In October 2024， the 75th World Medical Association General Assembly adopted the tenth revised version of the Declaration of Helsinki. Using textual analysis， this paper systematically compared the changes between the 2024 version and the 2013 version of the Declaration of Helsinki. This study found that， while maintaining the original framework， the new version incorporated the common achievements of the values and civilizational development of human society in recent years， mainly presenting changes in three aspects. First， the core terms were updated， and new concepts such as vulnerability， structural inequality， and environmental sustainability were introduced to further emphasize human dignity， rights and interests， and autonomy in terms of values. Second， the contents of the provisions were refined， especially focusing on the vulnerability of research subjects， free and full informed consent， ethical principles in public health emergencies， and the responsibilities of the ethics committee， as well as the standardization of implementation continued to be improved in the research process. Third， mandatory expressions were strengthened， and the justice of value pursuit was further reinforced in terms of research responsibilities. The revised contents reflected the “human-oriented” fundamental principle in medical research ethics， indicating the direction for future ethical development in medical research. In the future， China should strengthen the construction of ethics committees， actively build a protection system for research participants， and continuously promote international cooperation in medical ethics， to contribute Chinese wisdom to global medical research.

[Objective] To investigate the non-pathological influencing factors of the unqualified alanine aminotransferase (ALT) in the initial screening of blood donors in Changchun and the laboratory re-examination, so as to provide evidence for reducing the deferral of blood donors and the discarding of blood due to ALT disqualification. [Methods] The unqualified results of ALT from the laboratory of our center from September 1, 2023 to October 31, 2024 were collected. The unqualified rates of ALT were statistically analyzed according to the blood collection sites and the initial screening detection equipment. The samples after ALT pre-donation screening were tested in the laborator, and the unqualified rates of ALT in the initial screening and the laboratory, the non-conformity rate of the results and the distribution range of ALT values were statistically analyzed according to the blood collection sites and the initial screening detection equipment. A questionnaire survey was conducted on the blood donors before blood collection to statistically analyze the influence of the blood donors' living habits and diet on ALT test results. [Results] The statistical analysis of the unqualified rate of ALT in the laboratory showed statistically significant differences in the ALT disqualification rates among different blood collection sites and different initial screening detection devices (P<0.05). Comparison of the ALT unqualified rate for the same type of equipment at different sites showed that for Equipment 1, there were differences between the combined blood collection house and the whole blood house, and between the combined blood collection house and the blood donation vehicle (P<0.05); for Equipment 2, there were differences between the combined blood collection house and the blood donation vehicle, and between the whole blood house and the blood donation vehicle (P<0.05); there were no significant differences among other groups with the same equipment. The initial screening and the laboratory test results for the same samples were compared, with unqualified rates of ALT of 16.29% and 13.01%, respectively. There were statistically significant differences in the unqualified rates of ALT among different blood collection sites (P<0.05), but no significant differences in the ALT test results among different detection equipment (P>0.05).. The non-conformity rate between the initial screening and the laboratory results was 5.26%, of which 81.15% (99/122) were unqualified in the initial screening but qualified in the laboratory. There were statistically significant differences in those unqualified in the initial screening but qualified in the laboratory among different blood collection sites and different detection equipment (P<0.05). The median ALT level in the initial screening was 29.0 U/L (with a 5%-95% range of 14-75 U/L), and the median ALT level in the laboratory was 19 U/L (with a 5%-95% range of 8-65 U/L). The results of the questionnaire survey showed that 33.3% (2/6) of those who consumed alcohol within 24 hours before blood donation had unqualified ALT, and 10% (1/10) of those who stayed up late the night before blood donation had unqualified ALT. [Conclusion] The unqualified rates of ALT in the initial screening before blood collection and the laboratory re-examination of blood donors in Changchun are closely related to the blood collection sites, detection equipment, detection environment, detection personnel, samples, ALT thresholds and detection time. Drinking alcohol and staying up late within 24 hours before blood donation increase the risk of unqualified ALT detection.

BackgroundPrevention and intervention of procrastination in college students are of great practical significance， and studies have illustrated a pairwise correlation among mindfulness， self-control， insecure attachment and procrastination， whereas the mechanism by which insecure attachment leads to procrastination remains unclear， and the related mediation path is quite understudied. ObjectiveTo investigate the effect of insecure attachment on procrastination among college students and the pathway of mindfulness and self-control， so as to inform the design of interventions for procrastination among college students. MethodsRandom and cluster sampling method were utilized to enroll 514 college students from 4 colleges in Guangdong Province From February to April 2023. Subjects were assessed using Irrational Procrastination Scale （IPS）， Adult Attachment Scale （AAS）， Mindful Attention Awareness Scale （MAAS） and Brief Self-Control Scale （BSCS）. Pearson correlation analysis were adopted to identify the correlation among above scales， and the mediation effect was examined via Bootstrap procedure. ResultsAAS score was positively correlated with IPS score （r=0.382， P<0.01）， and negatively correlated with MAAS and BSCS scores （r=-0.242， -0.353， P<0.01）. IPS score was negatively correlated with MAAS and BSCS scores （r=-0.314， -0.682， P<0.01）. MAAS score was positively correlated with BSCS score （r=0.439， P<0.01）. Insecure attachment positively predicted procrastination （β=0.377， P<0.01）， and the prediction of procrastination by insecure attachment was mediated by self-control， with an indirect effect value of 0.163 （95% CI： 0.105~0.223）， accounting for 43.24% of the total effect value. The mindfulness and self-control exerted a chained mediation effect on the relationship between insecure attachment and procrastination， and the indirect effect value was 0.056 （95% CI： 0.028~0.089）， accounting for 14.85% of the total effect value. ConclusionInsecure attachment can influence procrastination among college students both directly and indirectly through the single mediation of self-control or the chained mediation of mindfulness and self-control. ［Funded by 2023 National College Student Innovation and Entrepreneurship Training Program （number， 202310570023）］

Objective To investigate the role of phospholipase A2 Group Ⅳ C(PLA2G4C)in diffuse large B-cell lymphoma(DLBCL)and its possible regulatory mechanism.Methods The protein expression of PLA2G4C in DLBCL tissues and cells was detected by Western blot.DLBCL cell lines with PLA2G4C overexpression or knockdown expression were constructed,and the cells were treated with autophagy inhibitor Chloroquine(CQ)or p38 inhibitor SB203580 for 24 h.Quantitative real time polymerase chain reaction(qRT-PCR)was used to detect the transfection efficiency of PLA2G4C;Western blot analysis was performed to detect the expression levels of PLA2G4C protein,mitochondrial autophagy related protein[microtubule-associated protein 1 light chain 3-Ⅱ/Ⅰ(LC3 Ⅱ/Ⅰ),Beclin1,p62,PTEN induced putative kinase 1(PINK1)and Parkin]and p38/mitogen activated protein kinases(MAPK)pathway-related protein[Phosphorylated p38/MAPK(p-p38/MAPK)];Cell proliferation,invasion and apoptosis were detected with CCK8,Transwell assay and the flow cytometry,respectively.The effects of PLA2G4C on tumor growth and mitochondrial autophagy in nude mice were further established.Results The PLA2G4C protein expression in lymphoma tissues of DLBCL patients was significantly higher than that in lymph nodes with reactive hyperplasia(3.47±0.42 vs 1.01±0.02),and the difference was statistically significant(t=-37.002,P<0.001).The PLA2G4C protein level in DLBCL cells was significantly higher than that in human lymphoblast-like cell lines and B-cell lymphoma cell lines,and the difference was statistically significant(F=73.771,P<0.001).Silencing PLA2G4C significantly decreased the viability and invasion ability of DLBCL cells,and induced apoptosis,with statistical significance(t=6.909～11.390),Overexpression of PLA2G4C gave the opposite result(t=2.392～19.778),and the differences were statistically significant(all P<0.001).PLA2G4C overexpression significantly promoted the occurrence of mitochondrial autophagy,while CQ or SB203580 treatment could significantly reverse the effects of PLA2G4C overexpression on the biological behavior of DLBCL cells and mitochondrial autophagy.In vivo nude mice experiments showed that PLA2G4C knockdown significantly inhibited tumor growth and mitochondrial autophagy related protein expression in transplanted nude mice,and the differences were statistically significant(t=13.816～25.926,all P<0.001).Conclusion PLA2G4C is up-regulated in DLBCL,which may promote tumor cell proliferation and invasion,inhibit cell apoptosis,and participate in the occurrence and development of DLBCL by promoting mitochondrial autophagy mediated by p38/MAPK signaling pathway.

Objective To investigate the prevalence of human parvovirus B19(B19V)infection among college students,so as to provide reference for the development of blood donor screening strategies and blood supply policies.Meth-ods From March 2023 to February 2024,blood donor samples from college students in Changchun were retrospectively an-alyzed using the principle of random numbers,with samples taken 1 to 3 days per month.B19V IgG/IgM were detected by ELISA,and B19V DNA and viral load were measured by real-time quantitative PCR.Results Among 1 456 blood donor samples from college students,the positive rates for B19V IgG,IgM and DNA were 11.54%,0.34%and 2.68%,respec-tively.The viral load in 39 B19V DNA-positive samples ranged from 5.60×102 IU/mL to 9.10×106 IU/mL,with 28 samples(1.92%)having a viral load above 104 IU/mL.There were 11 samples(0.76%)that were positive for B19V DNA but neg-ative for IgG/IgM.Conclusion The college students have a low prevalence of past B19V infection,but a higher risk of in-fections and a higer proportion of acute infections with high viral loads in individuals who are]B19V IgG negative,presenting a risk of transmission through blood transfusion.Targeted blood safety monitoring is necessary for college students to track the prevalence of B19V DNA.

Objective To investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion(I/R)injury in mice and explore the underlying mechanism.Methods A total of 100 C57BL/6 mice were randomly divided into 5 groups,including a sham-operated group,cerebral I/R model group,and 3 leptin treatment groups with intraperitoneal injections of 0.5,1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery.At 24 h after reperfusion,neurological function scores of the mice were assessed,and TTC staining was used to determine the area of cerebral infarction.The pathological changes in the cortical brain tissue of the mice were observed using HE staining,and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining.The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting.In another 45 C57BL/6 mice with sham operation,I/R modeling,or leptin(1 mg/kg)treatment,glutamic acid in the cortical brain tissue was detected using glutamate assay,and cortical glutamate-aspartate transporter(GLAST)and glutamate transporter-1(GLT-1)protein expressions were detected using immunohistochemistry.Results Compared with the I/R model mice,the leptin-treated mice had significantly lower neurological deficit scores,smaller cerebral infarct area,milder pathologies in the cortical brain tissue,and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes.Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.Conclusion Exogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice,mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.

Objective:To analyze the types and functions of CD34 + cells in full-thickness skin defect wounds of normal mice and diabetic mice by single-cell RNA sequencing. Methods:This study was an experimental study. The CD34 + cell lineage tracing mouse was produced, and the visualization of CD34 + cells under the fluorescent condition was realized. Six male CD34 + cell lineage tracing mice aged 7-8 weeks (designated as diabetic group) were intraperitoneally injected with streptozotocin to establish a diabetic model, and full-thickness skin defect wounds were prepared on their backs when they reached 13 weeks old. Another 6 male CD34 + cell lineage tracing mice aged 13 weeks (designated as control group) were also subjected to full-thickness skin defect wounds on their backs. On post-injury day (PID) 4, wound tissue was collected from 3 mice in control group and 2 mice in diabetic group, and digested to prepare single-cell suspensions. CD34 + cells were screened using fluorescence-activated cell sorting, followed by single-cell RNA sequencing. The Seurat 4.0.2 program in the R programming language was utilized for dimensionality reduction, visualization, and cell clustering analysis of CD34 + cell types, and to screen and annotate the marker genes for each CD34 + cell subpopulation. Kyoto encyclopedia of genes and genomes (KEGG) and gene ontology (GO) enrichment analysis was performed to analyze the differentially expressed genes (DEGs) of CD34 + fibroblasts (Fbs), smooth muscle cells (SMCs), keratinocytes (KCs), and chondrocyte-like cells (CLCs) in the wound tissue of two groups of mice for exploring cellular functions. Results:On PID 4, CD34 + cells in the wound tissue of both groups of mice were consisted of 7 cell types, specifically endothelial cells, Fbs, KCs, macrophages, T cells, SMCs, and CLCs. Among these, Fbs were further classified into 5 subpopulations. Compared with those in control group, the proportions of CD34 + endothelial cells, Fbs subpopulation 1, Fbs subpopulation 4, KCs, and CLCs in the wound tissue of mice were increased in diabetic group, while the proportions of CD34 + Fbs subpopulation 2, Fbs subpopulation 3, and SMCs were decreased. The marker genes for annotating CD34 + CLCs, endothelial cells, Fbs subpopulation 1, Fbs subpopulation 2, Fbs subpopulation 3, Fbs subpopulation 4, Fbs subpopulation 5, KCs, macrophages, SMCs, and T cells were respectively metastasis-associated lung adenocarcinoma transcript 1, fatty acid binding protein 4, Gremlin 1, complement component 4B, H19 imprinted maternally expressed transcript, Dickkopf Wnt signaling pathway inhibitor 2, fibromodulin, keratin 5, CD74 molecule, regulator of G protein signaling 5, and inducible T-cell co-stimulator molecule. KEGG and GO enrichment analysis revealed that, compared with those in control group, DEGs with significant differential expression (SDE) in CD34 + Fbs from the wound tissue of mice in diabetic group on PID 4 were significantly enriched in terms related to inflammatory response, extracellular matrix (ECM) organization, regulation of cell proliferation, and aging (with Pvalues all <0.05), DEGs with SDE in CD34 + SMCs were significantly enriched in terms related to cell migration, apoptotic process, positive regulation of transcription, and phagosome (with P values all <0.05), DEGs with SDE in CD34 + KCs were significantly enriched in terms related to mitochondrial function, transcription, and neurodegenerative diseases (with P values all <0.05), and DEGs with SDE in CD34 + CLCs were significantly enriched in terms related to rhythm regulation, ECM, and viral infection (with P values all <0.05). Conclusions:CD34 + cells display high heterogeneity in the healing process of full-thickness skin defect wounds in both normal mice and diabetic mice. The significantly enriched functions of DEGs with SDE in CD34 + cell subpopulations in the wound tissue of the two mouse groups are closely related to the wound healing process.

Objective To analyze the effect of inspection efficiency of large medical equipment on surgery-related time.Methods Data of surgical patients in a provincial top-three hospital in Anhui province from March to July 2023 were collected.A single-group intermittent time series analysis(ITSA)design was used to explore the changing trend of operation-related time before and after the improvement of inspection efficiency of large medical equipment,with preoperative waiting time,postoperative recovery time and hospital stay as the observational indicators.Results After the improvement of inspection efficiency of large medical equipment,the preoperative waiting time(β3=-0.010,P=0.048),postoperative recovery time(β3=-0.020,P＜0.001)and hospital stay(β3=-0.029,P＜0.001)were all decreased,and the differences were statistically significant.Con-clusion The improvement of inspection efficiency of large medical equipment can effectively reduce the operation related time,which can promote the utilization efficiency of medical resources and improve the medical experience of patients.

Objective:To identify risk variables for prolonged postoperative length of stay (PPOLOS) in hip fracture patients by machine learning algorithms and construct Nomogram models.Methods:A retrospective case-control study was conducted to select 248 patients with hip fracture diagnosed and treated in Yingtan 184th Hospital from June 2019 to June 2023 by convenient sampling method. Two machine learning algorithms were used (least absolute shrinkage and selection operator, LASSO and support vector machine-Recursive Feature Elimination, SVM-RFE) to screen PPOLOS risk variables. Construct a Nomogram model to predict the risk of PPOLOS in patients with hip fracture based on intersection risk variables. The model was validated using internal data sets.Results:Among the 248 patients with hip fracture, there were 79 males and 169 females, aged (64.49 ± 8.02). The mean postoperative length of hospital stay of 248 patients was (7.98 ± 5.68) d, and the median was 7 d. LASSO algorithm identifies 7 risk variables, the SVM-RFE algorithm identified 8 risk variables. Intersectional risk variables were age, body mass index (BMI), Charlson comorbidity index (CCI), type of surgery, and central granulocytocyte ratio (NLR). Multivariate Logistic regression analysis(intersection risk variables) showed that age [ OR=1.649(1.235-2.202)], BMI [1.603(1.204-2.134)], CCI [ OR=1.670(1.236-2.258)], type of surgery [ OR=1.620(1.209-2.170), 1.699(1.243-2.321)], and NLR [ OR=3.258(2.299-4.617)] were independently associated with the risk of PPOLOS (all P<0.05). The results showed that the conformity index of the Nomogram model was 0.865 (95% CI=0.768-0.945). The area under the curve was 0.852 (95% CI=0.748-0.962). When the risk threshold was >0.08, it could provide significant clinical net benefit. The clinical impact curve showed effective identification of PPOLOS patients in high-risk groups. Conclusions:This Nomogram model can guide medical staff to make clinical diagnosis and treatment decisions as soon as possible to avoid risks, allocate medical resources rationally, and improve nursing quality.

Objective To investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion(I/R)injury in mice and explore the underlying mechanism.Methods A total of 100 C57BL/6 mice were randomly divided into 5 groups,including a sham-operated group,cerebral I/R model group,and 3 leptin treatment groups with intraperitoneal injections of 0.5,1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery.At 24 h after reperfusion,neurological function scores of the mice were assessed,and TTC staining was used to determine the area of cerebral infarction.The pathological changes in the cortical brain tissue of the mice were observed using HE staining,and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining.The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting.In another 45 C57BL/6 mice with sham operation,I/R modeling,or leptin(1 mg/kg)treatment,glutamic acid in the cortical brain tissue was detected using glutamate assay,and cortical glutamate-aspartate transporter(GLAST)and glutamate transporter-1(GLT-1)protein expressions were detected using immunohistochemistry.Results Compared with the I/R model mice,the leptin-treated mice had significantly lower neurological deficit scores,smaller cerebral infarct area,milder pathologies in the cortical brain tissue,and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes.Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.Conclusion Exogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice,mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.