In order to achieve the construction goal of a"trinity"smart hospital,Sun Yat-sen Memorial Hospital of Sun Yat-sen University uses information technology to build a hospital logistics security operation and maintenance platform based on"BIM+Internet of Things"technology,integrates logistics business systems,improves standardized logistics services,and im-proves the efficiency of hospital logistics services.Visualization of logistics energy,environment,equipment,security and materi-al supply,standardization of business processes,precision of data,and exploration of a multi-district intelligent logistics manage-ment innovation model to help hospitals develop in high quality.

Objective:To investigate the correlation between gallbladder polyps and colon polyps of different locations.Methods:Healthy subjects who underwent colonoscopy in the Physical Examination Center of the Affiliated Hospital of Yangzhou University from January 2020 to October 2022 were included. They were divided into the proximal colon group and the distal colon group according to the location of colon polyps. Gallbladder polyps were compared with other known risk factors for colon cancer. Different parts and types of polyps were further explored.Results:A total of 2 811 patients had colon polyps, including 1 668 males and 1 143 females, with an average age of 47.3 years. One hundred and seventy-one (6.1%) had gallstones, and 459 (16.3%) had gallbladder polyps. The incidence of gallbladder polyps was higher in the proximal colon polyp group (21.7%, 93/429). Gallbladder polyps were independently associated with proximal colon polyps, including hyperplastic polyps ( OR=1.525, P=0.029) and adenomatous polyps ( OR=1.425, P=0.017). There was no significant correlation between gallbladder polyps and distal colon polyps. Conclusion:Gallbladder polyps are associated with proximal colon polyps, and colonoscopy screening is recommended for people with gallbladder polyps.

Objective:To investigate the changes and significance of granulocyte-like myeloid-derived suppressor cells (G-MDSC) in the acute phage of Kawasaki disease (KD).Methods:Forty-two children with acute KD were enrolled in the present study and 32 age-matched healthy children were selected as control group. The proportion of HLA-DR -CD11b + CD33 + CD14 -CD15 + G-MDSC, the concentration of reactive oxygen species (ROS) and the expression of arginase-1 (Arg-1), programmed death-ligand 1 (PD-L1), cytotoxic T lymphocyte associated protein 4 (CTLA4), glycoprotein 130 (gp130) and phosphorylated signal transducer and activator of transcription 3 (pSTAT3) at protein level were detected by flow cytometry. Quantitative real-time PCR was used to measure the expression of inducible nitric oxide synthase (iNOS), interferon regulatory factor 8 (IRF-8), IL-6 receptor α subunit (IL-6Rα), granulocyte colony-stimulating factor receptor (G-CSFR), CCAAT/enhancer binding protein β (C/EBPβ), suppressor of cytokine signaling 1 (SOCS1) and SOCS3 at mRNA level in G-MDSC. Chromatin immunoprecipitation was performed to detect the acetylation of histone H3 at the promoters of SOCS1 and SOCS3 genes. Plasma concentrations of IL-6 and granulocyte colony-stimulating factor (G-CSF) and protein levels of IL-10, transforming growth factor-β (TGF-β) and nitric oxide (NO) in the culture supernatant of G-MDSC stimulated with LPS were measured by ELISA. Results:(1) Compared with the control group, the proportion of HLA-DR -CD11b + CD33 + CD14 -CD15 + G-MDSC as well as the concentration of ROS and the expression of inhibitory molecules (Arg-1, PD-L1 and CTLA4) in G-MDSC increased significantly in patients with acute KD ( P<0.05). Moreover, the concentrations of IL-10 and TGF-β in culture supernatant of G-MDSC were also higher than those of the control group after stimulation with lipopolysaccharide for 48 h ( P<0.05). All of the seven afore-mentioned indexes in KD patients with coronary artery lesion (CAL group ) were lower than those in patients without coronary artery lesion (NCAL group) ( P<0.05), and restored to some extent after IVIG therapy ( P<0.05). There were no statistical differences in iNOS expression or NO concentration in culture supernatant of G-MDSC among different groups ( P<0.05). (2) Plasma concentrations of IL-6 and G-CSF, and the expression of IL-6Rα, gp130, G-CSFR, pSTAT3 and C/EBPβ increased remarkably during acute phase of KD ( P<0.05). The expression of IRF-8 at transcription level in patients with acute KD was found to be lower than that of healthy controls ( P<0.05), and restored significantly after IVIG therapy ( P<0.05). Moreover, the plasma concentrations of IL-6 and G-CSF and the expression of IL-6Rα, gp130, G-CSFR and IRF-8 in the CAL group were higher than those in the NCAL group ( P<0.05), while the expression of pSTAT3 and C/EBPβ was lower in the CAL group ( P<0.05), which were restored by IVIG therapy ( P<0.05). (3) In patients with acute KD, the expression of SOCS1 and SOCS3 at mRNA level and histone acetylation at the promoters of SOCS1 and SOCS3 genes were reduced significantly in comparison with those in healthy controls ( P<0.05) , but were increased remarkably after IVIG treatment( P<0.05). The four indexes were higher in the CAL group than in the NCAL group ( P<0.05). Pearson correlation analysis showed the expression of SOCS1 and SOCS3 was negatively correlated with the protein level of pSTAT3 in G-MDSC of patients with acute KD ( r=-0.46 and -0.32, P<0.05). Conclusions:Changes in the number and function of G-MDSC caused by aberrant histone acetylation at SOCS1 and SOCS3 genes might contribute to the immune dysfunction and vascular damage in patients with KD.

Objective:To investigate the changes of monocytic myeloid-derived suppressor cells (M-MDSC) in children with acute Kawasaki disease (KD) and its roles in the immunological pathogenesis of KD.Methods:A total of 38 children with acute KD were enrolled in the present study and 32 age-matched healthy children were selected as control group. The proportions of HLA-DR -CD11b + CD33 + CD15 -CD14 + M-MDSC and CD4 + CD25 + CD127 - regulatory T cells (Treg) in peripheral blood, concentrations of reactive oxygen species (ROS) and expression of arginase-1 (Arg-1), CD39, CD73, CD40, CD40L and CCR5 at protein levels were detected by flow cytometry. Quantitative real-time PCR was used to evaluate the transcription levels of inducible nitric oxide synthase (iNOS) in M-MDSC and the transcription levels of cytotoxic T-lymphocyte associated antigen 4 (CTLA4) and lymphocyte-activation gene 3 (LAG3) in Treg. Concentrations of NO, CCL3, CCL4, CCL5, IL-10 and TGF-β in the supernatants of cell culture were measured by ELISA. Results:(1) The proportion of HLA-DR -CD11b + CD33 + CD15 -CD14 + M-MDSC, the concentration of intracellular ROS and the expression of iNOS, CD39 and CD73 in M-MDSC decreased significantly in patients with acute KD as compared with those in the control group ( P<0.05), and the concentrations of NO, IL-10 and TGF-β in culture supernatant of M-MDSC were lower than those in the control group upon lipopolysaccharide (LPS) stimulation for 48 h ( P<0.05). All of the aforementioned indexes restored to some extent after intravenous immunoglobulin (IVIG) therapy ( P<0.05). No statistical differences were found in Arg-1 expression between healthy controls and patients with KD before or after IVIG therapy ( P<0.05). (2) CD40 expression on M-MDSC was significantly lower in the acute KD group than in the control group ( P<0.05). The concentrations of CCL3, CCL4 and CCL5 in the culture supernatants of M-MDSC were lower in the acute KD group than in the control group after LPS stimulation ( P<0.05). With IVIG treatment, all of the indexes were up-regulated significantly ( P<0.05), although CD40 expression was still lower in the acute KD group than in the control group ( P<0.05). (3) The proportion of CD4 + CD25 + CD127 -Treg and the expression of CTLA4, LAG3, CD40L and CCR5 reduced significantly in patients with acute KD as compared those in healthy controls ( P<0.05), and all increased remarkably after IVIG therapy ( P<0.05). Pearson correlation analysis showed a positive correlation between the proportions of M-MDSC and Treg in patients with acute KD ( r=0.58, P<0.05). Conclusions:Insufficiency and impaired function of M-MDSC might be a major cause of immune dysfunction in patients with acute KD.

Objective:To evaluate the microstructural changes of brain parenchyma in patients with essential hypertension by diffuse kurtosis imaging (DKI) and enhanced T2 star weighted angiography (ESWAN).Methods:A prospective study was performed; 27 patients with essential hypertension, admitted to our hospital from April 2019 to September 2019, and 16 healthy subjects matched with gender, age and education level were enrolled in our study. According to the presence or absence of cerebral microbleeds (CMBs), patients with essential hypertension were divided into essential hypertension with CMBs group ( n=8) and essential hypertension without CMBs group ( n=19). MRI, DKI and ESWAN were performed on all subjects. The mean kurtosis (MK), mean diffusivity (MD) and fractional anisotropy (FA) of bilateral hippocampal gyrus, centrum semiovale, caudate head, posterior limb of internal capsule, thalamus, red nucleus, substantia nigra, pons, and cerebellum were measured. Results:As compared with the healthy subjects, the patients with essential hypertension had significantly lower MK values in the left semioval center, bilateral caudate head, left posterior limb of internal capsule, and bilateral thalamus, significantly higher MD value in the right thalamus, and statistically lower FA value in the left posterior limb of internal capsule ( P<0.05). The essential hypertension with CMBs group had significantly lower MK values in left hippocampus gyrus, left centrum semiovale, bilateral caudate head, left posterior limb of internal capsule, bilateral thalamus, and left substantia nigra, significantly higher MD value in right thalamus, and significantly lower FA value in left posterior limb of internal capsule as compared with essential hypertension without CMBs group and healthy control group ( P<0.05). Conclusion:In patients with essential hypertension, the brain microstructural changes are found in the hippocampus, centrum semiovale, caudate head, posterior limb of internal capsule, thalamus and substantia nigra; these changes are more obvious in essential hypertension patients with CMBs; DKI and ESWAN can effectively assess the early brain microstructure changes in patients with essential hypertension.

Objective:To investigate the histone acetylation of interleukin-4(IL-4) gene and its roles in immunological pathogenesis of Kawasaki disease (KD).Methods:Thirty-six children with KD and 28 age-matched healthy children in Shenzhen Children′s Hospital from October 2016 to December 2018 were recruited in this study.Peripheral venous blood samples were collected from healthy controls (28 cases) and patients with KD during acute phase and 4 to 5 days after effective intravenous immunoglobulin (IVIG) treatment.Co-immunoprecipitation followed by real-time PCR was used to assess histone H4 acetylation levels of IL-4 promoter and Va enhancer, and binding abilities of p300 and CREB-binding protein (CBP) with promoter and Va enhancer of IL-4 gene in peripheral blood CD4 + T cells.Flow cytometry was performed to analyze the proportion of CD4 + IL-4 + T cells (Th2) and protein le-vels of phosphorylated signal transducer and activator of transcription 6 (pSTAT6), GATA binding protein 3 (GATA3), nuclear factor 1 of activated T cells(NFAT1), transforming growth factor-β receptor Ⅱ (TGF-βRⅡ), and phosphorylated L-type amino acid transporter 1(pLAT1). Quantitative real-time PCR was used to evaluate the transcription levels of IL-4, IL-5, IL-13, IL-4 receptor α (IL-4Rα), transforming growth factor-β receptor Ⅰ (TGF-βRⅠ) and sex-determining region Y(SRY)-box 4 (SOX4) in CD4 + T cells.Plasma concentrations of IL-4 and transforming growth factor-β(TGF-β) were measured by enzyme-linked immunosorbent assay. Results:(1)Compared with control group, the proportion of Th2 cells, expression levels of Th2-associated cytokines (IL-4, IL-5 and IL-13) and histone H4 acetylation levels associating with IL-4 promoter and Va enhancer, increased remarkably during acute KD(all P<0.05), and restored after IVIG therapy(all P<0.05). Meanwhile, all the former items in KD patients with coronary artery lesions (CAL) were higher than those in patients with non-coronary artery lesions (NCAL) (all P<0.05). (2) Compared with control group, binding abilities of p300 and CBP with IL-4 promoter and Va enhancer in CD4 + T cells were up-regulated significantly during acute KD (all P<0.05), and decreased in varying degrees after IVIG treatment (all P<0.05). Positive correlations between binding abilities of p300 with IL-4 (promoter and Va enhancer) and the expression of IL-4 promoter and Va enhancer were detected in patients with acute KD ( r=0.72, 0.43, all P<0.05). Furthermore, binding abilities of p300 and CBP with IL-4 promoter and Va enhancer in CAL group were higher than those in NCAL group (all P<0.05). (3) Compared with control group, patients with acute KD had remarkably increased plasma concentration of IL-4, and expression levels of IL-4Rα/STAT6/GATA-3 and pLAT1/NFAT1 in CD4 + T cells (all P<0.05), and significantly down-regulated plasma concentration of TGF-β and expression level of TGF-βRⅡ/TGF-βRⅠ/SOX4 (all P<0.05). All the items mentioned above restored in varying degrees after IVIG treatment (all P<0.05). Simultaneously, the 6 items aforementioned in CAL group were found to be higher than those in NCAL group (all P<0.05), while the latter four items were lower than those in NCAL group (all P<0.05). Conclusion:Histone hyperacetylation of IL-4 gene may be related to immune dysfunction in patients with KD.

Objective: To analyze the impact of the activation mode on the results of space closure in the mandibular arch using a double keyhole loop (DKHL) with a typodont model and reverse engineering technique to provide guidance for clinical treatment. Methods: Nine normal mandibular typodont models after leveling were randomly divided into 3 groups, which then underwent three types of DKHL activation for space closure. Each model was assessed at the initial stage and after the warm water bath, and the images were superimposed to measure the displacement of special crown and root mark points. All statistical analysis of the data was performed using SPSS 19.0 Results: After equal activation times, the root retraction of anterior teeth and the crown forward position of posterior teeth in groups activated at the distal loop (conditions 2 and 3) were much greater than those in the group activated horizontally (condition 1). Activation between mesial and distal loops (condition 3) induced significant anterior tooth intrusion, together with elongation and buccal inclination of posterior teeth. The displacement of mark points among the three conditions showed a statistically significant difference. Conclusion The movement of mandibular anterior and posterior teeth could be flexibly controlled through different DKHL activation modes, which should be chosen carefully according to individual conditions.

Objective To investigate the effects of p300/CBP on histone acetylation of Foxp3 gene and its roles in the immunological pathogenesis of Kawasaki disease (KD).Methods Forty-six children with KD and twenty-eight age-matched health children were consented to participate in this study.Co-immunoprecipitation and real-time PCR were performed to detect Foxp3-associated acetylation levels of histone H4 and binding abilities of p300, CBP, pSmad3 (phosphorylated mothers against decapentaplegic homolog 3) and NF-AT (nuclear factor of activated T cells) with Foxp3 gene in CD4+ T cells.The percentages of CD4+CD25high Foxp3+ cells (Treg) and the expression of Foxp3, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), p300, CBP, TGF-βRⅡ (transforming growth factor β receptor Ⅱ) and pLAT1 at protein level were analyzed by flow cytometry.Quantitative real-time PCR was used to measure the expression of Foxp3, IL-10, TGF-β, TGF-βRⅠ, Egr-1 (early growth response protein 1), RARα (retinoic acid receptor α) and PLCγ1 (phospholipase C-γ1) in Treg cells at mRNA level.Plasma concentrations of TGF-β and retinol acid (RA) were measured by enzyme-linked immunosorbent assay.Results (1) The percentages of Treg cells, levels of Foxp3 and molecules associated with suppressive function of Treg cells (TGF-β, IL-10 and CTLA4), acetylation levels of histone H4 associated with promoter, conserved non-coding DNA sequence 1 (CNS1) and CNS2 of Foxp3 gene decreased remarkably during acute KD (P<0.05), but were restored after IVIG therapy (P<0.05).Meanwhile, all of the aforementioned items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) (P<0.05).No significant differences in histone H4 acetylation associated with CNS3 were found among different groups (P>0.05).(2) The levels of p300 and CBP in Treg cells and their binding abilities with Foxp3 gene were down-regulated significantly during acute KD (P<0.05), but were restored to some extent after IVIG treatment (P<0.05).The Foxp3-associated histone acetylation was positively correlated with the expression of p300 and CBP at mRNA level during acute KD (r=0.65, 0.42, P<0.05).Furthermore, the expression of p300 and CBP and their binding abilities with Foxp3 gene in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(3) Compared with healthy subjects, plasma concentrations of TGF-β and RA and the expression of TGF-βRⅠ/Ⅱ/Egr-1, RARα and pLAT1/PLCγ1 were down-regulated during acute KD (P<0.05);the binding abilities of pSmad3 and NFAT with Foxp3 gene were reduced remarkably in patients with acute KD (P<0.05).All the items mentioned above were restored after IVIG treatment (P<0.05).Moreover, the ten items aforementioned in KD-CAL+ group were lower than those in KD-CAL-group (P<0.05).(4) Higher acetylation levels of histone H4 associated with promoter, CNS1 and CNS2, and enhanced binding abilities of p300 and CBP with Foxp3 gene were found in CD4+ T cells isolated from patients with acute KD after co-stimulation with TGF-β, RA and anti-CD3/CD28 antibodies as compared with those in CD4+ T cells without stimulation (P<0.05).However, no statistical difference in the acetylation level of histone H4 associated with CNS3 was found between the two groups (P>0.05).Conclusion Hypoacetylation of histone H4 associated with Foxp3 gene caused by insufficient expression of p300/CBP and their impaired binding abilities might be involved with immune dysfunction in KD.IVIG therapy regulates the expression of p300/CBP and their binding abilities with Foxp3 gene through up-regulating TGF-β signal.

Objective To investigate the effects of SMYD3 and MLL5 on histone methylation of Transcription factor forkhead box protein 3 (Foxp3) gene and its roles in the immunological pathogenesis of Kawasaki disease (KD). Methods Forty-two children with KD and 26 age-matched healthy children were consented to participate in this study. Co-Immunoprec-ipitation and real-time polymerase chain reaction (PCR) was performed to determine Foxp3-associated histone methylation levels of H3K4me3 and H3K27me3, and binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells. The proportion of CD4+CD25high Foxp3+cells (Treg) and protein levels of Foxp3, cytotoxic T lymphocyte associated antigen-4 (CTLA4), TGF-βRⅡand pSmad3 were analyzed by flow cytometry. Quantitative real-time PCR was used to evaluate levels of Foxp3, interleukin (IL)-10, GITR, TGF-βRⅠand RARαmRNA in CD4+T cells. Plasma concentrations of TGF-βand retinol acid (RA) were measured by enzyme-linked Immunosorbent assay. Independent-samples t-test was used as the statistical method in this study. Results ① The proportion of Treg, expression levels of Foxp3 and molecules associated with suppressive function of Treg cells(IL-10, GITR and CTLA4), and histone methylation levels of H3K4me3 associating with promoter, conserved non-coding DNA sequence (CNS) 1 and CNS2 of Foxp3 gene decreased remarkably during acute KD [Promoter:(5.4±1.8)%vs (9.1±2.2)%;CNS1:(2.6±0.9)% vs (3.8±1.1)%; CNS2: (2.4±0.8)% vs (4.2±1.0)%; t=5.50, 6.02, 9.56, 7.92, 7.97, 4.76, 7.73, 5.01, 8.66; P<0.05], and restored after intravenous immunoglobulins (IVIG) therapy [Promoter: (7.2 ±2.1)% vs (5.4 ±1.8)%; CNS1:(3.6±1.4)% vs (2.6±0.9)%; CNS2: (3.6±1.4)% vs (2.4±0.8)%; t=5.56, 4.59, 7.01, 6.04, 5.89, 4.83, 4.45, 4.00, 5.12; P<0.05]. Meanwhile, the nine former items in KD patients with coronary artery lesions (KD-CAL+) were lower than those without coronary artery lesions (KD-CAL-) [Promoter: (4.11±1.45)% vs (6.16±1.93)%; CNS1:(1.99±0.87)%vs (2.96±1.10)%;CNS2: (1.75±0.63)%vs (2.72±1.16)%;t=6.28, 3.24, 4.56, 3.69, 3.38, 4.40, 3.65, 3.00, 3.51; P<0.05]. No significant difference of H3K4me3 associated with CNS3 and H3K27me3 were found among the groups (t=1.03, 0.91, 1.48 and 0.79, 0.82, 1.53; P>0.05). ② Binding levels of SMYD3 and MLL5 with Foxp3 gene in CD4+T cells were down-regulated significantly during acute KD (t=6.63, 6.15; P<0.05), and restored to some extent after IVIG treatment (t=5.36, 4.56; P<0.05). Positive correlations between binding levels of SMYD3 and MLL5 and expression level of Foxp3 mRNA were detected in patients with acute KD (r=0.62、0.45, P<0.05). Furthermore, Binding levels of SMYD3 and MLL5 with Foxp3 gene in KD-CAL+group were lower than those in KD-CAL- group (t=4.11, 4.31; P<0.05). ③ Compared with healthy controls, plasma concentration of TGF-β and RA, and expressions of TGF-βRⅡ, TGF-βRⅠ, pSmad3 and RARα were down-regulated during acute KD (t=11.54, 12.81, 7.43, 16.10, 8.25, 12.06; P<0.05), and elevated remarkably after IVIG treatment (t=8.40, 6.24, 5.94, 11.78, 6.27, 8.30; P<0.05). Simultaneously, all the items aforementioned in KD-CAL+ group were found to be lower than those in KD-CAL-group (t=3.58, 3.30, 3.82, 5.27, 4.71, 3.78; P<0.05). Conclusion Hypomethylation of H3K4me3 associated with Foxp3 gene caused by insufficient binding levels of SMYD3/MLL5 may be involved with immune dysfunction in Kawasaki disease.

Objective: To investigate the impacts of ash2 (absent, small, or homeotic)-like (Ash2L) and Jumonji domain-containing protein 3 (Jmjd3) on histone methylation of interferon-gamma(IFN-γ) gene and association with vascular damage of Kawasaki disease (KD) in acute phase. Methods: This study was performed among 36 children with KD in acute phase (KD group) and 28 age-matched health children (control group), who were treated or underwent physical examination in our hospital between February 2015 and June 2016. Patients were further divided into KD groups with or without coronary artery lesions (KD-CAL⁺ , 16 cases; KD-CAL^-, 20 cases). All KD patients were treated with intravenous immunoglobulin. The proportion of type 1 helper T(Th1) cells and protein levels of IFN-γ, T-box expressed in T cells(T-bet), phosphorylated signal transducer and activator of transcription 1(pSTAT1) and phosphorylated signal transducer and activator of transcription 4(pSTAT4) were analyzed by flow cytometry.Chromatin immunoprecipitation was performed to determine histone methylation (histone H3 tri-methyl K4(H3K4me3), histone H3 tri-methyl K27(H3K27me3)) and binding levels of Ash2L, Jmjd3 and Ezh2 associated with IFN-γ in CD4⁺ T cells. Quantitative real-time PCR was used to determine mRNA levels of IFN-γ, interferon γ receptor 1(IFN-γR1), interferon γ receptor 2(IFN-γR2), interleukin 12 receptor subunit beta 1(IL-12Rβ1), interleukin 12 receptor subunit beta 2(IL-12Rβ2), interleukin 18 receptor subunit beta α(IL-18Rα), interleukin 18 receptor subunit beta β(IL-18Rβ), tumor necrosis factor receptor 1(TNFR1), toll-like receptor 4(TLR4), receptor interacting serine/threonine kinase 1(RIP-1) and myeloid differentiation primary response gene 88(MyD88) in CD4⁺ T cells. Plasma concentrations of IFN-γ, interleukin 12(IL-12), interleukin 18(IL-18) and tumor necrosis factor α(TNF-α) were measured by enzyme-linked Immunosorbent assay. Results: (1)The proportion of Th1 and its protein level of IFN-γ were significantly higher in KD group than those in control group and higher in KD-CAL⁺ group than in KD-CAL^- group (all P<0.05), and lower after treatment than before treatment (all P<0.05). (2)Compared with control group, mRNA level of IFN-γ and IFN-γ-associating H3K4me3 was increased, while level of IFN-γ associating H3K27me3 in CD4⁺ T cells was reduced in KD group (all P<0.05), which resulted in a higher rate of H3K4me3/H3K27me3 (P<0.05) in KD group, which was positively correlated with IFN-γ mRNA in KD group(r=0.55, P<0.05). Similar results were found between KD-CAL⁺ group and KD-CAL^- group (all P<0.05). Level of IFN-γ associating H3K27me3 was increased, and mRNA level of IFN-γ and IFN-γ associating H3K4me3 was decreased after treatment than before treatment (all P<0.05). (3)Expression of T-bet protein and binding levels of Ash2L and Jmjd3 with IFN-γ gene were significantly higher in KD group than those in control group(all P<0.05), higher in KD-CAL⁺ group than those in KD-CAL^- group (all P<0.05). These parameters were significantly lower after treatment than before treatment (all P<0.05). Binding level of Ezh2 with IFN-γ gene was similar among various groups (all P>0.05). (4)In comparison with control or after treatment, surface receptors(IFN-γR1/2, IL-12Rβ1/2, IL-18Rα/β, TNFR1 and TLR4) and its downstream molecules(pSTAT1, pSTAT4, RIP₁ and MyD88) in CD4⁺ T cells, and plasma concentrations of inflammatory cytokines(IFN-γ, IL-12, IL-18 and TNF-α) were found to be higher in KD group(all P<0.05). These parameters were also higher in KD-CAL⁺ group than in KD-CAL^- group (all P<0.05). Conclusion Aberrant histone methylation of IFN-γ associating H3K4me3 and H3K27me3 caused by over-binding of Ash2L and Jmjd3 might be involved in immune dysfunction and vascular damage in KD in the acute phase.