1.Risk factors and prevention and treatment strategies for perforation caused by endoscopic retrograde cholangiopancreatography
Jingjing LIU ; Yarong GUO ; Bao CHAI
Journal of Clinical Hepatology 2025;41(5):996-1000
Endoscopic retrograde cholangiopancreatography (ERCP), as an advanced endoscopic diagnostic and therapeutic technique, plays an important role in clinical practice. However, due to its complex operation and high technical requirements, it may lead to a series of severe complications, among which perforation is an important issue of concern. Perforation not only increases pain and treatment difficulty, but also threatens the life of patients. In order to guarantee good clinical outcomes, it is necessary to further improve the standard processes for the prediction, diagnosis, and management of perforation due to ERCP. This article discusses the risk factors, diagnostic methods, preventive measures, and treatment strategies for ERCP-related gastrointestinal perforation, in order to provide a reference for identifying high-risk populations and developing individualized treatment regimens in clinical practice.
2.Clinical efficacy of donafenib combined with PD-1 inhibitor and vascular intervention therapy in the treatment of unresectable hepatocellular carcinoma
Lan SU ; Jinghan ZHU ; Mingming LIU ; Yarong YANG ; Yu ZHANG ; Zutao CHEN
China Pharmacy 2025;36(21):2692-2698
OBJECTIVE To observe the clinical efficacy of donafenib combined with programmed death-1 (PD-1) inhibitors and vascular intervention therapy in the treatment of unresectable hepatocellular carcinoma (HCC). METHODS This retrospective study included 165 patients with unresectable HCC who were treated at the Fourth and First Affiliated Hospitals of Soochow University between June 2022 and March 2023. Among them, 89 patients received PD-1 inhibitors (tislelizumab or sintilimab, similarly hereinafter) plus vascular intervention (control group) and 76 patients received donafenib in combination with PD-1 inhibitors and vascular intervention (observation group). Short-term efficacy (3 months after treatment), long-term efficacy (2 years after treatment), the levels of liver function indexes [serum alanine amino-transferase (ALT), aspartate transferase (AST), and total bilirubin (TBil)] and tumor biomarkers [alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and des-gamma-carboxy prothrombin (DCP)] before treatment and after 3 months of treatment, as well as the occurrence of adverse drug reaction (ADR) during treatment, were compared between the two groups. In addition, overall response rate (ORR) stratified by PD-1 inhibitor type was analyzed. RESULTS After treatment, the ORR was significantly higher in the observation group than in the control group (P<0.05); although the disease control rate was higher in the observation group compared to the control group, the difference was not statistically significant (P>0.05). The median overall survival of patients in the observation group was 16.9 months [95% confidence interval (CI): 14.2 to 19.1 months], which was significantly longer than that in the control group (12.4 months, 95%CI: 10.1 to 15.3 months) (P<0.05). Subgroup analysis result indicated that therapeutic advantage was consistent across both sintilimab and tislelizumab subgroups, with no significant heterogeneity (P>0.1, I 2<0.001%). Before treatment, there were no significant differences in liver function indexes or tumor marker levels between 2 groups (P>0.05). After treatment, both groups showed significant declines in these indicators compared with baseline (P<0.05), with greater reductions observed in the observation group (P<0.05). There were no statistically significant differences in overall incidence of ADR and grade ≥3 ADRs between the two groups (P>0.05). CONCLUSIONS For patients with unresectable HCC, the combination of donafenib, PD-1 inhibitors and vascular intervention therapy may achieve superior clinical outcomes without increasing the risk of treatment-related ADR.
3.Telpegfilgrastim for chemotherapy-induced neutropenia in breast cancer: A multicenter, randomized, phase 3 study.
Yuankai SHI ; Qingyuan ZHANG ; Junsheng WANG ; Zhong OUYANG ; Tienan YI ; Jiazhuan MEI ; Xinshuai WANG ; Zhidong PEI ; Tao SUN ; Junheng BAI ; Shundong CANG ; Yarong LI ; Guohong FU ; Tianjiang MA ; Huaqiu SHI ; Jinping LIU ; Xiaojia WANG ; Hongrui NIU ; Yanzhen GUO ; Shengyu ZHOU ; Li SUN
Chinese Medical Journal 2025;138(4):496-498
4.Transient Formation of Stress Granules Disturbs Neural Stem Cell Differentiation.
Mengmeng WANG ; Yarong WANG ; Hongyu MA ; Hanze LIU ; Yating LU ; Yaozhong ZHANG ; Zhihui HUANG ; Songqi DONG ; Kun ZHANG ; Shengxi WU ; Yazhou WANG
Neuroscience Bulletin 2025;41(11):2078-2082
5.Mechanism of Wenyang Shengji Ointment in treating diabetic wounds based on network pharmacology and animal experiments
Yarong DING ; Chenlei XIE ; Shuihua FENG ; Zhonghang YUAN ; Wei WANG ; Mulin LIU ; Zhongzhi ZHOU ; Li CHEN
Digital Chinese Medicine 2024;7(1):79-89
Objective To explore the mechanism of Wenyang Shengji Ointment(温阳生肌膏,WYSJO)in the treatment of diabetic wounds from the perspective of network pharmacology,and to veri-fy it by animal experiments. Methods The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP)and related literature were used to screen active compounds in WYSJO and their corresponding targets.GeneCards,Online Mendelian Inheritance in Man(OMIM),DrugBank,PharmGkb,and Therapeutic Target Database(TTD)databases were employed to identify the targets associated with diabetic wounds.Cytoscape 3.9.0 was used to map the ac-tive ingredients in WYSJO,which was the diabetic wound target network.Search Tool for the Retrieval of Interaction Gene/Proteins(STRING)platform was utilized to construct protein-protein interaction(PPI)network.Kyoto Encyclopedia of Genes and Genomes(KEGG)and Gene Ontology(GO)enrichment analyses were performed to identify signaling pathways be-tween WYSJO and diabetic wounds.AutoDock 1.5.6 was used for molecular docking of core components in WYSJO to their targets.Eighteen rats were randomly divided into control,model,and WYSJO groups(n=6).The model and WYSJO groups were used to prepare the model of refractory wounds in diabetes rats.The wound healing was observed on day 0,5,9,and 14 after treatment,and the wound tissue morphology was observed by hematoxylin-eosin(HE)staining.The expression levels of core genes were detected by quantitative real-time polymerase chain reaction(qPCR). Results A total of 76 active compounds in WYSJO,206 WYSJO drug targets,3 797 diabetic wound targets,and 167 diabetic wound associated WYSJO targets were screened out through network pharmacology.With the use of WYSJO-diabetic wound target network,core targets of seven active compounds encompassing quercetin,daidzein,kaempferol,rhamnetin,rham-nocitrin,strictosamide,and diisobutyl phthalate(DIBP)in WYSJO were found.GO enrich-ment analysis showed that the treatment of diabetes wounds with WYSJO may involve lipopolysaccharide,bacteria-derived molecules,metal ions,foreign stimuli,chemical stress,nutrient level,hypoxia,and oxidative stress in the biological processes.KEGG enrichment analysis showed that the treatment of diabetes wounds with WYSJO may involve advanced glycation end products(AGE-RAGE),p53,interleukin(IL)-17,tumor necrosis factor(TNF),hypoxia inducible factor-1(HIF-1),apoptosis,lipid,atherosclerosis,etc.The results of animal experiments showed that WYSJO could significantly accelerate the healing process of diabetic wounds(P<0.05),alleviate inflammatory response,promote the growth of granulation tis-sues,and down-regulate the expression levels of eight core genes[histone crotonyltrans-ferase p300(EP300),protoc gene-oncogene c-Jun(JUN),myelocytomatosis(MYC),hypoxia inducible factor 1A(HIF1A),mitogen-activated protein kinase 14(MAPK14),specificity pro-tein 1(SP1),tumor protein p53(TP53),and estrogen receptor 1(ESR1)]predicted by the net-work pharmacology(P<0.05). Conclusion The mechanism of WYSJO in treating diabetes wounds may be closely related to AGE-RAGE,p53,HIF-1,and other pathways.This study can provide new ideas for the phar-macological research of WYSJO,and provide a basis for its further transformation and appli-cation.
6.Correlation study on TCM syndrome distribution of patients with chronic heart failure and their cardiopulmonary function
Yarong LIU ; Dezhi REN ; Jing AN ; Xiangcong BIAN
International Journal of Traditional Chinese Medicine 2024;46(12):1565-1570
Objective:To explore correlation between the distribution of TCM syndromes in patients with chronic heart failure (CHF) and its cardiopulmonary function.Methods:The general data and cardiopulmonary function test results of 220 hospitalized patients with CHF in the Cardiology Department of Shaanxi Provincial Hospital of Traditional Chinese Medicine from June 2018 to June 2023 were retrospectively analyzed, and they were divided into 95 cases with deficiency in nature syndrome and 125 cases with excess in superficiality syndrome according to TCM syndrome diagnosis criteria. The difference of cardiopulmonary function indexes among patients with different TCM syndromes was observed, and the correlation between the distribution of TCM syndromes and cardiopulmonary function indexes was analyzed.Results:In 95 patients with deficiency in nature syndrome, qi-deficiency syndrome (21.82%, 48/220) accounted for the highest proportion, and in 125 patients with excess in superficiality, water-drinking syndrome (39.09%, 86/220) accounted for the highest proportion. Left ventricular ejection fraction (LVEF) [(48.84±5.14) % vs. (56.55±6.01) %, t=10.02], stroke cardiac output (SV) [(55.99±6.23) ml vs. (62.86±6.47) ml, t=7.93], cardiac output (CO) [(2.60±0.59) L/min vs. (2.99±0.51) L/min, t=5.25], cardiac index (CI) [(1.54±0.39) L/min?m 2vs. (1.82±0.42) L/min?m 2, t=5.05] of patients with deficiency in nature syndrome were lower than patients with excess in superficiality syndrome ( P<0.001). FVC [(2.16±0.37) L vs. (2.51±0.48) L, t=5.90], maximum vital capacity (VC max) [(2.66±0.42) L vs. (3.01±0.49) L, t=5.58], FEV1 [(2.73±0.42) L vs. (3.15±0.53) L, t=6.35] of patients with deficiency in nature syndrome were lower than those in patients with excess in superficiality syndrome ( P<0.001). Point-biserial correlation analysis showed that patients of CHF excess in superficiality syndrome were significantly correlated with LVEF, SV, CO, CI, FVC, VC max, and FEV1 ( r values are 0.698, 0.705, 0.684, 0.675, 0.719, 0.742, and 0.640, respectively, P<0.05). Conclusions:The deficiency in nature syndrome of CHF patients is qi-deficiency syndrome, and the excess in superficiality syndrome is water-drinking syndrome. The cardiopulmonary function of patients with excess in superficiality syndrome is at a lower level, and there is a significant correlation between patients with excess in superficiality syndrome and cardiopulmonary function. It can provide reference for TCM syndrome diagnosis of CHF patients by monitoring cardiopulmonary function.
7. Study on the mechanism of astragalus glycyrrhiza decoction regulating SIRT1 / FOXO1 pathway to prevent QT interval prolongation induced by arsenic trioxide based on metabolomics
Lan XU ; Ke REN ; Yarong ZHANG ; Haoshi CAO ; Dongling LIU ; Yang HAI
Chinese Journal of Clinical Pharmacology and Therapeutics 2024;29(2):130-138
AIM: To explore the protective effect of astragalus glycyrrhiza decoction (AGD) on arsenic trioxide (ATO)-induced QT interval prolongation and its mechanism based on metabonomics. METHODS: The model of ATO-induced QT interval prolongation in rats was established, and ECG, blood routine, and metabonomics were detected, and the key targets were collected combined with network pharmacology. The possible candidate genes and pathways for the protective effect of AGD were screened by GO and KEGG enrichment analysis and then verified by experiments in vitro. RESULTS: AGD could significantly alleviate the ATO-induced QT interval of SD rats. GO enrichment analysis was mainly related to inflammatory response, reactive oxygen species, oxidative stress, inner cell vesicles, folds, inner cell vesicles, SMAD binding, R-SMAD binding, and signal receptor activator activity. KEGG analysis showed that it was mainly concentrated in the PI3K-Akt signal pathway, lipid and arteriosclerosis, FOXO signal pathway, TNF signal pathway, HIF-1, and other signal pathways. Through the H9c2 cell model in vitro, it was verified that AGD could reverse the expression of SIRT1 and FOXO1 proteins. CONCLUSION: AGD may improve the ATO-induced QT interval prolongation and reduce the cardiotoxicity of ATO by regulating the SIRT1 / FOXO1 signal pathway.
8.Expert consensus on digital intraoral scanning technology
Jie YOU ; Wenjuan YAN ; Liting LIN ; Wen-Zhen GU ; Yarong HOU ; Wei XIAO ; Hui YAO ; Yaner LI ; Lihui MA ; Ruini ZHAO ; Junqi QIU ; Jianzhang LIU ; Yi ZHOU
Journal of Prevention and Treatment for Stomatological Diseases 2024;32(8):569-577
Digital intraoral scanning is a hot topic in the field of oral digital technology.In recent years,digital intra-oral scanning has gradually become the mainstream technology in orthodontics,prosthodontics,and implant dentistry.The precision of digital intraoral scanning and the accuracy and stitching of data collection are the keys to the success of the impression.However,the operators are less familiar with the intraoral scanning characteristics,imaging process-ing,operator scanning method,oral tissue specificity of the scanned object,and restoration design.Thus far,no unified standard and consensus on digital intraoral scanning technology has been achieved at home or abroad.To deal with the problems encountered in oral scanning and improve the quality of digital scanning,we collected common expert opin-ions and sought to expound the causes of scanning errors and countermeasures by summarizing the existing evidence.We also describe the scanning strategies under different oral impression requirements.The expert consensus is that due to various factors affecting the accuracy of digital intraoral scanning and the reproducibility of scanned images,adopting the correct scanning trajectory can shorten clinical operation time and improve scanning accuracy.The scanning trajec-tories mainly include the E-shaped,segmented,and S-shaped methods.When performing fixed denture restoration,it is recommended to first scan the abutment and adjacent teeth.When performing fixed denture restoration,it is recommend-ed to scan the abutment and adjacent teeth first.Then the cavity in the abutment area is excavated.Lastly,the cavity gap was scanned after completing the abutment preparation.This method not only meets clinical needs but also achieves the most reliable accuracy.When performing full denture restoration in edentulous jaws,setting markers on the mucosal tissue at the bottom of the alveolar ridge,simultaneously capturing images of the vestibular area,using different types of scanning paths such as Z-shaped,S-shaped,buccal-palatal and palatal-buccal pathways,segmented scanning of dental arches,and other strategies can reduce scanning errors and improve image stitching and overlap.For implant restora-tion,when a single crown restoration is supported by implants and a small span upper structure restoration,it is recom-mended to first pre-scan the required dental arch.Then the cavity in the abutment area is excavated.Lastly,scanning the cavity gap after installing the implant scanning rod.When repairing a bone level implant crown,an improved indi-rect scanning method can be used.The scanning process includes three steps:First,the temporary restoration,adjacent teeth,and gingival tissue in the mouth are scanned;second,the entire dental arch is scanned after installing a standard scanning rod on the implant;and third,the temporary restoration outside the mouth is scanned to obtain the three-di-mensional shape of the gingival contour of the implant neck,thereby increasing the stability of soft tissue scanning around the implant and improving scanning restoration.For dental implant fixed bridge repair with missing teeth,the mobility of the mucosa increases the difficulty of scanning,making it difficult for scanners to distinguish scanning rods of the same shape and size,which can easily cause image stacking errors.Higher accuracy of digital implant impres-sions can be achieved by changing the geometric shape of the scanning rods to change the optical curvature radius.The consensus confirms that as the range of scanned dental arches and the number of data concatenations increases,the scanning accuracy decreases accordingly,especially when performing full mouth implant restoration impressions.The difficulty of image stitching processing can easily be increased by the presence of unstable and uneven mucosal mor-phology inside the mouth and the lack of relatively obvious and fixed reference objects,which results in insufficient ac-curacy.When designing restorations of this type,it is advisable to carefully choose digital intraoral scanning methods to obtain model data.It is not recommended to use digital impressions when there are more than five missing teeth.
9.Research progress on the role and mechanism of copper overload mediating athero-sclerosis
Tian WANG ; Hongfei WU ; Min DAI ; Yarong LIU
Chinese Journal of Arteriosclerosis 2024;32(8):719-727
Atherosclerosis(As)is a chronic inflammatory disease associated with lipid deposition.Copper is con-sidered to be an important trace element and is closely related to the occurrence and development of As.Excessive accu-mulation of copper ions in cells can induce cell death,a new type of cell death named"cuproptosis".Under normal con-ditions,the body's copper metabolism can control the copper level in a stable range.When the disease occurs,copper ho-meostasis is destroyed,intracellular copper overload produces cytotoxicity,induces oxidative stress,inflammation,cell py-roptosis and cuproptosis,and promotes the occurrence and development of As.This article summarizes the relationship between copper levels and As,and discusses the mechanism of cuproptosis and the pathological mechanism of copper over-load promoting As from the perspective of the body's copper regulation,and reviews the relevant drug intervention,expec-ting to provide a new therapeutic target for As.
10.Analysis of novel gene mutations in a family with hereditary coagulation factor XI deficiency
Rui LI ; Yarong XIE ; Wei ZHU ; Xiaoyan LI ; Hao LIU
Chinese Journal of Laboratory Medicine 2024;47(8):952-957
Objective:To explore the molecular mechanism of clinical bleeding in a family with hereditary coagulation factor Ⅺ (FⅪ) deficiency caused by a novel mutation of the coagulation factor Ⅺ (FⅪ) gene.Methods:A male proband with hereditary coagulation factor XI deficiency who was admitted to Yuncheng Central Hospital Affiliated to Shanxi Medical University due to "adenoid hypertrophy" on February 23, 2023 and his family members (5 people in 3 generations) were selected as research subjects. The clinical data of the proband and family members were collected; the relevant coagulation indexes of all members were tested; those with abnormal coagulation indexes (prolonged activated partial thromboplastin time (APTT), normal thrombin time (PT) and fibrinogen (Fib)) were selected for APTT correction experiment; those with corrected Rosner index (RI) less than 10% were selected to detect FⅪ activity (FⅪ:C) by one-step method, FⅪ antigen (FⅪ:Ag) by ELISA method, and whole exon sequence by Illumina sequencing method. New mutation sites were rated according to the American College of Medical Genetics and Genomics (ACMG) related variation rating guidelines, and bioinformatics software was used to predict the impact of new mutations on protein structure and function.Results:The APTT of the proband, his father and his daughter were all prolonged and their RI were all less than 10%. Further tests revealed that FⅪ:C and FⅪ:Ag of the three were all decreased. Illumina sequencing revealed a new frameshift mutation c.1223dupC (P.Ser409Leufs*32) in exon 11 of FⅪ of the three people, and a missense mutation c.G1253T (p.Gly418Val) in exon 11 of FⅪ of the proband′s father. ACMG rated the new mutation as pathogenic, and c.G1253T was a reported possible pathogenic mutation.Conclusion:The heterozygous frameshift mutation c.1223dupC (P.Ser409Leufs*32) in exon 11 of FⅪ may be the main molecular mechanism of the disease in this family.


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