To identify recruit movement dysfunction based on military joint function screening and assessment, implement targeted corrective training, explore the impact of this assessment-correction system on knowledge-attitude-belief-practice (KABP) related factors, and scientifically evaluate its efficacy in preventing recruit military training injuries within the knowledge-attitude-belief-practice theoretical framework.

A cluster randomized controlled trial was conducted at a recruit training base of the Joint Logistics Support Force from March to May 2025, enrolling 446 recruits. Participants were randomly assigned to an experimental group (n=223) or control group (n=223) using a random number table. The control group followed the routine training program, while the experimental group additionally received a 2-month targeted corrective training for movement dysfunction alongside the established training tasks. Knowledge-attitude-belief-practice questionnaires were administered to both groups at the initial, intermediate, and advanced stages of the corrective training. Univariate logistic regression was used to preliminarily screen KABP-related factors, and a multivariate logistic regression model was further constructed to analyze the role of KABP factors in the corrective training.

The experimental group had a cumulative training injury incidence of 40 cases (17.9%), which was significantly lower than that of the control group (83 cases, 37.2%; χ²=20.757, P<0.001). The experimental group showed varying degrees of improvement in knowledge, attitude and belief, and practice dimensions (P<0.05), while the control group exhibited no significant changes in the three KABP dimensions across the three surveys. Logistic regression analysis revealed: In the first round, total practice score was significantly negatively associated with training injury incidence rate (OR=0.863, 95%CI: 0.822~0.906, P<0.001), whereas knowledge and attitude-belief dimensions showed no significant association; In the second round, both total knowledge score (OR=0.925, 95%CI: 0.903~0.946, P<0.001) and total practice score (OR=0.906, 95%CI: 0.874~0.940, P<0.001) significantly reduced the risk of military training injuries, with attitude-belief dimension still showing no significant effect; In the third round, all three KABP dimensions were significantly negatively associated with military training injury incidence rate (knowledge: OR=0.905, 95%CI: 0.884~0.926, P<0.001; attitude and belief: OR=0.942, 95%CI: 0.899~0.988, P=0.013; behavior: OR=0.882, 95%CI: 0.841~0.924, P<0.001).

Joint function screening and corrective training can significantly reduce the incidence of recruit training injuries, primarily by optimizing knowledge mastery and movement behavior; belief cultivation, however, requires long-term practical accumulation.

To investigate the mechanism by which suppressor of cytokine signaling 3 (SOCS3) regulates microglial inflammation through nuclear factor-kappaB (NF-κB), providing novel mechanistic insights into microglial involvement in Parkinson’s disease (PD) pathogenesis.

① Ten male C57BL/6 mice (12 weeks old, weighing 20~25 g) were subjected to intraperitoneal injection of 15 mg/kg MPTP to establish a PD model. Rotarod test was used to assess motor function. Western blotting was employed to detect the protein expression of tyrosine hydroxylase (TH) and ionized calcium-binding adapter molecule 1 (IBA-1) in the substantia nigra. RT-qPCR was utilized to measure the mRNA level of SOCS3 in the substantia nigra. Immunohistochemistry was performed to assess NF-κB p65 subunit expression. The expression of SOCS3, NF-κB and p-NF-κB was measured with Western blotting. ② Microglial cell line BV2 was stimulated with 1 000 ng/mL lipopolysaccharide (LPS) for 6 h to establish an inflammatory model. Subsequently, SOCS3 was knocked down. NF-κB inhibitor BAY 11-7082 was used to treat the cells. RT-qPCR and Western blotting were used to measure the expression of SOCS3 at mRNA and protein levels. Western blotting was also applied to detect the expression of NF-κB and p-NF-κB, and ELISA was conducted to measure TNF-α and IL-1β levels in the culture supernatant. Immunofluorescence assay was carried out to localize NF-κB (nuclear vs cytoplasmic). ③ A co-culture system of BV2 microglia and N2a neuroblastoma cells was established to investigate the regulatory effects of microglia on neuronal cells. MTT assay and TUNEL staining were used respectively to determine cell viability and apoptosis of N2a cells.

① Compared to the control mice, the PD mouse model exhibited reduced rotarod fall latency, down-regulation in TH and SOCS3(P<0.01), up-regulation in IBA-1 and increased p-NF-κB/NF-κB ratio (P<0.01). ② In BV2 cells, LPS stimulation increased TNF-α, IL-1β, and p-NF-κB/NF-κB ratio(P<0.01), while down-regulated SOCS3 expression(P<0.01). SOCS3 knockdown in LPS-stimulated BV2 cells further increased the p-NF-κB/NF-κB ratio (P<0.01), increased nuclear localization of NF-κB, and elevated TNF-α and IL-1β levels (P<0.01). BAY 11-7082 treatment in these SOCS3-knockdown, LPS-stimulated cells resulted in reduced p-NF-κB/NF-κB ratio, TNF-α, and IL-1β (P<0.01), and decreased NF-κB nuclear distribution. ③ LPS-stimulated BV2 cells reduced cell viability and increased cell apoptosis in N2a cells(P<0.01). SOCS3 knockdown in BV2 cells exacerbated the reduction in N2a cell viability (P<0.01) and the increase in cell apoptosis in N2a cells (P<0.01). BAY 11-7082 treatment of these SOCS3-knockdown BV2 microglia attenuated the reduction in N2a cell viability and decreased apoptosis in N2a cells (P<0.01).

SOCS3 inhibits microglia inflammatory response through down-regulation of NF-kB activity, and in turn attenuates neuronal cell death and ameliorates PD nerve injury.

To investigate the protective effect of mitochondrial division inhibitor 1 (Mdivi-1), a mitophagy inhibitor, on cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol.

A total of 72 neonatal SD rats (half male and half female, aged 7 d, weighing 16.14±3.08 g) were randomly divided into 4 groups (n=18): blank control group (CON), Mdivi-1+blank control group (MCON), propofol+hypoxia group (PH), and Mdivi-1+propofol+ hypoxia group (MPH). The MCON group and MPH group were pretreated with 2.4 mg/kg Mdivi-1 in 30 min in advance, and subsequently, 50 mg/kg propofol was respectively given to the PH group and the MPH group. Immediately after the intraperitoneal injections were completed, the corresponding rats were transferred into a constant temperature chamber containing 18%O₂. Then the rats were continuously monitored until resuming the reversing reflex and then transferred to a normoxic environment. The hypoxic treatment was carried out once per day for 7 consecutive days. Transcriptome sequencing was used to screen for differential expressed genes (DEGs), and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis was employed to conduct functional analysis. Morris water maze test was applied to exam spatial learning and memory abilities. HE staining was used to observe the morphological changes of neurons in the hippocampal CA1 region. Morphological changes of mitochondria in hippocampal neurons were observed by transmission electron microscopy (TEM). Western blotting was utilized to detect the expression of Parkin Rbr E3 ubiquitin protein ligase (Parkin) and PTEN-induced putative kinase 1 (PINK1) in the hippocampal tissues.

KEGG analysis results indicated that the mitophagy pathway was more significantly enriched in the PH group when compared with the CON group. Morris water maze test revealed that the PH group exhibited obviously prolonged escape latency (P<0.05), reduced frequency of crossing the platform (P<0.05), and shortened residence time in the target quadrant (P<0.01) when compared with the CON group and the MPH group. HE staining demonstrated that the cells in the PH group were in disordered arrangement, with great loss in cell count in some areas, and widened intercellular spaces. Although the cell arrangement in the MPH group also showed a sparse state, but the condition was milder than that in the PH group, with slightly widened intercellular space. In the CON group and the MCON group, the cells exhibited round in shape, good morphological structure, relatively clear contours, and uniform cell nuclei. TEM revealed that in the hippocampal neurons of the PH group, the mitochondria were swollen and deformed, and mitochondrial cristae were disordered, dissolved and disappeared. In the MPH group, only some mitochondria were swollen and the cristae were reduced. However, the mitochondrial morphology of the CON and MCON groups was relatively complete, and the matrix was uniform. Western blot analysis showed that the expression levels of Parkin and PINK1 in the hippocampus were up-regulated in the PH group than the CON group (P<0.05), and reduced in the MPH group than the PH group (P<0.05).

Mdivi-1 may reduce hippocampal neuron damage by inhibiting excessive mitophagy and then improve cognitive dysfunction in immature SD rats induced by hypoxia combined with propofol.

To explore the protective effect of L-carnitine on myocardial systolic dysfunction in sepsis and its underlying mechanism.

A mouse sepsis model was established by cecal ligation and puncture (CLP). Ten-week-old male SPF-grade C57BL/6 mice (body weight 20~30 g) were randomly divided into 5 groups via random number table: Sham group, Sepsis group, L-carnitine group, L-carnitine+Etomoxir (Eto) group, and Eto group. Echocardiography assessed cardiac function, ELISA measured serum creatine kinase isoenzyme MB (CK-MB) levels, and 72-hour survival rates were recorded to evaluate L-carnitine’s effects on cardiac function. Cardiomyocytes were isolated, and a cell microtensiometer was used to detect cardiomyocyte contractile function and calcium transients. Myocardial tissues were collected from each group, and ELISA was used to determine the contents of triglyceride (TG), free fatty acid (FFA), and adenosine triphosphate (ATP).An in vitro sepsis model was constructed by stimulating HL-1 cardiomyocytes with lipopolysaccharide (LPS) for 12 hours, which was divided into 5 groups: control (CTRL) group, LPS group, L-carnitine group, L-carnitine + Eto group, and Eto group. ELISA was used to detect the contents of TG, FFA, and ATP as well as the activity of carnitine palmitoyltransferase 1A (CPT1A) in cardiomyocytes. A cellular energy metabolism analysis system was employed to measure fatty acid oxidation capacity, and Western blot was used to detect the protein expression of CPT1A in cardiomyocytes. BODIPY-FL-C16 (green fluorescently labeled palmitic acid) was utilized to detect the distribution of fatty acids in the cytoplasm and mitochondria via immunofluorescence technology, thereby observing the ability of cells to transport fatty acids into mitochondria.

Compared with the Sham group, cardiac function was significantly impaired in the Sepsis group, as evidenced by decreased ejection fraction and mean arterial pressure (P<0.05), along with elevated levels of the cardiac injury marker CK-MB (P<0.05). Treatment with L-carnitine significantly improved myocardial function, restored blood pressure in septic mice, and increased their survival rate from 12.50% to 81.25% (P<0.05).Compared with the Sham group, the contractile function and calcium transients of acutely isolated single cardiomyocytes were significantly reduced in the Sepsis group (P<0.05), while L-carnitine treatment remarkably restored the contractile function and calcium release capacity of septic cardiomyocytes (P<0.05).Both in vivo and in vitro experiments showed that TG and FFA levels were significantly increased (P<0.05), and ATP levels was significantly decreased (P<0.05) in the Sepsis and LPS groups—effects significantly reversed by L-carnitine treatment. Compared with the CTRL group, the basal oxidation rate and maximum oxidation capacity of fatty acids in cardiomyocytes of the LPS group were significantly reduced (P<0.05), and L-carnitine treatment notably improved these indicators.Compared with the CTRL group, the expression and activity of CPT1A in cardiomyocytes of the LPS group were significantly decreased (P<0.05), while L-carnitine treatment significantly increased the expression and activity of CPT1A (P<0.05). In LPS group cardiomyocytes, green fluorescently labeled palmitic acid primarily formed numerous granular/clumpy aggregates in the cytoplasm with minimal mitochondrial colocalization. In the L-carnitine group, the green fluorescent granules in the cytoplasm of cardiomyocytes were smaller, and colocalization with mitochondria was increased. However, the L-carnitine + Eto group exhibited similar phenomena to the LPS group.In addition, both in vivo and in vitro experiments demonstrated that treatment with the CPT1A inhibitor Eto reversed the effect of L-carnitine. Compared with the L-carnitine group, the ATP content in the L-carnitine + Eto group was significantly decreased (P<0.05), while the FFA content was significantly increased (P<0.05).

L-carnitine facilitates fatty acid entry into mitochondria for β-oxidation via a CPT1A-dependent mechanism, thereby ameliorating fatty acid oxidation dysfunction in septic cardiomyocytes and improving myocardial contractile function.

To investigate how vismodegib (Vis) influences the pathogenesis of basal cell carcinoma (BCC) via a chromatin remodeling factor, bromodomain containing protein 9 (BRD9), and to analyze the expression profile of BRD9 in BCC and its relationship with the immune checkpoint, programmed cell death-1 ligand 1 (PD-L1) and the Hedgehog (Hh) signaling pathway.

① A UVB-induced BCC model was established in SKH-1 hairless background Ptch1^+/-; LacZ reporter mice. Then the mice were treated with Vis, and those without treatment served as control. X-gal staining, immunohistochemistry (IHC) staining, immunofluorescence (IF) assay, and Western blotting were used to assess the expression and localization of BRD9 and PD-L1 in tumor tissues and to evaluate immune-cell infiltration. ② In vitro, mouse BCC cell line ASZ001 (ASZ cells) were treated with Vis or a BRD9 degrader (dBRD9), and BRD9-overexpressing cells were generated. Cell viability and the protein and mRNA levels of BRD9, PD-L1, Gli1, and cyclin D1 (Ccnd1) were measured. ChIP-qPCR was performed to examine BRD9 and H3K27ac enrichment at the PD-L1 promoter, including the promoter-proximal site (P1) and an upstream active segment (P2).

① At the tissue level, BRD9 was highly expressed in BCC, and co-localization of BRD9 and PD-L1 was observed within tumor regions, with evident immune-cell infiltration. Vis markedly suppressed UVB-induced BCC formation, reduced the probability of large-volume tumors (by probability-density analysis), decreased the X-gal-positive lesion area(P<0.000 1), down-regulated BRD9(P=0.024 9), and attenuated immune-cell infiltration. ② At the cellular level, Vis treatment reduced cell viability and down-regulated BRD9, Gli1, and Ccnd1 in ASZ cells(P<0.000 1). dBRD9 inhibited ASZ cell viability in a dose-dependent manner and decreased PD-L1, Gli1, and Ccnd1(P<0.000 1), whereas its overexpression increased the expression of these molecules(P<0.000 1). In ASZ cells, BRD9 and H3K27ac were enriched at the PD-L1 promoter P1/P2 regions. Treatment with dBRD9 or Vis reduced BRD9 and H3K27ac enrichment at P1/P2 regions(P<0.000 1).

In BCC, BRD9 maintains chromatin activation at the proximal PD-L1 promoter and modulates Hh/Gli1 signaling, thereby promoting immune evasion. Vis remodels the tumor immune microenvironment by inhibiting the Hh-BRD9-PD-L1 axis.

To investigate the role and mechanism of ferroptosis in cochlear hair cell injury induced by exposure to ammonium 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)propanoate (GenX).

Mouse cochlear hair cell line HEI-OC1 was assigned to control, GenX, ferrostatin-1 (Fer-1), and GenX+Fer-1 groups. CCK-8 assay was used to assess the cytotoxicity of GenX and the rescue effect of Fer-1 co-treatment. Western blotting and qRT-PCR were employed to measure the protein and transcriptional expression of ferroptosis markers, cochlear function indicators, blood labyrinth barrier markers, and ferroptosis-related pathway. FerroOrange, Bodipy(C11), mitochondrial membrane potential assay kit (JC-1), and adenosine triphosphate (ATP) assay were applied to detect Fe²⁺ accumulation, lipid peroxidation, mitochondrial membrane dysfunction, and cellular ATP levels, respectively.

Exposure to 200 μmol/L GenX for 12 h significantly reduced the viability of HEI-OC1 cells (P<0.01), down-regulated the protein levels of glutathione peroxidase 4 (Gpx4), solute carrier family 7 member 11 (Slc7a11), and ferroptosis suppressor protein 1 (Fsp1) (P<0.05), whereas up-regulated acyl-coa synthetase long-chain family member 4 (Acsl4) (P<0.01), and decreased the expression of cochlear hair-cell function genes and blood labyrinth barrier genes (P<0.05). These changes were accompanied with Fe²⁺ accumulation, elevated lipid peroxidation, mitochondrial membrane damage, and reduced ATP production (P<0.001). Addition of Fer-1 restored cell viability (P<0.05), restored the expression of ferroptosis related proteins (P<0.05), and improved the expression of several hair-cell function and blood labyrinth barrier genes (P<0.05). In parallel, the GenX+Fer-1 group exhibited reduced Fe²⁺ accumulation, lower lipid peroxidation, attenuated mitochondrial membrane damage, and increased ATP level (P<0.001).

GenX induces iron-metabolism dysregulation and lipid peroxidation, and then leads to differentiation impairment of cochlear hair cells and barrier functions via the ferroptotic System Xc⁻-Gpx4-Fsp1 axis.

To investigate the potential mechanism by which dihydromyricetin (DHM) ameliorates diabetic nephropathy (DN), and to screen and validate its possible key molecular targets.

A DN model was established using db/db mice, and 100 mg/(kg·d) DHM was administered via gavage 5 d per week for totally 10 weeks. Renal morphological changes were observed after staining to evaluate the effects of DHM. GSE161885 and GSE270526 datasets were obtained from the Gene Expression Omnibus (GEO) database and analyzed in combination with the GeneCards database to screen for DN-related differentially expressed genes (DEGs). Protein-protein interaction (PPI) network and molecular docking were employed to predict potential DHM targets. Western blotting and immunofluorescence staining were performed to detect the effects of DHM on pyroptosis-related pathways in the renal tissues of db/db mice and in high glucose (HG)-induced human renal tubular epithelial cells (HK-2). The specific NLR family pyrin domain containing protein 3 (NLRP3) inhibitor MCC950 was also used to validate the predicted mechanism.

In vivo experiments showed that DHM significantly ameliorated renal pathological damage in db/db mice, alleviated glomerular hypertrophy and mesangial expansion, and markedly reduced Paller scores (P<0.001). Immunofluorescence staining revealed significantly weakened fluorescence signals for α-smooth muscle actin (α-SMA), fibronectin, and collagen Ⅰ in renal tissues. Western blot results showed that the expression levels of collagen Ⅰ, collagen Ⅲ, α-SMA, and transforming growth factor beta 1 (TGF-β1) were significantly decreased (P<0.05). A total of 16 DN-related DEGs were identified. Enrichment analysis revealed that these genes were primarily enriched in pathways such as viral protein interactions, cytokine-cytokine receptor interaction, and the AGE-RAGE signaling pathway in diabetic complications, and were primarily involved in gene functions such as the positive regulation of lymphocyte-mediated immunity, positive regulation of adaptive immune response, and chemokine activity. Molecular docking confirmed NLRP3 as a potential target of DHM. In vivo validation showed that DHM significantly down-regulated gasdermin-D (GSDMD) fluorescence signals and inhibited the expression of pyroptosis-related proteins including NLRP3, Caspase 1, Cleaved-Caspase 1, interleukin 18 (IL-18), and GSDMD (P<0.05). In vitro studies further confirmed that both DHM and the specific NLRP3 inhibitor MCC950 alleviate high glucose-induced fibrosis and pyroptosis in HIC-2 cells.

DHM can ameliorate the progression of DN, and its mechanism is related to inhibiting NLRP3 inflammasome-mediated pyroptosis, thereby alleviating renal inflammation and fibrosis.

To investigate the effects of cinnamic aldehyde (CA) on Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak) in vascular endothelial cells of diabetic ulcer wound tissues, as well as on cell apoptosis.

① Forty-eight healthy SPF-grade male SD rats (5 weeks old, weighing 180~220 g) were randomly assigned to a control group (12 rats) and a diabetes group (36 rats). The diabetic model was established with an intraperitoneal injection of 50 mg/kg STZ-citrate sodium solution and high-fat diet feeding. The diabetes group was further randomly divided into Model group, CA group, and the rb-bFGF group, with 12 animals in each group. Wounds in the Con and Model groups were disinfected and topically treated with normal saline, CA group received topical application of 4 µmol/L CA in PEG 400 gel, and those of the rb-bFGF group were treated with bevacizumab gel. The wound healing rate of each group was calculated at 3, 7 and 14 d after intervention. At 14 d after intervention, pathological changes in the wounds were observed with HE staining, and the expression levels of Bax and Bak were detected by Western blotting. ② Human umbilical vein endothelial cell line EA.hy926 was treated with 175 mmol/L glucose for 48 h to establish a cell model of high glucose injury. The experimental cells were divided into control group, model group and CA treatment group. Cell scratch test and tube formation test were performed respectively to determine the migration ability and angiogenesis of the cells. The expression levels of Bax and Bak was detected with immunofluorescence assay, and cell apoptosis was detected by TUNEL staining.

①The diabetic rats in the Model group exhibited significantly higher blood glucose level (P<0.05), declined wound healing rate at 7 and 14 d after intervention (P<0.05), and enhanced expression levels of Bax and Bak (P<0.05) when compared with the control group. Pathological observation revealed that, at 14 d after intervention, accompanied with inflammatory reactions, dense infiltration of inflammatory cells, fewer new blood vessels, and continuous fluid exudation in the wound were observed in the Model group, but the control group presented complete epithelialization in full-thickness skin. Compared with the conditions in the Model group, both CA and rb-bFGF treatment improved the epithelialization process, with mature granulation tissues, showing good healing condition, promoted wound healing rate (P<0.05), and decreased the expression levels of Bax and Bak (P<0.05). ② The results of cell experiments showed that the cells of the model group showed significantly reduced migration ability and tube formation ability (P<0.05), reduced protein levels of Bax and Bak (P<0.05), and lower apoptotic rate (P<0.05) when compared with the cells in the model group.

CA can inhibit the expression of apoptosis-related proteins Bax and Bak, promote the migration and tube formation of vascular endothelial cells, and inhibit the cell apoptosis under high glucose condition, which may be an important reason for its promoting wound healing in diabetic ulcer rats.

To explore the repair effect and mechanism of human amniotic mesenchymal stem cells (hAMSCs) on endometrial injury.

hAMSCs were isolated using a two-enzyme digestion and then cultured. The third-passage (P3) cells were harvested to detect the surface markers by flow cytometry and to identify their trilineage differentiation potentials. Eighteen nulliparous female SD rats (8~9 weeks old, weighing 250~280 g) were randomly divided into 3 groups (n=6): normal control group, model group, and hAMSCs group. A rat model of intrauterine adhesions (IUA) was established in SD rats by using curettage combined with lipopolysaccharide (LPS) infection. In 2 weeks after modeling, the hAMSCs group received a bilateral uterine horn transplantation of 0.2 mL hAMSCs (1.0×10⁶ cells/mL), while the model group received a same volume of PBS into both uterine horns. All rats were sacrificed in 2 weeks after transplantation. HE and Masson staining was used to observe endometrial thickness and gland number as well as endometrial fibrosis area. RT-qPCR and Western blotting were performed to detect the mRNA and protein levels of TGF-β1, Smad3, Smad7, epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin), fibrosis factor α-SMA, and endometrial estrogen receptor (ER) and progesterone receptor (PR) in endometrial tissues.

The obtained cells were identified as hAMSCs due to the characteristics of surface markers and differentiation potentials. Compared with the normal control group, the model group showed decreased endometrial thickness, reduced gland number, increased fibrosis area, and enhanced mRNA and protein levels of fibrosis-related factors TGF-β1, Smad3, Vimentin, and α-SMA (P<0.01), while down-regulation of fibrosis-inhibiting molecule Smad7, the EMT marker E-cadherin, and endometrial receptors ER and PR at both mRNA and protein levels (P<0.01). hAMSCs transplantation increased endometrial thickness and gland number, decreased fibrosis area, and down-regulated mRNA expression of the aforementioned fibrosis-related factors (P<0.01), and up-regulated the mRNA expression levels of Smad7, E-cadherin, ER, and PR (P<0.01). The hAMSCs group also exhibited obviously down-regulated protein levels of TGF-β1, Smad3, and α-SMA (P<0.05), while enhanced protein levels of Smad7 and PR (P<0.05).

Intrauterine transplantation of hAMSCs can promote the repair of endometrial injury, and inhibits endometrial EMT and fibrosis through the TGF-β1/Smad7 signaling pathway.

To determine the median effective concentration (EC₅₀) of ropivacaine at the volume of 0.5 mL/kg for ultrasound-guided interscalene brachial plexus block in children aged 6 to 10 years.

A prospective dose-finding trial was conducted based a sequential Dixon up-and-down allocation. We recruited children aged 6 to 10 years who were scheduled for unilateral surgery on upper extremity regions in our hospital from April to December 2022. All of them were subjected to general intravenous anaesthesia combined with ultrasound-guided interscalene brachial plexus block. The ropivacaine volume for each patient was 0.5 mL/kg. The concentration of 0.2% for the first patient, subsequent concentrations were adjusted based on the block effect of previous patient, increase or decrease by 0.02%. The trial was stopped when there were 7 turning points. Isotonic regression and Bootstrap were used to calculate the values of EC₅₀ and 95% effective concentration (EC₉₅), along with their 95% confidence intervals (CI). General data, incidence of adverse events, and score of postoperative pain were recorded.

A total of 26 children aged 6 to 10 years were included. The EC₅₀ of ultrasound-guided interscalene brachial plexus block was determined to be 0.091% (95%CI: 0.077%~0.105%), and the EC₉₅ was estimatedto be 0.117% (95%CI: 0.110%~0.118%). Successful blockade was achieved in 16 cases (61.5%), while 10 cases (38.5%) failed. No statistical differences existed between successful and failed cases regarding sex, age, body weight, surgical site, surgical laterality, operative time, or anesthesia duration. None of the patients experienced adverse events such as pneumothorax, vascular injury, or Horner’s syndrome, and the score of postoperative pain were all <6 by modified Children’s Hospital of Eastern Ontario Pain Scale.

In children aged 6 to 10 years, the EC₅₀ of ropivacaine is 0.091% at a volume of 0.5 mL/kg for ultrasound-guided interscalene brachial plexus block, and this low dose of regional anesthetic can reduce the risks such as systemic toxicity and direct neurotoxicity.