BACKGROUND:Ubiquitination is a fundamental biological process that plays several critical roles in cellular regulation. In recent years, extensive research worldwide has investigated the involvement of ubiquitination in the pathogenesis of various brain diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), ischemic stroke, and glioblastoma (GBM). However, to date, no comprehensive bibliometric analysis has systematically examined the research landscape concerning the role of ubiquitination in brain diseases. METHODS:A detailed exploration of the Web of Science Core Collection (WoSCC) database was carried out, encompassing studies from 1999 to 2024, to evaluate the interplay between ubiquitination mechanisms and various brain disorders. The database was retrieved on January 20, 2025. Bibliometric and visualization analyses were performed using various tools such as Microsoft Excel, VOSviewer, CiteSpace, the R package 'bibliometrix', and an online bibliometric platform. RESULTS:A marked growth in scholarly articles investigating ubiquitination's role in brain diseases has been observed over the 25-year period from 1999 through 2024. A total of 1,658 articles were published in 539 journals. The United States leads in national research output, with the Chinese Academy of Sciences ranking first among all institutions in terms of publication output. Among authors, Ted M. Dawson has contributed the most articles, and the Journal of Biological Chemistry has the highest number of publications. Research on ubiquitination in brain diseases primarily focuses on AD, PD, ischemic stroke, and GBM. DISCUSSION:The rapid expansion of this field highlights ubiquitination as a key regulatory mechanism in brain diseases. Future studies should focus on mechanistic depth and translational potential, particularly targeting ubiquitin related pathways for therapeutic intervention. CONCLUSION:Increasing attention is being paid to the research field exploring the relationship between brain diseases and ubiquitination. The insights from our findings may serve as a valuable reference for scholars interested in investigating ubiquitination in brain disorders in the future.

Post-stroke depression (PSD) is the most prevalent neuropsychological disorder among stroke survivors, affecting over 30% of patients. It significantly impairs patients’ quality of life and imposes a substantial burden on individuals, families, and society. Currently, the primary treatment for PSD focuses on conventional antidepressant therapies, with a lack of innovative approaches. Therefore, there is an urgent need to develop novel targeted therapies for PSD. This review synthesizes PSD pathogenesis as a multi-system network disorder involving monoamine deficits, neuroinflammation, HPA axis dysfunction, and neurotrophic imbalance. Within this framework, mesenchymal stem cells (MSCs) transplantation, as an emerging therapeutic strategy, may exert beneficial effects through anti-inflammatory, neuroprotective mechanisms, and the provision of neurotrophic factors. This review provides a preclinical framework that highlights the potential of MSC-based strategies, while emphasizing the need for further validation in PSD-specific models before clinical translation.

Poly-ether-ketone-ketone (PEKK) exhibits a bone-matching elastic modulus, commendable modifiability, and 3D-printable processability. These attributes enable its application in customized porous implants with optimized mechanical compatibility and osteogenic potential, particularly for orthopedic and dental regenerative therapies. This review evaluates the chemical characteristics, crystallization behavior, and mechanical properties of PEKK, alongside current strategies for material modification and additive manufacturing tailored to clinical requirements. Thus, PEKK-based restorative solutions exhibit great flexibility and adaptability when facing complex restorative demands of orthopedics and dentistry. The potential of PEKK in fields such as orthopedic surgery, dentistry, tissue engineering, drug delivery, and regenerative medicine is promising, with a possibility to serve as an alternative to traditional metal materials. However, the advantages of PEKK are not yet sufficient to supplant currently widely used implant material and further in-depth research and long-term evaluation is required.

Glaucomatous optic neuropathy represents a prevalent optic nerve degenerative disease. Neuroinflammation is recognized as a significant mechanism underlying optic nerve damage in glaucoma; however, the precise mechanisms driving neuroinflammation remain largely elusive. Existing studies have indicated that microglia-driven neuroinflammation is pivotal for neuroinflammation onset and progression. Mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) damage, metabolic deficiencies, and quality control impairments, is upstream of microglial activation and neuroinflammation. Thus, a deeper comprehension of the link between mitochondrial dysfunction and microglial activation in glaucoma may provide valuable insights into the underlying pathogenesis. As a result of these findings, promising avenues for developing effective interventions to mitigate optic nerve damage and preserve visual function in glaucoma patients have been identified.

Leptospirosis is a zoonotic infectious disease that can involve multiple organ systems. Neurological involvement is uncommon, and long-term neuropsychiatric sequelae have rarely been described. We report the case of a previously healthy adult who developed acute leptospiral infection complicated by multifocal central nervous system (CNS) lesions. The patient presented with fever, convulsions, altered mental status. Chest computed tomography (CT) scan revealed diffuse ground-glass opacities and patchy consolidations in both lungs. Brain magnetic resonance (MRI) demonstrated multifocal CNS lesions. Cerebrospinal fluid Metagenomic Next-generation Sequencing (mNGS) confirmed leptospiral infection. The patient received appropriate antimicrobial therapy and recovered fully, with follow-up imaging showing resolution of cortical lesions. Three years later, the patient developed new-onset psychiatric symptoms, including delusions, hallucinations, or personality changes, without evidence of recurrent infection or other organic causes. This case highlights that leptospiral infection may cause multifocal CNS lesions and lead to delayed psychiatric sequelae years after apparent recovery.

Excessive accumulation of reactive oxygen species (ROS) in Parkinson's disease (PD) leads to oxidative stress, which induces neuroinflammation and accelerates disease progression. To address this, we developed mPDA@MSC, a nanosystem consisting of mesoporous polydopamine (mPDA) nanoparticles coated with a mesenchymal stem cell membrane (MSCm), which exhibits ROS-scavenging properties. The mPDA structure significantly enhanced ROS-scavenging and anti-inflammatory activities, while the surface-encapsulated MSCm enabled effective blood-brain barrier traversal and targeted the lesion site in the PD brain. Both in vitro and in vivo studies demonstrated that mPDA@MSC exerted anti-Parkinsonian effects through multiple mechanisms, including ROS scavenging, modulation of mitochondrial dysfunction, and promotion of the transition from pro-inflammatory to anti-inflammatory microglial phenotypes. This resulted in the reversal of dopaminergic neuron damage, inhibition of α-synuclein (α-syn) production, and improvement in behavioral deficits and other phenotypes. These findings highlight the potential of mPDA@MSC as a therapeutic agent for PD and introduce a novel approach to anti-PD therapy.

IntroductionDrug target identification is a fundamental step in drug discovery and plays a pivotal role in new therapies development. Existing computational methods focus on the direct interactions between drugs and targets, often ignoring the complex interrelationships between drugs, targets and various biomolecules in the human system.MethodTo address this limitation, we propose a novel prediction model named DTGHAT (Drug and Target Association Prediction using Heterogeneous Graph Attention Transformer based on Molecular Heterogeneous). DTGHAT utilizes a graph attention transformer to identify novel targets from 15 heterogeneous drug-gene-disease networks characterized by chemical, genomic, phenotypic, and cellular networks.ResultIn a 5-fold cross-validation study, DTGHAT achieved an area under the receiver operating characteristic curve (AUC) of 0.9634, which is at least 4% higher than current state-of-the-art methods. Characterization ablation experiments highlight the importance of integrating biomolecular data from multiple sources in revealing drug-target interactions. In addition, a case study on cancer drugs further validates DTGHAT’s effectiveness in predicting novel drug target identification. DTGHAT is free and available at: https://github.com/stella-007/DTGHAT.git.

Spinal cord injury (SCI) is a pathological condition that damages the central nervous system. Due to the persistence of neuroinflammation after injury, the prognosis is often poor. Recent studies have found that local transplantation of mesenchymal stem cells (MSCs) can improve SCI. However, MSCs retain and engraft at the injured site limit, which may be the reason their effectiveness is greatly reduced. A gelatin sponge (GS), commonly used in clinical practice, was selected as a scaffold to deliver olfactory mucosal mesenchymal stem cells (OM-MSCs). This was done to to enhance local reparative of MSCs at the injury site. We also paid special attention to the biocompatibility of GS co-cultured with OM-MSCs in vitro, and then applied acellular GS and GS loaded with OM-MSCs to the rat SCI model, respectively. After the scaffold was transplanted into rat complete spinal cord injury, behavioral scores and hindlimb movement scores were improved evidently. Local inflammation in the spinal cords of transplanted rats was reduced, and the changes were related to cell pyroptosis. In addition, we found that gelatin sponges and OM-MSC transplantation did not damage other organs in rats. In conclusion, the GS scaffold loaded with OM-MSCs can reduce the local inflammatory microenvironment and facilitate neurological recovery, providing a potential and practical strategy for therapeutic approach of spinal cord injury.

Background Pulmonary fibrosis (PF) is a progressive fibrosing interstitial pneumonia that leads to respiratory failure and other complications, which is ultimately fatal. Mesenchymal stem cells (MSCs) transplant is a promising strategy to solve this problem, while the procurement of MSCs from the patient for autotransplant remains a challenge. Methods Here, we presented olfactory mucosa mesenchymal stem cells (OM-MSCs) from mouse turbinate and determined the preventing efficacy of allotransplant for PF. We demonstrated the antiinflammation and immunomodulatory effects of OM-MSCs. Flow cytometric analysis was used to verify the effect of OM-MSCs on monocyte-derived macrophage populations in the lung. Results Administration of OM-MSCs reduces inflammation, attenuates the matrix metallopeptidase 13 (MMP13) expression level and restores the bleomycin (BLM)-induced pulmonary fibrosis by assessing the architecture of lung, collagen type I; (COL1A1), actin alpha 2, smooth muscle, aorta (ACTA2/α-SMA) and hydroxyproline. This therapeutic effect of OM-MSCs was related to the increase in the ratio of nonclassical monocytes to proinflammatory monocytes in the lung. Conclusions This study suggests that transplant of OM-MSCs represents an effective and safe treatment for PF.

Retinoic acid (RA), a vitamin A derivative, is an effective cell differentiating factor which plays critical roles in neuronal differentiation induction and the production of neurotransmitters in neurons. However, the specific changes in phosphorylation levels and downstream signalling pathways associated with RA remain unclear. This study employed qualitative and quantitative phosphoproteomics approaches based on mass spectrometry to investigate the phosphorylation changes induced by RA in C17.2 neural stem cells (NSCs). Dimethyl labelling, in conjunction with TiO2 phosphopeptide enrichment, was utilized to profile the phosphoproteome of self-renewing and RA-induced differentiated cells in C17.2 NSCs. The results of our study revealed that, qualitatively, 230 and 14 phosphoproteins were exclusively identified in the self-renewal and RA-induced groups respectively. Quantitatively, we successfully identified and quantified 177 unique phosphoproteins, among which 70 exhibited differential phosphorylation levels. Analysis of conserved phosphorylation motifs demonstrated enrichment of motifs corresponding to cyclin-dependent kinase and MAPK in the RA-induced group. Additionally, through a comprehensive literature and database survey, we found that the differentially expressed proteins were associated with the Wnt/β-catenin and Hippo signalling pathways. This work sheds light on the changes in phosphorylation levels induced by RA in C17.2 NSCs, thereby expanding our understanding of the molecular mechanisms underlying RA-induced neuronal differentiation.

BackgroundCerebral ischemia-reperfusion (I/R) injury often leads to neuronal death through persistent neuroinflammatory responses. Recent research has unveiled a unique inflammatory programmed cell death mode known as PANoptosis. However, direct evidence for PANoptosis in ischemic stroke-induced neuronal death has not been established. Although it is widely thought that modulating the balance of microglial phenotypic polarization in cerebral I/R could mitigate neuroinflammation-mediated neuronal death, it remains unknown whether microglial polarization influences PANoptotic neuronal death triggered by cerebral I/R. Our prior study demonstrated that curcumin (CUR) preconditioning could boost the neuroprotective properties of olfactory mucosa-derived mesenchymal stem cells (OM-MSCs) in intracerebral hemorrhage. Yet, the potential neuroprotective capacity of curcumin-pretreated OM-MSCs (CUR-OM-MSCs) on reducing PANoptotic neuronal death during cerebral I/R injury through modulating microglial polarization is uncertain.MethodsTo mimic cerebral I/R injury, We established in vivo models of reversible middle cerebral artery occlusion (MCAO) in C57BL/6 mice and in vitro models of oxygen-glucose deprivation/reoxygenation (OGD/R) in HT22 neurons and BV2 microglia.ResultsOur findings indicated that cerebral I/R injury caused PANoptotic neuronal death and triggered microglia to adopt an M1 (pro-inflammatory) phenotype both in vivo and in vitro. Curcumin pretreatment enhanced the proliferation and anti-inflammatory capacity of OM-MSCs. The CUR-OM-MSCs group experienced a more pronounced reduction in PANoptotic neuronal death and a better recovery of neurological function than the OM-MSCs group. Bioinformatic analysis revealed that microRNA-423-5p (miRNA-423-5p) expression was obviously upregulated in CUR-OM-MSCs compared to OM-MSCs. CUR-OM-MSCs treatment induced the switch to an M2 (anti-inflammatory) phenotype in microglia by releasing miRNA-423-5p, which targeted nucleotide-binding oligomerization domain 2 (NOD2), an upstream regulator of NF-kappaB (NF-κB) and Mitogen-Activated Protein Kinase (MAPK) signaling pathways, to attenuate PANoptotic neuronal death resulting from cerebral I/R.ConclusionThis results provide the first demonstration of the existence of PANoptotic neuronal death in cerebral I/R conditions. Curcumin preconditioning enhanced the ameliorating effect of OM-MSCs on neuroinflammation mediated by microglia polarization via upregulating the abundance of miRNA-423-5p. This intervention effectively alleviates PANoptotic neuronal death resulting from cerebral I/R. The combination of curcumin with OM-MSCs holds promise as a potentially efficacious treatment for cerebral ischemic stroke in the future.

BACKGROUND:Parkinson's disease (PD) is a neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra (SN). Activation of the neuroinflammatory response has a pivotal role in PD. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic approach for various nerve injuries, but there are limited reports on their use in PD and the underlying mechanisms remain unclear. METHODS:We investigated the effects of clinical-grade hypoxia-preconditioned olfactory mucosa (hOM)-MSCs on neural functional recovery in both PD models and patients, as well as the preventive effects on mouse models of PD. To assess improvement in neuroinflammatory response and neural functional recovery induced by hOM-MSCs exposure, we employed single-cell RNA sequencing (scRNA-seq), assay for transposase accessible chromatin with high-throughput sequencing (ATAC-seq) combined with full-length transcriptome isoform-sequencing (ISO-seq), and functional assay. Furthermore, we present the findings from an initial cohort of patients enrolled in a phase I first-in-human clinical trial evaluating the safety and efficacy of intraspinal transplantation of hOM-MSC transplantation into severe PD patients. RESULTS:A functional assay identified that transforming growth factor-β1 (TGF-β1), secreted from hOM-MSCs, played a critical role in modulating mitochondrial function recovery in dopaminergic neurons. This effect was achieved through improving microglia immune regulation and autophagy homeostasis in the SN, which are closely associated with neuroinflammatory responses. Mechanistically, exposure to hOM-MSCs led to an improvement in neuroinflammation and neural function recovery partially mediated by TGF-β1 via activation of the anaplastic lymphoma kinase/phosphatidylinositol-3-kinase/protein kinase B (ALK/PI3K/Akt) signaling pathway in microglia located in the SN of PD patients. Furthermore, intraspinal transplantation of hOM-MSCs improved the recovery of neurologic function and regulated the neuroinflammatory response without any adverse reactions observed in patients with PD. CONCLUSIONS:These findings provide compelling evidence for the involvement of TGF-β1 in mediating the beneficial effects of hOM-MSCs on neural functional recovery in PD. Treatment and prevention of hOM-MSCs could be a promising and effective neuroprotective strategy for PD. Additionally, TGF-β1 may be used alone or combined with hOM-MSCs therapy for treating PD.

Background: Short-chain fatty acids (SCFAs) are thought to play a key role in the microbe-gut-brain axis and involve in the pathogenesis of a variety of neurological diseases. This study aimed to identify research hotspots and evolution trends in SCFAs in central nervous diseases (CNS) and examine current research trends. Methods: The bibliometric analysis was performed using CiteSpace, and the results were visualized via network maps. Results: From 2002 to 2022, 480 publications in the database met the criteria. On the country level, China produced the highest number of publications, while the United States had the highest centrality. On the institutional level, University College Cork contributed to the most publications, and John F. Cryan from this university was the key researcher with considerable academic influence. The article, the role of short-chain fatty acids in microbiota-gut-brain, written by Boushra Dalile et al., in 2019 was the most cited article. Furthermore, the journal Nutrients had the maximum number of publications, while Plos One was the most cited journal. “Gut microbiome”, “SCFAs”, and “central nervous system” were the three most frequent keywords. Among them, SCFAs had the highest centrality. “Animal model” was the keyword with the highest burst strength, with the latest burst keywords being “social behavior”, “pathogenesis”, and “insulin sensitive”. In addition, the research topics on SCFAs in CNS diseases from 2002 to 2022 mainly focused on following aspects: SCFAs plays a key role in microbe-gut-brain crosstalk; The classification and definition of SCFAs in the field of CNS; Several CNS diseases that are closely related to SCFAs research; Mechanism and translational studies of SCFAs in the CNS diseases. And the hotspots over the past 5 years have gradually increased the attention to the therapeutic potential of SCFAs in the CNS diseases. Conclusion: The research of SCFAs in CNS diseases is attracting growing attention. However, there is a lack of cooperation between countries and institutions, and additional measures are required to promote cooperation. The current evidence for an association between SCFAs and CNS diseases is preliminary and more work is needed to pinpoint the precise mechanism. Moreover, large-scale clinical trials are needed in the future to define the therapeutic potential of SCFAs in CNS diseases.

Mesenchymal stem cells (MSCs) are ubiquitous multipotent cells exhibiting significant therapeutic potential for various diseases. It is generally accepted that clinical application requires massive expansion of MSCs, which is often accompanied by the occurrence of replicative senescence. Additionally, senescent MSCs exhibit significantly reduced proliferation, differentiation, and therapeutic potential. The scale-up of MSCs production and cellular senescence are major challenges for translational applications. This study first collected extracellular vesicles (EVs) from gingival MSCs (GMSCs) under hypoxia preconditioning combined with 3D dynamic culture (obtained EVs designed as H-3D-EVs). Subsequently, we further explored the effects and mechanisms of H-3D-EVs on aging-GMSCs. The results showed that H-3D-EVs improved the proliferation ability and cell activity of aging-GMSCs, and ameliorated their senescence. mRNA sequencing reveals transcriptomic changes in aging-GMSCs. It was found that H-3D-EVs up-regulated genes related to mitochondrial dynamics, cell cycle, and DNA repair, while down-regulated aging-related genes. Furthermore, we verified that H-3D-EVs corrected the mitochondrial dysfunction of aging-GMSCs by improving mitochondrial dynamics. In summary, this study provides a promising strategy for improving the culture methods of GMSCs and avoiding its senescence in large-scale production.

Abstract Background and aims Refractory epilepsy is also known as drug-resistant epilepsy with limited clinical treatment. Benefitting from its safety and easy availability, olfactory mucosa mesenchymal stem cells (OM-MSCs) are considered a preferable MSC source for clinical application. This study aims to investigate whether OM-MSCs are a promising alternative source for treating refractory epilepsy clinically and uncover the mechanism by OM-MSCs administration on an epileptic mouse model. Methods OM-MSCs were isolated from turbinal and characterized by flow cytometry. Autologous human OM-MSCs treatment on a patient was carried out using intrathecal administration. Epileptic mouse model was established by 1 mg/kg scopolamine and 300 mg/kg pilocarpine treatment (intraperitoneal). Stereotaxic microinjection was employed to deliver the mouse OM-MSCs. Mouse electroencephalograph recording was used to investigate the seizures. Brain structure was evaluated by magnetic resonance imaging (MRI). Immunohistochemical and immunofluorescent staining of GFAP, IBA1, MAP2, TUBB3, OLIG2, CD4, CD25, and FOXP3 was carried out to investigate the neural cells and Treg cells. QRT-PCR and ELISA were performed to determine the cytokines (Il1b, Il6, Tnf, Il10) on mRNA and protein level. Y-maze, the object location test, and novel object recognition test were performed to measure the cognitive function. Footprint test, rotarod test, balance beam test, and grip strength test were conducted to evaluate the locomotive function. Von Frey testing was carried out to assess the mechanical allodynia. Results Many beneficial effects of the OM-MSC treatment on disease status, including seizure type, frequency, severity, duration, and cognitive function, and no apparent adverse effects were observed at the 8-year follow-up case. Brain MRI indicated that autologous OM-MSC treatment alleviated brain atrophy in epilepsy patients. A study in an epileptic mouse model revealed that OM-MSC treatment recruited Treg cells to the brain, inhibited inflammation, rebuilt the neural network, and improved the cognitive, locomotive, and perceptive functions of epileptic mice. Conclusions Autologous OM-MSC treatment is efficacious for improving chronic refractory epilepsy, suggesting a future therapeutic candidate for epilepsy. Trial registration: The study was registered with Chinese Clinical Trial Registry (ChiCTR2200055357).

Parkinson's disease (PD) is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons in the substantia nigra (SN); the etiology and pathological mechanism of the disease are still unclear. Recent studies have shown that the activation of a neuroimmune response plays a key role in the development of PD. Alpha-synuclein (α-Syn), the primary pathological marker of PD, can gather in the SN and trigger a neuroinflammatory response by activating microglia which can further activate the dopaminergic neuron’s neuroimmune response mediated by reactive T cells through antigen presentation. It has been shown that adaptive immunity and antigen presentation processes are involved in the process of PD and further research on the neuroimmune response mechanism may open new methods for its prevention and therapy. While current therapeutic regimens are still focused on controlling clinical symptoms, applications such as immunoregulatory strategies can delay the symptoms and the process of neurodegeneration. In this review, we summarized the progression of the neuroimmune response in PD based on recent studies and focused on the use of mesenchymal stem cell (MSC) therapy and challenges as a strategy of disease-modifying therapy with multiple targets.

In cell transplantation therapy, mesenchymal stem cells(MSCs)are ideal seed cells due to their easy acquisition and cultivation, strong regenerative capacity, multi-directional differentiation abilities, and immunomodulatory effects. Autologous MSCs are better applicable compared with allogeneic MSCs in clinical practice. The elderly are the main population for cell transplantation therapy, but as donor aging, MSCs in the tissue show aging-related changes. When the number of generations of in vitro expansion is increased, MSCs will also exhibit replicative senescence. The quantity and quality of MSCs decline during aging, which limits the efficacy of autologous MSCs transplantation therapy. In this review, we examine the changes in MSC senescence as a result of aging, discuss the progress of research on mechanisms and signalling pathways of MSC senescence, and discuss possible rejuvenation strategies of aged MSCs to combat senescence and enhance the health and therapeutic potential of MSCs.

Oxidative stress is essential in brain injury after intracerebral hemorrhage (ICH). Ferroptosis, iron-dependent oxidative cell death, overwhelms the antioxidant system. Recently, Olfactory mucosa-derived mesenchymal stem cells (OM-MSCs) hold great potential for treating ferroptosis-mediated oxidative brain damage after ICH. However, massive grafted cell death, possibly caused by a hostile host brain microenvironment, lessens the effectiveness of OM-MSCs. Therefore, it is necessary to develop strategies to upregulate the therapeutic efficacy of OM-MSCs in ICH. Curcumin, a well-established traditional herbal substance, has potent antioxidant property. In the present study, curcumin preconditioning might enhance the anti-oxidative activity of OM-MSCs, thereby augmenting the therapeutic efficacy of OM-MSCs in ICH. In vitro model of ICH, we demonstrated that curcumin-preconditioned OM-MSCs co-culture is more effective in attenuating the cell injury, oxidative stress, and ferroptosis of neuronal cells compared to the native OM-MSCs treatment. In vivo model of ICH, transplantation of curcumin-preconditioned OM-MSCs also showed better neuroprotective effects. Moreover, curcumin pretreatment promoted the survival of OM-MSCs under a conditioned medium from hemin-insulted neurons by improving the anti-oxidative capacities of OM-MSCs. Collectively, our investigation suggested that curcumin preconditioning effectively enhanced the survival and neuroprotective effects of OM-MSCs in the ICH model by upregulating the anti-oxidative capacities of OM-MSCs. Curcumin-preconditioned OM-MSCs might be taken as a novel therapeutic strategy for treating ICH.

目的 探讨某院普通外科患者超长住院日影响因素,为有效缩短平均住院日提供参考依据.方法 采用回顾性研究方法,收集某院2017年1月1日-2020年12月31日普通外科患者住院病案首页信息,将住院日大于第95百分位数定义为超长住院,共纳入12512例患者,其中超长住院日患者592例.对研究对象进行统计描述、单因素及多因素logistic回归分析.结果 2017年-2020年普通外科剔除超长住院日患者后,平均住院日减少1.43日.多因素logistic回归分析结果显示,手术(OR=2.975,P<0.001)、B、C、D型病例(OR值分别为2.052,4.092,4.962,P值均小于0.001)、输血(OR=4.570,P<0.001)、年龄(≥65岁,OR=3.627,P=0.014)、住院次数(≥3次,OR=1.569,P=0.012)和疾病分类(肿瘤,损伤、中毒和外因的某些其他后果、其他;OR值分别为3.564,6.341,1.840,P值均小于0.001)是延长患者住院日的危险因素.结论 超长住院日与患者社会和临床因素有关.医院应全面提升医疗服务能力,严格完成临床路径管理,鼓励开展微创手术,积极探索有效统计方法预测住院天数,缩减患者住院日.

1Key Laboratory of Protein Chemistry and Developmental Biology of Ministry of Education, College of Life Sciences, Hunan Normal University, Changsha 410081, Hunan, P.R. China 2Department of Neurosurgery, Second Affiliated Hospital of Hunan Normal University, Changsha 410003, Hunan, P.R. China 3Hunan Provincial Key Laboratory of Neurorestoration, Second Affiliated Hospital of Hunan Normal University, Changsha 410003, Hunan, P.R. China 4Department of Gastrointestinal Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China 5Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, P.R. China *Equal contribution