Objective To investigate the role of p300 in lipid metabolism disorders.Methods Bioinformatics analysis was performed to analyze the expression patterns of p300 in lipid metabolism disorder-related diseases and its correlation with SREBP-1c and downstream lipid metabolic enzymes.Immunofluorescence assay was used to detect the expression of p300 in the liver tissues of the patients with varying disease severity of non-alcoholic fatty liver disease(NAFLD).A mouse model of lipid metabolism disorder was established in male C57BL/6J mice by feeding high-fat diet(HFD)for 12 weeks.Western blotting was employed to assess p300 expression level in the liver tissues of HFD-fed mice.A cell model of lipid metabolism disorder was established in HepG2/AML-12 cells induced with free fatty acid(FFA).The effects of siRNA-mediated knockdown of p300 was observed to measure the levels of intracellular total cholesterol(TC)and triglyceride(TG),lipid deposition,and production of reactive oxygen species(ROS).Results Clinically,p300 was highly expressed in lipid metabolism disorders,and its level was positively correlated with NAFLD severity(P<0.05).Gene Set Enrichment Analysis(GSEA)revealed that p300 expression was significantly associated with fatty acid metabolism,cholesterol homeostasis,lipogenesis,PPAR signaling pathway,and peroxisome pathway.In vivo,p300 was significantly up-regulated in the livers of HFD-fed mice(P<0.01).In vitro,FFA stimulation markedly increased p300 expression in both HepG2 and AML-12 cells(P<0.01),whereas p300 knockdown significantly reduced intracellular TG and TC levels(P<0.01),attenuated lipid droplet accumulation,and reversed FFA-induced ROS elevation(P<0.01).Furthermore,p300 expression was positively correlated with the expression of SREBP-1c and its downstream key lipid synthesis enzymes.Conclusion p300 may promote hepatic lipid accumulation by acetylating and activating SREBP-1c and regulating downstream lipid metabolic enzymes,thereby affecting lipid synthesis and oxidative stress.These findings suggest that p300 may be a potential therapeutic target for lipid metabolism disorder-related diseases.

Objective To investigate the CT and MRI findings of rhabdomyosarcoma(RMS).Methods A retrospective analysis was conducted on CT and/or MRI data of 19 cases of pathologically confirmed RMS.The growth location,morphology,density/sig-nal intensity,enhancement pattern,and infiltration scope of the lesions were analyzed.Results Among the 19 patients,12 lesions were located in the head and neck regions(sinuses,nasal cavity,masseter muscle,infratemporal fossa,nasopharynx,and gum),2 in the lower extremities,1 in the left heart,1 in the mediastinum,1 in the prostate,1 in the testicle,and 1 in the pelvis.On CT scans,the lesions appeared as homogeneously iso-or hypodensity compared to the muscle,with homogeneous or inhomogeneous enhancement on contrast-enhanced scans.On MRI,the lesions exhibited iso-or hypointense signals on T1WI and inhomogeneous hyperintense signals on T2WI,with inhomogeneous enhancement on contrast-enhanced scans.All lesions had irregular morphologies but clear boundaries,and no calcification or hemorrhage was observed within the lesions.Lesions in the sinuses often invaded adjacent sinus cavities or the nasal cavity and orbit,and some lesions could involve the intracranial cavity through the cranial base foramina.Bone destruction could occurred.Regional lymph node enlargement in the drainage area was observed in some cases.One case exhibited multiple osseous metastases.Conclusion RMS can occur in various parts of the body,with the head and neck being the most common site.Most cases lack specificity,but CT and MRI is helpful to understand the location of the disease,its invasion of surrounding tissues,and the presence of metastasis,thereby assisting in treatment and prognosis evaluation.

Objective To investigate the CT and MRI findings of rhabdomyosarcoma(RMS).Methods A retrospective analysis was conducted on CT and/or MRI data of 19 cases of pathologically confirmed RMS.The growth location,morphology,density/sig-nal intensity,enhancement pattern,and infiltration scope of the lesions were analyzed.Results Among the 19 patients,12 lesions were located in the head and neck regions(sinuses,nasal cavity,masseter muscle,infratemporal fossa,nasopharynx,and gum),2 in the lower extremities,1 in the left heart,1 in the mediastinum,1 in the prostate,1 in the testicle,and 1 in the pelvis.On CT scans,the lesions appeared as homogeneously iso-or hypodensity compared to the muscle,with homogeneous or inhomogeneous enhancement on contrast-enhanced scans.On MRI,the lesions exhibited iso-or hypointense signals on T1WI and inhomogeneous hyperintense signals on T2WI,with inhomogeneous enhancement on contrast-enhanced scans.All lesions had irregular morphologies but clear boundaries,and no calcification or hemorrhage was observed within the lesions.Lesions in the sinuses often invaded adjacent sinus cavities or the nasal cavity and orbit,and some lesions could involve the intracranial cavity through the cranial base foramina.Bone destruction could occurred.Regional lymph node enlargement in the drainage area was observed in some cases.One case exhibited multiple osseous metastases.Conclusion RMS can occur in various parts of the body,with the head and neck being the most common site.Most cases lack specificity,but CT and MRI is helpful to understand the location of the disease,its invasion of surrounding tissues,and the presence of metastasis,thereby assisting in treatment and prognosis evaluation.

Objective:To explore the effects and mechanism of anti IL-9 antibody on malignant ascites ( MA) of hepatic carci-noma in mice.Methods:A mouse model of MA was established by mouse H 22 cell line.45 mice were divided randomly into experi-mental group,negative control group and blank control group at 24 hours after modeling,with 15 mice in each group.The experimental group was injected intraperitoneally with anti IL-9 antibody;the negative control group was injected with isotype IgG antibody;the blank control group was injected with normal saline .The weight and behavior of the mice were measured before each injection .Five mice of each group was sacrificed at 24 hours after the last injection to measure the volume of MA .The level of VEGF,MMP-2,IL-9 and IFN-γin MA were determined with ELISA assay;the survival time of rest mice were recorded and compared .Results:The mean volume of MA of experimental group,negative control group and blank control group were (6.70±1.52)ml,(10.28±1.75)ml,(10.36±2.30) ml,respectively,the MA volume of experimental group were lower as compared to negative control group and blank control group ( P<0.05).The mean survival time of experimental group was (17.2±2.1)d,which was significantly prolonged compared with the negative control group (14.5±1.2)d and the blank control group (14.8±1.4)d (P<0.05).The levels of VEGF of MA in experimental group was significantly lower compared to the negative control group and blank control group (P<0.05).The levels of IL-9 of MA in experi-mental group was significantly lower compared to the negative control group (P<0.05).The levels of MMP-2 and IFN-γin experimental group had no significant difference compared with the negative control group and blank control group ( P>0.05 ) .Conclusion:Intraper-itoneal injection anti IL-9 antibody on H22 ascites-bearing mice can effectively inhibit the generation of the MA .The mechanism may be related to the inhibition of the expression of the VEGF and IL-9.

Objective:To investigate the effects and mechanisms of interleukin-22(IL-22) on inhibiting liver fibrosis induced by HSC,and explore the role of Wnt/β-catenin pathway in the activation of hepatic stellate cells(HSC).Methods:Rat HSC was activated by TGF-β1,and the mRNA and protein levels of β-catenin and α-SMA were detected by q-PCR and Western blot,respectively.HSC was treated with different hours and concentration of recombinant rat protein IL-22.The cell proliferation rates were detected by CCK8,cell apoptosis rates were tested by flow cytometry.HSC were treated with optimal concentration of IL-22 after activated by TGF-β1,the cell proliferation rates,mRNA and protein levels of β-catenin and α-SMA were compared of before and after intervention.Results:The mRNA and the protein levels of β-catenin and α-SMA were significantly increased after activated by TGF-β1(P<0.05).IL-22 inhibiting the proliferation of HSC in a dose-and time-dependent manner (P<0.05) and decreased the mRNA and the protein expression level of β-catenin and α-SMA(P<0.05),but had no significant effect on apoptosis rates(P>0.05).IL-22 significantly inhibited the activation of HSC induced by TGF-β1 and remarkably decreased the mRNA and the protein expression level of β-catenin and α-SMA(P<0.05).Conclusion:The Wnt/β-catenin pathway may participates in the process of HSC activation and α-SMA secretion,and IL-22 inhibits biological function of HSC in a dose-and time-dependent manner.This effect probably via inhibited the Wnt/β-catenin signal pathway.

Objective The purpose of this study was to explore the relationship between the loss of the gene deleted in colorectal carcinoma (DCC) gene expression in ovarian carcinoma and the transformation, progression of the tumor and its clinicopathological factors. Methods DCC gene mRNA expression were examined by reverse transcription polymerase chain reaction (RT-PCR) in 34 malignant, 10 benign and 10 normal ovarian samples. To clarify the expression of DCC gene by the DNA cloning and the DNA sequencing analysis in normal ovarian sample. Results The expression of DCC gene was lost in no normal ovarian tissues, in 2 (2/10) benign lesions, while the loss of DCC gene expression was found in 19(19/34,56%) carcinomas ( P