Objective To analyze the problems in the operation and management of drug clinical trials and put forward targeted suggestion. Methods An electronic questionnaire survey was conducted among medical staff in about 80 hospitals in the yangtze river delta region. Results 606 valid questionnaires were received. 71% of the respondents expressed their willingness to study and participate in drug clinical trials. There were significant differences in the cognitive demands, willingness and motivation of the respondents with different occupations and educational backgrounds about the drug clinical trial work （P<0.05）. During the operation of drug clinical trials, respondents reported the main factors affecting the quality of clinical trials which including good clinical practice (GCP) awareness and subjective enthusiasm of investigators （response rate 27%）, job stability of supervisors and research coordinators （27%）, compliance of subjects （45%）, quality control of the whole process of the circulation of test drugs, medical devices and biological samples （52%）, and the informatization level of clinical trial institutions （30%）. Conclusion Hospitals, institutions and project teams could take measures to cultivate and stabilize the drug clinical trial talent team, improve the quality management system of drug clinical trials, improve work efficiency, and promote the high-quality development of drug clinical trials in medical institutions.

Objective To analyze the main causes and risk factors of unplanned reoperation after liver transplantation. Methods The clinical data of 242 liver transplant recipients in the First Affiliated Hospital of Anhui Medical University from January 2015 to December 2024 were retrospectively analyzed. According to whether unplanned reoperation was performed during the same hospitalization after surgery, the recipients were divided into the reoperation group (n=36) and the non-reoperation group (n=206). The preoperative, intraoperative and postoperative data of the two groups, as well as donor and graft-related data, were compared to analyze the risk factors of unplanned reoperation after liver transplantation and the survival status of the two groups. Results Among the 242 liver transplant recipients, 36 underwent unplanned reoperations, with a total of 54 procedures including various laparotomies, endoscopic and interventional surgeries, among which there were 20 laparotomies, 18 endoscopic surgeries and 16 interventional surgeries. The most common cause of unplanned reoperation was biliary complications (20 times), followed by vascular complications (17 times). Compared with the non-reoperation group, the reoperation group had longer graft cold ischemia time, higher postoperative fatality rate of recipients, longer length of stay in the intensive care unit and postoperative hospital stay, and higher total hospitalization costs (all P<0.05). The incidence of unplanned reoperation was higher in recipients who underwent split liver transplantation (P<0.05). Multivariate analysis showed that intraoperative blood loss ≥1 000 mL, positive culture of graft perfusate and split liver transplantation were independent risk factors for unplanned reoperation (all P<0.05). The postoperative 7-day, 1-month, 3-month and 6-month survival rates of recipients in the reoperation group and the non-reoperation group were 100% vs. 98.1%, 88.9% vs. 94.2%, 69.4% vs. 90.8% and 66.7% vs. 90.8%, respectively, and the postoperative survival rate of recipients in the reoperation group was lower than that in the non-reoperation group (P<0.05). Conclusions The main causes of unplanned reoperation after liver transplantation are biliary complications, vascular complications, abdominal incision infection and intra-abdominal hemorrhage. Intraoperative massive blood loss, positive culture of graft perfusate and split liver transplantation are the risk factors associated with unplanned reoperation after liver transplantation.

Objective: To investigate the status and influencing factors of nutritional health knowledge awareness among primary and middle school students in Wenzhou City, Zhejiang Province, so as to provide a basis for carrying out targeted nutrition health education for students. Methods: The stratified cluster random sampling method was used to select students from 48 schools across 12 counties (cities and districts) in Wenzhou City as survey subjects from October 2023 to February 2024. Basic information, parental information, and nutritional health knowledge were collected using the Questionnaire on nutritional health knowledge for School-Age Children. The awareness rate of nutritional health knowledge was analyzed. Multivariable logistic regression model was used to analyze the influencing factors for nutritional health knowledge awareness among primary and middle school students. Results: The survey included 4 405 boys, accounting for 51.42%, and 4 161 girls, accounting for 48.58%. The sample consisted of 2 497 pupils in Grades 1-3 (29.15%), 2 591 pupils in Grades 4-6 (30.25%), 1 739 junior high school students (20.30%), and 1 739 senior high school students (20.30%). The median score of nutrition health knowledge was 75.00 (interquartile range, 19.00), and the awareness rate was 4 524 (52.81%). Multivariable logistic regression analysis showed that girls (OR=1.317, 95%CI: 1.198-1.447), primary school students (Grades 1-3, OR=7.830, 95%CI: 6.444-9.513; Grades 4-6, OR=1.276, 95%CI: 1.066-1.528), and those whose mothers had an educational level above junior high school (senior high school/technical secondary school/technical school/junior college, OR=1.188, 95%CI: 1.044-1.352; bachelor' s degree or above, OR=1.194, 95%CI: 1.024-1.392) had a higher likelihood of nutrition and health knowledge awareness. Conversely, students who were overweight or obese (OR=0.798, 95%CI: 0.671-0.950), lived in school (OR=0.763, 95%CI: 0.650-0.895), and had a daily outdoor activity duration of <30 minutes (OR=0.641, 95%CI: 0.570-0.721) had a lower likelihood of nutritional health knowledge awareness. Conclusions The awareness rate of nutritional health knowledge among primary and middle school students in Wenzhou City needs to be improved, and is mainly influenced by gender, educational stage, body mass index, mother' s educational level, and outdoor activity duration. It is recommended to implement differentiated health education strategies and build a "family-school-community" linkage mechanism to improve students' nutrition health literacy.

ObjectiveTo construct a risk prediction model for chronic atrophic gastritis （CAG） that combines disease and syndrome by integrating spleen deficiency and blood stasis syndrome scores， gastric stem cell marker analysis， and network pharmacology and to elucidate the mechanism link between spleen deficiency， blood stasis， and gastric stem cell dysregulation. MethodsA total of 60 patients were stratified into high-risk CAG， low-risk CAG， and non-atrophic groups based on the operative link for gastritis assessment （OLGA）/operative link for gastric intestinal metaplasia assessment （OLGIM） stages. General data and syndrome scores of the patients were collected. Immunohistochemistry was employed to measure the protein levels of leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， trefoil factor 2 （TFF2）， and β-catenin in gastric mucosa across groups. Transcriptomic data （GSE130823） from the Gene Expression Omnibus （GEO） database were analyzed to validate the expression of these molecular markers at the gene level. A Firth penalized maximum likelihood logistic regression model was employed to integrate clinical， molecular， and TCM syndrome data to develop a CAG risk prediction model. Finally， network pharmacology analysis was conducted on spleen-invigorating herbs （Astragali Radix， Atractylodis Macrocephalae Rhizoma， and Dioscorea Rhizoma） and blood-activating herbs （Hedyotis diffusa， Salviae Miltiorrhizae Radix et Rhizoma， and Curcumae Rhizoma） to identify overlapping targets between these herbs and differentially expressed genes between low-grade intraepithelial neoplasia （LGIN） and gastritis， thereby clarifying the role of spleen deficiency and blood stasis in CAG progression from a pharmacological perspective. ResultsHigh-risk CAG patients exhibited higher blood stasis scores （4.60±1.50，2.62±1.32， P<0.01）， progressive nuclear accumulation of β-catenin （A 0.28-0.53， P<0.01）， and an increased LGR5⁺/TFF2⁺ ratio （A 1.02-1.92， P<0.01）. Blood stasis scores were correlated with LGR5/TFF2 imbalance （P=0.03） and activation of the Wnt/β-catenin signaling pathway （CTNNB1 increase， log₂=0.78）. The integrated prediction model （blood stasis score≥5 + β-catenin>0.38 + LGR5/TFF2>1.5） outperformed a pure biomarker approach ［Area Under the Curve （AUC） 0.92，0.89， ΔAUC=0.03， P=0.02］. Moreover， network pharmacology revealed 66 overlapping targets between spleen-invigorating/blood-activating herbs and LGIN， which were functionally enriched in mucosal repair and anti-oxidative stress， and negatively correlated with the Wnt/β-catenin signaling pathway （P<0.01）. ConclusionThis study developed an integrated risk prediction model for CAG by combining TCM spleen deficiency and blood stasis syndromes with gastric stem cell molecular markers. Furthermore， it proposed for the first time the "blood stasis-Wnt/β-catenin-stem cell axis" hypothesis， preliminarily elucidating that spleen deficiency and blood stasis may exacerbate gastric stem cell dysregulation and promote malignant transformation of CAG through hypoxia-induced Wnt activation. This provides a theoretical foundation and a translational tool for risk stratification and multi-target TCM intervention in CAG.

ObjectiveTo develop an early - warning approach for influenza in Anhui province using the moving epidemic method （MEM）， offering a scientific basis for influenza prevention and control in the province. MethodsBased on the surveillance data reported weekly by influenza sentinel hospitals and network laboratories in the “China Influenza Surveillance Information System”， the weekly influenza virus detection positive rate （positive rate， PR） across the province was analyzed. The MEM was used to estimate the epidemic threshold and classification intensity threshold of influenza in Anhui province before and after the COVID-19 pandemic， respectively. The early warning effect of the MEM was evaluated using cross-validation. ResultsEpidemic and graded intensity thresholds of influenza were derived using PR and MEM. Prior to the COVID-19 pandemic， the starting， medium-intensity， high-intensity， extremely-high-intensity， and ending thresholds of influenza epidemics were 17.08%， 38.47%， 53.20%， 59.71%， and 12.34% respectively. At this point， the model exhibited sensitivity of 0.98， specificity of 0.86， Matthews correlation coefficient of 0.84， and Youden index of 0.84. After the COVID-19 pandemic， these thresholds were 25.61%， 43.81%， 63.29%， 74.46%， and 17.82% respectively. At this point， the model demonstrates sensitivity of 0.86， specificity of 0.92， Matthews correlation coefficient of 0.78， and Youden index of 0.77. ConclusionMEM shows good applicability in estimating the epidemic and graded intensity thresholds of influenza during the winter and spring in Anhui province. Both the influenza epidemic threshold and graded intensity thresholds after the COVID-19 pandemic are higher than those before the pandemic.

ObjectiveTo construct a risk prediction model for chronic atrophic gastritis （CAG） that combines disease and syndrome by integrating spleen deficiency and blood stasis syndrome scores， gastric stem cell marker analysis， and network pharmacology and to elucidate the mechanism link between spleen deficiency， blood stasis， and gastric stem cell dysregulation. MethodsA total of 60 patients were stratified into high-risk CAG， low-risk CAG， and non-atrophic groups based on the operative link for gastritis assessment （OLGA）/operative link for gastric intestinal metaplasia assessment （OLGIM） stages. General data and syndrome scores of the patients were collected. Immunohistochemistry was employed to measure the protein levels of leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， trefoil factor 2 （TFF2）， and β-catenin in gastric mucosa across groups. Transcriptomic data （GSE130823） from the Gene Expression Omnibus （GEO） database were analyzed to validate the expression of these molecular markers at the gene level. A Firth penalized maximum likelihood logistic regression model was employed to integrate clinical， molecular， and TCM syndrome data to develop a CAG risk prediction model. Finally， network pharmacology analysis was conducted on spleen-invigorating herbs （Astragali Radix， Atractylodis Macrocephalae Rhizoma， and Dioscorea Rhizoma） and blood-activating herbs （Hedyotis diffusa， Salviae Miltiorrhizae Radix et Rhizoma， and Curcumae Rhizoma） to identify overlapping targets between these herbs and differentially expressed genes between low-grade intraepithelial neoplasia （LGIN） and gastritis， thereby clarifying the role of spleen deficiency and blood stasis in CAG progression from a pharmacological perspective. ResultsHigh-risk CAG patients exhibited higher blood stasis scores （4.60±1.50，2.62±1.32， P<0.01）， progressive nuclear accumulation of β-catenin （A 0.28-0.53， P<0.01）， and an increased LGR5⁺/TFF2⁺ ratio （A 1.02-1.92， P<0.01）. Blood stasis scores were correlated with LGR5/TFF2 imbalance （P=0.03） and activation of the Wnt/β-catenin signaling pathway （CTNNB1 increase， log₂=0.78）. The integrated prediction model （blood stasis score≥5 + β-catenin>0.38 + LGR5/TFF2>1.5） outperformed a pure biomarker approach ［Area Under the Curve （AUC） 0.92，0.89， ΔAUC=0.03， P=0.02］. Moreover， network pharmacology revealed 66 overlapping targets between spleen-invigorating/blood-activating herbs and LGIN， which were functionally enriched in mucosal repair and anti-oxidative stress， and negatively correlated with the Wnt/β-catenin signaling pathway （P<0.01）. ConclusionThis study developed an integrated risk prediction model for CAG by combining TCM spleen deficiency and blood stasis syndromes with gastric stem cell molecular markers. Furthermore， it proposed for the first time the "blood stasis-Wnt/β-catenin-stem cell axis" hypothesis， preliminarily elucidating that spleen deficiency and blood stasis may exacerbate gastric stem cell dysregulation and promote malignant transformation of CAG through hypoxia-induced Wnt activation. This provides a theoretical foundation and a translational tool for risk stratification and multi-target TCM intervention in CAG.

ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg^-1）， a middle-dose SMI group（6 mL·kg^-1）， a high-dose SMI group（12 mL·kg^-1）， and a Ginaton group（4 mL·kg^-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.

Background: The genetic basis for hyperglycaemia in pregnancy remain unclear. This study aimed to uncover the genetic determinants of gestational diabetes mellitus (GDM) and investigate their applications. Methods: We performed a meta-analysis of genome-wide association studies (GWAS) for GDM in Chinese women (464 cases and 1,217 controls), followed by de novo replications in an independent Chinese cohort (564 cases and 572 controls) and in silico replication in European (12,332 cases and 131,109 controls) and multi-ethnic populations (5,485 cases and 347,856 controls). A polygenic risk score (PRS) was derived based on the identified variants. Results: Using the genome-wide scan and candidate gene approaches, we identified four susceptibility loci for GDM. These included three previously reported loci for GDM and type 2 diabetes mellitus (T2DM) at MTNR1B (rs7945617, odds ratio [OR], 1.64; 95% confidence interval [CI],1.38 to 1.96]), CDKAL1 (rs7754840, OR, 1.33; 95% CI, 1.13 to 1.58), and INS-IGF2-KCNQ1 (rs2237897, OR, 1.48; 95% CI, 1.23 to 1.79), as well as a novel genome-wide significant locus near TBR1-SLC4A10 (rs117781972, OR, 2.05; 95% CI, 1.61 to 2.62; Pmeta=7.6×10-9), which has not been previously reported in GWAS for T2DM or glycaemic traits. Moreover, we found that women with a high PRS (top quintile) had over threefold (95% CI, 2.30 to 4.09; Pmeta=3.1×10-14) and 71% (95% CI, 1.08 to 2.71; P=0.0220) higher risk for GDM and abnormal glucose tolerance post-pregnancy, respectively, compared to other individuals. Conclusion Our results indicate that the genetic architecture of glucose metabolism exhibits both similarities and differences between the pregnant and non-pregnant states. Integrating genetic information can facilitate identification of pregnant women at a higher risk of developing GDM or later diabetes.

Background: The genetic basis for hyperglycaemia in pregnancy remain unclear. This study aimed to uncover the genetic determinants of gestational diabetes mellitus (GDM) and investigate their applications. Methods: We performed a meta-analysis of genome-wide association studies (GWAS) for GDM in Chinese women (464 cases and 1,217 controls), followed by de novo replications in an independent Chinese cohort (564 cases and 572 controls) and in silico replication in European (12,332 cases and 131,109 controls) and multi-ethnic populations (5,485 cases and 347,856 controls). A polygenic risk score (PRS) was derived based on the identified variants. Results: Using the genome-wide scan and candidate gene approaches, we identified four susceptibility loci for GDM. These included three previously reported loci for GDM and type 2 diabetes mellitus (T2DM) at MTNR1B (rs7945617, odds ratio [OR], 1.64; 95% confidence interval [CI],1.38 to 1.96]), CDKAL1 (rs7754840, OR, 1.33; 95% CI, 1.13 to 1.58), and INS-IGF2-KCNQ1 (rs2237897, OR, 1.48; 95% CI, 1.23 to 1.79), as well as a novel genome-wide significant locus near TBR1-SLC4A10 (rs117781972, OR, 2.05; 95% CI, 1.61 to 2.62; Pmeta=7.6×10-9), which has not been previously reported in GWAS for T2DM or glycaemic traits. Moreover, we found that women with a high PRS (top quintile) had over threefold (95% CI, 2.30 to 4.09; Pmeta=3.1×10-14) and 71% (95% CI, 1.08 to 2.71; P=0.0220) higher risk for GDM and abnormal glucose tolerance post-pregnancy, respectively, compared to other individuals. Conclusion Our results indicate that the genetic architecture of glucose metabolism exhibits both similarities and differences between the pregnant and non-pregnant states. Integrating genetic information can facilitate identification of pregnant women at a higher risk of developing GDM or later diabetes.

Background: The genetic basis for hyperglycaemia in pregnancy remain unclear. This study aimed to uncover the genetic determinants of gestational diabetes mellitus (GDM) and investigate their applications. Methods: We performed a meta-analysis of genome-wide association studies (GWAS) for GDM in Chinese women (464 cases and 1,217 controls), followed by de novo replications in an independent Chinese cohort (564 cases and 572 controls) and in silico replication in European (12,332 cases and 131,109 controls) and multi-ethnic populations (5,485 cases and 347,856 controls). A polygenic risk score (PRS) was derived based on the identified variants. Results: Using the genome-wide scan and candidate gene approaches, we identified four susceptibility loci for GDM. These included three previously reported loci for GDM and type 2 diabetes mellitus (T2DM) at MTNR1B (rs7945617, odds ratio [OR], 1.64; 95% confidence interval [CI],1.38 to 1.96]), CDKAL1 (rs7754840, OR, 1.33; 95% CI, 1.13 to 1.58), and INS-IGF2-KCNQ1 (rs2237897, OR, 1.48; 95% CI, 1.23 to 1.79), as well as a novel genome-wide significant locus near TBR1-SLC4A10 (rs117781972, OR, 2.05; 95% CI, 1.61 to 2.62; Pmeta=7.6×10-9), which has not been previously reported in GWAS for T2DM or glycaemic traits. Moreover, we found that women with a high PRS (top quintile) had over threefold (95% CI, 2.30 to 4.09; Pmeta=3.1×10-14) and 71% (95% CI, 1.08 to 2.71; P=0.0220) higher risk for GDM and abnormal glucose tolerance post-pregnancy, respectively, compared to other individuals. Conclusion Our results indicate that the genetic architecture of glucose metabolism exhibits both similarities and differences between the pregnant and non-pregnant states. Integrating genetic information can facilitate identification of pregnant women at a higher risk of developing GDM or later diabetes.