JC, Franklin BA et al. · Obesity reviews : an official journal of the International Association for the Study of Obesity · (2026) · View on PubMed ↗ · Free PDF ↗
Restoration of neuromuscular function by mitochondrial transplantation in injured mouse skeletal muscle.
This mouse study investigated whether mitochondrial transplantation (MT) restores neuromuscular function after cardiotoxin-induced injury in skeletal muscle and whether moderate electrically evoked contractions affect recovery. The key finding was that exogenous mitochondrial transplantation (delivered via tail-vein injection after cardiotoxin injury) enhanced restoration of contractile/neuromuscular function compared with controls (PBS) under injury conditions. Scientifically, it suggests MT could be a therapeutic approach to improve functional recovery after muscle injury while informing how rehabilitation-like electrical stimulation interacts with repair.
Alway SE, Ferrandi PJ, Paez HG et al. · The Journal of physiology · (2026) · View on PubMed ↗ · Free PDF ↗
General Translational Methods, Trial Design & Research Governance
Identifying Novel Biomarkers and Therapeutic Targets for Endometriosis: Integrative Analysis of the Plasma Proteome and Genome.
This integrative study identified endometriosis (EM) biomarkers and therapeutic targets by combining plasma proteome quantitative trait loci (pQTLs) from the UK Biobank Pharma Proteomics Project with EM genetic associations from FinnGen. The key finding was that proteins with causal genetic evidence (tested via cis-Mendelian randomization and supported by colocalization and protein–protein interaction analyses) were associated with EM risk and could be validated using GWAS catalog data. The clinical significance is a prioritized list of candidate EM biomarkers and drug targets grounded in genetic causality rather than correlation alone.
Zheng J, Yao YL, Chen XZ et al. · Mediators of inflammation · (2026) · View on PubMed ↗ · Free PDF ↗
AI-induced never-skilling in medical education.
This Perspective discusses how AI tools used during early medical education could impair trainees’ development of foundational clinical reasoning skills, focusing on medical trainees rather than practicing clinicians. It argues that reliance on AI can cause “never-skilling” (a failure to acquire core competencies) and can also contribute to “mis-skilling” when trainees internalize AI errors as clinical knowledge. The significance is that medical training frameworks should proactively govern AI use to prevent long-term safety and competence deficits.
Ke Y, Jin L, Ong JCL et al. · Nature medicine · (2026) · View on PubMed ↗
Soma-to-germline miRNA inheritance through yolk promotes stress resilience in progeny.
This study investigated whether yolk in the nematode Caenorhabditis elegans can transmit gene-regulatory microRNAs (miRNAs) from mother to offspring, focusing on soma-to-germline inheritance via yolk. It found that yolk granules contain miRNAs and that the lipoprotein yolk receptor RME-2 mediates transport of maternal intestinal miRNAs into embryos, where they regulate developing larval transcriptomes and enhance stress resilience. The significance is that it identifies a concrete RNA inheritance route (yolk-delivered miRNAs via RME-2) that can program progeny stress responses.
Aupérin N, Singh M, Bourdon L et al. · Nature structural & molecular biology · (2026) · View on PubMed ↗ · Free PDF ↗
Treatment Effect Reanalysis of the Randomized Individual Screening Trial of Innovative Glioblastoma Therapy in Newly Diagnosed Glioblastoma With External Control Data.
This reanalysis compared internal versus matched external control data for a randomized phase II platform trial (INSIGhT; NCT02977780) in newly diagnosed O6-methylguanine-DNA methyltransferase-unmethylated glioblastoma, focusing on three experimental arms treated with abemaciclib, neratinib, and CC-11. The study assessed whether treatment effect estimates remain valid when external datasets are integrated instead of using only internal trial controls. This has scientific and regulatory significance for accelerating glioblastoma drug development by improving the credibility and efficiency of external-control trial designs.
Rudra Gupta T, Polley MC, Redd R et al. · Journal of clinical oncology : official journal of the American Society of Clinical Oncology · (2026) · View on PubMed ↗
53BP1 orchestrates sequence feature of RAG targets to balance DNA repair outcomes during V(D)J recombination.
This mechanistic study investigated how the DNA damage response factor 53BP1 shapes DNA repair outcomes during V(D)J recombination by controlling sequence features of RAG targets. Loss of 53BP1 specifically increased junctional microhomology of cryptic RSS (cRSS) recombination rather than canonical RSS recombination, with partial phenocopy by depletion of RIF1 or Shieldin, indicating a 53BP1-dependent end-joining program. These insights are clinically relevant for understanding how DDR pathway variation can influence the quality of immune-receptor rearrangements and potentially affect genomic stability.
Luo S, Zha H, Yang Z et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Developmental candidate GHP-88310/EIDD-3608 with high tolerability and oral efficacy in measles and respiratory paramyxovirus models.
The study developed the orthoparamyxovirus polymerase inhibitor clinical candidate analog GHP-88310 (EIDD-3608) and evaluated its activity and tolerability against measles virus (MeV) and respiratory paramyxoviruses in nonrodent models (ferrets and dogs) and related virus models. GHP-88310 showed broad antiviral activity against human parainfluenza virus type 3 (HPIV3), Sendai virus (SeV), MeV, and canine distemper virus (CDV), with 7-day tolerability at daily doses up to 2000 mg/kg in higher mammals. These findings support GHP-88310/EIDD-3608 as an orally efficacious, broadly acting candidate for orthoparamyxovirus infections with improved translational tolerability.
Lieber CM, Wolf JD, Govindarajan M et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Genetic-Proteomic Integration Identifies Predictive Plasma Proteins for Multiple Sclerosis.
This study used genetic-proteomic integration to identify cis-acting protein quantitative trait loci (pQTL) for 2,545 plasma proteins (n=80,824) and then applied Mendelian randomization and colocalization to test predicted protein levels for association with multiple sclerosis (MS) risk in 14,802 cases and 26,703 controls. It identified plasma proteins that are predictive of MS susceptibility and evaluated their prediagnostic value and links to disease severity. The work is significant because it provides genetically supported blood biomarker candidates that may enable earlier risk stratification before clinical MS onset.
Ding Y, Hamitouche D, Thebault S et al. · Annals of neurology · (2026) · View on PubMed ↗ · Free PDF ↗
Engineering precision oncology: Targeting tumors and immune cells with lentiviral vectors.
This review studied lentiviral vector (LV) engineering strategies for precision oncology, focusing on how pseudotyping and targeting approaches can direct LV tropism to tumors and immune cells while improving in vivo safety and efficacy. The key finding was that moving beyond standard VSV-G pseudotyping—using natural viral envelopes (e.g., measles virus, baboon endogenous retrovirus, Nipah virus, Sindbis virus) and engineered targeting/multicomponent glycoprotein systems—enables more selective vector delivery. Clinically and scientifically, it provides a framework for designing next-generation LV gene therapies with improved targeting for cancer treatment.
Rossi J, Martinello C, Sorrentino R et al. · Molecular therapy. Oncology · (2026) · View on PubMed ↗ · Free PDF ↗
Inflammation, Innate Immunity & Inflammasome Biology
TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.
This study investigated the role of the E3 ubiquitin ligase TRIM21 in inflammasome assembly and autoinflammatory disease, focusing on inflammasome components such as ASC and cytokine maturation. It found that TRIM21 facilitates inflammasome assembly and contributes to ASC particle assembly/release, thereby promoting IL-1β and IL-18 inflammatory outputs and supporting chronic inflammation relevant to autoinflammatory disease. The significance is that TRIM21 emerges as a regulator of inflammasome activation that could be targeted to modulate autoinflammatory pathology.
Carriere J, Yun C, Khare S et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Manganese enhances macrophage bactericidal activity in mice with Staphylococcus aureus osteomyelitis via Sirt3-mitophagy axis.
This mouse study tested whether manganese (Mn2+) enhances macrophage bactericidal activity during Staphylococcus aureus osteomyelitis and defined the Sirt3-dependent pathway involved. It found that Mn2+ boosts killing of intracellular S. aureus in infected macrophages by repressing Sirt3, which inhibits S. aureus-induced mitophagy via the PINK1/parkin axis and increases mitochondrial reactive oxygen species to eradicate bacteria. The significance is that it links a trace-metal intervention (manganese) to a defined Sirt3–mitophagy mechanism that could inform adjunct therapies for persistent osteomyelitis.
Guan X, Yang B, Bai B et al. · Nature communications · (2026) · View on PubMed ↗ · Free PDF ↗
Endocrine/Metabolic Pathophysiology (Non-cancer) & Aging Mechanisms
The pathophysiology of pre-eclampsia.
This Nature Reviews Nephrology article synthesizes current evidence on the pathophysiology of pre-eclampsia, focusing on maternal endothelial dysfunction and placental contributions across pregnancy. It highlights that placental dysfunction produces toxins that drive systemic endothelial injury—especially in kidney, liver, and cerebral vascular beds—leading to hypertension and proteinuria and contributing to severe complications such as stroke, acute kidney injury, and liver dysfunction. The significance is that it frames pre-eclampsia as a placenta-to-maternal-system disease process, guiding mechanistic research and potential therapeutic targets.
Hennessy A, Ng J, Makris A · Nature reviews. Nephrology · (2026) · View on PubMed ↗
Effects of a 6-week subcutaneous infusion of native GIP alone or as add-on to semaglutide in people with type 2 diabetes: a single-centre, double-blind, parallel-group, randomised, placebo-controlled trial.
This single-centre, double-blind, parallel-group, randomized, placebo-controlled trial tested whether a 6-week subcutaneous infusion of native GIP alone or added to semaglutide improves glycemic control in adults with type 2 diabetes. The study evaluated changes in glycemic outcomes (e.g., HbA1c and related measures) across GIP monotherapy, GIP+semaglutide, and placebo arms. Scientifically, the trial clarifies whether augmenting GLP-1 receptor agonism with native GIP provides additive benefit for type 2 diabetes management.
Helsted MM, Fonnesbech-Wulff C, Schaltz NL et al. · The lancet. Diabetes & endocrinology · (2026) · View on PubMed ↗
In vivo single-cell ribosome profiling reveals cell-type-specific translational programs during aging.
This study developed and applied an in vivo single-cell ribosome profiling approach to map cell-type-specific translational programs during aging in the epidermis. Using ribosomal elongation-inhibited cell isolation and RNase I to enable in vivo single-cell ribosome profiling, the authors characterized how aging reshapes translation across epidermal cell types. These data provide a mechanistic framework for how stemness-associated low protein synthesis and aging interact at the translational level.
Duré C, Ghoshdastider U, Weber R et al. · Molecular cell · (2026) · 1 citations · View on PubMed ↗ · Free PDF ↗
Uric Acid to HDL-C Ratio as a Novel Biomarker for Sarcopenia: A National Study with Machine Learning Insights.
This national cohort study analyzed 9,853 middle-aged and older adults from the China Health and Retirement Longitudinal Study (CHARLS) to test whether the uric acid to HDL-C ratio (UHR) predicts sarcopenia defined by AWGS 2019 criteria, using multivariable logistic regression, restricted cubic splines, mediation analyses, and machine-learning insights. The UHR was associated with higher sarcopenia risk, with mediation suggesting roles for insulin resistance (TyG index) and renal function (eGFR). If validated, UHR could become a practical biomarker for risk stratification and early intervention in aging populations.
Yang R, Cheng Z, Yang P et al. · The journals of gerontology. Series A, Biological sciences and medical sciences · (2026) · View on PubMed ↗ · Free PDF ↗
P2X7R of synovial fibroblasts is a potential therapeutic target associated with refractory rheumatoid arthritis.
This study investigated the role of the P2X7 receptor (P2X7R) in rheumatoid arthritis (RA) by profiling expression in synovial fibroblasts from RA patients and identifying cell subsets associated with refractory disease. P2X7R was robustly expressed in RA synovium, correlated with synovitis and systemic inflammation, and single-cell transcriptomics showed enrichment in specific synovial fibroblast populations linked to refractory RA; treatment with the selective human P2X7R antagonist EVT-401 was then used to test therapeutic potential. Targeting P2X7R in defined synovial fibroblast subsets could provide a mechanism-based strategy for treating refractory RA.
Rao P, Jin S, Xiao S et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Shifting IRES versus Cap-initiated translation during homeostatic stem cell differentiation and stress.
This study used an IRES/Cap reporter mouse to quantify shifts between internal ribosome entry site (IRES)-mediated and cap-dependent translation during homeostatic stem cell differentiation and stress. Caloric stress increased IRES/Cap translation as expected, but IRES/Cap progressively increased during hematopoietic and epithelial lineage commitment, indicating differentiation-state–dependent regulation of translation initiation mode. Understanding how stress and lineage programs rebalance IRES versus cap translation is important for explaining how cells maintain proteostasis and adapt during development and stress.
Mazzola MC, Zhao T, Kiem A et al. · Science advances · (2026) · View on PubMed ↗ · Free PDF ↗
Age-related patterns of cardiometabolic risk factors for complications in type 2 diabetes.
This study analyzed age-related patterns of cardiometabolic risk factors for complications in people with type 2 diabetes using cross-sectional data from national health surveys in multiple countries (including AusDiab, NHANES, and Mauritius). The key finding is the comparison of whether younger age is associated with a more adverse risk-factor profile than older age among individuals with type 2 diabetes. Clinically, identifying age-specific risk-factor patterns can improve prevention strategies for diabetes complications by tailoring monitoring and intervention intensity to patient age.
Sajjadi SF, Sacre JW, Kowlessur S et al. · Diabetologia · (2026) · View on PubMed ↗
Neuroimmunology & Rare Neuroinflammatory Disorders
French NOMADMUS Cohort Overview: Landscape Evolution of AQP4+NMOSD and MOGAD From 2010 to 2024.
This retrospective French cohort study (NOMADMUS) analyzed clinical, imaging, and treatment data from 98 centers to characterize how aquaporin-4 IgG–seropositive neuromyelitis optica spectrum disorder (AQP4+NMOSD) and MOG antibody-associated disease (MOGAD) evolved from 2010 to 2024. The cohort included 769 AQP4+NMOSD and 957 MOGAD patients, with 68.6% female and a mean age at onset of 37.4 years, and the study documents changes in diagnostic and therapeutic approaches over time. These real-world trends are significant for understanding how evolving criteria and treatments affect disease course in rare neuroimmunologic disorders.
Roux T, Lejeune FX, Casey R et al. · Neurology · (2026) · View on PubMed ↗
Surgical/Procedural Standards & Postoperative Complications
Development and validation of a predictive model for hypothalamic obesity following craniopharyngioma resection.
This retrospective study of 136 craniopharyngioma patients evaluated risk factors for hypothalamic obesity (HO) after surgery and built/validated a logistic-regression predictive model using training and validation cohorts. The model identified preoperative and/or perioperative factors associated with postoperative HO and demonstrated predictive performance in the validation set. Clinically, it enables earlier identification of patients at high risk for HO, supporting targeted monitoring and preventive interventions after craniopharyngioma resection.
Li Q, Zhao L, Huang F et al. · BMC endocrine disorders · (2026) · View on PubMed ↗ · Free PDF ↗
Temporal relationship between hematoma resolution and functional recovery after middle meningeal artery embolization for chronic subdural hematoma.
This multicenter retrospective study evaluated the temporal relationship between hematoma resolution and functional recovery after middle meningeal artery embolization (MMAE) for chronic subdural hematoma (cSDH). It modeled hematoma thickness resolution trajectories using exponential decay functions and assessed factors associated with favorable outcomes measured by modified Rankin Scale (mRS) over follow-up intervals. The findings can help clinicians predict recovery timing and identify prognostic factors to optimize follow-up and management after MMAE.
DeMessie B, Essibayi MA, Salim HA et al. · Journal of neurosurgery · (2026) · View on PubMed ↗
Hypoparathyroidism Post Thyroidectomy: Prevention, Evaluation, Management, and Application of Recent Guidelines.
This narrative review studied prevention, evaluation, and management strategies for postsurgical hypoparathyroidism (HypoPT) in patients undergoing thyroidectomy, synthesizing evidence-based guidelines through December 2025. It found that postsurgical HypoPT—accounting for ~75% of all HypoPT cases—is largely preventable and that risk factors span patient-related, surgical, and sometimes presurgical domains, with guideline-based approaches for diagnosis and treatment. Clinically, applying these recent recommendations can reduce incidence and improve early detection and management of HypoPT after thyroid surgery.
Ali DS, Perrier ND, Khan AA · Thyroid : official journal of the American Thyroid Association · (2026) · View on PubMed ↗
Acceptability of Atropine Eyedrops Administered Sublingually for Sialorrhea Treatment Related to Neurological Conditions.
This multicenter, cross-sectional study assessed patient acceptability of sublingually administered atropine eye drops (off-label anticholinergic) for sialorrhea in neurological-condition patients in France using the CAST-ClinSearch Acceptability Score Test methodology. The key finding was that acceptability/willingness to use and administer atropine eyedrops sublingually is a critical determinant for safe and effective real-world therapy. Scientifically and clinically, the results support patient-centered feasibility considerations for repurposing ophthalmic atropine formulations for sialorrhea management in neurologic populations.
Michelon H, Lefèvre-Dognin C, Paquereau J et al. · Pharmacology research & perspectives · (2026) · View on PubMed ↗ · Free PDF ↗
Environmental Exposures & Epidemiology
Environmental Nonessential Element Exposure and Urologic Cancer: A Systematic Review and Meta-Analysis.
This systematic review and meta-analysis synthesized epidemiologic evidence on whether environmental exposure to nonessential chemical elements is associated with urologic cancer risk across human studies. The key finding (as reported in the full analysis) is the overall direction and strength of association between nonessential element exposure levels and urologic cancer incidence, based on pooled data from multiple databases searched through January 27, 2025. Clinically, clarifying these exposure–cancer relationships can inform risk assessment and guide future mechanistic and prospective studies on environmental carcinogenesis.
Deng Z, Li J, Ji R et al. · JAMA network open · (2026) · View on PubMed ↗ · Free PDF ↗
Regional and national burden of six major digestive cancers in Asia, 1990-2023: An analysis of the GBD Study 2023.
Using Global Burden of Disease (GBD) 2023 data, this study quantified and projected the regional and national burden (DALYs) of six major digestive cancers across 34 Asian countries/territories from 1990–2023 through 2040. It reported divergent trends, including declines in gastric cancer alongside increases in pancreatic and colorectal cancer in specific subregions, with pandemic-era shifts. These results are significant for public health planning and resource allocation to address changing digestive cancer burdens across Asia.
Zhang L, Li F, Zhang J · iScience · (2026) · View on PubMed ↗ · Free PDF ↗
Generated automatically on May 24, 2026 from PubMed’s trending articles. Summaries are AI-generated; always consult the original publication for clinical or research decisions.