The role of vitamin D through SphK1/S1P in the regulation of MS progression.

Sphingosine-1-phosphate (S1P) is biologically active lipid, leading to neuroinflammation and macrophage invasion in central nervous system, plays an important role in the development of multiple sclerosis (MS) model in experimental allergic encephalomyelitis (EAE) rats. Vitamin D is observed to be a key factor in regulating cell S1P levels. We detected vitamin D can alleviate the symptoms of EAE rats, but the exact mechanism is unclear. In PC12 cells, vitamin D can reverse S1P-induced cell death, but the signaling pathway unclear. This study was aimed to investigate S1P regulation mechanism or signaling pathway mediated by vitamin D in EAE and PC12 model. In our experiments, S1P and Sphingosine kinase type 1 (SphK1) mRNA and protein expression in EAE rats group, control group, vitamin D feeding group were detected by HPLC, ELISA, RT-PCR and western blot. PC12 cell death was detected by Propidium (PI) staining. VDR plasmid overexpression and RNA interference, immunofluorescence, real-time cell analysis, protein immunoblotting was used to detect SphK1 transcriptional regulation, cell-substrate attachment quality, the signaling pathway of cell apoptosis and inflammation related gene expression (Bax/Bcl-2, Casepase-3, Il-6, TGF-ß, TNF-α). Our study showed vitamin D can reverse the elevation of S1P level in EAE rats, reduce the severity and shorten the course of EAE. 1,25-(OH) 2D3 coupled with vitamin D receptor (VDR) inhibited SphK1 transcription. 1,25-(OH)2D3 significantly reduced PC12 cell death rate induced by S1P, in addition improved the cell substrate attachment quality. 1,25-(OH) 2D3 can block S1P-induced p-ERK activation and PI3K /Akt signaling pathway reduced Il-6, TGF-ß, TNF-α cytokine release and Bax/Bcl-2, Casepase-3 apoptosis protein expression. On the other hand, immunofluorescence staining showed 1,25-(OH) 2D3 can increase the expression of neuronal perinuclear protein MAP2 in PC12 cells probably protect nerve cells further. In summary, the ameliorative effect of vitamin D was derived from its ability to reduce S1P levels, provides an idea for vitamin D as a combination therapy for disease.

[Metabolomic changes of neonatal sepsis: an exploratory clinical study]. / æ–°ç”Ÿå„¿è´¥è¡€ç—‡çš„ä»£è°¢ç»„å­¦æ”¹å˜ï¼šä¸€é¡¹æŽ¢ç´¢æ€§ä¸´åºŠç ”ç©¶.

OBJECTIVES: To study the metabolic mechanism of neonatal sepsis at different stages by analyzing the metabolic pathways involving the serum metabolites with significant differences in neonates with sepsis at different time points after admission. METHODS: A total of 20 neonates with sepsis who were hospitalized in the Department of Neonatology, Hunan Provincial People's Hospital, from January 1, 2019 to January 1, 2020 were enrolled as the sepsis group. Venous blood samples were collected on days 1, 4, and 7 after admission. Ten healthy neonates who underwent physical examination during the same period were enrolled as the control group. Ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry was used for the metabonomic analysis of serum samples to investigate the change in metabolomics in neonates with sepsis at different time points. RESULTS: On day 1 after admission, the differentially expressed serum metabolites between the sepsis and control groups were mainly involved in the biosynthesis of terpenoid skeleton. For the sepsis group, the differentially expressed serum metabolites between days 1 and 4 after admission were mainly involved in pyruvate metabolism, and those between days 4 and 7 after admission were mainly involved in the metabolism of cysteine and methionine. The differentially expressed serum metabolites between days 1 and 7 after admission were mainly involved in ascorbic acid metabolism. CONCLUSIONS: The metabolic mechanism of serum metabolites varies at different stages in neonates with sepsis and is mainly associated with terpenoid skeleton biosynthesis, pyruvate metabolism, cysteine/methionine metabolism, and ascorbic acid metabolism.

Development and validation of a prediction model for deep vein thrombosis in older non-mild acute pancreatitis patients.

BACKGROUND: Deep vein thrombosis (DVT) may cause pulmonary embolus, leading to late deaths. The systemic inflammatory and hypercoagulable state of moderate and severe acute pancreatitis (non-mild acute pancreatitis, NMAP) patients may contribute to the development of venous thromboembolism. Accurate prediction of DVT is conducive to clinical decisions. AIM: To develop and validate a potential new prediction nomogram model for the occurrence of DVT in NMAP. METHODS: NMAP patient admission between 2013.1.1 and 2018.12.31 at the West China Hospital of Sichuan University was collected. A total of 220 patients formed the training set for nomogram development, and a validation set was constructed using bootstrapping with 100 resamplings. Univariate and multivariate logistic regression analyses were used to estimate independent risk factors associated with DVT. The independent risk factors were included in the nomogram. The accuracy and utility of the nomogram were evaluated by calibration curve and decision curve analysis, respectively. RESULTS: A total of 220 NMAP patients over 60 years old were enrolled for this analysis. DVT was detected in 80 (36.4%) patients. The final nomogram included age, sex, surgery times, D-dimer, neutrophils, any organ failure, blood culture, and classification. This model achieved good concordance indexes of 0.827 (95%CI: 0.769-0.885) and 0.803 (95%CI: 0.743-0.860) in the training and validation sets, respectively. CONCLUSION: We developed and validated a prediction nomogram model for DVT in older patients with NMAP. This may help guide doctors in making sound decisions regarding the administration of DVT prophylaxis.

Bosworth-type fibular entrapment fracture of the ankle without dislocation: a rare case report and a review of the literature.

Bosworth fracture-dislocation of ankle is a rare and irreducible type of ankle injury, with a high incidence of complication. This type of fracture was defined originally as entrapment of the proximal fragment of the fibula behind the posterior tubercle of the distal tibia. Recently, many variants of this type of fracture dislocation have been reported, but all of those reports included the syndesmosis ligament injury of ankle. Here, we report a case of a particularly rare variant of Bosworth fracture-dislocation without syndesmosis ligament injury of ankle. A 48-year-old male presented with a Bosworth fracture dislocation with entrapment of proximal fragment behind the tibia. After temporary treatment in emergency department was applied, emergency open reduction and internal fixation with a plate and screws was performed due to irreducibility of the fracture fragment. The fractured lateral malleolus was entrapped behind the tibia and rupture of the interosseous ligament was found intraoperatively. The anterior inferior tibiofibular ligament, a part of syndesmosis ligament of ankle, was grossly intact and no abnormal findings was seen by fluoroscopy with external rotational stress. Moreover, the deltoid ligament was found to be normal in ultrasonography. There were no complications after surgery and the patient showed full functional recovery at 2 years follow up. These fractures will frequently be irreducible and should be considered for open reduction and internal fixation with the careful evaluation of injury mechanisms with syndesmotic stability.

The elevated transcription of ADAM19 by the oncohistone H2BE76K contributes to oncogenic properties in breast cancer.

The recent discovery of the cancer-associated E76K mutation in histone H2B (H2BE76-to-K) in several types of cancers revealed a new class of oncohistone. H2BE76K weakens the stability of histone octamers, alters gene expression, and promotes colony formation. However, the mechanism linking the H2BE76K mutation to cancer development remains largely unknown. In this study, we knock in the H2BE76K mutation in MDA-MB-231 breast cancer cells using CRISPR/Cas9 and show that the E76K mutant histone H2B preferentially localizes to genic regions. Interestingly, genes upregulated in the H2BE76K mutant cells are enriched for the E76K mutant H2B and are involved in cell adhesion and proliferation pathways. We focused on one H2BE76K target gene, ADAM19 (a disintegrin and metalloproteinase-domain-containing protein 19), a gene highly expressed in various human cancers including breast invasive carcinoma, and demonstrate that H2BE76K directly promotes ADAM19 transcription by facilitating efficient transcription along the gene body. ADAM19 depletion reduced the colony formation ability of the H2BE76K mutant cells, whereas wild-type MDA-MB-231 cells overexpressing ADAM19 mimics the colony formation phenotype of the H2BE76K mutant cells. Collectively, our data demonstrate the mechanism by which H2BE76K deregulates the expression of genes that control oncogenic properties through a combined effect of its specific genomic localization and nucleosome destabilization effect.

Chain conformation transition induced host-guest assembly between triple helical curdlan and ß-CD for drug delivery.

The unique conformation transition from a triple helix to single coils for the triple helical ß-d-glucans has paved the way to fabricate various functional nanocomposites through the denaturing-renaturing process. This study firstly reports a novel kind of naturally derived supramolecular polymer micelle consisting of single-stranded chains of curdlan (CUR) and ß-CDs. It is proposed that ß-CDs as the host molecules were threaded onto single ß-glucan chains (denatured triplex CUR) via the host-guest interaction, thereby forming supramolecular micelles. The results from the 1H NMR, FT-IR, XRD and 2D 1H NOESY NMR studies confirmed the formation of the inclusion complex and the existence of the core-shell structure of the supramolecular assembly. TEM images and DLS revealed that the self-organized micelles displayed a regular spherical shape with an average diameter of ∼27 nm. Furthermore, the hydrophobic anticancer drug camptothecin (CPT) was selected as a model drug and successfully encapsulated into the CUR/ß-CD micelles. The drug-loaded micelles exhibited a steady sustained-release pattern regardless of the environmental pH. The flow cytometry and confocal laser scanning microscopy measurements confirmed that the CPT-loaded micelles could be well internalized into HepG 2 cells and continuously release the drug molecules inside the tumor cells. Meanwhile, the in vivo experiments demonstrated that CPT-loaded micelles could effectively inhibit tumor growth in comparison to free drugs. This concept will give a favorable platform to construct intelligent drug delivery systems for potential use.

Total pancreatectomy compared with pancreaticoduodenectomy: a systematic review and meta-analysis.

Aim: To assess whether total pancreatectomy (TP) is as feasible, safe, and efficacious as pancreaticoduodenectomy (PD). Materials and Methods: Major databases, including PubMed, EMBASE, Science Citation Index Expanded, Scopus and the Cochrane Library, were searched for studies comparing TP and PD between January 1943 and June 2018. The meta-analysis only included studies that were conducted after 2000. The primary outcomes were morbidity and mortality. Pooled odds ratios (ORs), weighted mean differences (WMDs) or hazard ratios (HRs) with 95 percent confidence intervals (CIs) were calculated using fixed effects or random effects models. The methodological quality of the included studies was evaluated by the Risk of Bias in Non-randomized Studies of Interventions (ROBINS-I) tool. Results: In total, 45 studies were included in this systematic review, and 5 non-randomized comparative studies with 786 patients (TP: 270, PD: 516) were included in the meta-analysis. There were no differences in terms of mortality (OR: 1.44, 95% CI: 0.66-3.16; P=0.36), hospital stay (WMD: -0.60, 95% CI: -1.78-0.59; P=0.32) and rates of reoperation (OR: 1.12; 95% CI: 0.55-2.31; P=0.75) between the two groups. In addition, morbidity was not significantly different between the two groups (OR: 1.41, 95% CI: 1.01-1.97; P=0.05); however, the results showed that the TP group tended to have more complications than the PD group. Furthermore, the operation time (WMD: 29.56, 95% CI: 8.23-50.89; P=0.007) was longer in the TP group. Blood loss (WMD: 339.96, 95% CI: 117.74-562.18; P=0.003) and blood transfusion (OR: 4.86, 95% CI: 1.93-12.29; P=0.0008) were more common in the TP group than in the PD group. There were no differences in the long-term survival rates between the two groups. Conclusion: This systematic review and meta-analysis suggested that TP may not be as feasible and safe as PD. However, TP and PD may have the same efficacy.

The oncological safety in minimally invasive versus open distal pancreatectomy for pancreatic ductal adenocarcinoma: a systematic review and meta-analysis.

The safety of minimally invasive distal pancreatectomy (MIDP) and open distal pancreatectomy (ODP) regarding oncological outcomes of pancreatic ductal adenocarcinoma (PDAC) remains inconclusive. Therefore, the aim of this study was to examine the oncological safety of MIDP and ODP for PDAC. Major databases including PubMed, Embase, Science Citation Index Expanded, and the Cochrane Library were searched for studies comparing outcomes in patients undergoing MIDP and ODP for PDAC from January 1994 to August 2018. In total, 11 retrospective comparative studies with 4829 patients (MIDP: 1076, ODP: 3753) were included. The primary outcome was long-term survival, including 3-year overall survival (OS) and 5-year OS. The 3-year OS (hazard ratio (HR): 1.03, 95% confidence interval (CI): 0.89, 1.21; P = 0.66) and 5-year OS (HR: 0.91, 95% CI: 0.65, 1.28; P = 0.59) showed no significant differences between the two groups. Furthermore, the positive surgical margin rate (weighted mean difference (WMD): 0.71, 95% CI: 0.56, 0.89, P = 0.003) was lower in the MIDP group. However, patients in the MIDP group had less intraoperative blood loss (WMD: -250.03, 95% CI: -359.68, -140.39; P < 0.00001), a shorter hospital stay (WMD: -2.76, 95% CI: -3.73, -1.78; P < 0.00001) and lower morbidity (OR: 0.57, 95% CI: 0.46, 0.71; P < 0.00001) and mortality (OR: 0.50, 95% CI: 0.31, 0.81, P = 0.005) than patients in the ODP group. The limited evidence suggested that MIDP might be safer with regard to oncological outcomes in PDAC patients. Therefore, future high-quality studies are needed to examine the oncological safety of MIDP.

Puerarin reverses cadmium-induced lysosomal dysfunction in primary rat proximal tubular cells via inhibiting Nrf2 pathway.

Previous studies have shown that oxidative stress-induced inhibition of autophagy plays a pivotal role in cadmium (Cd)-mediated cytotoxicity in primary rat proximal tubular (rPT) cells. The objective of this study is to explore the protective effect of puerarin (PU), a potent antioxidant, on Cd-induced autophagy inhibition and oxidative stress in rPT cells. First, Cd-induced blockage of autophagic flux in rPT cells was obviously restored by PU treatment, evidenced by immunoblot analysis of autophagy marker proteins and tandem fluorescent-tagged LC3 method. Resultantly, Cd-induced autophagosome accumulation was significantly alleviated by PU treatment. Also, Cd-induced lysosomal alkalinization and impairment of lysosomal degradation capacity were obviously recovered by PU, demonstrating that PU can restore Cd-induced lysosomal dysfunction. Moreover, Cd-induced lysosomal membrane permeabilization (LMP) was effectively blocked by PU. Cd-stimulated Nrf2 nuclear translocation and subsequent elevated expression of Nrf2-downstream targets were significantly inhibited by PU treatment. Simultaneously, Cd-elevated protein levels of antioxidant enzymes and glutathione synthesis-related proteins in rPT cells were markedly downregulated by PU treatment. In conclusion, these observations indicate that PU alleviates Cd-induced cytotoxicity in rPT cells through restoring autophagy, blocking LMP and inhibiting Nrf2 pathway, which is intimately related with its antioxidant activity.

Long noncoding RNA MIR22HG is down-regulated in prostate cancer.

Prostate cancer (PCa) is one of the most common cancer in males. Previous studies indicated that MIR22HG was a tumor suppressor in various cancers. However, the expression pattern and functional roles of MIR22HG in PCa remained to be further investigated. In this study, we for the first time showed MIR22HG was down-regulated in PCa. Furthermore, we observed the lower expression levels of MIR22HG were significantly related to higher Gleason score and T stage. Of note, we found that higher MIR22HG expression was associated with better disease-free survival and overall survival time in PCa. Moreover, we constructed a MIR22HG mediated co-expression network. Bioinformatics analysis showed MIR22HG was associated with regulating inflammatory response, regulation of transcription, cellular response to tumor necrosis factor, neutrophil chemotaxis, cell-cell signaling, and TNF signaling pathway. These results showed that MIR22HG could serve as a novel biomarker for prostate cancer.

Timing of Laparoscopic Cholecystectomy After Mild Biliary Pancreatitis: A Systematic Review and Meta-Analysis.

AIM: To compare the safety of cholecystectomy in early laparoscopic cholecystectomy (ELC) and delayed laparoscopic cholecystectomy (DLC). METHODS: We systematically searched PubMed, EMBASE, and Cochrane Library for studies that were published from January 1992 to March 2017. We included studies on patients with mild biliary pancreatitis and that reported the timing of cholecystectomy and the number of complications, readmissions, and conversion to open cholecystectomy. Moreover, we assessed the quality and bias risks of the included studies. RESULTS: After screening 4651 studies, we included 3 randomized clinical trials and 10 retrospective studies. The included studies described 2291 patients, of whom 1141 (49.8%) underwent ELC and 1150 (50.2%) underwent DLC. The reported rate of complications for ELC (6.8%) was lower than that for DLC (13.45%). The reported rate of readmission for ELC was lower than that for DLC. The length of hospital stay was longer with DLC than with ELC. ELC and DLC did not have significantly different rates of conversion to open cholecystectomy and duration of surgery. CONCLUSION: This meta-analysis provides evidence that ELC is better than DLC in many aspects for acute mild pancreatitis patients undergoing laparoscopic cholecystectomy. ELC associated with few complications and readmissions, as well as a short length of hospital stay.

miR-181a-5p is downregulated and inhibits proliferation and the cell cycle in prostate cancer.

Prostate cancer (PCa) is one of the most common cancers in men worldwide. However, the detailed molecular mechanisms underlying PCa tumorigenesis and progression remain largely unclear. MicroRNAs are key regulators of gene post-transcriptional expression in human cancer. In this study, we used public datasets, including GSE21036, GSE14857 and GSE45604 to analyze the expression of miR-181a in PCa. We also explored the potential role of miR-181a by using bioinformatics analysis and gain of function assay. miR-181a was down-regulated in PCa. Bioinformatics analysis revealed miR-181a was significantly involved in regulating cell metabolic process and gene expression. Of note, gain of function assay results showed overexpression of miR-181a could significantly inhibit cell proliferation by inducing G1 cell cycle arrest. Our results suggest miR-181a-5p may be adiagnostic and therapeutic biomarker for prostate cancer.

Trehalose protects against cadmium-induced cytotoxicity in primary rat proximal tubular cells via inhibiting apoptosis and restoring autophagic flux.

Autophagy has an important renoprotective function and we recently found that autophagy inhibition is involved in cadmium (Cd)-induced nephrotoxicity. Here, we aimed to investigate the protective effect of trehalose (Tre), a novel autophagy activator, against Cd-induced cytotoxicity in primary rat proximal tubular (rPT) cells. First, data showed that Tre treatment significantly decreased Cd-induced apoptotic cell death of rPT cells via inhibiting caspase-dependent apoptotic pathway, evidenced by morphological analysis, flow cytometric and immunoblot assays. Also, administration with Tre protected rPT cells against Cd-induced lipid peroxidation. Inhibition of autophagic flux in Cd-exposed rPT cells was markedly restored by Tre administration, demonstrated by immunoblot analysis of autophagy marker proteins and GFP and RFP tandemly tagged LC3 method. Resultantly, Cd-induced autophagosome accumulation was obviously alleviated by Tre treatment. Meanwhile, blockage of autophagosome-lysosome fusion by Cd exposure was noticeably restored by Tre, which promoted the autophagic degradation in Cd-exposed rPT cells. Moreover, Tre treatment markedly recovered Cd-induced lysosomal alkalinization and impairment of lysosomal degradation capacity in rPT cells, demonstrating that Tre has the ability to restore Cd-impaired lysosomal function. Collectively, these findings demonstrate that Tre treatment alleviates Cd-induced cytotoxicity in rPT cells by inhibiting apoptosis and restoring autophagic flux.

EphrinB2 Regulates Cardiac Fibrosis Through Modulating the Interaction of Stat3 and TGF-ß/Smad3 Signaling.

RATIONALE: Cardiac fibrosis is a common feature in left ventricular remodeling that leads to heart failure, regardless of the cause. EphrinB2 (erythropoietin-producing hepatoma interactor B2), a pivotal bidirectional signaling molecule ubiquitously expressed in mammals, is crucial in angiogenesis during development and disease progression. Recently, EphrinB2 was reported to protect kidneys from injury-induced fibrogenesis. However, its role in cardiac fibrosis remains to be clarified. OBJECTIVE: We sought to determine the role of EphrinB2 in cardiac fibrosis and the underlying mechanisms during the pathological remodeling process. METHODS AND RESULTS: EphrinB2 was highly expressed in the myocardium of patients with advanced heart failure, as well as in mouse models of myocardial infarction and cardiac hypertrophy induced by angiotensin II infusion, which was accompanied by myofibroblast activation and collagen fiber deposition. In contrast, intramyocardial injection of lentiviruses carrying EphrinB2-shRNA ameliorated cardiac fibrosis and improved cardiac function in mouse model of myocardial infarction. Furthermore, in vitro studies in cultured cardiac fibroblasts demonstrated that EphrinB2 promoted the differentiation of cardiac fibroblasts into myofibroblasts in normoxic and hypoxic conditions. Mechanistically, the profibrotic effect of EphrinB2 on cardiac fibroblast was determined via activating the Stat3 (signal transducer and activator of transcription 3) and TGF-ß (transforming growth factor-ß)/Smad3 (mothers against decapentaplegic homolog 3) signaling. We further determined that EphrinB2 modulated the interaction between Stat3 and Smad3 and identified that the MAD homology 2 domain of Smad3 and the coil-coil domain and DNA-binding domain of Stat3 mediated the interaction. CONCLUSIONS: This study uncovered a previously unrecognized profibrotic role of EphrinB2 in cardiac fibrosis, which is achieved through the interaction of Stat3 with TGF-ß/Smad3 signaling, implying a promising therapeutic target in fibrotic diseases and heart failure.

[A preliminary study on the autophagy level of human periodontal ligament cells regulated by nicotine].

OBJECTIVE: To explore the effect of nicotine on the autophagy level of human periodontal ligament cells (hPDLCs). METHODS: Periodontal tissues collected from premolars for orthodontic treatment reasons were used to culture hPDLCs. Western blot analysis was performed to test the most optimal time and concentration of nicotine on the autophagy level of the hPDLCs. Transmission electron microscope and immunofluorescence observation were carried out to detect the form of autophagosomes and expression of autophagy related protein LC3 in hPDLCs under this optimal condition. RESULTS: Protein expression of LC3Ⅱ was up regulated with the 12 h nicotine stimulating. Besides that, the up regulation of the protein expression of LC3Ⅱ was concentration dependent and nicotine with a concentration of 1×10⁻5 mol·L⁻¹ was the most optimal condition. Transmission electron microscope and immunofluorescence observations indicated that nicotine would activate the autophagy level of hPDLCs by increasing the number of autophagosomes and up regulating the expression of autophagy related protein LC3. CONCLUSIONS: Nicotine could increase autophagy level of hPDLCs, thus affecting the occurrence and development of smoking related periodontitis.

EphrinB2/EphB4 pathway in postnatal angiogenesis: a potential therapeutic target for ischemic cardiovascular disease.

Ischemic cardiovascular disease remains one of the leading causes of morbidity and mortality in the world. Proangiogenic therapy appears to be a promising and feasible strategy for the patients with ischemic cardiovascular disease, but the results of preclinical and clinical trials are limited due to the complicated mechanisms of angiogenesis. Facilitating the formation of functional vessels is important in rescuing the ischemic cardiomyocytes. EphrinB2/EphB4, a novel pathway in angiogenesis, plays a critical role in both microvascular growth and neovascular maturation. Hence, investigating the mechanisms of EphrinB2/EphB4 pathway in angiogenesis may contribute to the development of novel therapeutics for ischemic cardiovascular disease. Previous reviews mainly focused on the role of EphrinB2/EphB4 pathway in embryo vascular development, but their role in postnatal angiogenesis in ischemic heart disease has not been fully illustrated. Here, we summarized the current knowledge of EphrinB2/EphB4 in angiogenesis and their interaction with other angiogenic pathways in ischemic cardiovascular disease.

Intraoperative Identification of Liver Cancer Microfoci Using a Targeted Near-Infrared Fluorescent Probe for Imaging-Guided Surgery.

Difficulties in the highly sensitive detection of tumour microfoci represent a critical obstacle toward improved surgical intervention in liver cancer. Conventional preoperative imaging methods and surgeons' subjective experience are limited by their inability to effectively detect tumour lesions measuring less than 2 mm; however, intraoperative fluorescence molecular imaging may overcome this limitation. Here, we synthesised an arginine-glycine-aspartic acid (RGD)-conjugated mesoporous silica nanoparticle (MSN) highly loaded with indocyanine green (ICG) dye that could accurately delineate liver cancer margins and provide excellent tumour-to-normal tissue contrast intraoperatively. The increased ICG loading capacity and tumour specificity enabled the identification of residual microtumours and satellite lesions measuring less than 1 mm in living mice. Histological analysis validated the sensitivity and accuracy of this approach. We believe this technique utilising a new fluorescent nanoprobe with intraoperative optical imaging may offer a more sensitive and accurate method for liver cancer resection guidance, resulting in better surgical outcomes.