1.The expression of Wnt/beta-catenin signaling molecule in inflammatory bowel diseases treated with bone marrow mesenchymal stem cell transplantation
Yanfen XING ; Xuhong XIE ; Zhaohu YUAN ; Yejia CUI ; Yuyuan LI ; Yuqiang NIE ; Yaming WEI
Chinese Journal of Tissue Engineering Research 2015;(1):49-53
BACKGROUND:The Wnt/β-catenin signaling pathway is one of the most important signaling pathways in stem cel regulation, which is involved in regulation of cel proliferation and differentiation. OBJECTIVE:To investigate the expression of Wnt/β-catenin main signaling molecule in inflammatory bowel tissues treated with bone marrow mesenchymal stem cel transplantation. METHODS:2,4,6-Trinitrobenzene sulfonic acid was used for establishing inflammatory bowel diseases rat models. Bone marrow mesenchymal stem cels labeled with green fluorescent protein were transplanted into rat modelsviatail vein. Normal saline was injected as control. The expression of Wnt/β-catenin signaling molecule was detected in the large intestine tissue of inflammatory bowel disease rat models by quantitative RT-PCR at 14 and 28 days after transplantation. RESULTS AND CONCLUSION:Real-time quantitative PCR results showed that the expression of Wnt3a andβ-catenin in the inflammatory bowel tissue increased significantly (P < 0.05), while no difference in the expression of c-myc (P > 0.05). The expressions of Wnt3a, β-catenin and c-myc in the transplantation group were significantly lower than those in the control group after transplantation (P <0.05). These findings indicate that the Wnt/β-catenin signaling pathway plays important roles in inflammatory bowel disease and repair after bone marrow mesenchymal stem cel transplantation, while this pathway may promote stem cels differentiating into intestinal epithelium, promote recovery from inflammatory bowel disease, repair inflammatory area, and restore intestinal tissue homeostasis.
2.Evaluation of transesophageal echocardiography on the morphology and function of the left atrial appendage in nonvalvular atrial fibrillation
Xiaoxia WU ; Dongxing MA ; Lu ZHANG ; Fengyu ZHANG ; Yejia SHEN ; Yuezhi MENG ; Hong LI
Chinese Journal of Ultrasonography 2016;25(6):470-474
Objective To investigate the application value of the transesophageal echocardiography TEE in patients with nonvalvular atrial fibrillation about the size lobes morphology and function of left atrial appendage LAA Methods One hundred and forty-two patients underwent TEE were divided into nonvalvular atrial fibrillation group 98 cases and non atrial fibrillation group 44 cases The orifice diameter depth volume peak emptying velocity PEV of the LAA and the 1 eft atrial dimension LAD were measured The form and lobes of LAA thrombus and spontaneous echo contrast SEC in LAA were observed Results The LAA orifice diameter depth volume and LAD of patients with atrial fibrillation were significantly higher than those in the group without atrial fibrillation which showed statistical significance P < 0 05 Forty-one cases in atrial fibrillation group were found with the SEC and the number with thrombus in LAA was 22 The differences of PEV between chicken wings and non-chicken wings were statistically significant P <0 05 The SEC in LAA and the lobe number of LAA had no relevance Conclusions It was reliable to analyze the size morphologies lobes and hemodynamic parameters of LAA in patients with atrial fibrillation by TEE which provided reference for percutaneous LAA occlusion and anticoagulation therapy for the patients with atrial fibrillation.
3.Effect of atorvastatin on adventitial fibroblast phenotype differentiation in atherosclerosis of apolipoprotein E-knockout mice
Fang XU ; Ying LIU ; Jie QI ; Lei SHI ; Yejia HU ; Weichen WANG ; Hongjing CAI ; Wei LIU ; Yuling LI
Chinese Journal of Pathophysiology 2016;32(9):1599-1607
AIM: To explore the effect of atorvastatin on the expression of α-SMA and TGF-β1 in the adventi-tia of ApoE-/-mice with atherosclerosis, and to investigate the underlying mechanism of atorvastatin therapy.METHODS:Male ApoE-/-mice (n =40) at 6-weeks of age were used to establish the atherosclerosis model by feeding with high fat diet. The mice were randomly divided into model group and atorvastatin group.In atorvastatin group, the mice were lavaged with atorvastatin at dose of 20 mg? kg-1? d-1 .The mice in model group were given normal saline.C57BL/6 mice of the same age served as control group, feeding with ordinary food.The mice were respectively sacrificed at the time points of 10 and 15 weeks after feeding with different diets.The ascending aorta was removed for serial sectioning.Some sections were per-formed with Movat staining in order to observe the morphological changes of the tissues, and to measure the relative athero-sclerotic plaque area and the thickness of the adventitia.Some sections were stained with Sirius red to identify the collagen synthesis.Immunohistochemistry assay was prepared to observe the expression of α-SMA and TGF-β1 in the adventitia at different time points.The expression of TGF-β1 at mRNA and protein levels in the thoracoabdominal aorta was measured by RT-qPCR and Western blot.RESULTS: Compared with model group, the formation of plaque in atorvastatin group signifi-cantly descended.Meanwhile the adventitial thickness and collagen synthesis also decreased.The results of immunohisto-
chemical staining showed that compared with 10 weeks-model group, α-SMA and TGF-β1 in 15 weeks-model group was in-creased.The expression of α-SMA and TGF-β1 in atorvastatin group decreased significantly compared with model group. The expression of TGF-β1 at mRNA and protein levels in model group were higher than those in control group.They de-creased in atorvastatin group compared with model group.Compared with 10 weeks-model group, the mRNA and protein of TGF-β1 in 15 weeks-model group were increased.CONCLUSION: Atorvastatin modulates adventitial fibroblast phenotype differentiation by suppressing expression of TGF-β1 and intervenes atherosclerotic development in ApoE.
4.Analysis of Risk Factors for a Poor Prognosis in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis and Construction of a Prognostic Composite Score
Yejia MO ; Li WANG ; Libo ZHU ; Feng LI ; Gang YU ; Yetao LUO ; Meng NI
Journal of Clinical Neurology 2020;16(3):438-447
Background:
and Purpose: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most-common form of autoimmune encephalitis, but its early diagnosis is challenging.This study aimed to identify the risk factors for a poor prognosis in anti-NMDAR encephalitis and construct a prognostic composite score for obtaining earlier predictions of a poor prognosis.
Methods:
We retrospectively analyzed the clinical data, laboratory indexes, imaging findings, and electroencephalogram (EEG) data of 60 patients with anti-NMDAR encephalitis. The modified Rankin Scale (mRS) scores of patients were collected when they were discharged from the hospital. The mRS scores were used to divide the patients into two groups, with mRS scores of 3–6 defined as a poor prognosis. Logistic regression analysis was used to analyze independent risk factors related to a poor prognosis.
Results:
This study found that 23 (38.3%) and 37 (61.7%) patients had good and poor prognoses, respectively. Logistic regression analysis showed that age, disturbance of consciousness at admission, and ≥50% slow waves on the EEG were significantly associated with patient outcomes. An age, consciousness, and slow waves (ACS) composite score was constructed to predict the prognosis of patients with anti-NMDAR encephalitis at an early stage based on regression coefficients.
Conclusions
Age, disturbance of consciousness at admission, and ≥50% slow waves on the EEG were independent risk factors for a poor prognosis. The ACS prognostic composite score could play a role in facilitating early predictions of the prognosis of anti-NMDAR encephalitis.
5.Study on the effect of NNMT enzyme on iron death of hepatocellular carcinoma cells by mediating ROS
Jinchun WANG ; Yongqing DAI ; Yaqing WANG ; Jue CHEN ; Zuping LIU ; Yejia LI
China Modern Doctor 2024;62(23):30-34
Objective To explore the effect of nicotinamide transmethylase on intracellular reactive oxygen species(ROS)in iron death of hepatocellular carcinoma cells and its mechanism.Methods Methyl nicotinamide(MNA)expression in cells was detected using a tandem liquid chromatography-mass spectrometry.The average fluorescence intensity of ROS and lipid peroxidation was measured using a flow cytometer.Western blot was used to detect changes in the expression of human liver cancer cells(SK-Hep-1,Hep3B).Forty patients with primary hepatocellular carcinoma who received treatment in our hospital from March 2019 to February 2020 were selected as the study subjects,and their adjacent tissue samples and liver cancer tissue samples were collected.Immunohistochemical methods were used to detect the levels of nicotinamide N-methyltransferase(NNMT)and ROS in adjacent and liver cancer tissues.CCK-8 method was used to detect the survival activity of cells with different iron concentrations.Results The MNA levels in the liver cancer tissue group were higher than those in the adjacent tissue group(P<0.05).Compared with the adjacent tissue group,the average fluorescence intensity expression of ROS in the liver cancer tissue group increased,while the average fluorescence intensity expression of lipid peroxidation decreased(P<0.05).Compared with the adjacent tissue group,the expression levels of SK Hep-1 and Hep3B cells in the liver cancer tissue group increased(P<0.05).Compared with the control group,NNMT groups 2,10,20,and 25 μmol/L The cell survival activity level increased(P<0.05);Compared with the NNMT group,the iron inhibition group had different iron concentrations(2μmol/L,10μmol/L,20μmol/L,25μmol/L.The expression of cell viability decreased(P<0.05).Conclusion ROS mediated by nicotinamide methyltransferase can be guided to produce ROS and energy disorders,leading to increased tumor cell death.