ObjectiveTo investigate the inhibitory effects of curcumol （Cur） on the proliferation and metastasis of non-small cell lung cancer （NSCLC） cells and to explore the underlying mechanisms. MethodsIn vivo， a subcutaneous tumor xenograft model was established to evaluate the antiproliferative effect of Cur. In vitro， the cell counting kit-8 （CCK-8） assay was used to assess the effects of Cur at concentrations of 0， 60， 120， 240， 360， 480， 600， 720， 840， 960 μmol·L^-1 on the viability of NCI-A549 and NCI-H23 cells， and to evaluate its inhibitory effect on the proliferation of human bronchial epithelial BEAS-2B cells. Wound healing and Transwell migration assays were conducted to assess changes in cell migratory capacity following Cur treatment. Immunohistochemistry （IHC-P） was used to investigate the regulatory effect of Cur on the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway in tumor tissues. Western blot was performed to determine the protein expression levels of phosphorylated JAK2 （p-JAK2）， phosphorylated STAT3 （p-STAT3）， proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） in tumor tissues and cells. To further verify the role of the JAK2/STAT3 signaling pathway in the pharmacological effects of Cur， rescue experiments were performed using the pathway agonist colivelin. ResultsIn vivo experiments showed that， compared with the model group， the tumor volumes of subcutaneous xenografts in nude mice in both low- and high-dose Cur groups were significantly reduced （P<0.05）， and the tumor inhibition rates were significantly increased （P<0.05）. The inhibitory effect in the high-dose group was comparable to that of the cisplatin group， and the body weight of mice in the Cur groups remained stable throughout the experiment. In vitro， compared with the control group， Cur at concentrations of 120 and 240 μmol·L^-1 inhibited the proliferation of NCI-A549 and NCI-H23 cells in a concentration-dependent manner （P<0.05）， with a significant inhibitory effect observed at 360 μmol·L^-1 （P<0.01）， while no significant effect on the viability of BEAS-2B cells was observed. Migration assays demonstrated that， compared with the control group， Cur treatment significantly reduced the migration rates of both cell lines in a concentration-dependent manner （P<0.05）， with an inhibitory effect at 360 μmol·L^-1 comparable to that of the cisplatin group. Mechanistic validation showed that， compared with the control group， the protein expression levels of p-JAK2 and p-STAT3 in tumor tissues and cells were significantly downregulated in the Cur groups （P<0.01）， and the expression levels of downstream proteins PCNA， MMP-2， MMP-9， and VEGFA were also significantly decreased with increasing Cur concentration （P<0.05）. In the rescue experiments， compared with the control group， colivelin pretreatment increased cell proliferation and migration rates （P<0.05） and upregulated the expression of related proteins （P<0.05）. Compared with the Cur group， the colivelin+Cur group showed significantly increased proliferation and migration rates （P<0.05）， along with significantly upregulated protein expression levels （P<0.05）. ConclusionCur can significantly inhibit the proliferation and metastasis of NSCLC both in vivo and in vitro， and its mechanism of action is closely associated with the inhibition of JAK2/STAT3 signaling pathway activation.

ObjectiveTo investigate the mechanisms by which oxyresveratrol （OXY） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） through the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsCell counting kit-8 （CCK-8） assays were used to determine the survival rates of A549 and H1299 cells treated with different concentrations of OXY， and appropriate concentrations （0， 30， 60， 90 μmol·L^-1） were selected. The effects of OXY on the proliferation of A549 and H1299 cells were evaluated using 5-ethynyl-2′-deoxyuridine （EdU） assays and colony formation assays. Wound healing assays and Transwell invasion assays were performed to assess the effects of OXY on cell migration and invasion. Western blot （WB） was used to detect the expression levels of Snail， E-cadherin， N-cadherin， and Vimentin in A549 and H1299 cells. Network pharmacology and molecular docking were applied to predict the mechanism of action of OXY， and WB was used to evaluate the effects of OXY on proteins in the PI3K/Akt signaling pathway. Rescue experiments were conducted using the PI3K/Akt signaling pathway agonist 740Y-P. Under activation of the PI3K/Akt pathway， the effect of OXY on proliferation， migration， and invasion phenotypes， as well as on the expression levels of PI3K/Akt pathway-related proteins and EMT markers （Snail， E-cadherin， N-cadherin， and Vimentin）， were examined. ResultsIn the forward experiments， CCK-8 assay results showed that， compared with the control group， the survival rates of NSCLC cells in the OXY-treated groups （20-120 μmol·L^-1） were significantly decreased （P<0.05）. The half-maximal inhibitory concentration （IC₅₀） values of A549 and H1299 cells after 48 h of OXY treatment were 113.6 μmol·L^-1 and 92.53 μmol·L^-1， respectively. Therefore， concentrations of 0， 30， 60， 90 μmol·L^-1 were selected as the gradient for subsequent phenotypic and mechanistic studies. Compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the OXY groups （30， 60， and 90 μmol·L^-1） were significantly decreased （P<0.01， P<0.05）. WB results showed that， compared with the control group， the protein expression levels of Snail， N-cadherin， and Vimentin in NSCLC cells of the OXY groups were significantly decreased （P<0.05）， whereas E-cadherin expression was significantly increased （P<0.01）. Network pharmacology and molecular docking results indicated that OXY could act on the PI3K/Akt signaling pathway and exhibited good binding affinity with PI3K and Akt proteins. Further WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in NSCLC cells of the OXY groups， whereas the expression levels of phosphorylated PI3K （p-PI3K） and phosphorylated Akt （p-Akt） were significantly decreased （P<0.05）. In the rescue experiments， compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the 740Y-P group （15 μmol·L^-1） were significantly increased （P<0.01）. Compared with the control + OXY group （90 μmol·L^-1）， these indices in the 740Y-P + OXY group （15 μmol·L^-1 + 90 μmol·L^-1） were also significantly increased （P<0.01）. WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in the 740Y-P group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.01）. Compared with the control + OXY group， there were no statistically significant differences in PI3K and Akt protein expression in the 740Y-P + OXY group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.05）. ConclusionOXY inhibits the PI3K/Akt signaling pathway and suppresses the EMT process， thereby exerting anti-metastatic effects in NSCLC.

Lung cancer， particularly non-small cell lung cancer （NSCLC）， is the malignant tumor with the highest incidence and mortality in China and worldwide. In 2022， the global number of deaths reached 1.8 million， accounting for 18.7% of all cancer-related deaths， seriously threatening human health and life， and posing a severe challenge for prevention and treatment. Although treatment strategies for lung cancer have been continuously enriched in recent years， and progress has been made in targeted therapy and immunotherapy， long-term survival benefits remain limited due to primary or acquired drug resistance， low immune responsiveness， and chemotherapy-related toxicities. Therefore， there is an urgent need to explore safe and effective adjunctive therapeutic strategies. Traditional Chinese medicine （TCM）， with its advantages of holistic regulation and individualized syndrome differentiation， has played an increasingly prominent role in comprehensive cancer treatment. TCM holds that "Yang deficiency leads to accumulation" is a key pathogenesis of tumors. Based on the theory that "Yang transforms Qi， while Yin forms substance"， deficiency of Yang Qi results in impaired warming and transformation functions， leading to internal accumulation of Yin-cold. This is closely related to dysregulation of the immune microenvironment， "cold tumor" characteristics， and dysfunction of the neuroendocrine system in modern medicine. Accordingly， the therapeutic strategy of "warming Yang， supporting healthy Qi， and combating cancer" has gained increasing attention. In recent years， commonly used Yang-warming Chinese herbs， including Aconiti Lateralis Radix Praeparata， Zingiberis Rhizoma， Cinnamomi Cortex， Epimedii Folium， and Psoraleae Fructus， as well as their active constituents， have achieved notable progress in anti-lung cancer research by regulating multiple signaling pathways， inducing apoptosis， inhibiting metastasis， and reversing drug resistance. In addition， Yang-warming formulae such as Sini Tang and Yanghe Tang have shown promising effects in alleviating myelosuppression， improving cancer-related fatigue， managing malignant pleural effusion， and relieving cancer pain. These therapies exhibit toxicity-reducing and efficacy-enhancing effects， significantly improving patients' quality of life and survival benefits. To systematically summarize the roles and mechanisms of Yang-warming Chinese herbal medicines and compound formulae in lung cancer， this paper provides a comprehensive review of recent advances， aiming to offer insights for the clinical practice of TCM in the prevention and treatment of lung cancer.

ObjectiveTo investigate the inhibitory effects of curcumol （Cur） on the proliferation and metastasis of non-small cell lung cancer （NSCLC） cells and to explore the underlying mechanisms. MethodsIn vivo， a subcutaneous tumor xenograft model was established to evaluate the antiproliferative effect of Cur. In vitro， the cell counting kit-8 （CCK-8） assay was used to assess the effects of Cur at concentrations of 0， 60， 120， 240， 360， 480， 600， 720， 840， 960 μmol·L^-1 on the viability of NCI-A549 and NCI-H23 cells， and to evaluate its inhibitory effect on the proliferation of human bronchial epithelial BEAS-2B cells. Wound healing and Transwell migration assays were conducted to assess changes in cell migratory capacity following Cur treatment. Immunohistochemistry （IHC-P） was used to investigate the regulatory effect of Cur on the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway in tumor tissues. Western blot was performed to determine the protein expression levels of phosphorylated JAK2 （p-JAK2）， phosphorylated STAT3 （p-STAT3）， proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） in tumor tissues and cells. To further verify the role of the JAK2/STAT3 signaling pathway in the pharmacological effects of Cur， rescue experiments were performed using the pathway agonist colivelin. ResultsIn vivo experiments showed that， compared with the model group， the tumor volumes of subcutaneous xenografts in nude mice in both low- and high-dose Cur groups were significantly reduced （P<0.05）， and the tumor inhibition rates were significantly increased （P<0.05）. The inhibitory effect in the high-dose group was comparable to that of the cisplatin group， and the body weight of mice in the Cur groups remained stable throughout the experiment. In vitro， compared with the control group， Cur at concentrations of 120 and 240 μmol·L^-1 inhibited the proliferation of NCI-A549 and NCI-H23 cells in a concentration-dependent manner （P<0.05）， with a significant inhibitory effect observed at 360 μmol·L^-1 （P<0.01）， while no significant effect on the viability of BEAS-2B cells was observed. Migration assays demonstrated that， compared with the control group， Cur treatment significantly reduced the migration rates of both cell lines in a concentration-dependent manner （P<0.05）， with an inhibitory effect at 360 μmol·L^-1 comparable to that of the cisplatin group. Mechanistic validation showed that， compared with the control group， the protein expression levels of p-JAK2 and p-STAT3 in tumor tissues and cells were significantly downregulated in the Cur groups （P<0.01）， and the expression levels of downstream proteins PCNA， MMP-2， MMP-9， and VEGFA were also significantly decreased with increasing Cur concentration （P<0.05）. In the rescue experiments， compared with the control group， colivelin pretreatment increased cell proliferation and migration rates （P<0.05） and upregulated the expression of related proteins （P<0.05）. Compared with the Cur group， the colivelin+Cur group showed significantly increased proliferation and migration rates （P<0.05）， along with significantly upregulated protein expression levels （P<0.05）. ConclusionCur can significantly inhibit the proliferation and metastasis of NSCLC both in vivo and in vitro， and its mechanism of action is closely associated with the inhibition of JAK2/STAT3 signaling pathway activation.

ObjectiveTo investigate the mechanisms by which oxyresveratrol （OXY） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） through the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsCell counting kit-8 （CCK-8） assays were used to determine the survival rates of A549 and H1299 cells treated with different concentrations of OXY， and appropriate concentrations （0， 30， 60， 90 μmol·L^-1） were selected. The effects of OXY on the proliferation of A549 and H1299 cells were evaluated using 5-ethynyl-2′-deoxyuridine （EdU） assays and colony formation assays. Wound healing assays and Transwell invasion assays were performed to assess the effects of OXY on cell migration and invasion. Western blot （WB） was used to detect the expression levels of Snail， E-cadherin， N-cadherin， and Vimentin in A549 and H1299 cells. Network pharmacology and molecular docking were applied to predict the mechanism of action of OXY， and WB was used to evaluate the effects of OXY on proteins in the PI3K/Akt signaling pathway. Rescue experiments were conducted using the PI3K/Akt signaling pathway agonist 740Y-P. Under activation of the PI3K/Akt pathway， the effect of OXY on proliferation， migration， and invasion phenotypes， as well as on the expression levels of PI3K/Akt pathway-related proteins and EMT markers （Snail， E-cadherin， N-cadherin， and Vimentin）， were examined. ResultsIn the forward experiments， CCK-8 assay results showed that， compared with the control group， the survival rates of NSCLC cells in the OXY-treated groups （20-120 μmol·L^-1） were significantly decreased （P<0.05）. The half-maximal inhibitory concentration （IC₅₀） values of A549 and H1299 cells after 48 h of OXY treatment were 113.6 μmol·L^-1 and 92.53 μmol·L^-1， respectively. Therefore， concentrations of 0， 30， 60， 90 μmol·L^-1 were selected as the gradient for subsequent phenotypic and mechanistic studies. Compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the OXY groups （30， 60， and 90 μmol·L^-1） were significantly decreased （P<0.01， P<0.05）. WB results showed that， compared with the control group， the protein expression levels of Snail， N-cadherin， and Vimentin in NSCLC cells of the OXY groups were significantly decreased （P<0.05）， whereas E-cadherin expression was significantly increased （P<0.01）. Network pharmacology and molecular docking results indicated that OXY could act on the PI3K/Akt signaling pathway and exhibited good binding affinity with PI3K and Akt proteins. Further WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in NSCLC cells of the OXY groups， whereas the expression levels of phosphorylated PI3K （p-PI3K） and phosphorylated Akt （p-Akt） were significantly decreased （P<0.05）. In the rescue experiments， compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the 740Y-P group （15 μmol·L^-1） were significantly increased （P<0.01）. Compared with the control + OXY group （90 μmol·L^-1）， these indices in the 740Y-P + OXY group （15 μmol·L^-1 + 90 μmol·L^-1） were also significantly increased （P<0.01）. WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in the 740Y-P group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.01）. Compared with the control + OXY group， there were no statistically significant differences in PI3K and Akt protein expression in the 740Y-P + OXY group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.05）. ConclusionOXY inhibits the PI3K/Akt signaling pathway and suppresses the EMT process， thereby exerting anti-metastatic effects in NSCLC.

Lung cancer， particularly non-small cell lung cancer （NSCLC）， is the malignant tumor with the highest incidence and mortality in China and worldwide. In 2022， the global number of deaths reached 1.8 million， accounting for 18.7% of all cancer-related deaths， seriously threatening human health and life， and posing a severe challenge for prevention and treatment. Although treatment strategies for lung cancer have been continuously enriched in recent years， and progress has been made in targeted therapy and immunotherapy， long-term survival benefits remain limited due to primary or acquired drug resistance， low immune responsiveness， and chemotherapy-related toxicities. Therefore， there is an urgent need to explore safe and effective adjunctive therapeutic strategies. Traditional Chinese medicine （TCM）， with its advantages of holistic regulation and individualized syndrome differentiation， has played an increasingly prominent role in comprehensive cancer treatment. TCM holds that "Yang deficiency leads to accumulation" is a key pathogenesis of tumors. Based on the theory that "Yang transforms Qi， while Yin forms substance"， deficiency of Yang Qi results in impaired warming and transformation functions， leading to internal accumulation of Yin-cold. This is closely related to dysregulation of the immune microenvironment， "cold tumor" characteristics， and dysfunction of the neuroendocrine system in modern medicine. Accordingly， the therapeutic strategy of "warming Yang， supporting healthy Qi， and combating cancer" has gained increasing attention. In recent years， commonly used Yang-warming Chinese herbs， including Aconiti Lateralis Radix Praeparata， Zingiberis Rhizoma， Cinnamomi Cortex， Epimedii Folium， and Psoraleae Fructus， as well as their active constituents， have achieved notable progress in anti-lung cancer research by regulating multiple signaling pathways， inducing apoptosis， inhibiting metastasis， and reversing drug resistance. In addition， Yang-warming formulae such as Sini Tang and Yanghe Tang have shown promising effects in alleviating myelosuppression， improving cancer-related fatigue， managing malignant pleural effusion， and relieving cancer pain. These therapies exhibit toxicity-reducing and efficacy-enhancing effects， significantly improving patients' quality of life and survival benefits. To systematically summarize the roles and mechanisms of Yang-warming Chinese herbal medicines and compound formulae in lung cancer， this paper provides a comprehensive review of recent advances， aiming to offer insights for the clinical practice of TCM in the prevention and treatment of lung cancer.

Objective:To evaluate rapid on-site evaluation (ROSE) in endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) for pancreatic solid lesions, and to compare the difference in ROSE performance between cytopathologists and trained endoscopists.Methods:A total of 168 consecutive patients with pancreatic solid lesions who underwent EUS-FNA from January 2014 to December 2020 at Fuding Hospital, Fujian University of Traditional Chinese Medicine were recruited. The patients who did not receive ROSE from January 2014 to November 2017 were included in N-ROSE group ( n=67). Since December 2017, the patients who intended to receive EUS-FNA were divided into E-ROSE group ( n=59, patients who received EUS-FNA and ROSE by endoscopists trained with cytopathology) and C-ROSE group ( n=42,patients who received EUS-FNA by untrained endoscopists and ROSE by cytopathologists) according to random number table. The number of punctures, sample adequacy, cytological diagnosis, final diagnosis and diagnostic efficiency (including the sensitivity, the specificity, the positive predictive value, the negative predictive value and the accuracy) in 3 groups were compared. Results:(1) The puncture number in N-ROSE group (4.22±0.76) was significantly more than E-ROSE group (3.12±0.79, P<0.001) and C-ROSE group (3.24±0.91, P<0.001). (2) The proportions of adequate samples in N-ROSE group [82.09% (55/67)] was significantly lower than those of E-ROSE group [96.61% (57/59), χ2=5.308, P=0.021] and C-ROSE group [97.62% (41/42), χ2=4.541, P=0.033]. The proportion of negative cytological diagnosis in N-ROSE group [40.30% (27/67)] was significantly higher than those of E-ROSE group [20.34% (12/59), χ2=5.848, P=0.016] and C-ROSE group [19.05% (8/42), χ2=5.348, P=0.021]. (3) The sensitivity of N-ROSE group [74.07% (40/54)] was significantly lower than those of E-ROSE group [94.00% (47/50), χ2=6.151, P=0.013] and C-ROSE group [94.44% (34/36), χ2=4.817, P=0.028]. The accuracy in N-ROSE group [79.10% (53/67)] was significantly lower than those of E-ROSE group [94.92% (56/59), χ2=5.433, P=0.020] and C-ROSE group [95.24% (40/42), χ2=4.155, P=0.042]. (4) There was no significant difference in any observational index between E-ROSE group and C-ROSE group ( P>0.05). Conclusion:ROSE in EUS-FNA can improve sample adequacy, the diagnostic sensitivity and accuracy, and reduce the number of punctures. The sample adequacy and diagnostic efficiency of endoscopists trained with cytopathology are comparable to those of cytopathologists.

Objective:To evaluate the clinical application of LASEREO endoscopic system in early gastric cancer (EGC).Methods:A total of 68 patients diagnosed with EGC were retrospectively analyzed between August 2017 to December 2020 in Fuding Hospital Affiliated to Fujian University of Traditional Chinese Medicine. There were 50 males and 18 females finally enrolled with a median age of 64 years. EGCs were analyzed from subjective and objective aspect, as well as from magnification and non-magnification status. Six endoscopists evaluated the visibility of the EGC (RSC) and calculated the color difference (ΔEC) between EGC and the surrounding mucosa in white light imaging (WLI), blue light imaging-bright (BLI-Bri) and linked color imaging (LCI) modes. In the case of magnification (×80), the visibility of the microstructures and microvessels (RSV) was analyzed and the color difference (ΔEV) between microvessels and non-vessels areas were calculated in WLI, BLI and LCI modes. The visibility was evaluated using visibility ranking scale(RS) and the color difference (ΔE) was calculated using L*a*b* color space.Results:In WLI, BLI-Bri, and LCI modes, the mean (±SD) RSC were 2.56±0.68, 2.63±0.59 and 3.17±0.50, and the mean(±SD) ΔEC were 15.71±5.58, 12.04±3.73, and 22.84±8.46, respectively, which in LCI were higher than those in WLI and BLI-Bri modes ( P<0.001).Regarding the data evaluated by senior endoscopists, the RSC was higher in BLI-Bri than that in WLI mode (2.98±0.58 vs. 2.79±0.73, P<0.001), but as to those evaluated by junior endoscopists, there were no significant differences between the WLI and BLI-Bri modes(2.29±0.72 vs. 2.23±0.72,P =0.218).In magnifying endoscopy with WLI, BLI, and LCI modes, the mean(±SD) RSV were 2.95±0.28, 3.46±0.40, and 3.38±0.33, and the mean (±SD) ΔEV were 21.68±7.52, 44.29±10.94, and 45.38±14.29, respectively.The RSV and ΔEV in LCI and BLI were higher than that in WLI mode ( P<0.001). Conclusions:LCI improves the visibility of EGC by increasing ΔEC, especially in junior endoscopists. Both BLI and LCI improve the visibility of microstructures and microvessels under magnification.

Objective To investigate the diagnostic value of blue light imaging-bright (BLI-bright) and linked color imaging (LCI) for early esophageal cancer (EEC).Methods:Data of 63 consecutive patients with EEC who underwent gastroscopy under BLI-bright, LCI and white-light imaging (WLI) and endoscopic submucosal dissection (ESD) from May 2018 to August 2020 at Fuding Hospital Affiliated to Fujian University of Traditional Chinese Medicine were analyzed retrospectively in the cohort study. Subjective visibility analysis was performed by 6 endoscopists who were divided into 2 groups (expert group and trainee group) with 3 endoscopists in each group. The main observation index was the visibility score (ranking score, RS). The objective color difference (Δ E) between lesions of EEC and surrounding mucosa under 3 modes were analyzed by using the L *a *b * color space. Results:The overall RS of 6 endoscopists under WLI mode (2.57±0.81) was significantly lower than that under LCI (3.25±0.67) ( t=9.71, P<0.001) and BLI-bright (3.18±0.67) ( t=9.31, P<0.001). In the expert group, the RS of WLI (2.71±0.80) was significantly lower than that of LCI (3.33±0.66) ( t=7.16, P<0.001) and BLI-bright (3.42±0.62) ( t=8.09, P<0.001). In the trainee group, the RS of WLI (2.40±0.90) was also significantly lower than that of LCI (3.15±0.83) ( t=9.62, P<0.001) and BLI-bright (2.89±0.92) ( t=5.69, P<0.001), and the RS of LCI was higher than that of BLI-bright ( t=4.07, P<0.001). The Δ E between lesions of EEC and surrounding mucosa under WLI (11.52±3.40) was significantly lower than that under LCI (16.64±4.70) ( t=7.10, P<0.001) and BLI-bright (15.72±3.84) ( t=7.88, P<0.001). Conclusion:BLI-bright and LCI can effectively improve EEC visibility and color difference between EEC and surrounding mucosa. Furthermore, LCI is more conducive to the detection of EEC for the trainees.

Objective:To evaluate the efficacy of linked color imaging (LCI) for the colorectal polyp detection, especially detection of adenoma.Methods:A retrospective analysis was conducted on the patients who underwent LCI or white light imaging(WLI) mode of LASEREO colonoscopy from May 2018 to March 2019.The differences of the detection rates in the global polyps, adenomatous polyps, flat polyps, small polyps (≤5 mm) and right-sided polyps under two modes were compared. Color differences between the adenomatous polyps and surrounding mucosa (ΔE) were examined under two modes, based on L *a *b * color space by the Commission Internationale de L′Eclairage in 1976. Results:The global polyp detection rate, especially adenoma detection rate, in LCI group was higher than that in WLI group(45.53% VS 32.83%, P=0.038; 53.65% VS 39.62%, P=0.009). The color difference(ΔE) between adenomatous polyps and surrounding mucosa in LCI group was significantly higher than that in WLI group(27.24±8.67 VS 15.28±6.68, P<0.001). In addition, the detection rates of flat polyps, small polyps and right-sided polyps in LCI group were higher than those in WLI group (61.98% VS 47.17%, P=0.005; 60.94% VS 42.77%, P=0.001; 45.83% VS 32.70%, P=0.012). Conclusion:LCI can effectively improve the colorectal polyp detection rate, especially adenoma detection rate, which is worthy of clinical application.