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.

In order to realize the diagnosis of slit lamp in cross-regional patients and improve the real-time and convenience of diagnosis,a remote slit lamp diagnosis platform based on Internet of Things(IoT)technology is designed.Firstly,the feasibility of remote slit lamp is analyzed.Secondly,the IoT platform architecture of doctor/server/facility(D/S/F)is proposed and a remote slit lamp is designed.Finally,the performance of the remote slit lamp diagnostic platform is tested.The platform solves the communication problem of distributed slit lamps and realizes respectively numerical control of multi-area slit lamp by multi-eye experts.The test results show that the remote control delay of the platform is less than 20 ms,which supports multiple experts to diagnose multiple patients separately.

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 risk factors for frailty in older adult patients with chronic obstructive pulmonary disease (COPD) and its correlation with oxidative stress.Methods:A total of 168 patients with COPD aged 60 years and above, who were treated at Pingxiang People's Hospital from August 2022 to August 2023, were selected as the study subjects using the convenient sampling method. The FRAIL scale was utilized to assess frailty status. Patients were divided into two groups based on their FRAIL scale scores: the frail group (≥ 3 points, n = 109), the non-frail/pre-frail group (< 3 points, n = 59). Patients in the non-frail/pre-frail group were sub-divided into the pre-frail group (1-2 points, n = 23), and the non-frail group (0 points, n = 36). Serum levels of 8-hydroxydeoxyguanosine and malondialdehyde, and total antioxidant capacity were measured. One-way analysis of variance was performed to compare differences between groups, and correlation analysis was conducted. Logistic regression was used to identify the risk factors for frailty. Results:The incidence of frailty among 168 older adult patients with COPD was 64.9% (109/168). Multivariable logistic regression analysis revealed that age ( OR = 1.59, 95% CI 1.02-2.25), body mass index ( OR = 4.11, 95% CI 2.02-8.42), comorbidities ( OR = 2.57, 95% CI 1.31-5.02), activities of daily living ( OR = 3.07, 95% CI 1.54-6.06), malnutrition ( OR = 2.97, 95% CI 1.56-5.41), and cognitive impairment ( OR = 2.87, 95% CI 1.42-5.88) were risk factors for frailty in older patients with COPD ( P < 0.05). The frailty scores of older adult patients with COPD were significantly positively correlated with serum levels of 8-hydroxydeoxyguanosine and malondialdehyde ( γ= 0.67, 0.65, P = 0.008, 0.006), and negatively correlated with total antioxidant capacity ( γ= -0.54, P = 0.012). Conclusion:Age, body mass index, comorbidities, activities of daily living, malnutrition, and cognitive impairment are risk factors for frailty in older adult patients with COPD, and the severity of frailty is markedly associated with levels of oxidative stress products.

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 develop a deep learning method for volumetric assessment of traumatic intracerebral hemorrhage(TICH)using the Trans-UNet model and to compare its performance with traditional formula-based methods.Methods CT data from 141 TICH patients admitted to Army Medical Center of PLA between May 2018 and May 2023 were collected.A deep learning method based on the Trans-UNet model was established.Manual delineation via picture archiving and communication system(PACS)was served as the gold standard for comparing the accuracy,consistency,and time efficiency of our method against 10 different formula-based methods for measuring the amount of TICH.Results The median volume of TICH,as manual delineation via PACS,was 1.167 mL,with a median measurement time of 135 s per patient.The median percentage error in volume between the deep learning method and manual delineation via PACS was 3.59％.Spearman correlation coefficient was 0.999(P＜0.001),and a median measurement time was only 4.38 s per patient.In contrast,in the formula-based methods,the lowest median percentage error in volume was 16.451％,the highest Spearman correlation coefficient was 0.986(P＜0.001),and the lowest median measurement time was 20 s for a single patient.The statistical differences were observed in percentage error in volume and measurement time between the 2 types of methods(all P＜0.001).Conclusion Our developed deep learning method for volumetric assessment of TICH is superior to the formula-based methods in terms of measurement accuracy and time efficiency.

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 analyze the risk factors of heart failure in patients with coronary heart disease(CHD),and to construct and verify a nomogram prediction model for the risk of heart failure in patients with CHD.Methods The clinical data of 453 patients with CHD who were hospitalized in the Second Affiliated Hospital of Shenyang Medical College from January to December 2022 were retrospectively analyzed,including 278 patients with CHD combined with heart failure and 175 patients without heart failure.The patients were divided into training group(318 cases)and validation group(135 cases)according to the ratio of 7:3.R software was applied to perform LASSO regression to screen the risk factors,and Logistic regression to establish a prediction model and construct a nomogram.The calibration curve and receiver operating characteristic(ROC)curve were used to evaluate the calibration and discrimination of the model.Results LASSO regression analysis ultimately screened five risk factors from 22 variables,and Logistic regression results showed that age,smoking,history of myocardial infarction,New York Heart Association(NYHA)cardiac function class Ⅳ,and left ventricular ejection fraction(LVEF)were all independent risk factors for heart failure in CHD patients(P＜0.05).The model formula was Z=-2.927+0.045 × age+0.886 × smoking+0.808 × history of myocardial infarction-2.829 × NYHA cardiac function class Ⅳ+0.037×LVFF.Internal validation of the model showed that area under the curve was 0.727(95％CI:0.588-0.752),the sensitivity was 40.4％,the specificity was 84.3％,and the Youden index was 0.247.According to the calibration curve,the predicted value of the calibration curve was highly consistent with the actual value,and the Brier score was 0.106.Conclusion The risk prediction model for heart failure in patients with CHD based on LASSO regression has good discrimination and prediction efficiency,which can be used as an evaluation tool for medical staff to predict the risk of patients.

As a natural drug delivery carrier with rough and porous surface and hollow core， yeast microcapsules have good safety， high targeting and high stability， and have excellent application prospects in oral drug delivery systems. Yeast cells can be treated and washed with acid-base and organic solvents to obtain loose and porous yeast microcapsules. Yeast microcapsules can encapsulate drugs through electrostatic interactions， passive diffusion， hydrophobic interaction and other methods. The surface of yeast microcapsules is mainly composed of β-glucan， which can maintain stability in the gastrointestinal environment； it can be recognized by the surface-related receptors of immune cells， thus activating the immune response， and can be transported to the lesion site with the movement of lymphocytes after being ingested. Yeast microcapsules are safe and very suitable for delivering vaccines， anti-inflammatory drugs， and anti-tumor drugs. They can not only achieve oral delivery of the aforementioned drugs， but also enhance drug efficacy and improve drug targeting. In the future， more research on systemic transport mechanisms or the development of more efficient combination drug delivery systems can be carried out to fully exhibit the clinical value of yeast microcapsules.