ObjectiveMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS); however, its underlying neurological pathogenic mechanisms remain incompletely understood. Endogenous formaldehyde (FA), a metabolic byproduct of methylation-demethylation cycles, has recently been implicated in neurotoxicity, oxidative damage, and cognitive impairment. This study aimed to investigate whether excessive FA contributes to myelin sheath demyelination in mice and to evaluate the protective effects and mechanisms of two FA-elimination strategies: sodium bisulfite (NaHSO₃), a classical FA scavenger, and polyethylene glycol-modified astaxanthin nanoparticles (PEG-ATX@NPs), a brain-targeted nano-antioxidant formulation. MethodsA chronic demyelination model was established by feeding female C57BL/6J mice a diet containing 0.2% cuprizone (CPZ) for four weeks, followed by a two-week intervention period. Eighty mice were randomly assigned to four groups: NS (normal saline), CPZ+NS, CPZ+NaHSO₃, and CPZ+PEG-ATX@NPs. Behavioral tests, including open-field, Y-maze, and pole-climbing assays, were conducted to assess locomotor activity, motor coordination, and working memory. FA levels in serum, corpus callosum, and spinal cord were measured using an Na-FA fluorescent probe and quantified via in vivo and ex vivo fluorescence imaging. Neuroinflammatory responses were evaluated by measuring TNF-α, IL-1β, and IL-6 levels using ELISA, while oxidative stress was assessed by reactive oxygen species (ROS) fluorescence intensity. Demyelination was examined via Luxol fast blue staining, and microglial activation was analyzed by Iba1 immunofluorescence. Correlation analyses were performed to explore relationships among FA levels, inflammatory cytokines, ROS intensity, and behavioral parameters. ResultsCompared with the NS group, mice in the CPZ+NS group exhibited significant weight loss, impaired motor coordination and memory, and markedly reduced myelin regeneration (P<0.05). FA levels and pro-inflammatory cytokines were significantly elevated in serum, corpus callosum, and spinal cord (P<0.05). FA-associated fluorescence in brain and spinal tissues, as well as ROS intensity across all tissues examined, also increased substantially (P<0.05). CPZ treatment induced pronounced microglial activation and severe demyelination in the corpus callosum (P<0.01). Both NaHSO₃ and PEG-ATX@NPs effectively reduced FA accumulation in the brain and spinal cord, attenuated demyelination, suppressed microglial activation, decreased inflammatory cytokine levels, and improved motor and cognitive performance. These results confirm that CPZ induced severe demyelination accompanied by oxidative stress, neuroinflammation, and abnormal FA accumulation. Following intervention with either NaHSO₃ or PEG-ATX@NPs, endogenous FA levels in the CNS were substantially reduced. Both treatments alleviated demyelination and significantly decreased the number of activated microglia. Levels of TNF-α, IL-1β, and IL-6 in serum, corpus callosum, and spinal cord were downregulated. Behavioral performance improved significantly, as evidenced by enhanced locomotor activity, better coordination, and improved memory function. These findings indicate that both FA-scavenging agents mitigate CPZ-induced biochemical and behavioral abnormalities. ConclusionThis study demonstrates that excessive endogenous FA is closely associated with cognitive impairment, inflammatory dysregulation, and demyelination in a CPZ-induced chronic demyelination mouse model. Clearing abnormally elevated FA effectively reduces neuroinflammation, suppresses microglial overactivation, decreases oxidative stress, and alleviates demyelination, ultimately improving motor and cognitive outcomes in mice. These results suggest that targeting endogenous FA represents a promising therapeutic strategy for MS and other demyelinating disorders. Further investigations are warranted to explore the long-term safety, dosage optimization, and molecular pathways involved in FA-mediated neurotoxicity.

ObjectiveMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS); however, its underlying neurological pathogenic mechanisms remain incompletely understood. Endogenous formaldehyde (FA), a metabolic byproduct of methylation-demethylation cycles, has recently been implicated in neurotoxicity, oxidative damage, and cognitive impairment. This study aimed to investigate whether excessive FA contributes to myelin sheath demyelination in mice and to evaluate the protective effects and mechanisms of two FA-elimination strategies: sodium bisulfite (NaHSO₃), a classical FA scavenger, and polyethylene glycol-modified astaxanthin nanoparticles (PEG-ATX@NPs), a brain-targeted nano-antioxidant formulation. MethodsA chronic demyelination model was established by feeding female C57BL/6J mice a diet containing 0.2% cuprizone (CPZ) for four weeks, followed by a two-week intervention period. Eighty mice were randomly assigned to four groups: NS (normal saline), CPZ+NS, CPZ+NaHSO₃, and CPZ+PEG-ATX@NPs. Behavioral tests, including open-field, Y-maze, and pole-climbing assays, were conducted to assess locomotor activity, motor coordination, and working memory. FA levels in serum, corpus callosum, and spinal cord were measured using an Na-FA fluorescent probe and quantified via in vivo and ex vivo fluorescence imaging. Neuroinflammatory responses were evaluated by measuring TNF-α, IL-1β, and IL-6 levels using ELISA, while oxidative stress was assessed by reactive oxygen species (ROS) fluorescence intensity. Demyelination was examined via Luxol fast blue staining, and microglial activation was analyzed by Iba1 immunofluorescence. Correlation analyses were performed to explore relationships among FA levels, inflammatory cytokines, ROS intensity, and behavioral parameters. ResultsCompared with the NS group, mice in the CPZ+NS group exhibited significant weight loss, impaired motor coordination and memory, and markedly reduced myelin regeneration (P<0.05). FA levels and pro-inflammatory cytokines were significantly elevated in serum, corpus callosum, and spinal cord (P<0.05). FA-associated fluorescence in brain and spinal tissues, as well as ROS intensity across all tissues examined, also increased substantially (P<0.05). CPZ treatment induced pronounced microglial activation and severe demyelination in the corpus callosum (P<0.01). Both NaHSO₃ and PEG-ATX@NPs effectively reduced FA accumulation in the brain and spinal cord, attenuated demyelination, suppressed microglial activation, decreased inflammatory cytokine levels, and improved motor and cognitive performance. These results confirm that CPZ induced severe demyelination accompanied by oxidative stress, neuroinflammation, and abnormal FA accumulation. Following intervention with either NaHSO₃ or PEG-ATX@NPs, endogenous FA levels in the CNS were substantially reduced. Both treatments alleviated demyelination and significantly decreased the number of activated microglia. Levels of TNF-α, IL-1β, and IL-6 in serum, corpus callosum, and spinal cord were downregulated. Behavioral performance improved significantly, as evidenced by enhanced locomotor activity, better coordination, and improved memory function. These findings indicate that both FA-scavenging agents mitigate CPZ-induced biochemical and behavioral abnormalities. ConclusionThis study demonstrates that excessive endogenous FA is closely associated with cognitive impairment, inflammatory dysregulation, and demyelination in a CPZ-induced chronic demyelination mouse model. Clearing abnormally elevated FA effectively reduces neuroinflammation, suppresses microglial overactivation, decreases oxidative stress, and alleviates demyelination, ultimately improving motor and cognitive outcomes in mice. These results suggest that targeting endogenous FA represents a promising therapeutic strategy for MS and other demyelinating disorders. Further investigations are warranted to explore the long-term safety, dosage optimization, and molecular pathways involved in FA-mediated neurotoxicity.

OBJECTIVE To systematically evaluate the influential factors for all-cause mortality in patients with carbapenem-resistant Gram-negative bacteria （CR-GNB） treated with polymyxin B. METHODS PubMed， Embase， the Cochrane Library， Web of Science， Wanfang Data， VIP， CBM and CNKI were searched to collect clinical studies on all-cause death within 30 days or 28 days after treatment with polymyxin B in patients with CR-GNB infection from database establishment to July 2025. After literature screening， data extraction and evaluation of literature quality， meta-analysis was performed using RevMan 5.4 software. RESULTS A total of 12 studies were included， involving 1 326 patients， among whom 529 patients died， with a mortality rate of 39.89%. Meta-analysis results showed that combined with cardiovascular disease [OR＝2.06， 95%CI （1.37， 3.09）， P ＝0.005 ] ， increased Sequential Organ Failure Assessment （SOFA） score [OR＝1.20， 95%CI （1.07， 1.35）， P ＝0.003 ] ， mechanical ventilation [OR＝2.35， 95%CI （1.65， 3.34）， P ＜0.001 ] ， continuous renal replacement therapy （CRRT） [OR＝2.58， 95%CI （1.67， 3.97）， P ＜0.001 ] ， bloodstream infection [OR＝3.24， 95%CI （2.19， 4.78）， P ＜0.001 ] ， multiple-site infection [OR＝1.51， 95%CI （1.03， 2.20）， P ＝0.03 ] ， septic shock [OR＝3.19， 95%CI （1.94， 5.24）， P ＜0.001 ] ， use of vasoactive drugs [OR＝2.90， 95%CI （1.97， 4.27）， P ＜0.001 ] ， and the occurrence of acute kidney injury （AKI） [OR＝2.17， 95%CI （1.41， 3.36）， P ＜0.001 ] were risk factors for all-cause mortality in patients with CR-GNB infection treated with polymyxin B. Conversely， an extended duration of polymy xin B treatment [OR＝0.92， 95%CI （0.86， 0.99）， P ＝0.03 ] and early administration after CR-GNB infection [OR＝0.47， 95%CI （0.25， 0.85）， P ＝0.01 ] were protective factors. CONCLUSIONS Patients with cardiovascular disease， receiving mechanical ventilation or CRRT， having bloodstream infection， multiple-site infection or septic shock， combining with vasoactive drugs， with AKI and increased SOFA scores have a higher risk of all-cause mortality. Conversely， extending the duration of polymyxin B treatment （beyond 7 days） and early administration within 48 hours after confirmed CR-GNB infection can significantly reduce the risk of all-cause mortality.

Objective To investigate the drug resistance phenotype/genotype and virulence gene carrying status, serotype, and sequence typing (ST) of Campylobacter jejuni in Fengtai District in 2024. Methods The drug resistance phenotype was detected by agar dilution method, and serotyping was performed by real-time fluorescence quantitative polymerase chain reaction (PCR). The whole genome sequencing was used to analyze drug resistance genes, virulence genes, and other characteristics. Results Among the 35 Campylobacter jejuni strains analyzed, the antibiotics with the highest resistance rates were nalidixic acid and ciprofloxacin (both 82.86%), followed by tetracycline (74.89%). All strains exhibited a 100.00% sensitivity rate to erythromycin. The multiple drug resistance rate was 77.14%. The predominant drug resistance genes were gyrA-T86I (94.29%) and tetO (74.29%). The most common serotype was HS:2, accounting for 25 strains. A total of 132 virulence genes were detected. There were 12 clonal complexes (CC) and 24 ST types. Conclusion The drug resistance situation of Campylobacter jejuni in Fengtai District is relatively severe, and the drug resistance phenotype is related to specific genetic mutations to some extent. The serotypes are diverse, the virulence genes are complex, and the pathogenic potential is significant, posing a notable risk for inducing Guillain-Barré syndrome (GBS). The high number of ST types indicates substantial genetic diversity.

Sarcopenia, an age-related degenerative skeletal muscle disorder characterized by progressive loss of muscle mass, diminished strength, and impaired physical function, poses substantial challenges to global healthy aging initiatives. The pathogenesis of this condition is fundamentally rooted in mitochondrial dysfunction, manifested through defective energy metabolism, disrupted redox equilibrium, imbalanced dynamics, and compromised organelle quality control. This comprehensive review elucidates the central role of exercise-induced mitochondrial hormesis as a critical adaptive mechanism counteracting sarcopenia. Mitohormesis represents an evolutionarily conserved stress response wherein sublethal mitochondrial perturbations, particularly transient low-dose reactive oxygen species (ROS) generated during muscle contraction, activate cytoprotective signaling cascades rather than inflicting macromolecular damage. The mechanistic foundation of this process involves ROS functioning as essential signaling molecules that activate the Keap1 nuclear factor erythroid 2 related factor 2 (Nrf2) antioxidant response element pathway. This activation drives transcriptional upregulation of phase II detoxifying enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GPx), thereby enhancing cellular redox buffering capacity. Crucially, Nrf2 engages in bidirectional molecular crosstalk with peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC-1α), the principal regulator orchestrating mitochondrial biogenesis through coordinated induction of nuclear respiratory factors 1 and 2 (NRF1/2) along with mitochondrial transcription factor A (Tfam), collectively facilitating mitochondrial DNA replication and respiratory complex assembly. Concurrently, exercise-induced alterations in cellular energy status, specifically diminished ATP to AMP ratios, potently activate AMP activated protein kinase (AMPK). This energy-sensing kinase phosphorylates PGC-1α while concomitantly stimulating NAD dependent deacetylase sirtuin 1 (SIRT1) activity, which further potentiates PGC-1α function through post-translational deacetylation. The integrated AMPK/PGC-1α/SIRT1 axis coordinates mitochondrial biogenesis, optimizes network architecture through regulation of fusion proteins mitofusin 1 (Mfn1), mitofusin 2 (Mfn2) and optic atrophy protein 1 (OPA1), and enhances clearance of damaged organelles via selective activation of mitophagy receptors BCL2 interacting protein 3 (Bnip1) and FUN14 domain containing 1 (FNDC1). Exercise further stimulates the mitochondrial unfolded protein response (UPRmt), increasing molecular chaperones such as heat shock protein 60 (HSP60) and HSP10 to preserve proteostasis. Within the mitochondrial matrix, SIRT3 fine-tunes metabolic flux through deacetylation of electron transport chain components, improving phosphorylation efficiency while attenuating pathological ROS emission. Distinct exercise modalities differentially engage these pathways. Aerobic endurance training primarily activates AMPK/PGC-1α signaling and UPRmt to expand mitochondrial volume and oxidative capacity. Resistance training exploits mechanical tension to acutely stimulate mechanistic target of rapamycin complex 1 (mTORC1) mediated protein synthesis while modulating dynamin related protein 1 (Drp1) phosphorylation dynamics to support mitochondrial network reorganization. High intensity interval training generates potent metabolic oscillations that rapidly amplify AMPK/PGC-1α and Nrf2 activation, demonstrating particular efficacy in insulin-resistant phenotypes. Strategically designed concurrent training regimens synergistically integrate these adaptations. Mitochondrial-nuclear communication through tricarboxylic acid cycle metabolites and mitochondrially derived peptides such as mitochondrial open reading frame of 12s rRNA-c (MOTS-c) coordinates systemic metabolic reprogramming, with exercise-responsive myokines including fibroblast growth factor 21 (FGF-21) mediating inter-tissue signaling to reduce inflammation and enhance insulin sensitivity. This integrated framework provides the scientific foundation for precision exercise interventions targeting mitochondrial pathophysiology in sarcopenia, incorporating biomarker monitoring and exploring pharmacological potentiators including nicotinamide riboside and MOTS-c mimetics. Future investigations should delineate temporal dynamics of mitohormesis signaling and epigenetic regulation to optimize therapeutic approaches for age-related muscle decline.

Amblyopia is a common visual development disorder and is the main cause of monocular vision impairment in children and adults. Photobiomodulation(PBM), a non-invasive treatment method, has gradually gained attention in the field of ophthalmology. This paper begins with the macroscopic manifestation of light on the animal model of amblyopia. Additionally, it discusses the pathological changes of the amblyopic retina and the human eye's central nervous system, as well as the influence and mechanism of PBM on the visual perception and processing system and its chemical effect on the visual system through dopamine and melatonin. It examines its mechanism of action, current clinical application status, and future development direction in order to provide new ideas and theoretical foundation for amblyopia treatment.

ObjectiveTo observe ovarian microvascular damage in rats with cold coagulation and blood stasis syndrome and to explore the mechanism by which Liangfang Wenjing decoction improves this condition in rats. MethodsFifty SPF female SD rats were randomly divided into a blank group， a model group， low-dose （8.1 g·kg^-1） and high-dose groups （16.2 g·kg^-1） of Liangfang Wenjing decoction， and a 4-phenylbutyric acid （0.1 g·kg^-1） group， with 10 rats in each group. The ice-water bath method was employed to establish the rat model of cold coagulation and blood stasis syndrome. Concurrent with modeling， Liangfang Wenjing decoction was administered continuously for 21 days， once daily. The rats' syndrome manifestations and estrous cycles were recorded. The enzyme-linked immunosorbent assay （ELISA） was used to detect serum reproductive hormone levels and levels of endothelin-1 （ET-1）， nitric oxide （NO）， thrombomodulin （TM）， and von Willebrand factor （vWF） in ovarian tissue. Prothrombin time （PT）， activated partial thromboplastin time （APTT）， thrombin time （TT）， and fibrinogen （FIB） were measured. The ovarian microcirculatory blood perfusion was detected by laser speckle contrast imaging. Hematoxylin-eosin （HE） staining was performed to observe the ovarian histopathology， flow cytometry to detect ovarian apoptosis rate， and transmission electron microscopy to observe the ultrastructure of ovarian microvascular endothelial cells. Western blot was employed to detect the protein expression of endothelial nitric oxide synthase （eNOS）， phosphorylated eNOS （p-eNOS）， Caspase-3， B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， glucose-regulated protein 78 （GRP78）， C/EBP homologous protein （CHOP）， inositol-requiring enzyme1α （IRE1α）， p-IRE1α， apoptosis signal-regulating kinase 1 （ASK1）， p-ASK1， c-Jun N-terminal kinase （JNK）， and p-JNK. Immunofluorescence was used to detect ovarian Bax and Bcl-2 expression in microvascular endothelial cells. ResultsCompared with the blank group， the model group showed signs of cold coagulation and blood stasis syndrome， prolonged estrus cycles， and reproductive hormone disorders. Histopathological results revealed a decrease in follicle counts at all stages and disorganized granulosa cell arrangement. Ovarian microcirculatory perfusion was significantly decreased （P<0.01）. PT， APTT， and TT were reduced （P<0.05， P<0.01）， while FIB levels were increased （P<0.05）. In ovarian tissue， NO content was decreased， while ET-1， vWF， and TM levels were increased significantly （P<0.01）. The apoptosis rate of ovarian cells was markedly increased （P<0.01）. Furthermore， p-eNOS/eNOS and Bcl-2 were decreased （P<0.05）， whereas Bax， cleaved-Caspase-3/Caspase-3， GRP78， CHOP， p-IRE1α/IRE1α， p-ASK1/ASK1， and p-JNK/JNK expression showed significant increases （P<0.05， P<0.01）. Compared with the model group， Liangfang Wenjing decoction intervention alleviated the symptoms of cold coagulation and blood stasis， gradually restored the estrus cycle， and improved ovarian histopathology and endothelial cell ultrastructure. Microcirculatory blood perfusion was significantly elevated （P<0.05）. NO content in ovarian tissue was elevated， while ET-1， vWF， and TM levels were significantly decreased （P<0.05， P<0.01）. The p-eNOS/eNOS ratio and Bcl-2 expression were significantly elevated （P<0.05）， while the expression of Bax， cleaved-Caspase-3/Caspase-3， GRP78， CHOP， p-IRE1α/IRE1α， p-ASK1/ASK1， and p-JNK/JNK was significantly decreased （P<0.05， P<0.01）. ConclusionLiangfang Wenjing decoction may regulate the IRE1α/ASK1/JNK signaling pathway to inhibit endoplasmic reticulum stress， attenuate apoptosis， and improve microvascular endothelial injury in ovaries of rats with cold coagulation and blood stasis syndrome.

Objective Using female mice to investigate the reparative effects of human umbilical cord mesenchymal stem cells on radiation-induced ovarian injury. Methods Mice were randomly divided into three groups: a blank control group, a radiation model group, and a cell therapy group. Mice in the radiation model group and the cell therapy group received a single whole-body irradiation of 5 Gy X-rays. Within 2 hours post-irradiation, mice in the cell therapy group underwent ovarian transplantation of UC-MSCs. On days 1, 7, and 14 post-irradiation, body weight was measured, ovarian index was calculated, histopathological changes in ovarian tissue were examined, serum levels of reproductive hormones (follicle-stimulating hormone, anti-Müllerian hormone, and estradiol) were determined, and the colonization of implanted UC-MSCs in the mice was observed. Results On days 1, 7, and 14 post-irradiation, both the cell therapy group and the radiation model group showed decreased body weight compared to the blank control group (P < 0.05). On day 1 post-irradiation compared to day 1 pre-irradiation within the same group, the radiation model group exhibited a greater decrease in body weight than the cell therapy group (P < 0.05). On days 1, 7, and 14 post-irradiation, the ovarian index decreased in both the radiation model group and the cell therapy group compared to the blank control group (P < 0.05). On days 7 and 14 post-irradiation, the ovarian index in the cell therapy group was significantly higher than that in the radiation model group (P < 0.05). Ovarian tissue in the radiation model group exhibited atrophy and a reduction in the number of follicles at all stages. In contrast, follicles in the cell therapy group were large and abundant. On days 1, 7, and 14 post-irradiation, serum follicle-stimulating hormone levels in the cell therapy group were lower than those in the radiation model group, while anti-Müllerian hormone and estradiol levels were higher than those in the radiation model group (P < 0.01). In vivo fluorescence imaging demonstrated that UC-MSCs successfully colonized the ovarian tissue on days 1, 7, and 14 after transplantation. Conclusion UC-MSCs exert a repair effect on radiation-induced ovarian injury in mice.

Objective To analyze the molecular epidemiology of Candida tropicalis(C.tropicalis)isolates from bloodstream infections,and to investigate preliminarily the underlying mechanisms of fluconazole resistance.Methods Clinical C.tropicalis isolates were collected from bloodstream infections at West China Hospital,Sichuan University and other hospitals in Sichuan Province.All the collected isolates were identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry,and the antifungal susceptibility test was performed by the broth microdilution method.Multilocus sequence typing(MLST)was conducted using the first generation sequencing technique.Genes associated with drug-resistance were sequenced and the mutation sites were identified.The relative expression levels of genes associated with drug-resistance were analyzed using reverse transcription-quantitative polymerase chain reaction(RT-qPCR).Results A total of 39 C.tropicalis isolates from bloodstream infections were collected.The MLST phylogenetic tree showed that most of the strains clustered in the phylogenetic tree shared identical or similar minimal inhibitory concentrations(MICs).All MLST types were not matched with the isolates in the PubMLST database,representing new diploid sequence types(DSTs).A total of 3 sense mutations,including Ser154Phe,Tyr132Phe,and Tyr257His were identified in ERG11,and were present only in drug-resistant strains.UPC2 contained 4 sense mutations,including Ala251Thr,Gln289Leu,Ser279Glu,and Gln313His,which were also present only in drug-resistant strains.Ser279Glu and Gln313His were previously unreported.There were two sense mutations in ERG3,namely Ser112Gly and Ala48Ser,both being previously unreported,and Ser112Gly was found only in drug-resistant strains.The expression levels of ERG11(14.48 vs 7.109,P=0.003)and UPC2(1.922 vs 0.832,P=0.04)in non-sensitive group(MIC>2 mg/L)were higher than those in sensitive group(MIC≤2 mg/L),and the difference was statistically significant.Conclusion There may be a unique genetic relationship among C.tropicalis isolates from Sichuan province,and the MICs of fluconazole against C.tropicalis are associated with molecular typing.ERG11 mutations were the major mechanism underlying fluconazole resistance in C.tropicalis isolates.The upregulation of ERG11 and UPC2 was associated with fluconazole resistance in C.tropicalis.

Objective To determine the median effective dose(ED50)of remimazolam for preoperative sedation in pediatric patients aged 1-6 years using the modified Dixon sequential method.Methods This is a prospective clinical study.Pediatric patients scheduled for elective short surgery(surgery time≤1 h)under general anesthesia from January to July 2023 were selected.Inclusion criteria were age 1-6 years,an ASA physical status Ⅰ-Ⅱ and the preoperative parent separation anxiety scale(PSAS)score≥3 points.Remimazolam was administered intravenously preoperatively,and its sedative effect was assessed.The modified Dixon sequential method was used to determine the ED50 of remimazolam,with the initial dose set at 0.10 mg/kg and the dose increment set at 0.02 mg/kg.Sedation was considered successful(positive,included in positive group)if the child with sedation score≥2 points,preoperative PSAS score<3 points,and the mask acceptance score of 4 points during anesthesia induction.If any criterion was not met,sedation was considered failure(negative,included in negative group),and the next patient's dosage was increased by 0.02 mg/kg based on the previous patient's dosage.The test was completed after 7 consecutive positive and negative turning points appeared alternately.Probabilistic unit regression analysis was used to determine the ED50,ED95 and the corresponding 95%confidence interval(CI)of remimazolam for preoperative sedation.Postoperative recovery time and adverse events such as airway spasm,respiratory depression,hypotension,nausea and vomiting during anesthesia were recorded.Results A total of 23 pediatric patients were included,with 13 in positive group and 10 in negative group.There were no statistically significant differences in mean arterial pressure,pulse oxygen saturation or heart rate before and after sedation(P>0.05).Compared with negative group,positive group showed a significant reduction in preoperative parent separation anxiety and an increase in mask acceptance during anesthesia(P<0.05).There was no significant difference in sedation score and anesthesia awakening time between two groups(P>0.05).The ED50 of remimazolam for preoperative sedation in pediatric patients aged 1-6 years was 0.051 mg/kg(95%CI 0.033-0.065 mg/kg),and the ED95 was 0.077 mg/kg(95%CI 0.064-0.161 mg/kg).No adverse events such as airway spasm,respiratory depression,hypotension,nausea and vomiting occurred during anesthesia in any of pediatric patients.Conclusion The ED50 of intravenous administration of remimazolam for preoperative sedation in pediatric patients aged 1-6 years is 0.051 mg/kg(95%CI 0.033-0.065 mg/kg).