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Author Correction: A mouse brain stereotaxic topographic atlas with isotropic 1-μm resolution
Nature, Published online: 07 September 2026; doi:10.1038/s41586-026-11094-2
Author Correction: A mouse brain stereotaxic topographic atlas with isotropic 1-μm resolutionPerioperative Modulation of the Gut-Liver Axis in Liver Surgery: Clinical Evidence and Future Directions
J Vis Exp. 2026 Sep 1;(235). doi: 10.3791/73747.
ABSTRACT
Liver resection and liver transplantation remain cornerstone treatments for many hepatobiliary diseases, yet postoperative infection, impaired liver regeneration, and post-hepatectomy liver failure (PHLF) remain serious complications. Perioperative stressors can disrupt the gut-liver axis by altering the intestinal microbiota, epithelial barrier integrity, microbial metabolites, bile acid signaling, and host immunity. This review examines how these alterations relate to clinical outcomes and evaluates evidence for microbiota-targeted interventions, including probiotics, synbiotics, nutritional optimization, antibiotic stewardship, bile acid modulation, and emerging multiomics strategies. We distinguish liver resection from living-donor and deceased-donor liver transplantation because the patient populations, graft or remnant anatomy, ischemia-reperfusion exposures, immune status, and outcome definitions differ. Clinical evidence most consistently supports selected pro-/synbiotic strategies for reducing postoperative infection in higher-risk settings, whereas microbiome-based prediction of PHLF, fecal microbiota transplantation (FMT), bile acid-directed therapy, and precision multiomics-guided pathways remain investigational. Future work should use transparent literature identification, standardized perioperative protocols, risk-defined populations, external validation, and prospective multicenter trials. A better understanding of gut-liver interactions may help preserve beneficial host-microbial signals while limiting translocation and inflammation during recovery.
PMID:42683887 | DOI:10.3791/73747
AffordTissue: Dense Affordance Prediction for Tool-Action Specific Tissue Interaction
Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35
Cell Oncol (Dordr). 2026 Mar 23;49(2):60. doi: 10.1007/s13402-026-01194-6.
ABSTRACT
Glycolytic reprogramming is closely associated with the occurrence and progression of gastric cancer. Specifically, the energy derived from glucose metabolism and the cellular proteins by its intermediate products influence gastric cancer development. However, as an important branch of glucose metabolism, sialic acid metabolism and its mediated sialylation modifications remain insufficiently studied in gastric cancer, and their specific relationship with malignant tumor progression requires further exploration. This study employed a multi‑omics approach, integrating metabolomics, single‑cell RNA sequencing, and bulk RNA sequencing analyses, to investigate the metabolic landscape of gastric cancer and its associated alterations. The results indicated that sialic acid is a characteristic metabolite in malignant gastric cancer tissues. It modulates biological functions such as immune response, proliferative activity, and metabolic remodeling within gastric cancer tissues by influencing sialylation modifications. Furthermore, we identified the drug WZ35, which can inhibit the malignant proliferation of gastric cancer by targeting both sialic acid metabolism and sialylated protein modifications. We put forward a conjecture that the metabolism and modification of sialic acid promote the malignant development of gastric cancer, and we discovered that the drug WZ35 has an inhibitory effect on the sialic acid metabolism of gastric cancer.
GRAPHICAL ABSTRACT:
PMID:41870836 | PMC:PMC13009457 | DOI:10.1007/s13402-026-01194-6
Avoiding Over-smoothing in Social Media Rumor Detection with Pre-trained Propagation Tree Transformer
Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35
Cell Oncol (Dordr). 2026 Mar 23;49(2):60. doi: 10.1007/s13402-026-01194-6.
NO ABSTRACT
PMID:41870836 | DOI:10.1007/s13402-026-01194-6
Global Evolutionary Steering: Refining Activation Steering Control via Cross-Layer Consistency
SAW: Toward a Surgical Action World Model via Controllable and Scalable Video Generation
METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translation
Oncogene, Published online: 13 March 2026; doi:10.1038/s41388-026-03706-y
METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translation