The construction of a training system for visiting physicians in the department of rare diseases in China is an important measure to improve the overall diagnosis and treatment capacity for rare diseases and address the critical challenge of insufficient knowledge and skills among clinicians in practice. This article systematically describes the visiting physician training system established by the Department of Rare Diseases at Peking Union Medical College Hospital. It summarizes the training objectives and positioning, design logic, and learning modules of the system, aiming to provide a reference for the construction of the specialized talent team for rare diseases in China.

To investigate the clinical efficacy of neoadjuvant imatinib in the treatment of rectal gastrointestinal stromal tumor (GIST).

ObjectiveTo construct a competing endogenous RNA （ceRNA） network involving long non-coding RNA NOTCH1 （lncRNA NOTCH1） and investigate whether Xianglian Huazhuo prescription （XLHZ） ameliorates gastric mucosal injury via regulating ferroptosis through the lncRNA NOTCH1/microRNA-138-5p （miR-138-5p）/silent information regulator 1 （SIRT1） axis. MethodsLncRNA sequencing and bioinformatics tools were used to construct the ceRNA network involving lncRNA NOTCH1. In the animal experiments， a chronic atrophic gastritis （CAG） model was induced by N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） in mice. Mice were randomized into normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.6， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups （n=10）. Transmission electron microscopy was adopted to assess gastric pathology. Real-time PCR was employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， nuclear factor erythroid 2-related factor 2 （Nrf2）， and glutathione peroxidase 4 （GPX4）. Western blot was adopted to quantify the protein levels of SIRT1， Nrf2， and GPX4 in the gastric tissue. In the cell experiment， dual-luciferase assay was employed to verify the targeting among lncRNA NOTCH1， miR-138-5p， and SIRT1. MNNG was used to treat GES-1 cells for disease modeling. The effects of NOTCH1 mimics on the expression of lncRNA NOTCH1， miR-138-5p， and SIRT1， as well as the effects of miR-138-5p inhibitor on the expression of miR-138-5p and SIRT1， were observed. The rescue experiment with XLHZ was designed with five groups： GES-1， GES-1+MNNG （Model）， Model+XLHZ， Model+NOTCH1 inhibitor+XLHZ， and Model+NOTCH1 inhibitor+miR-138-5p mimics+XLHZ. Real-time PCR and immunofluorescence assay were employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， Nrf2， and GPX4 and the Fe²⁺ content， respectively， in GES-1 cells. ResultsThe modeled mice showed mitochondrial damage with shrinkage and cristae loss， downregulated mRNA/protein levels of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， and upregulated expression of miR-138-5p （P<0.01）. Compared with the model group， drug treatments reduced mitochondrial structural damage and the membrane density decreased， partially recovered the crista structure， downregulated the expression of miR-138-5p， and upregulated the mRNA and protein levels of lncRNA NOTCH1， SIRT1， Nrf2， and GPX4 （P<0.05， P<0.01）. In the cell experiments， the dual-luciferase assays confirmed lncRNA NOTCH1 bound to miR-138-5p and miR-138-5p bound to SIRT1， both suppressing luciferase activity （P<0.05， P<0.01）. Compared with the blank control group， the model group showed decreased expression of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， increased expression of miR-138-5p， and enhanced Fe²⁺ fluorescence （P<0.01）. NOTCH1 mimics or miR-138-5p inhibitor reversed these changes （P<0.05， P<0.01）. Rescue experiments showed that NOTCH1 inhibitor reversed XLHZ-induced miR-138-5p decrease and SIRT1 increase （P<0.01）， while miR-138-5p overexpression suppressed SIRT1 expression （P<0.05， P<0.01）. The results confirmed that lncRNA NOTCH1 negatively regulated miR-138-5p， which in turn negatively regulated SIRT1. ConclusionXLHZ effectively alleviates gastric mucosal injury and curbs CAG progression by inhibiting ferroptosis through modulation of the lncRNA NOTCH1/miR-138-5p/SIRT1 axis.

ObjectiveTo explore the mechanism of Xianglian Huazhuo prescription （XLHZ） in ameliorating chronic atrophic gastritis （CAG） by regulating lysosomal iron metabolism. MethodsIn the animal experiments， a mouse model of CAG was established through a combined modeling approach， including free drinking of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG， 100 mg·L^-1）， gavage of ranitidine （8 g·L^-1）， and irregular feeding. Mice were randomly assigned into the normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.2， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups. In the cell experiments， GES-1 cells were treated with MNNG to construct a cell model of CAG， and cells were allocated into the GES-1， GES-1+MNNG （Model）， and Model+XLHZ groups. The general physical conditions of mice in each group were observed. Hematoxylin-eosin （HE） staining was used to detect the pathological morphology of the gastric mucosa. Transmission electron microscopy was employed to observe the ultrastructure of gastric mucosal cells. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and interleukin-10 （IL-10） in the serum. Western blot was used to determine the protein levels of lysosome-associated membrane protein 1 （LAMP1）， nuclear receptor coactivator 4 （NCOA4）， ferritin heavy chain 1 （FTH1）， six-transmembrane epithelial antigen of prostate 3 （Steap3）， and transient receptor potential mucolipin 1 （TRPML1） in the gastric tissue. Immunohistochemistry was employed to detect the positive expression of glutathione peroxidase 4 （GPX4） and 8-hydroxy-2′-deoxyguanosine （8-OHdG） in the gastric tissue. Fluorescent probe method was used to detect the levels of Fe²⁺ and reactive oxygen species （ROS）. Immunofluorescence assay was applied to observe the co-localization of FTH1 and LAMP1. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited poor mental status and hair condition， accompanied by decreased locomotor activity， food and water intake， and even reduced body weight. HE staining results showed that the gastric mucosal epithelium of model mice presented poor continuity， significantly decreased mucosal thickness， irregular gastric fovea morphology with widened spacing， dilated glandular cavities， reduced and disarranged glands with obvious atrophy， and extensive inflammatory cell infiltration. Transmission electron microscopy revealed that the mitochondria were markedly shrunken with condensed and deeply stained matrix， drastically reduced and irregularly arranged cristae， and even vacuolization， and the outer mitochondrial membrane shrank and ruptured. In addition， the model group showed elevated serum levels of IL-6 and IL-1β （P<0.01）， declined serum level of IL-10 （P<0.01）， upregulated protein levels of LAMP1， NCOA4， Steap3， and TRPML1 （P<0.01）， downregulated protein level of FTH1 （P<0.01） in the gastric tissue， reduced positive expression of GPX4 （P<0.01）， and increased positive expression of 8-OHdG （P<0.01）. Compared with the model group， all the treatment groups showed improved mental state and hair appearance， increased locomotor activity， food and water intake， as well as gradual body weight gain in mice. HE staining demonstrated that the gastric mucosal epithelium of mice in each treatment group was continuous and intact， with normalized gastric fovea morphology， narrowed glandular cavities， increased and neatly arranged glands， and alleviated inflammatory cell infiltration. Transmission electron microscopy results showed that the mitochondria in mice from each treatment group possessed intact structures with recovered normal volume， increased and regularly arranged cristae， and homogeneous density of the mitochondrial membrane. The mice treated with high and medium doses of XLHZ exhibited declined serum levels of IL-6 and IL-1β （P<0.01） and elevated serum level of IL-10 （P<0.01）. Low-dose XLHZ reduced serum IL-1β level in mice （P<0.05）. The expression levels of LAMP1， NCOA4， Steap3 and TRPML1 protein in gastric tissue of mice in XLHZ high- and medium-dose groups were decreased （P<0.05， P<0.01）， and the expression level of FTH1 protein was increased （P<0.05， P<0.01）. The positive expression of GPX4 in the gastric tissue was increased in the high- and medium-dose XLHZ groups （P<0.05， P<0.01）， and that of 8-OHdG was decreased in all treatment groups （P<0.01）. The cell experiments showed that compared with the GES-1 group， the fluorescence intensities of Fe²⁺ and ROS， as well as the co-localization of FTH1 and LAMP1， were significantly increased in the GES-1 + MNNG group （P<0.01）. Compared with the GES-1 + MNNG group， the fluorescence intensities of Fe²⁺ and ROS were markedly decreased in the Model + XLHZ group （P<0.01）， while the co-localization of FTH1 and LAMP1 was reduced （P<0.05）. ConclusionXLHZ can effectively regulate lysosomal iron metabolism and ameliorate gastric mucosal and cellular injury induced by CAG.

ObjectiveTo construct a competing endogenous RNA （ceRNA） network involving long non-coding RNA NOTCH1 （lncRNA NOTCH1） and investigate whether Xianglian Huazhuo prescription （XLHZ） ameliorates gastric mucosal injury via regulating ferroptosis through the lncRNA NOTCH1/microRNA-138-5p （miR-138-5p）/silent information regulator 1 （SIRT1） axis. MethodsLncRNA sequencing and bioinformatics tools were used to construct the ceRNA network involving lncRNA NOTCH1. In the animal experiments， a chronic atrophic gastritis （CAG） model was induced by N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） in mice. Mice were randomized into normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.6， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups （n=10）. Transmission electron microscopy was adopted to assess gastric pathology. Real-time PCR was employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， nuclear factor erythroid 2-related factor 2 （Nrf2）， and glutathione peroxidase 4 （GPX4）. Western blot was adopted to quantify the protein levels of SIRT1， Nrf2， and GPX4 in the gastric tissue. In the cell experiment， dual-luciferase assay was employed to verify the targeting among lncRNA NOTCH1， miR-138-5p， and SIRT1. MNNG was used to treat GES-1 cells for disease modeling. The effects of NOTCH1 mimics on the expression of lncRNA NOTCH1， miR-138-5p， and SIRT1， as well as the effects of miR-138-5p inhibitor on the expression of miR-138-5p and SIRT1， were observed. The rescue experiment with XLHZ was designed with five groups： GES-1， GES-1+MNNG （Model）， Model+XLHZ， Model+NOTCH1 inhibitor+XLHZ， and Model+NOTCH1 inhibitor+miR-138-5p mimics+XLHZ. Real-time PCR and immunofluorescence assay were employed to measure the mRNA levels of lncRNA NOTCH1， miR-138-5p， SIRT1， Nrf2， and GPX4 and the Fe²⁺ content， respectively， in GES-1 cells. ResultsThe modeled mice showed mitochondrial damage with shrinkage and cristae loss， downregulated mRNA/protein levels of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， and upregulated expression of miR-138-5p （P<0.01）. Compared with the model group， drug treatments reduced mitochondrial structural damage and the membrane density decreased， partially recovered the crista structure， downregulated the expression of miR-138-5p， and upregulated the mRNA and protein levels of lncRNA NOTCH1， SIRT1， Nrf2， and GPX4 （P<0.05， P<0.01）. In the cell experiments， the dual-luciferase assays confirmed lncRNA NOTCH1 bound to miR-138-5p and miR-138-5p bound to SIRT1， both suppressing luciferase activity （P<0.05， P<0.01）. Compared with the blank control group， the model group showed decreased expression of lncRNA NOTCH1， SIRT1， Nrf2， GPX4， increased expression of miR-138-5p， and enhanced Fe²⁺ fluorescence （P<0.01）. NOTCH1 mimics or miR-138-5p inhibitor reversed these changes （P<0.05， P<0.01）. Rescue experiments showed that NOTCH1 inhibitor reversed XLHZ-induced miR-138-5p decrease and SIRT1 increase （P<0.01）， while miR-138-5p overexpression suppressed SIRT1 expression （P<0.05， P<0.01）. The results confirmed that lncRNA NOTCH1 negatively regulated miR-138-5p， which in turn negatively regulated SIRT1. ConclusionXLHZ effectively alleviates gastric mucosal injury and curbs CAG progression by inhibiting ferroptosis through modulation of the lncRNA NOTCH1/miR-138-5p/SIRT1 axis.

ObjectiveTo explore the mechanism of Xianglian Huazhuo prescription （XLHZ） in ameliorating chronic atrophic gastritis （CAG） by regulating lysosomal iron metabolism. MethodsIn the animal experiments， a mouse model of CAG was established through a combined modeling approach， including free drinking of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG， 100 mg·L^-1）， gavage of ranitidine （8 g·L^-1）， and irregular feeding. Mice were randomly assigned into the normal， model， Morodan （2.0 g·kg^-1）， and high-， medium-， and low-dose （7.2， 3.8， 1.9 g·kg^-1， respectively） XLHZ groups. In the cell experiments， GES-1 cells were treated with MNNG to construct a cell model of CAG， and cells were allocated into the GES-1， GES-1+MNNG （Model）， and Model+XLHZ groups. The general physical conditions of mice in each group were observed. Hematoxylin-eosin （HE） staining was used to detect the pathological morphology of the gastric mucosa. Transmission electron microscopy was employed to observe the ultrastructure of gastric mucosal cells. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the serum levels of interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and interleukin-10 （IL-10） in the serum. Western blot was used to determine the protein levels of lysosome-associated membrane protein 1 （LAMP1）， nuclear receptor coactivator 4 （NCOA4）， ferritin heavy chain 1 （FTH1）， six-transmembrane epithelial antigen of prostate 3 （Steap3）， and transient receptor potential mucolipin 1 （TRPML1） in the gastric tissue. Immunohistochemistry was employed to detect the positive expression of glutathione peroxidase 4 （GPX4） and 8-hydroxy-2′-deoxyguanosine （8-OHdG） in the gastric tissue. Fluorescent probe method was used to detect the levels of Fe²⁺ and reactive oxygen species （ROS）. Immunofluorescence assay was applied to observe the co-localization of FTH1 and LAMP1. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited poor mental status and hair condition， accompanied by decreased locomotor activity， food and water intake， and even reduced body weight. HE staining results showed that the gastric mucosal epithelium of model mice presented poor continuity， significantly decreased mucosal thickness， irregular gastric fovea morphology with widened spacing， dilated glandular cavities， reduced and disarranged glands with obvious atrophy， and extensive inflammatory cell infiltration. Transmission electron microscopy revealed that the mitochondria were markedly shrunken with condensed and deeply stained matrix， drastically reduced and irregularly arranged cristae， and even vacuolization， and the outer mitochondrial membrane shrank and ruptured. In addition， the model group showed elevated serum levels of IL-6 and IL-1β （P<0.01）， declined serum level of IL-10 （P<0.01）， upregulated protein levels of LAMP1， NCOA4， Steap3， and TRPML1 （P<0.01）， downregulated protein level of FTH1 （P<0.01） in the gastric tissue， reduced positive expression of GPX4 （P<0.01）， and increased positive expression of 8-OHdG （P<0.01）. Compared with the model group， all the treatment groups showed improved mental state and hair appearance， increased locomotor activity， food and water intake， as well as gradual body weight gain in mice. HE staining demonstrated that the gastric mucosal epithelium of mice in each treatment group was continuous and intact， with normalized gastric fovea morphology， narrowed glandular cavities， increased and neatly arranged glands， and alleviated inflammatory cell infiltration. Transmission electron microscopy results showed that the mitochondria in mice from each treatment group possessed intact structures with recovered normal volume， increased and regularly arranged cristae， and homogeneous density of the mitochondrial membrane. The mice treated with high and medium doses of XLHZ exhibited declined serum levels of IL-6 and IL-1β （P<0.01） and elevated serum level of IL-10 （P<0.01）. Low-dose XLHZ reduced serum IL-1β level in mice （P<0.05）. The expression levels of LAMP1， NCOA4， Steap3 and TRPML1 protein in gastric tissue of mice in XLHZ high- and medium-dose groups were decreased （P<0.05， P<0.01）， and the expression level of FTH1 protein was increased （P<0.05， P<0.01）. The positive expression of GPX4 in the gastric tissue was increased in the high- and medium-dose XLHZ groups （P<0.05， P<0.01）， and that of 8-OHdG was decreased in all treatment groups （P<0.01）. The cell experiments showed that compared with the GES-1 group， the fluorescence intensities of Fe²⁺ and ROS， as well as the co-localization of FTH1 and LAMP1， were significantly increased in the GES-1 + MNNG group （P<0.01）. Compared with the GES-1 + MNNG group， the fluorescence intensities of Fe²⁺ and ROS were markedly decreased in the Model + XLHZ group （P<0.01）， while the co-localization of FTH1 and LAMP1 was reduced （P<0.05）. ConclusionXLHZ can effectively regulate lysosomal iron metabolism and ameliorate gastric mucosal and cellular injury induced by CAG.

Immunoglobulin G4-related disease (IgG4-RD) is a rare systemic immune-mediated disorder characterized by infiltration of IgG4-positive plasma cells and multiorgan fibrosis. Among them, cases with multiple pancreatic cystic lesions as the prominent manifestation are relatively rare, and they are easily misdiagnosed as pancreatic tumors or pancreatitis in clinical practice. Herein, we report one patient with IgG4-RD admitted to Peking Union Medical College Hospital. The patient initially presented with multiple pancreatic cystic lesions and aneurysmal dilatation of the abdominal aorta, accompanied by markedly elevated serum IgG4 levels. Combined with pathological findings from submandibular gland biopsy, the diagnosis of IgG4-RD was ultimately established. After treatment with a regimen of glucocorticoids combined with cyclophosphamide, the patient′s condition improved. Meanwhile, we performed a literature review of cases with IgG4-RD-related pancreatic cystic lesions, aiming to improve clinicians′ understanding of this rare disease phenotype.

Objective:To explore the risk factors of pulmonary infection in patients with non-small cell lung cancer (NSCLC) after thoracoscopic lobectomy and evaluate their predictive value.Methods:A retrospective analysis was conducted on the clinical data of 152 NSCLC patients who underwent thoracoscopic lobectomy at the Central Hospital of Tongchuan Mining Bureau in Shaanxi Province from May 2021 to May 2024. Among them, 45 cases were diagnosed with pulmonary infection by postoperative lung CT examination (postoperative infection group), while the remaining 107 cases did not develop pulmonary infection (non infection group). The levels of serum procalcitonin, serum amyloid A (SAA), and soluble triggering receptor expressed on myeloid cell-1 (sTREM-1) between two groups of patients before and after surgery were compared, and conduct a multivariate logistic regression analysis on the risk factors of pulmonary infection in NSCLC patients undergoing thoracoscopic lobectomy was conducted to evaluate the predictive value of each indicator for pulmonary infection in NSCLC patients after thoracoscopic lobectomy. The normally distributed quantitative data was represented by xˉ± s. Independent sample t-test was used for comparison between two groups, and paired t-test was used for comparison before and after treatment; The count data was presented as an example (%), and the comparison between groups was conducted using the chi square test. The risk factors for postoperative pulmonary infection in NSCLC patients were analyzed using multiple logistic regression analysis. Receiver operating characteristic (ROC) curves were plotted to analyze the predictive value of each indicator for pulmonary infection after thoracoscopic lobectomy. Results:No difference were found in the levels of serum procalcitonin, SAA, and sTREM-1 between two groups of patients before surgery(all P>0.05); 24 hours after surgery, the levels of serum procalcitonin, SAA, and sTREM-1 in both groups of patients were higher than before surgery [Postoperative infection group: (1.16±0.29) μg/L compared to (0.34±0.09) μg/L, (10.2±1.8) mg/L compared to (7.3±0.9) mg/L, (20.3±4.8) ng/L compared to (8.0±1.2) ng/L, t-values were 20.70, 9.70, and 16.89, respectively, all P<0.001; The uninfected group (0.84±0.14) μg/L compared to (0.32±0.08) μg/L, (8.2±1.1) mg/L compared to (7.4±0.9) mg/L, and (13.5±6.3) ng/L compared to (8.1±1.2) ng/L, with t-values of 33.36, 6.13, and 8.73, respectively, all P<0.001, and the infected group was higher than the uninfected group ( t-values of 9.18, 8.32, and 6.52, respectively, all P<0.001). The results of multivariate logistic regression analysis showed that serum procalcitonin, SAA, and sTREM-1 levels at 24 hours after surgery were all risk factors for pulmonary infection in NSCLC patients undergoing thoracoscopic lobectomy (odds ratios of 2.40, 1.61, 1.60, 95% confidence intervals: 1.14~5.04, 1.09~2.38, 1.13~2.26, P values of 0.021, 0.017, 0.009, respectively). The area under curve(AUC) of serum procalcitonin, SAA, and sTREM-1 predicting pulmonary infection after thoracoscopic lobectomy in NSCLC patients 24 hours after surgery were 0.84, 0.74, and 0.79, respectively, with cutoff values of 1.03 μg/L, 9.74 mg/L, and 16.85 ng/L, respectively. Conclusions:The levels of serum procalcitonin, SAA, and sTREM-1 24 hours after surgery are all risk factors for pulmonary infection in NSCLC patients undergoing thoracoscopic lobectomy, and all three had a high predictive value for postoperative pulmonary infection.

ObjectiveTo establish a rapid analytical method for identifying the differential components in Poria cocos medicinal materials based on ultra performance liquid chromatography-quadrupole-electrostatic field orbital trap high-resolution mass spectrometry（UPLC-Q-Orbitrap-MS）， combined with mass defect filtering（MDF） and molecular network integration techniques. MethodsUPLC-Q-Orbitrap-MS was used for MS data acquisition and identification of P. cocos medicinal materials， with the help of MDF for the study of cleavage behavior and structural identification of triterpenoids. According to the similarity of MS/MS fragmentation patterns of each component， global natural product social molecular network（GNPS） was established， and Cytoscape 3.6.1 was used to screen molecular clusters with similar structures and the the structure of main compound classes were identified and confirmed. Multivariate statistical analyses such as principal component analysis（PCA） and orthogonal partial least squares-discriminant analysis（OPLS-DA） were used to screen the differential components of the five P. cocos medicinal materials with the variable importance in the projection（VIP） value>1 and P<0.05 as the criteria. ResultsA total of 66 compounds were identified by database comparison， 8 compounds were newly identified by MDF， 28 compounds were newly identified by GNPS， and a total of 102 chemical compounds were identified， including 43 triterpenoids， 16 saccharides， 26 amino acids and peptides， 3 nucleosides， and 14 other compounds. Triterpenoids were predominant in Poriae Cutis and wild Fushen， amino acids and peptides were the most abundant in Poria and cultivated Fushen， carbohydrates were the most abundant in Poriae Cutis. Type Ⅰ and Ⅱ triterpenoids had higher amounts in Poria and cultivated Fushen， type Ⅲ triterpenoids were more abundant in Poriae Cutis， all four types of triterpenoids were higher in Fushenmu， and type Ⅰ， Ⅱ， and Ⅳ triterpenoids were higher in wild Fushen. A total of 12 common differential chemical constituents were screened， including serine， guanosine， gallic acid， 2-octenal， maltotriose， trametenolic acid， dehydroeburicoic acid， dehydrotrametenolic acid， poricoic acid A， poricoic acid B， poricoic acid E and G， but the relative contents of them varied significantly among different medicinal materials. ConclusionAmong the five P. cocos medicinal materials， the types of constituents are generally similar， but their relative contents differed significantly among these medicinal materials， especially in the distribution of triterpenoids. The integration of UPLC-Q-Orbitrap-MS， MDF and GNPS can provide a reference for the rapid qualitative analysis of other Chinese medicines.

ObjectiveTo establish a rapid analytical method for identifying the differential components in Poria cocos medicinal materials based on ultra performance liquid chromatography-quadrupole-electrostatic field orbital trap high-resolution mass spectrometry（UPLC-Q-Orbitrap-MS）， combined with mass defect filtering（MDF） and molecular network integration techniques. MethodsUPLC-Q-Orbitrap-MS was used for MS data acquisition and identification of P. cocos medicinal materials， with the help of MDF for the study of cleavage behavior and structural identification of triterpenoids. According to the similarity of MS/MS fragmentation patterns of each component， global natural product social molecular network（GNPS） was established， and Cytoscape 3.6.1 was used to screen molecular clusters with similar structures and the the structure of main compound classes were identified and confirmed. Multivariate statistical analyses such as principal component analysis（PCA） and orthogonal partial least squares-discriminant analysis（OPLS-DA） were used to screen the differential components of the five P. cocos medicinal materials with the variable importance in the projection（VIP） value>1 and P<0.05 as the criteria. ResultsA total of 66 compounds were identified by database comparison， 8 compounds were newly identified by MDF， 28 compounds were newly identified by GNPS， and a total of 102 chemical compounds were identified， including 43 triterpenoids， 16 saccharides， 26 amino acids and peptides， 3 nucleosides， and 14 other compounds. Triterpenoids were predominant in Poriae Cutis and wild Fushen， amino acids and peptides were the most abundant in Poria and cultivated Fushen， carbohydrates were the most abundant in Poriae Cutis. Type Ⅰ and Ⅱ triterpenoids had higher amounts in Poria and cultivated Fushen， type Ⅲ triterpenoids were more abundant in Poriae Cutis， all four types of triterpenoids were higher in Fushenmu， and type Ⅰ， Ⅱ， and Ⅳ triterpenoids were higher in wild Fushen. A total of 12 common differential chemical constituents were screened， including serine， guanosine， gallic acid， 2-octenal， maltotriose， trametenolic acid， dehydroeburicoic acid， dehydrotrametenolic acid， poricoic acid A， poricoic acid B， poricoic acid E and G， but the relative contents of them varied significantly among different medicinal materials. ConclusionAmong the five P. cocos medicinal materials， the types of constituents are generally similar， but their relative contents differed significantly among these medicinal materials， especially in the distribution of triterpenoids. The integration of UPLC-Q-Orbitrap-MS， MDF and GNPS can provide a reference for the rapid qualitative analysis of other Chinese medicines.