[Objective] To analyze the loss rate of platelet donors and evaluate the strategies for establishing a platelet donor bank. [Methods] A total of 1 443 donors who joined the HLA and HPA gene donor bank for platelets in Henan Province from 2018 to 2020 were included in this study. Data on the total number of apheresis platelet donations, annual donation frequency, age at enrollment, donation habits (including the number of platelets donated per session and whether they had previously donated whole blood), and enrollment location were collected from the platelet donor information management system. Donor loss was determined based on the date of their last donation. The loss rates of different groups under various conditions were compared to assess the enrollment strategies. [Results] By the time the platelet bank was officially operational in 2022, 421 donors had been lost, resulting in an loss rate of 29% (421/1 443). By the end of 2023, the overall cumulative loss rate reached 52% (746/1 443). The loss rate was lower than the overall level in groups meeting any of the following conditions: total apheresis platelet donations exceeding 50, annual donation frequency of 10 or more, age at enrollment of 40 years or older, donation of more than a single therapeutic dose per session, or a history of whole blood donation two or more times. Additionally, loss rates varied across different enrollment locations, with higher enrollment numbers generally associated with higher loss rates. [Conclusion] Through a comprehensive analysis of donor loss, our center has adjusted its strategies for establishing the donor pool. These findings also provide valuable insights for other blood collection and supply institutions in building platelet donor banks.

BACKGROUND:The specific molecular mechanisms underlying common degenerative bone diseases,such as osteoarthritis,osteoporosis,and intervertebral disc degeneration,are currently unclear and may involve endoplasmic reticulum stress.At present,research on the systematic role of endoplasmic reticulum stress in the pathogenesis of these common skeletal diseases and related therapeutic progress is relatively limited. OBJECTIVE:To review the role of endoplasmic reticulum stress in common degenerative bone diseases,explore the molecular mechanisms of these diseases in depth,and provide new ideas and perspectives for prevention and treatment of these diseases. METHODS:Relevant literature from 2000 to 2024 was searched in CNKI,WanFang,VIP,PubMed and Web of Science databases using the search terms of"endoplasmic reticulum stress,bone disease,unfolded protein response,osteoarthritis,osteoporosis,intervertebral disc degeneration,autophagy,apoptosis,ferroptosis,pyroptosis"in Chinese and English.After removal of duplicates and older literature,a total of 115 articles met the inclusion criteria. RESULTS AND CONCLUSION:Endoplasmic reticulum stress has a dual effect in regulating cell physiology.Mild endoplasmic reticulum stress promotes osteogenic differentiation and extracellular matrix synthesis;however,persistent excessive endoplasmic reticulum stress leads to cell death.Endoplasmic reticulum stress-induced cell autophagy and apoptosis are closely related to osteoarthritis,osteoporosis,and intervertebral disc degeneration.Aging,drug side effects,metabolic disorders,calcium imbalance,poor lifestyle habits and other reasons may lead to long-term activation of endoplasmic reticulum stress,which causes bone remodeling disorders,cartilage damage,nucleus pulposus cell death and other pathological manifestations,ultimately leading to the occurrence of osteoarthritis,osteoporosis and intervertebral disc degeneration.Intervention in the relevant mechanisms triggering endoplasmic reticulum stress is expected to play a role in the prevention and treatment of common degenerative bone diseases,such as osteoarthritis,osteoporosis and intervertebral disc degeneration.

ObjectiveThis study aimed to investigate the intervention effect of Renqing Mangjue on the malignant transformation of gastric mucosal epithelial cells induced by N-methyl-N′-nitro-N-nitrosoguanidine （MNNG） and to explore its molecular mechanism in preventing precancerous lesions of gastric cancer based on the cyclic guanosine monophosphate （cGMP）/protein kinase G （PKG）/mitogen-activated protein kinase （MEK）/extracellular signal-regulated kinase （ERK） signaling pathway. MethodsHuman gastric mucosal epithelial cells （GES-1） were initially induced by MNNG to establish a precancerous cell model （MC cells）. The effective concentration of MNNG for inducing malignant transformation in GES-1 cells was screened using the cell proliferation activity decection （CCK-8） assay， and the effective concentration of Renqing Mangjue for inhibiting the proliferation of transformed GES-1 cells was also determined. GES-1 cells were divided into a blank control group， a model group， and treatment groups with Renqing Mangjue at concentrations of 1， 3， 10， and 30 mg·L^-1. Furthermore， the effects of Renqing Mangjue on the migratory ability and epithelial-mesenchymal transition （EMT） characteristics of GES-1 malignant transformed cells were evaluated using Transwell migration assays， wound healing assays， and real-time quantitative reverse transcription polymerase chain reaction （Real-time PCR）. Additionally， candidate chemical components and target sites of Renqing Mangjue were obtained from the TCMIP v2.0 database， and disease targets at various stages of gastric cancer precursors were sourced from the Gene Expression Omnibus （GEO） database. Pathway enrichment analysis was performed using the Metascape database to predict the potential mechanisms of action of Renqing Mangjue. Finally， the protective mechanism of Renqing Mangjue against gastric cancer precursors was validated through Western blot analysis. ResultsAt a concentration of 20 μmol·L^-1， MNNG exhibited an inhibition rate of approximately 50% on GES-1 cells （P<0.01）， and at this concentration， the GES-1 cells displayed biological characteristics indicative of malignant transformation. In contrast， Renqing Mangjue had no significant effect on the proliferation of normal GES-1 cells， but significantly inhibited the proliferation of MC cells （P<0.01） and markedly reduced their migratory capacity （P<0.01）. Moreover， it also increased the mRNA expression level of E-cadherin during the EMT process （P<0.05）， while inhibiting the expression of both N-cadherin and the transcription factor Snail mRNA （P<0.05， P<0.01）. Network predictions suggested that Renqing Mangjue may prevent gastric cancer precursors through modulating the cGMP/PKG and MAPK/ERK signaling pathways. Furthermore， Western blot results indicated that Renqing Mangjue upregulated the expression of PKG and NPRB （B-type natriuretic peptide receptor） proteins in the cGMP/PKG pathway （P<0.01）， while downregulating the expression of the downstream proteins MEK and ERK （P<0.05， P<0.01）. ConclusionIn summary， Renqing Mangjue can prevent gastric cancer precursors by inhibiting the proliferation and migration of malignant transformed GES-1 cells， thereby delaying the EMT process. The underlying mechanisms may be related to the activation of the cGMP/PKG pathway and the inhibition of the MEK/ERK signaling pathway.

Objective To analyze the core genes of lung ischemia-reperfusion injury and construct a competitive endogenous RNA (ceRNA) network. Methods Original data of GSE145989 were downloaded from the Gene Expression Omnibus (GEO) database as the training set, and the GSE172222 and GSE9634 datasets were used as the validation sets, and the differentially-expressed genes (DEG) were identified. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. Protein-protein interaction (PPI) network was constructed, and the core genes were screened, and the diagnostic values of these core genes and the immune infiltration levels of immune cells were evaluated. The ceRNA network was constructed and validated. The targeted drugs based on ceRNA network were assessed. Results A total of 179 DEG were identified, including 61 down-regulated and 118 up-regulated genes. GO analysis showed that DEGs were associated with multiple biological processes, such as cell migration, differentiation and regulation, etc. They were correlated with cell components, such as vesicle membrane, serosa and membrane raft, etc. They were also associated with multiple molecular functions, such as chemokine receptor, G protein-coupled receptor, immune receptor activity and antigen binding, etc. KEGG pathway enrichment analysis revealed that DEG were involved in tumor necrosis factor (TNF), Wnt, interleukin (IL)-17 and nuclear factor (NF)-κB signaling pathways, etc. PPI network suggested that CD8A, IL2RG, STAT1, CD3G and SYK were the core genes of lung ischemia-reperfusion injury. The ceRNA network prompted that miR-146a-3p, miR-28-5p and miR-593-3p were related to the expression level of CD3G. The miR-149-3p, miR-342-5p, miR-873-5p and miR-491-5p were correlated with the expression level of IL-2RG. The miR-194-3p, miR-512-3p, miR-377-3p and miR-590-3p were associated with the expression level of SYK. The miR-590-3p and miR-875-3p were related to the expression level of CD8A. The miR-143-5p, miR-1231, miR-590-3p and miR-875-3p were associated with the expression level of STAT1. There were 13 targeted drugs for CD3G, 4 targeted drugs for IL-2RG, 28 targeted drugs for SYK and 3 targeted drugs for lncRNA MUC2. No targeted drugs were identified for CD8A, STAT1 and other ceRNA network genes. Conclusions CD8A, IL2RG, STAT1, CD3G and SYK are the core genes of lung ischemia-reperfusion injury. The research and analysis of these core genes probably contribute to the diagnosis of lung ischemia-reperfusion injury and providing novel research ideas and therapeutic targets.

ObjectiveTo investigate risk factors for postoperative sore throat in patients with double-lumen endotracheal intubation. MethodsThe data used in this post-hoc analysis were prospectively collected from a randomized， controlled trial. Age from 18 to 65 years old， ASAI-Ⅲ patients undergoing general anesthesia with a double-lumen endotracheal tube were enrolled. The perioperative data collected retrospectively were as follows： gender， age， smoking history， endotracheal tube diameter， duration of endotracheal tube， dose of Sufentanil， use of Flurbiprofen Axetil， cough after extubation， etc..Dynamometer was applied to assess extubation force. According to occurrence of postoperative sore throat， patients were divided into two groups： those who experienced sore throats and those who did not. Comparative analysis and multivariate logistic regression analysis were performed to screen the risk factors. ROC curve was used for predicting the predictive value of risk factors. ResultsAmong the 163 patients ， 74 （45.4%） had postoperative sore throat vs 89 （54.6%） not had. Multivariate logistic regression showed female ［OR95%CI=3.83（1.73， 8.50）， P=0.000 1］ and extubation force ［OR95%CI=1.78（1.45， 2.17）， P＜0.001］ were independent risk factors for postoperative sore throat. AUC value showed the extubation force was 0.773［95%CI（0.701， 0.846）， P＜0.001］. Youden index was 0.447， and the cut-off valve of extubation force was 13N. ConclusionFemale and extubation force were risk factors for sore throat in patients with double lumen endotracheal intubation.

Evoked Potentials ; Social Isolation ; Attention ; Humans

ObjectiveTo identify the pharmacodynamic material basis of Ruyi Zhenbaowan in relieving neuropathic pain by integrating the calculation of biological network proximity and pharmacokinetic characterization. MethodThe interaction network of "drug candidate target-related gene of disease" was constructed by Cytoscape 3.8.2， and the average shortest path value of each drug putative target acting on neuropathic pain-related genes in this network was calculated by Pesca 3.8.0 tool so as to evaluate the network proximity between them， and screen prescription candidate targets with strong intervention efficiency and their corresponding potential effect components. After that， plasma and cerebrospinal fluid samples were collected from rats after administration of Ruyi Zhenbaowan at set time points， and the contents of potential effect components in samples was quantified by ultra performance liquid chromatography-quadrupole-ion trap mass spectrometry（UPLC-Q-TRAP/MS）， and drug concentration-time curves were plotted， then the pharmacokinetic parameters were calculated by DAS 2.1.1. ResultBy evaluating the network proximity between candidate targets and neuropathic pain-related genes in the interaction network， a total of 40 putative targets of Ruyi Zhenbaowan with strong intervention effects on neuropathic pain-related genes， such as estrogen receptor 1（ESR1）， cyclic adenosine monophosphate（cAMP）-dependent protein kinase catalytic subunit alpha（PRKACA） and protein kinase B1 （Akt1）， and 10 corresponding potential effect components， such as glycyrrhizic acid and betulinic acid， were obtained. Pharmacokinetic characterization showed that among the 10 potential effect components， gallic acid， apigenin-7-O-glucuronide， glycyrrhizic acid and apigenin were well absorbed and metabolized in plasma and cerebrospinal fluid， with long onset time and good bioavailability. ConclusionFrom the perspective of efficacy-target-constituent-pharmacokinetic， this study analyzes the main effective materials of Ruyi Zhenbaowan， such as glycyrrhizic acid， gallic acid， apigenin-7-O-glucuronide and apigenin， which have a high exposure in plasma or cerebrospinal fluid and have a strong intervention effect on neuropathic pain. The related results provide reliable experimental evidences for clarifying the material basis and developing quality standards of Ruyi Zhenbaowan.

Objective:To assess the enhancement characteristics of responsibility plaque of patients with intracranial artery stenosis(ICAS)and explore the correlation between that and stroke by using three dimensional high-resolution magnetic resonance imaging(3D-HR-MRI).Methods:A total of 72 ICAS patients who admitted to Beijing Huairou Hospital from April 2019 to April 2022 were retrospectively selected as the study objects,with a total of 96 atherosclerotic stenosis plaques.The plaques were divided into mild to moderate stenosis group(33 cases)and severe stenosis group(63 cases)according to the results of whole brain digital subtraction angiography.They were also were divided into sub-acute/acute plaque group(within 1 month)(47 cases)and non-acute plaque group(including chronic and non-responsible plaques)(49 cases)according to the time of occurring plaque.The imaging characteristics of the 3D-HR-MRI results were assessed by two radiologists.The degrees of plaque enhancement referred to the degrees of pituitary enhancement,and the degrees of plaque enhancement were divided into significant enhancement group(52 cases)and non-significant enhancement group that included moderate enhancement group and non-enhancement group(44 cases).The relationships between ICAS,degree of plaque enhancement and stroke were analyzed.Results:A total of 96 atherosclerotic stenosis plaques were confirmed in 72 patients.The statistical analysis of Kruskal-Wallis H test of multiple samples showed that there was a significant correlation between the time of occurring plaque and the degree of plaque enhancement(H=3.294,P＜0.05).Univariate Logistic regression analysis indicated that the difference between the acute plaque group and the non-acute plaque group was respectively significant correlations with ICAS degree[P＜0.05,OR(95%CI)=1.0(0.3-2.6)]and degree of plaque enhancement[P＜0.05,OR(95%CI)=1.0(0.4-2.0)].The multivariate Logistic regression analysis demonstrated that both severe arterial stenosis[P＜0.05,OR(95%CI)=1.0(0.3-1.9)]and significant enhancement of plaque[P＜0.05,OR(95%CI)=1.0(0.4-2.1)]were independent risk factors of stroke.Conclusion:Severe ICAS and significant plaque enhancement are the independent risk factors of stroke,which can provide effective basis for clinical prevention,diagnosis and treatment of stroke.

To describe and evaluate the clinical studies of postoperative pain sensitization caused by sleep deprivation through the evidence map system, understand the distribution of evidence in this field, and provide reference for subsequent evidence research.

Adipose-derived mesenchymal stem cell (ADSC) has become a research hotspot in the field of regenerative medicine and stem cells in recent years because of its rich stock, easy access and low immunogenicity. ADSC can regulate immune system not only directly by interacting with immune cells, such as T cells, macrophages and B cells, but also indirectly via secreting soluble cytokines, such as interleukin (IL), growth factors and extracellular vesicles. Meanwhile, the immunomodulatory effects of ADSC have been demonstrated in vitro and in vivo experiments and applied to treat various of immune-related diseases with good results, such as systemic scleroderma, systemic lupus erythematosus and atopic dermatitis, etc. In this article, the direct and indirect immunomodulatory mechanisms and clinical applications of ADSC are described, its research direction and application prospect are also prospected.