Objective To investigate the temporal changes in pathological damage and macrophage polarization in liver and spleen tissues of mice infected with Angiostrongylus cantonensis, and to preliminarily unravel the peripheral immune responses during the early stage of A. cantonensis infection. Methods Forty female BALB/c mice at ages of 6 to 8 weeks were randomly divided into four groups, including the control group and 7-, 14-, and 21-day infection groups, with 10 mice in each group. Each mouse in the infection groups was inoculated with 30 third-stage (L3) larvae of A. cantonensis by oral gavage, and five mice were randomly selected from each infection group on days 7, 14, and 21 post-infection, while mice in the control group were given the same volume of physiological saline and five mice were randomly selected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled. The histopathological changes of mouse liver and spleen tissues were observed using hematoxylin and eosin (HE) staining, and the percentage of positive staining area and the co-localization positive rates of the macrophage surface antigens F4/80, CD86, and CD206 were quantified in mouse liver and spleen tissues using immunohistochemical and immunofluorescence staining. In addition, five mice were collected from each infection group on days 7, 14, and 21 post-infection, and five mice were collected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled for detection of macrophage markers CD86 and CD206 and macrophage phenotyping using flow cytometry, and the expression of M1 macrophage markers, including inducible nitric oxide synthase (Nos2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and M2 markers, including arginase 1 (Arg1), mannose receptor C-type 1 (Mrc1) and chitinase-like protein 3 (Chil3) was quantified in mouse liver and spleen tissues using real-time quantitative PCR (RT-qPCR) assay. Results Proliferative lesions of the hepatocyte were observed in mouse liver tissues and the follicular structures of the mouse spleen white pulp were disrupted 21 days post-infection with A. cantonensis. Immunohistochemical staining showed that there were significant differences in the percentages of F4/80, CD86 and CD206 positive staining areas in the liver and spleen tissues among the four groups of mice (F = 242.40, 197.14, 183.19, 157.65, 242.35 and 146.24; all P values < 0.001), and the percentages of positive staining in the liver and spleen tissues of mice in the 14-day infection group [(4.45 ± 0.51)%, (3.74 ± 0.67)%, (8.32 ± 0.72)%, (16.56 ± 1.14)%, (11.62 ± 0.52)%, and (8.29 ± 0.72)%, respectively] and the 21-day infection group [(3.70 ± 0.11)%, (3.22 ± 0.43)%, (11.53 ± 1.03)%, (12.59 ± 1.05)%, (9.02 ± 0.83)%, and (11.67 ± 1.10)%, respectively] were higher than in the control group [(0.35 ± 0.16)%, (0.40 ± 0.02)%, (0.93 ± 0.05)%, (2.78 ± 0.26)%, (2.33 ± 0.20)%, and (1.85 ± 0.20)%, respectively] (all P values < 0.05). Immunofluorescence staining showed significant differences in the positive rates of F4/80 co-localization with CD86 and CD206 in mouse liver and spleen tissues among the four groups (F = 24.42, 25.28, 54.51 and 130.55; all P values < 0.001). Flow cytometry detected significant differences in the proportions of CD86⁺ and CD206⁺ macrophages in mouse liver and spleen tissues among the four groups (F = 67.98, 18.41, 29.77, 172.80; all P values < 0.001), and the proportions of CD206⁺ macrophages in the liver and spleen of the 21-day infection group were significantly higher than those in the control group [(9.25 ± 2.55)% vs (3.83 ± 0.72)%, and (4.22 ± 0.56)% vs (0.47 ± 0.18)%, respectively] (both P values < 0.05). In addition, RT-qPCR assay quantified significant differences in the relative mRNA expression of M1 macrophage markers (IL-1β, TNF-α and Nos2) and M2 macrophage markers (Arg1, Chil3 and Mrc1) in mouse liver and spleen tissues among the four groups (F = 41.30, 31.82, 199.33, 19.96, 62.01, 119.76, 23.67, 95.90, 72.27, 82.59, 123.41 and 29.75; all P values < 0.05). Conclusions A. cantonensis infection may cause progressive pathological damage in mouse liver and spleen tissues, accompanied by dynamic temporal changes in macrophage polarization. M1 macrophage polarization predominates at the early stage of A. cantonensis infection and shifts towards M2 polarization at the later stages, suggesting that M2 polarization may participate in immune regulation at late stages of A. cantonensis infection by suppressing excessive inflammatory responses and promoting tissue repair.

Aim To investigate the effect of p-AMPK activity on autophagy in different subtypes of MDA-MB-231(triple-negative breast cancer cells)and MCF-7(estrogen receptor-positive cells)and its regulatory mechanism.Methods MDA-MB-231 cells were trea-ted with EBSS,Baf-A1,and EBSS+Baf-A1 for four hours,and MCF-7 cells for eight hours.The effects of autophagy on cell proliferation and apoptosis were ob-served,mitochondrial morphology was examined,and the expression of autophagy markers LC3B,P62,LAMP1,TOM20,AMPK,p-AMPK,ULK1,and Bec-lin1/VPS34 proteins was detected.The autophagy pathway was validated by inhibiting AMPK activity.Results Breast cancer cells underwent autophagy af-ter starvation induction(EBSS),with inconsistent au-tophagy processes observed in different subtypes of breast cancer cells.Autophagy inhibited cell prolifera-tion.In MDA-MB-231 cells,autophagy led to an in-crease in p-AMPK levels and a decrease in ULK1 lev-els,initiating autophagy through p-AMPK activation of ULK1.In MCF-7 cells,both p-AMPK and ULK1 levels decreased after autophagy,suggesting that autophagy might not be mediated by p-AMPK activation.Conclu-sions MDA-MB-231 cells primarily initiate autophagy by directly activating ULK1 by p-AMPK,independent of the MTOR pathway.In MCF-7 cells autophagy might be triggered by inhibiting MTOR through AMPK activity or directly activating MTOR through other up-stream factors.Regulating p-AMPK activity based on the autophagy pathways in different cell subtypes could enable more precise targeting and treatment of different types of breast cancer.

Aim To investigate the effect of p-AMPK activity on autophagy in different subtypes of MDA-MB-231(triple-negative breast cancer cells)and MCF-7(estrogen receptor-positive cells)and its regulatory mechanism.Methods MDA-MB-231 cells were trea-ted with EBSS,Baf-A1,and EBSS+Baf-A1 for four hours,and MCF-7 cells for eight hours.The effects of autophagy on cell proliferation and apoptosis were ob-served,mitochondrial morphology was examined,and the expression of autophagy markers LC3B,P62,LAMP1,TOM20,AMPK,p-AMPK,ULK1,and Bec-lin1/VPS34 proteins was detected.The autophagy pathway was validated by inhibiting AMPK activity.Results Breast cancer cells underwent autophagy af-ter starvation induction(EBSS),with inconsistent au-tophagy processes observed in different subtypes of breast cancer cells.Autophagy inhibited cell prolifera-tion.In MDA-MB-231 cells,autophagy led to an in-crease in p-AMPK levels and a decrease in ULK1 lev-els,initiating autophagy through p-AMPK activation of ULK1.In MCF-7 cells,both p-AMPK and ULK1 levels decreased after autophagy,suggesting that autophagy might not be mediated by p-AMPK activation.Conclu-sions MDA-MB-231 cells primarily initiate autophagy by directly activating ULK1 by p-AMPK,independent of the MTOR pathway.In MCF-7 cells autophagy might be triggered by inhibiting MTOR through AMPK activity or directly activating MTOR through other up-stream factors.Regulating p-AMPK activity based on the autophagy pathways in different cell subtypes could enable more precise targeting and treatment of different types of breast cancer.

Objective To explore the effect of microRNA-381-3p(miR-381-3p)/MuRF1 axis on cardiopulmonary injury in hypoxia-induced pulmonary hypertension(HPH)mice and its potential mechanisms.Methods Sixty mice were randomly assigned to four groups:the normal control group(NC),the hypobaric hypoxia-induced pulmonary hypertension(HPH)group,the HPH+agomir control group and the HPH+miR-381-3p agomir analog group(HPH+miR-381-3p agomir),with 15 mice in each group.The HPH mouse model was established using a low-pressure and hypoxic artificial chamber.Three weeks prior to the establishment of the HPH model,miR-381-3p agomir and its corresponding control agomir were prepared by dissolving them in RNA-free phosphate-buffered saline(PBS)according to the experimental requirements.These solutions were administered via tail vein injection at a dose of 10 mg/kg,twice weekly for three consecutive weeks.Right heart function was assessed using echocardiography.Right ventricular systolic pressure(RVSP)was measured via cardiac catheterization.Pulmonary vascular remodeling was evaluated through hematoxylin and eosin(HE)staining.Levels of inflammatory cytokines in bronchoalveolar lavage fluid were quantified using enzyme-linked immunosorbent assay(ELISA).Real-time quantitative fluorescent PCR(RT-qPCR)was employed to analyze the mRNA expression levels of miR-381-3p and MuRF1.Potential targets of miR-381-3p were predicted,and pathway enrichment analysis was conducted.A dual-luciferase reporter gene assay was performed to confirm the direct regulatory effect of miR-381-3p on MuRF1.Results Compared with the NC group,the mRNA expression of miR-381-3p was significantly decreased in both the HPH group and the HPH+agomir control group,whereas the mRNA expression of MuRF1 was significantly increased(P＜0.05).In contrast,compared with the HPH group and the HPH+agomir control group,the mRNA expression of miR-381-3p was significantly increased in the HPH+miR-381-3p agomir group,while the mRNA expression of MuRF1 was significantly decreased(P＜0.05).Additionally,compared with the NC group,RVSP,right ventricular anterior wall thickness(RVAW),right ventricular hypertrophy index(RVHI),right ventricular collagen volume fraction(CVF),distal pulmonary artery wall thickness ratio(WT),pulmonary artery wall area ratio(WA),as well as IL-1β,IL-6 and TNF-α levels in alveolar lavage fluid were significantly increased in the HPH group and the HPH+agomir control group,whereas the right ventricular diameter(RVID)was significantly decreased(P＜0.05).Conversely,compared with the HPH group and the HPH+agomir control group,RVSP,RVAW,RVHI,right ventricular CVF,WT,Wa and RVID were decreased in the HPH+miR-381-3p agomir group,and IL-1β,IL-6,and TNF-α levels of alveolar lavage fluid were significantly decreased(P＜0.05).Furthermore,the downstream target genes of miR-381-3p were predicted in the database,and MuRF1 was a potential target,and the Cytoskeleton in muscle cells ranked first in the significant enrichment of target genes.Compared with WT-MuRF1+mimic control group,the luciferase activity was decreased in the WT-MuRF1+miR-381-3p mimic group(P＜0.05).There was no significant difference in the luciferase activity between the Mut-MuRF1+mimic control group and the Mut-MuRF1+miR-381-3p mimic group.Conclusion Overexpression of miR-381-3p can improve cardiopulmonary injury in HPH mice,and the mechanism may be related to the targeted inhibition of MuRF1 by miR-381-3p.

Radiochemotherapy-induced oral mucositis (OM) is a common oral complication in patients with tumors following head and neck radiotherapy or chemotherapy. Erosion and ulcers are the main features of OM that seriously affect the quality of life of patients and even the progress of tumor treatment. To date, differences in clinical prevention and treatment plans for OM have been noted among doctors of various specialties, which has increased the uncertainty of treatment effects. On the basis of current research evidence, this expert consensus outlines risk factors, clinical manifestations, clinical grading, ancillary examinations, diagnostic basis, prevention and treatment strategies and efficacy indicators for OM. In addition to strategies such as basic oral care, anti-inflammatory and analgesic agents, anti-infective agents, pro-healing agents, and photobiotherapy recommended in previous guidelines, we also emphasize the role of traditional Chinese medicine in OM prevention and treatment. This expert consensus aims to provide references and guidance for dental physicians and oncologists in formulating strategies for OM prevention, diagnosis, and treatment, standardizing clinical practice, reducing OM occurrence, promoting healing, and improving the quality of life of patients.
Humans ; Chemoradiotherapy/adverse effects* ; Consensus ; Risk Factors ; Stomatitis/etiology*

Rapid and ultrasensitive detection of pathogen-associated biomarkers is vital for the early diagnosis and therapy of bacterial infections. Herein, we developed a close-packed and ordered Au@AgPt array coupled with a cascade triggering strategy for surface-enhanced Raman scattering (SERS) and colorimetric identification of the Staphylococcus aureus biomarker micrococcal nuclease (MNase) in serum samples. The trimetallic Au@AgPt nanozymes can catalyze the oxidation of 3,3',5,5'-tetramethylbenzidine (TMB) molecules to SERS-enhanced oxidized TMB (oxTMB), accompanied by the color change from colorless to blue. In the presence of S. aureus, the secreted MNase preferentially cut the nucleobase AT-rich regions of DNA sequences on magnetic beads (MBs) to release alkaline phosphatase (ALP), which subsequently mediated the oxTMB reduction for inducing the colorimetric/SERS signal fade away. Using this "on-to-off" triggering strategy, the target S. aureus can be recorded in a wide linear range with a limit of detection of 38 CFU/mL in the colorimetric mode and 6 CFU/mL in the SERS mode. Meanwhile, the MNase-mediated strategy characterized by high specificity and sensitivity successfully discriminated between patients with sepsis (n = 7) and healthy participants (n = 3), as well as monitored the prognostic progression of the disease (n = 2). Overall, benefiting from highly active and dense "hot spot" substrate, MNase-mediated cascade response strategy, and colorimetric/SERS dual-signal output, this methodology will offer a promising avenue for the early diagnosis of S. aureus infection.

The chemical constituents of sesquiterpenes from 95% ethanol extract of Aquilariae Lignum Resinatum were isolated and purified by various column chromatography techniques, including silica gel, Sephadex LH-20, octadecylsilyl(ODS), and semi-preparative high performance liquid chromatography(HPLC). Their planar structures and absolute configurations were elucidated by ultraviolet(UV) spectrometry, infrared(IR) spectroscopy, mass spectrometry(MS), nuclear magnetic resonance(NMR), electronic circular dichroism(ECD), and other techniques. Eight sesquiterpenoids were isolated and identified as(+)-(7R,10R)-selina-4,11-dien-12-dimethoxy-15-al(1),(+)-(7R,10R)-selina-4,11-diene-12,15-dial(2), agalleudesmanol B(3), aquisinenoid C(4), 12,15-dioxo-α-selinen(5), agarospiranic aldehyde B(6), neopetasane(7), and eremophila-7(11),9-dien-8-one(8). Compound 1 was a new compound, and it was the first time to find a dimethoxy substitution on the side chain of eudesmane-type sesquiterpene skeleton.
Sesquiterpenes/isolation & purification* ; Thymelaeaceae/chemistry* ; Molecular Structure ; Drugs, Chinese Herbal/isolation & purification* ; Magnetic Resonance Spectroscopy

Objective To investigate the changes in the prevalence of Babesia microti infections, spleen morphology and proportions of splenic immune cells in BALB/c mice following intravenous and intraperitoneal injections, so as to provide insights into unraveling the immune regulatory mechanisms of Babesia infections. Methods Laboratory - maintained B. microti strains were prepared into whole blood samples with 10% prevalence of B. microti infection. A total of 75 BALB/c mice were randomly divided into three groups, including the normal control group, intravenous injection group, and intraperitoneal injection group, of 25 mice in each group. Mice in the intravenous and intraperitoneal injection groups were administered 100 μL of whole blood samples with 10% prevalence of B. microti infection, with the day of injection recorded as d0, and animals in the normal control group were given no treatments. Blood was sampled from mice in each group via the tail tip on d7, d14, d21, d28 and d35, and prepared into thin-film blood smears, and B. microti infection was observed in red blood cells. Five mice were randomly sampled from each group and sacrificed on d7, d14, d21, d28 and d35, and spleen was collected for measurement of spleen size and weight. In addition, splenic cells were isolated, and the proportions of CD3e⁺ T cells, CD45R⁺ B cells, CD49b⁺ nature killer (NK) cells, and F4/80⁺ macrophages were detected in CD45⁺ lymphocytes using flow cytometry. Results The prevalence of B. microti infection in the intravenous (22.80%) and intraperitoneal injection groups (44.82%) peaked on d7 (χ² = 8.141, P < 0.01) and then rapidly decreased, and no parasites were observed on d35. The longest mouse spleen length [(32.91 ± 2.20) mm] and width [(9.82 ± 0.43) mm], and the greatest weight [(0.78 ± 0.10) g] were found on d14 in the intravenous injection group, and the longest spleen length [(32.42 ± 3.21) mm] and width [(10.25 ± 0.73) mm], and the greatest weight [(0.73 ± 0.09) g] were seen in the intra-peritoneal injection group on d21, d7 and d14, respectively. There were significant differences among the intravenous injection group, intraperitoneal injection group and the normal control group in terms of spleen length (F = 10.310, P < 0.05), width (F = 9.824, P < 0.05), and weight (F = 10.672, P < 0.05) on d21, and the mouse spleen length, width and weight were all significantly greater in the intraperitoneal injection group than in the intravenous injection group (allP values < 0.05). The proportions of splenic CD3e⁺ T cells [(60.60 ± 6.20)% and (39.68 ± 7.62)%], CD45R⁺ B cells [(43.32 ± 2.08)% and (49.53 ± 4.90)%], CD49b⁺ NK cells [(6.88 ± 1.34)% and (7.71 ± 1.59)%], and F4/80⁺ macrophages [(2.21 ± 0.29)% and (3.80 ± 0.35)%] peaked on d14, d21, d21 and d14 in the intravenous and intraperitoneal injection groups, respectively. There were significant differences in the proportions of CD3e⁺ T cells (F = 16.730, P < 0.05) and F4/80⁺ macrophages (F = 15.941, P < 0.05) among the intravenous injection group, intraperitoneal injection group and normal control group on d14, and a higher proportion of CD3e⁺ T cells and a lower proportion of F4/80⁺ macrophages were detected in the intravenous injection group than in the intraperitoneal injection group (both P values < 0.01). There were significant differences among the intravenous injection group, intraperitoneal injection group and normal control group on d21 in terms of proportions of splenic CD3e⁺ T cells (F = 9.252, P < 0.05), CD45R⁺ B cells (F = 14.349, P < 0.05), CD49b⁺ NK cells (F = 13.436,P < 0.05), and F4/80⁺ macrophages (F = 8.180, P < 0.05), and a higher proportion of CD3e⁺ T cells and lower proportions of CD45R⁺ B cells and F4/80⁺ macrophages were detected in the intravenous injection group than in the intraperitoneal injection group (all P values < 0.01). In addition, there was a significant difference in the proportion of CD3e⁺ T cells among the intravenous injection group, intraperitoneal injection group and normal control group on d28 (F = 9.772,P < 0.05), and a lower proportion of CD3e⁺ T cells was found in the intravenous injection group than in the intraperitoneal injection group (P < 0.01). Conclusions Both intraperitoneal and intravenous routes are effective to induce B. microti infections in BALB/c mice, and the prevalence of B. microti infections is higher in BALB/c mice through the intraperitoneal route than through the intravenous route. Intraperitoneal and intravenous injections with B. microti cause diverse spleen morphologies and proportions of splenic immune cells in mice, indicating routes of B. microti infections cause different impacts on immune response mechanisms in mice.

Objective:To investigate the reliability and validity of different measurement methods under 30° arthroscopy for quantifying the proportion of glenoid bone defect in bony Bankart lesions of the shoulder joint and validate its preliminary application effect.Methods:Eight intact shoulder glenoid specimens were selected, with no existing defects or deformities, from donors of 4 females and 4 males, with their age at death of 43-67 years [(54.4±8.0)years]. Bone defects of 12.5% and 25% were created in the glenoid at 0° and 45° relative to the longitudinal axis, with two specimens per defect category. The defect proportion in each specimen was quantified using direct measurement and CT-based digital reconstruction and these values served as reference standards for subsequent statistical analysis. Using a combined approach of arthroscopic simulation equipment and cadaveric study, five investigators performed simulated examinations through the standard posterior portal (2 cm medial and 1.5 cm inferior to the posterolateral acromial corner) and the modified posteroinferior portal (2 cm medial and 3 cm inferior to the posterolateral acromial corner) separately. Under 30° arthroscopy, the glenoid bone loss percentage was measured using the bare spot method and secant chord method. The reliability was analyzed for these measurements. Furthermore, using direct physical measurements and CT-based three-dimensional reconstruction data from the same specimens as reference standards, the comprehensive validity of four measurement methods was evaluated (standard posterior portal-bare spot method, standard posterior portal-secant chord method, modified posteroinferior portal-bare spot method, and modified posteroinferior portal-secant chord method). The independent validity of each method was assessed according to bone defect morphology classification to determine differences in measurement accuracy across defect types. In an arthroscopic procedure for a patient with Bigliani type IIIB bony Bankart lesion, the standard posterior portal-secant chord method was applied to quantify the proportion of glenoid bone defects.Results:The mean reference values from direct measurement and CT measurement of glenoid bone defect proportion in eight bony Bankart lesion specimens were 12.71%/12.37%, 13.17%/13.10%, 25.71%/24.9%, 26.6%/26.95%, 13.41%/13.10%, 12.90%/12.59%, 26.42%/25.94%, and 26.73%/27.06%, respectively. Measurements obtained by the five investigators showed intraclass correlation coefficients (ICCs) all greater than 0.90, indicating excellent interobserver agreement. In the validity analysis, the standard posterior portal-secant chord method demonstrated the highest overall validity. Using direct measurement and CT-based measurement as reference standards, the overall validity was (0.90±0.38)% and (1.07±0.53)% for the standard posterior portal-bare spot method, (1.33±0.40)% and (1.51±0.54)% for the modified posteroinferior portal-bare spot method, and (0.53±0.17)% and (0.70±0.38)% ( P<0.05) for the modified posteroinferior portal-secant chord method. In contrast, the standard posterior portal-secant chord method showed an overall validity of (0.10±0.10)% and (0.28±0.39)% ( P>0.05). In subsequent independent validity analyses, the standard posterior portal-secant chord method also demonstrated superior validity across all bone defect subtypes over the other three methods. In a patient with a Bigliani type IIIB bony Bankart lesion, we used the standard posterior portal-secant chord method to quantify the glenoid bone loss in 2 minutes, revealing a defect proportion of 26.6%. An arthroscopic autologous iliac bone graft procedure with single-tunnel elastic fixation guided by this measurement achieved favorable outcomes, with stable reduction, secure internal fixation and favorable recovery of shoulder function at 2 months postoperatively. Conclusion:For various types of bony Bankart lesions, the 30° arthroscopic standard posterior portal-secant chord method provides the most accurate quantification of glenoid bone loss and its preliminary clinical application yields satisfactory results.

Objective:To investigate the reliability and validity of different measurement methods under 30° arthroscopy for quantifying the proportion of glenoid bone defect in bony Bankart lesions of the shoulder joint and validate its preliminary application effect.Methods:Eight intact shoulder glenoid specimens were selected, with no existing defects or deformities, from donors of 4 females and 4 males, with their age at death of 43-67 years [(54.4±8.0)years]. Bone defects of 12.5% and 25% were created in the glenoid at 0° and 45° relative to the longitudinal axis, with two specimens per defect category. The defect proportion in each specimen was quantified using direct measurement and CT-based digital reconstruction and these values served as reference standards for subsequent statistical analysis. Using a combined approach of arthroscopic simulation equipment and cadaveric study, five investigators performed simulated examinations through the standard posterior portal (2 cm medial and 1.5 cm inferior to the posterolateral acromial corner) and the modified posteroinferior portal (2 cm medial and 3 cm inferior to the posterolateral acromial corner) separately. Under 30° arthroscopy, the glenoid bone loss percentage was measured using the bare spot method and secant chord method. The reliability was analyzed for these measurements. Furthermore, using direct physical measurements and CT-based three-dimensional reconstruction data from the same specimens as reference standards, the comprehensive validity of four measurement methods was evaluated (standard posterior portal-bare spot method, standard posterior portal-secant chord method, modified posteroinferior portal-bare spot method, and modified posteroinferior portal-secant chord method). The independent validity of each method was assessed according to bone defect morphology classification to determine differences in measurement accuracy across defect types. In an arthroscopic procedure for a patient with Bigliani type IIIB bony Bankart lesion, the standard posterior portal-secant chord method was applied to quantify the proportion of glenoid bone defects.Results:The mean reference values from direct measurement and CT measurement of glenoid bone defect proportion in eight bony Bankart lesion specimens were 12.71%/12.37%, 13.17%/13.10%, 25.71%/24.9%, 26.6%/26.95%, 13.41%/13.10%, 12.90%/12.59%, 26.42%/25.94%, and 26.73%/27.06%, respectively. Measurements obtained by the five investigators showed intraclass correlation coefficients (ICCs) all greater than 0.90, indicating excellent interobserver agreement. In the validity analysis, the standard posterior portal-secant chord method demonstrated the highest overall validity. Using direct measurement and CT-based measurement as reference standards, the overall validity was (0.90±0.38)% and (1.07±0.53)% for the standard posterior portal-bare spot method, (1.33±0.40)% and (1.51±0.54)% for the modified posteroinferior portal-bare spot method, and (0.53±0.17)% and (0.70±0.38)% ( P<0.05) for the modified posteroinferior portal-secant chord method. In contrast, the standard posterior portal-secant chord method showed an overall validity of (0.10±0.10)% and (0.28±0.39)% ( P>0.05). In subsequent independent validity analyses, the standard posterior portal-secant chord method also demonstrated superior validity across all bone defect subtypes over the other three methods. In a patient with a Bigliani type IIIB bony Bankart lesion, we used the standard posterior portal-secant chord method to quantify the glenoid bone loss in 2 minutes, revealing a defect proportion of 26.6%. An arthroscopic autologous iliac bone graft procedure with single-tunnel elastic fixation guided by this measurement achieved favorable outcomes, with stable reduction, secure internal fixation and favorable recovery of shoulder function at 2 months postoperatively. Conclusion:For various types of bony Bankart lesions, the 30° arthroscopic standard posterior portal-secant chord method provides the most accurate quantification of glenoid bone loss and its preliminary clinical application yields satisfactory results.