Analysis and risk factors of deep vein catheterization-related bloodstream infections in neonates.

To investigate the incidence, risk factors, and pathogenic characteristics of catheter-related bloodstream infection caused by peripherally inserted central venous catheter in neonates, and to provide references for reducing the infection rate of peripherally inserted central venous catheter. The clinical data of 680 neonates who underwent peripherally inserted central catheter (PICC) in the neonatal intensive care unit from June 2020 to June 2023 were retrospectively analyzed. The risk factors and independent risk factors of catheter-related bloodstream infection caused by PICC were determined by univariate and multivariate analysis, respectively. Catheter-related bloodstream infection occurred in 38 of 680 neonates who underwent PICC. The infection rate was 4.74%. The proportions of fungi, gram-positive bacteria, and gram-negative bacteria were 42.11%, 36.84%, and 21.05%, respectively. Candida parapsilosis was the main fungus (18.42%), coagulase negative Staphylococcus was the main gram-positive bacteria (23.68%), and Klebsiella pneumoniae and Escherichia coli were the main gram-negative bacteria (7.89%). Univariate analysis showed that gestational age ≤32 weeks, birth weight ≤1500 g, congenital diseases, nutritional support, catheterization time, 5-minute APGAR score ≤7, and neonatal respiratory distress syndrome were associated with catheter-related bloodstream infection caused by PICC. Multivariate analysis showed that premature delivery, low birth weight, parenteral nutrition, long catheterization time, and 5-minute APGAR score ≤7 were associated with catheter-related bloodstream infection caused by PICC. Among the pathogens detected, there were 6 cases of K pneumoniae, 5 cases of coagulase negative staphylococci, and 2 cases of fungi. Low birth weight, premature delivery, off-site nutrition, long catheterization time, and 5-minute APGAR score ≤7 are independent risk factors for catheter-related bloodstream infection in neonates with peripherally inserted central venous catheters. The pathogenic bacteria are fungi and multidrug-resistant bacteria.

Dual-Stage Surficial Microstructure to Enhance the Sensitivity of MXene Pressure Sensors for Human Physiological Signal Acquisition.

Accompanying the rapid growth of wearable electronics, flexible pressure sensors have received great interest due to their promising application in health monitoring, human-machine interfaces, and intelligent robotics. The high sensitivity over a wide responsive range, integrated with excellent repeatability, is a crucial requirement for the fabrication of reliable pressure sensors for various wearable scenes. In this work, we developed a highly sensitive and long-life flexible pressure sensor by constructing surficial microarrayed architecture polydimethylsiloxane (PDMS) film as a substrate and Ti3C2TX MXene/bacterial cellulose (BC) hybrid as an active sensing layer. The specific surficial morphology of PDMS couples with nanointercalated structure of Ti3C2Tx MXene/BC can effectively improve the sensitivity through controlling the stress distribution and layer spacing under different levels of pressure loading. In addition, abundant spontaneous hydrogen bonds between BC and Ti3C2Tx MXene nanosheets endow the MXene coating with highly adhesive strength on the PDMS surface; hence, the cyclic stability of the pressure sensor is greatly boosted. As a result, the obtained MXene/BC/PDMS (MBP) pressure sensor delivers high sensitivity (528.87 kPa-1), fast response/recovery time (45 ms/29 ms), low detection limit (0.6 Pa), and outstanding repeatability of up to 8000 cycles. Those excellent sensing properties of the MBP sensor allow it to serve as a reliable wearable device to monitor full-range human physiological motions, and it is expected to be applied in next-generation portable electronics, such as E-skins, smart healthcare, and the Internet of Things technology.

Insight of novel biomarkers for papillary thyroid carcinoma through multiomics.

Introduction: The overdiagnosing of papillary thyroid carcinoma (PTC) in China necessitates the development of an evidence-based diagnosis and prognosis strategy in line with precision medicine. A landscape of PTC in Chinese cohorts is needed to provide comprehensiveness. Methods: 6 paired PTC samples were employed for whole-exome sequencing, RNA sequencing, and data-dependent acquisition mass spectrum analysis. Weighted gene co-expression network analysis and protein-protein interactions networks were used to screen for hub genes. Moreover, we verified the hub genes' diagnostic and prognostic potential using online databases. Logistic regression was employed to construct a diagnostic model, and we evaluated its efficacy and specificity based on TCGA-THCA and GEO datasets. Results: The basic multiomics landscape of PTC among local patients were drawn. The similarities and differences were compared between the Chinese cohort and TCGA-THCA cohorts, including the identification of PNPLA5 as a driver gene in addition to BRAF mutation. Besides, we found 572 differentially expressed genes and 79 differentially expressed proteins. Through integrative analysis, we identified 17 hub genes for prognosis and diagnosis of PTC. Four of these genes, ABR, AHNAK2, GPX1, and TPO, were used to construct a diagnostic model with high accuracy, explicitly targeting PTC (AUC=0.969/0.959 in training/test sets). Discussion: Multiomics analysis of the Chinese cohort demonstrated significant distinctions compared to TCGA-THCA cohorts, highlighting the unique genetic characteristics of Chinese individuals with PTC. The novel biomarkers, holding potential for diagnosis and prognosis of PTC, were identified. Furthermore, these biomarkers provide a valuable tool for precise medicine, especially for immunotherapeutic or nanomedicine based cancer therapy.

Loss of hepatic FTCD promotes lipid accumulation and hepatocarcinogenesis by upregulating PPARγ and SREBP2.

Background & Aims: Exploiting key regulators responsible for hepatocarcinogenesis is of great importance for the prevention and treatment of hepatocellular carcinoma (HCC). However, the key players contributing to hepatocarcinogenesis remain poorly understood. We explored the molecular mechanisms underlying the carcinogenesis and progression of HCC for the development of potential new therapeutic targets. Methods: The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) and Genotype-Tissue Expression (GTEx) databases were used to identify genes with enhanced expression in the liver associated with HCC progression. A murine liver-specific Ftcd knockout (Ftcd-LKO) model was generated to investigate the role of formimidoyltransferase cyclodeaminase (FTCD) in HCC. Multi-omics analysis of transcriptomics, metabolomics, and proteomics data were applied to further analyse the molecular effects of FTCD expression on hepatocarcinogenesis. Functional and biochemical studies were performed to determine the significance of loss of FTCD expression and the therapeutic potential of Akt inhibitors in FTCD-deficient cancer cells. Results: FTCD is highly expressed in the liver but significantly downregulated in HCC. Patients with HCC and low levels of FTCD exhibited worse prognosis, and patients with liver cirrhosis and low FTCD levels exhibited a notable higher probability of developing HCC. Hepatocyte-specific knockout of FTCD promoted both chronic diethylnitrosamine-induced and spontaneous hepatocarcinogenesis in mice. Multi-omics analysis showed that loss of FTCD affected fatty acid and cholesterol metabolism in hepatocarcinogenesis. Mechanistically, loss of FTCD upregulated peroxisome proliferator-activated receptor (PPAR)γ and sterol regulatory element-binding protein 2 (SREBP2) by regulating the PTEN/Akt/mTOR signalling axis, leading to lipid accumulation and hepatocarcinogenesis. Conclusions: Taken together, we identified a FTCD-regulated lipid metabolic mechanism involving PPARγ and SREBP2 signaling in hepatocarcinogenesis and provide a rationale for therapeutically targeting of HCC driven by downregulation of FTCD. Impact and implications: Exploiting key molecules responsible for hepatocarcinogenesis is significant for the prevention and treatment of HCC. Herein, we identified formimidoyltransferase cyclodeaminase (FTCD) as the top enhanced gene, which could serve as a predictive and prognostic marker for patients with HCC. We generated and characterised the first Ftcd liver-specific knockout murine model. We found loss of FTCD expression upregulated peroxisome proliferator-activated receptor (PPAR)γ and sterol regulatory element-binding protein 2 (SREBP2) by regulating the PTEN/Akt/mTOR signalling axis, leading to lipid accumulation and hepatocarcinogenesis, and provided a rationale for therapeutic targeting of HCC driven by downregulation of FTCD.

Al Foil-Supported Carbon Nanosheets as Self-Supporting Electrodes for High Areal Capacitance Supercapacitors.

Self-supporting electrode materials with the advantages of a simple operation process and the avoidance of the use any binders are promising candidates for supercapacitors. In this work, carbon-based self-supporting electrode materials with nanosheets grown on Al foil were prepared by combining hydrothermal reaction and the one-step chemical vapor deposition method. The effect of the concentration of the reaction solution on the structures as well as the electrochemical performance of the prepared samples were studied. With the increase in concentration, the nanosheets of the samples became dense and compact. The CNS-120 obtained from a 120 mmol zinc nitrate aqueous solution exhibited excellent electrochemical performance. The CNS-120 displayed the highest areal capacitance of 6.82 mF cm-2 at the current density of 0.01 mA cm-2. Moreover, the CNS-120 exhibited outstanding rate performance with an areal capacitance of 3.07 mF cm-2 at 2 mA cm-2 and good cyclic stability with a capacitance retention of 96.35% after 5000 cycles. Besides, the CNS-120 possessed an energy density of 5.9 µWh cm-2 at a power density of 25 µW cm-2 and still achieved 0.3 µWh cm-2 at 4204 µW cm-2. This work provides simple methods to prepared carbon-based self-supporting materials with low-cost Al foil and demonstrates their potential for realistic application of supercapacitors.

Inactivated whole-virion SARS-CoV-2 vaccines and long-term clinical outcomes in patients with coronary atherosclerosis disease in China: a prospective cohort study.

AIMS: Publicized adverse events after vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) raised concern among patients with coronary atherosclerosis disease (CAD). We sought to study the association between SARS-CoV-2 vaccines and long-term clinical outcomes including ischaemic and bleeding events among patients with CAD. METHODS AND RESULTS: Inpatients diagnosed with CAD by coronary angiography, without a history of SARS-CoV-2 infection and vaccination, were included between 1 January and 30 April 2021, and underwent follow-up until 31 January 2022. Two doses of inactivated whole-virion SARS-CoV-2 vaccine (CoronaVac, BBIBPCorV, or WIBP-CorV) were available after discharge, and the group was stratified by vaccination. The primary composite outcomes were cardiovascular death, non-fatal myocardial infarction, stent thrombosis, unplanned revascularization, ischaemic stroke, venous thrombo-embolism, or peripheral arterial thrombosis. The bleeding outcomes were Bleeding Academic Research Consortium (BARC) type 3 or 5 bleeding. Cox regression models with vaccination status as a time-dependent covariate were used to calculate the hazard ratio (HR) for the outcomes. A propensity score matching method was used to reduce confounding biases. This prospective cohort study included 2078 individuals with CAD, 1021 (49.1%) were vaccinated. During a median follow-up of 9.1 months, 45 (4.3%) primary composite outcomes occurred in the unvaccinated group, and 33 (3.2%) in the vaccinated group. In Cox regression, the adjusted HR was 1.13 [95% confidence interval (CI) 0.65-1.93]. The adjusted HR for the bleeding outcomes associated with vaccination was 0.81 [95% CI 0.35-1.19]. After matching, the adjusted HR for the primary composite outcomes associated with vaccination was 1.06 [95% CI 0.57-1.99] and for the bleeding outcomes was 0.91 [95% CI 0.35-2.38]. Similar results were found in the seven prespecified subgroups. No grade 3 adverse reactions after vaccination were recorded. CONCLUSION: Our results indicated no evidence of an increased ischaemic or bleeding risk after vaccination with inactivated SARS-CoV-2 vaccine among Chinese patients with CAD, with limited statistical power.

The significance of galactose-deficient immunoglobulin A1 staining in kidney diseases with IgA deposition.

BACKGROUND: This study investigated the significance of galactose-deficient immunoglobulin A1 staining in kidney diseases with IgA deposition. METHODS: A total of 120 patients with IgA-dominant deposition in kidney tissues were enrolled and divided into four groups: primary IgA nephropathy (PIgAN), secondary IgA nephropathy (SIgAN), monotypic IgA nephropathy (MIgAN), and IgA variant monoclonal gammopathy of renal significance (IgA-MGRS). KM55 (the antibody of galactose-deficient immunoglobulin A1), IgA subtypes, and complement pathway factors (properdin, C4d, and C1q) were detected through immunofluorescence or immunohistochemistry analysis. RESULTS: KM55 and IgA double staining showed colocalization within glomeruli in all cases except for IgA-MGRS, which showed negative or weak staining of KM55 but strong staining of IgA. The PIgAN group showed the highest intensity of KM55 and KM55/IgA ratio, while these values in the IgA-MGRS group were the lowest (P < 0.01). A KM55/IgA quantified ratio of 0.78 was the optimal cut-off value to distinguish PIgAN from SIgAN, whereas a cut-off value of 0.21 was optimal to distinguish between MIgAN and IgA-MGRS. The clinicopathological characteristics showed significant differences as the groups were divided by diseases with optimal cut-off values, and these differences corresponded to the pathogenesis of each disease entity. CONCLUSIONS: PIgAN, SIgAN, and MIgAN are caused by the deposition of abnormally glycosylated IgA1 whereas IgA-MGRS is not. The KM55/IgA quantified ratio is valuable in distinguishing PIgAN from SIgAN, as well as MIgAN from IgA-MGRS.

Sustained activation of EGFR-ERK1/2 signaling limits the response to tigecycline-induced mitochondrial respiratory deficiency in liver cancer.

BACKGROUND: Identification of tumor dependencies is important for developing therapeutic strategies for liver cancer. METHODS: A genome-wide CRISPR screen was performed for finding critical vulnerabilities in liver cancer cells. Compounds screen, RNA sequencing, and human phospho-receptor tyrosine kinase arrays were applied to explore mechanisms and search for synergistic drugs. FINDINGS: We identified mitochondrial translation-related genes associated with proliferation for liver cancer cells. Tigecycline induced deficiency of respiratory chain by disturbing mitochondrial translation process and showed therapeutic potential in liver cancer. For liver cancer cells extremely insensitive to tigecycline, a compounds screen was applied to identify MEK inhibitors as synergistic drugs to tigecycline-insensitive liver cancer cells. Mechanistically, sustained activation of EGFR-ERK1/2-MYC cascade conferred the insensitivity to tigecycline, which was mediated by enhanced secretion of EREG and AREG. Moreover, glycolytic enzymes, such as HK2 and PKM2 were upregulated to stimulate glycolysisin a MYC-dependent manner. Tigecycline induced respiratory chain deficiency in combination with cutting off EGFR-ERK1/2-MYC cascade by MEK inhibitors or EGFR inhibitors, resulting in decrease of both oxidative phosphorylation and glycolysis in liver cancer cells. INTERPRETATION: Our study proved that blocking EGFR-ERK1/2-MYC cascade combined with tigecycline could be a potential therapeutic strategy for liver cancer. FUNDING: This work was funded by grants from the National Natural Science Foundation of China (82073039,82222047, 81920108025), Program of Shanghai Academic/Technology Research Leader (22XD1423100), Shanghai Municipal Science and Technology Project (20JC1411100), 111 Project (B21024), Innovative Research Team of High-level Local Universities in Shanghai (SHSMU-ZDCX20212700, SHSMU-ZDCX20210802) and Shanghai Jiao Tong University School of Medicine (YG2019GD01).

cFLIP suppression and DR5 activation sensitize senescent cancer cells to senolysis.

Senolytics, drugs that kill senescent cells, have been proposed to improve the response to pro-senescence cancer therapies; however, this remains challenging due to a lack of broadly acting senolytic drugs. Using CRISPR/Cas9-based genetic screens in different senescent cancer cell models, we identify loss of the death receptor inhibitor cFLIP as a common vulnerability of senescent cancer cells. Senescent cells are primed for apoptotic death by NF-κB-mediated upregulation of death receptor 5 (DR5) and its ligand TRAIL, but are protected from death by increased cFLIP expression. Activation of DR5 signaling by agonistic antibody, which can be enhanced further by suppression of cFLIP by BRD2 inhibition, leads to efficient killing of a variety of senescent cancer cells. Moreover, senescent cells sensitize adjacent non-senescent cells to killing by DR5 agonist through a bystander effect mediated by secretion of cytokines. We validate this 'one-two punch' cancer therapy by combining pro-senescence therapy with DR5 activation in different animal models.

Visualization of Polymer-Surfactant Interaction by Dual-Emissive Gold Nanocluster Labeling.

Polymer-surfactant interaction decides the performance of corresponding complexes, making its rapid and intuitionistic visualization important for enhancing the performance of products and/or processing in related fields. In this study, the fluorescence visualization of the interaction between cationic hyperbranched polyethyleneimine and anionic sodium dodecyl sulfonate surfactant was realized by dual-emissive gold nanocluster labeling. The sensing mechanism was due to the interaction-induced polymer conformation change, which regulated the molecular structure and subsequent photoradiation process of the gold nanoclusters. All three inflection points of the interactions between the polymers and the surfactants were obtained by the change in fluorescence emission ratio of the designed dual-emissive gold nanoclusters. Moreover, these inflection points are verified by the hydrodynamic diameter and zeta potential measurements.

The effect of chronic exposure to a low concentration of perfluorooctanoic acid on cognitive function and intestinal health of obese mice induced by a high-fat diet.

Perfluorooctanoic acid (PFOA) is a persistent organic pollutant associated with many adverse health risks. Evidence suggests that obese individuals may be more susceptible to environmental substances. In the present work, we explored the effects of PFOA exposure on the cognitive function and intestinal health of obese mice. Obese mice induced by a high-fat diet were exposed to PFOA (0.5 mg/kg (bw)/day) via drinking water for 100 days. After exposure to PFOA, decreased body weight, enlarged liver, abnormal behavior, impaired synapse structure, neuroinflammation, activated glial cell, decreased nerve growth factor, altered gut microbiota, and disturbed serum metabolites were observed, while the gut inflammation and intestinal barrier were not significantly influenced. These results suggest that exposure to PFOA is associated with cognitive impairment in obese mice.

Progress in the use of organic potassium salts for the synthesis of porous carbon nanomaterials: microstructure engineering for advanced supercapacitors.

Porous carbon nanomaterials (PCNs) are widely applied in energy storage devices. Traditionally, PCNs were mainly synthesized by activation and templating methods, which are time-consuming, tedious, corrosive and relatively high cost. Therefore, the development of easier and greener methods to produce PCNs is of great significance. Recently, organic potassium salts (OPSs) emerged as versatile reagents for synthesizing PCNs. The OPS-based synthesis of PCNs can avoid the use of large amounts of corrosive chemical agents. Potassium carbonate generated in situ from the decomposition of OPSs could serve as both a green activation agent and a water-removable template to produce nanopores. Potassium oxide and potassium formed at higher temperature could generate additional porosity, contributing to a highly porous architecture. The carbon-rich organic moiety could function as a carbon precursor and chemical blowing agent. This review aims to elucidate the multifunctionality of OPSs in the synthesis of PCNs and the capacitive performance of the corresponding PCNs. To this end, recent progress on the capacitive performance of PCNs synthesized from OPSs is summarized. This review provides constructive viewpoints for the cost-effective and green synthesis of PCNs with the aid of OPSs for application in supercapacitors.

Coronaviruses in wild animals sampled in and around Wuhan at the beginning of COVID-19 emergence.

Over the last several decades, no emerging virus has had a profound impact on the world as the SARS-CoV-2 that emerged at the end of 2019 has done. To know where severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) originated from and how it jumped into human population, we immediately started a surveillance investigation in wild mammals in and around Wuhan when we determined the agent. Herein, coronaviruses were screened in the lung, liver, and intestinal tissue samples from fifteen raccoon dogs, seven Siberian weasels, three hog badgers, and three Reeves's muntjacs collected in Wuhan and 334 bats collected around Wuhan. Consequently, eight alphacoronaviruses were identified in raccoon dogs, while nine betacoronaviruses were found in bats. Notably, the newly discovered alphacoronaviruses shared a high whole-genome sequence similarity (97.9 per cent) with the canine coronavirus (CCoV) strain 2020/7 sampled from domestic dog in the UK. Some betacoronaviruses identified here were closely related to previously known bat SARS-CoV-related viruses sampled from Hubei province and its neighbors, while the remaining betacoronaviruses exhibited a close evolutionary relationship with SARS-CoV-related bat viruses in the RdRp gene tree and clustered together with SARS-CoV-2-related bat coronaviruses in the M, N and S gene trees, but with relatively low similarity. Additionally, these newly discovered betacoronaviruses seem unlikely to bind angiotensin-converting enzyme 2 because of the deletions in the two key regions of their receptor-binding motifs. Finally, we did not find SARS-CoV-2 or its progenitor virus in these animal samples. Due to the high circulation of CCoVs in raccoon dogs in Wuhan, more scientific efforts are warranted to better understand their diversity and evolution in China and the possibility of a potential human agent.

[Laparoscopic Common Bile Duct Exploration for Treatment of Common Bile Duct Stones:Clinical Analysis of 158 Cases].

Objective To evaluate the safety and effectiveness of laparoscopic common bile duct exploration in the treatment of common bile duct stones. Methods A retrospective analysis was conducted for 158 patients with cholecystolithiasis and choledocholithiasis admitted to the Number One Hospital of Zhangjiakou from January 2015 to December 2019.The patients were assigned into three groups according to the diameters of cystic duct and common bile duct,degrees of abdominal infection and tissue edema,and operation method.Group A(16 cases):laparoscopic cholecystectomy,transcystic choledochoscopic exploration for stone removal;Group B(94 cases):laparoscopic cholecystectomy,common bile duct incision exploration combined with choledochoscopy for stone removal,T tube drainage;Group C(48 cases):laparoscopic cholecystectomy,common bile duct incision exploration combined with choledochoscopy for stone removal,primary closure of the common bile duct.The operation time,residual rate of stones,and complication(bleeding,bile leakage,and wound infection) rate were compared between groups. Results The operation time of groups A,B,and C was(95.1±14.7),(102.2±18.1),(110.1±16.4) minutes,respectively,which showed no statistical difference between each other(F=0.020,P=0.887).One case in group A had residual stones,while no residual stone appeared in groups B and C.The overall stone clearance rate was 99.4% and the overall complication rate was 1.9%.There was no perioperative death. Conclusion It is generally safe and effective to carry out laparoscopic cholecystectomy and common bile duct exploration for stone removal in suitable populations.

Activation of TRPV4 Induces Exocytosis and Ferroptosis in Human Melanoma Cells.

TRPV4 (transient receptor potential vanilloid 4), a calcium permeable TRP ion channel, is known to play a key role in endocytosis. However, whether it contributes to exocytosis remains unclear. Here, we report that activation of TRPV4 induced massive exocytosis in both melanoma A375 cell and heterologous expression systems. We show here that, upon application of TRPV4-specific agonists, prominent vesicle priming from endoplasmic reticulum (ER) was observed, followed by morphological changes of mitochondrial crista may lead to cell ferroptosis. We further identified interactions between TRPV4 and folding/vesicle trafficking proteins, which were triggered by calcium entry through activated TRPV4. This interplay, in turn, enhanced TRPV4-mediated activation of folding and vesicle trafficking proteins to promote exocytosis. Our study revealed a signaling mechanism underlying stimulus-triggered exocytosis in melanoma and highlighted the role of cellular sensor TRPV4 ion channel in mediating ferroptosis.

Catechin-inspired gold nanocluster nanoprobe for selective and ratiometric dopamine detection via forming azamonardine.

The sensitive and selective perception of dopamine (DA, a typical neurotransmitter) is important to evaluate the biological environment. In this study, a catechin-functionalized gold nanocluster (C-Au NC) nanoprobe has been explored for the ratiometric DA sensing. The detection mechanism is based on the formation of azamonardine via selective DA-catechin chemical reaction and subsequent enhanced fluorescence emission. Using Au NC emission as the internal reference, ratiometric fluorescence variation is realized, which allows sensitive DA analysis with a limit of detection of 1.0 nM (S/N = 3) and linear response concentration range from 0 to 500 nM. The characteristic chemical reaction between catechin and DA affords favorable selectivity over other amino acids, metal ions and small molecules. In addition, the practical application of the proposed nanoprobe is validated by the accurate detection of DA content in urea and cell lysate samples.

NAT10 regulates mitotic cell fate by acetylating Eg5 to control bipolar spindle assembly and chromosome segregation.

Cell fate of mitotic cell is controlled by spindle assembly. Deficient spindle assembly results in mitotic catastrophe leading to cell death to maintain cellular homeostasis. Therefore, inducing mitotic catastrophe provides a strategy for tumor therapy. Nucleolar acetyltransferase NAT10 has been found to regulate various cellular processes to maintain cell homeostasis. Here we report that NAT10 regulates mitotic cell fate by acetylating Eg5. NAT10 depletion results in multinuclear giant cells, which is the hallmark of mitotic catastrophe. Live-cell imaging showed that knockdown of NAT10 dramatically prolongs the mitotic time and induces defective chromosome segregation including chromosome misalignment, bridge and lagging. NAT10 binds and co-localizes with Eg5 in the centrosome during mitosis. Depletion of NAT10 reduces the centrosome loading of Eg5 and impairs the poleward movement of centrosome, leading to monopolar and asymmetrical spindle formation. Furthermore, NAT10 stabilizes Eg5 through its acetyltransferase function. NAT10 acetylates Eg5 at K771 to control Eg5 stabilization. We generated K771-Ac specific antibody and showed that Eg5 K771-Ac specifically localizes in the centrosome during mitosis. Additionally, K771 acetylation is required for the motor function of Eg5. The hyper-acetylation mimic Flag-Eg5 K771Q but not Flag-Eg5 rescued the NAT10 depletion-induced defective spindle formation and mitotic catastrophe, demonstrating that NAT10 controls mitosis through acetylating Eg5 K771. Collectively, we identify Eg5 as an important substrate of NAT10 in the control of mitosis and provide K771 as an essential acetylation site in the stabilization and motor function of Eg5. Our findings reveal that targeting the NAT10-mediated Eg5 K771 acetylation provides a potential strategy for tumor therapy.