1.Efficacy and immune of gamma globulin in treatment of dilated cardiomyopathy complicating heart failure *
Xinling MO ; Fusheng XIE ; Guangdao HOU
Chongqing Medicine 2013;(27):3249-3250,3254
Objective To observe the anti-cardiac myosin heavy chain IgG changes and efficacy of the antibody titration during the treatment of dilated cardiomyopathy (DCM ) complicating heart failure by a large number of gamma globulin .Methods 28 inpa-tients with dilated cardiomyopathy complicating heart failure were taken as the experimental group ,28 cases of healthy examination as the control group .The anti-cardiac myosin heavy chain IgG antibodies were detected by ELISA ;moreover ,among the patients with heart failure treated by the conventional therapy ,14 cases were selected and added large dose of gamma globulin for observing the curative effect .The remaining 14 cases were taken as the standard control group of this experiment .The anti-cardiac myosin heavy chain IgG antibodies were detected by ELISA .Results The anti-cardiac myosin heavy chain IgG antibodies before gamma globulin therapy in the DCM complicating heart failure group had statistical difference compared with the healthy examination goup (P<0 .05);in the 14 cases of heart failure treated by large dose of gamma globulin ,11 cases (78 .57% ) in the treatment group were improved ,while 5 cases(35 .71% ) in the standard control group were improved ,the anti-cardiac myosin heavy chain IgG antibody had no significant differences between the gamma globulin treatment group and the healthy examination group .The left ventricular ejection fraction(LVEF) in the gamma globulin treatment group was increased from (36 .12 ± 9 .98)% to (46 .15 ± 12 .18)% ,the left ventricular end-diastolic diameter was decreased from (59 .68 ± 9 .60) mm to (50 .05 ± 10 .20) mm ,the effects after gamma glob-ulin treatment were more significant than the conventional traditional control group .Conclusion Large dose of gamma globulin for treating dilated cardiomyopathy complicating heart failure has more significant effect than the traditional method ,reduces the titra-tion of in vivo anti-cardiac myosin heavy chain IgG antibody and contributes to explain the drug action mechanism from immune mechanism .
2.Effects of myocardial PPAR-gamma expression change on reperfusion arrhythmias in ischemia/reperfusion rats
Hua CHEN ; Xinling MO ; Xueshu HE ; Ting XIE
Chongqing Medicine 2017;46(17):2313-2315
Objective To investigate the effects of PPAR-gamma expression on reperfusion arrhythmias in different precon ditioning myocardial ischemia/reperfusion(I/R) animal model.Methods Thirty-two SD rats were randomly divided into 4 groups(n =8):rosiglitazone+ I/R group (ROS group),GW9662 + I/R group(GW group),I/R group and sham group (Sham group).The I/ R animal model was constructed by ligation of the left anterior descending coronary artery,with ischemia for 30 min and reperfusion for 120 min.The dynamic limb Ⅱ lead electrocardiogram monitoring was performed;PPAR-gamma mRNA was detected by fluorescent quantitative PCR and the change of PPAR-gamma protein expression was detected by Western blot.Results The increasing range of QRS wave width detected before operation,at 30 min of ischemia,at 1,2 h of reperfusion from large to small were in turn the ROS group,I/R group,GW group and Sham group;the reperfusion arrhythmia score in the ROS group was significantly higher than that in the other groups(P<0.05),while the GW group was relatively reduced.The expression level of PPAR-gamma mRNA in the ROS group detected by fluorescent quantitative PCR was significantly up-regulated(P<0.05),while which in the GW group was down-regulated compared with the I/R group and ROS group(P<0.05).The expression of PPAR-gamma protein was similar to that of PPAR-gamma mRNA.Conclusion Up-regulation of myocardial PPAR-gamma expression may increase the occurrence of reperfusion arrhythmias in myocardial I/R animal model.
3.Relationship of serum levels of homocysteine,cystain-C and serum uric acid with carotid atherosclerosis in H-type hypertension patients
Ting XIE ; Xueshu HE ; Xiheng YANG ; Rixin DAI ; Xinling MO
Tianjin Medical Journal 2015;(6):620-623
Objective To investigate the relationship of serum levels of homocysteine, cystain C and uric acid with ca?rotid atherosclerosis in H-type hypertension patients. Methods A total of 132 H-type hypertension patients were collected to be studied. Their carotid intima-media thickness (IMT) was measured by Doppler ultrasonography. And according to the result of carotid artery atherosclerosis, all patients were divided into normal cIMT group (n=40),thickened cIMT group (n=43) and plague formation group (n=49). Their serum Hcy, Cyst-C, UA, blood glucose, blood lipid, blood urea nitrogen and se?rum creatinine were compared among three group and their relationship with cIMT were analyzed. Logistic regression was used to screen risk factors for carotid atherosclerosis. Results There was no significant difference in serum levels of blood glucose,blood urea nitrogen, creatinine, serum creatinine (Scr), triglyceride (TG), total cholesterol (TC), low density lipppro?tein cholesterol (LDL-c) among these three groups (P>0.05). The level of high-density lipoprotein (HDL-c) in thickened cIMT group was higher than that in plague formation group, and lower than normal cIMT group, while both serum levels of Cyst-c and UA were lower in thickened cIMT group than those in plague formation group but higher than those in normal cIMT group (P<0.05). In addition, serum level of Hcy in normal cIMT group was higher than that in thickened cIMT group and plague formation group. The cIMT grade was positively correlated with serum levels of Hcy, Cyst-C and UA (r=0.26, 0.30, 0.23, P<0.05), but was negative correlated with HDL-c(r=-0.38, P<0.05). Further more, Logistic regression analy?sis showed that Hcy,Cyst-C and UA were independent risk factors for cIMT. Conclusion Serum levels of Hcy, Cyst-C and UA are closely related to the cIMT,which indicates that they are independent risk factors of cIMT and may be used as mark?ers in judging the developments and preventions of arteriosclerosis.
4.Effects of PPARγon malignant arrhythmia in myocardial ischemia/reperfusion model rats
Xueshu HE ; Xinling MO ; Hua CHEN ; Ting XIE
Tianjin Medical Journal 2015;43(5):488-490
Objective To investigate the effects of peroxisome proliferator activated receptor gamma (PPARγ) on malignant arrhythmia in myocardial of ischemia/reperfusion(I/R) rats. Methods Twenty-four SD rats were randomly divided into four groups:Sham group, I/R group, rosiglitazone (ROS) group and PPARγ inhibitor GW9662 (GW) group. The myocardial I/R injury was induced by ligation of the left anterior descending coronary artery, with ischemia for 30 min and reperfusion for 2 h. The whole process limb Ⅱ lead electrocardiogram was applied to observe the frequency of malignant arrhythmia and record the corrected changes of QT(QTc) interval. RT-PCR was used to detect the expression of PPARγ mRNA. Results There were 5 cases of malignant arrhythmia in ROS group, 2 in I/R and 1 in GW group, 0 was found in Sham group. There was a prolongation of the QTc interval in ROS group than the other groups after ischemic stage (P<0.05). Compared with I/R group and ROS group, the QTc intervals were shorten in ischemia 30 min and reperfusion process in GW group (P<0.05). Compared with sham group, the expression of PPARγ mRNA was significantly increased in other three groups (P<0.05). The expression level of PPARγ mRNA was the highest in ROS group. The expression level of PPARγ mRNA was reduced in GW group compared with that of I/R group and ROS group (P<0.05). Conclusion Over expression of PPARγ may lead to the occurrence of malignant arrhythmia in myocardial ischemia/reperfusion rats.
5.Effect of levcromakalim on ET-1 induced proliferation and expression of protein kinase C in vascular smooth muscle cells
Wenxin HUANG ; Biwen MO ; Yaozhong YANG ; Chunsheng FANG ; Zhonghua XIA ; Dihua PAN ; Tongtong XU ; Xinling MO
Chinese Journal of Clinical Pharmacology and Therapeutics 2002;0(06):-
AIM:To observe the effect of levcromakalim(Lev) on endthelin-1(ET-1) induced proliferation and the expression of protein kinase C(PKC) in cultured rat vascular smooth muscle cells(VSMCs).METHODS: VSMCs were isolated from rat aorta and were cultured with different concentrations of Lev in vitro after stimulated to proliferation by ET-1(10~(-8)(mol?L~(-1))).Vitality of VSMCs was detected by MTT;DNA replication was evaluated by 3H-TdR method.Flow cytometry was used to analyze cell cycle and apoptosis.The expression of PKC? protein and mRNA were determined by Western blot and reverse transcription-polymerase chain reaction(RT-PCR).RESULTS:Vitality of VSMCs and 3H-TdR intermingle rate were decreased(P
6.The value of 320 slice volume CT venography and ultrasound in diagnosis of lower extremity deep vein thrombosis
Junwei WANG ; Xinling CHENG ; Jianbo GAO ; Zhihui DONG ; Hua WANG ; Wei ZENG ; Peng GAO ; Zheheng MO
Journal of Practical Radiology 2016;32(10):1578-1581
Objective To study the value of 320 slice volume CT venography (CTV)and ultrasound in the diagnosis of lower limb deep vein thrombosis(DVT).Methods 51 patients with DVT confirmed by DSA were analyzed retrospectively,with comparing detection rate by direct method of CTV and ultrasound of the emboli in different parts of lower limb.Results In 5 1 patients,48 cases with DVTs were detected by CTV,including 124 thrombi,and 46 cases by ultrasound,finding 86 thrombi.CT diagnosed 34 pelvic deep vein thrombi,and ultrasound found 10.CT diagnosed 25 tibiofibular vein thrombi,and ultrasound found 5.CT diagnosed 2 femoral deep vein thrombi,and ultrasound found 1 1.Conclusion Direct method of CTV and ultrasound have high clinical value in the diagnosis of deep venous thrombosis,the former is better for the thrombosis in the pelvic deep veins and tibiofibular vein,while the latter is better for the thrombosis in the femoral deep vein.
7.Changes and clinical significance of correlated inflammatory factor and cytokine level following coronary stent implantation
Xinling MO ; Fusheng ME ; Jianyi ZHANG ; Quanzhong LI ; Zhonghua XIA ; Yaozhong YANG ; Dihua PAN
Chinese Journal of Tissue Engineering Research 2009;13(39):7763-7766
OBJECTIVE: To observe the correlated serum inflammatory factor and cytokine changes in patients with coronary stent implantation, and to explore the significance of these changes.METHODS: Chinese Journal Full-Text Database was retrieved with search terms of coronary artery disease, percutaneous coronary interventions, inflammation, intimal hyperplasia, apoptosis and platelet-derived growth factor from 1995 to 2008. The language was restrained Chinese. A total of 17 literatures were collected, which concerns the changes of correlated inflammatory factor and cytokine levels and its significance. The literatures were sorted according to research object, experimental grouping,sample collection, assay method, experimental result, as well as experimental conclusion. Simultaneously, the patients received coronary stent implantation was analyzed to explore the significance of inflammatory factor and cytokine changes.RESULTS: The dynamic changed serum inflammatory factor and cytokine in patients with coronary stent implantation may be associated with the following mechanisms:①Endothelial cells were easily damaged in the balloon dilatation or stent implantation,therefore, inflammatory mediators or inflammatory factors were exposed to blood circulation, which stimulating neutrophilic granulocytes and up-regulating leukocyte adhesion molecule CD11b expression. ②Many stimulus could arise nuclear factor induced inflammatory reaction, produce interleukin 6, and stimulate C-reactive protein generation. ③The level of angiotensin Ⅱ increased at several days following stent implantation, and heightened with time prolonged, the proliferation of angiotensin Ⅱ was regulated by platelet-derived growth factor. By increasing the expression of endothelin, the synthesis of endothelin was accelerated, the proliferation and migration of vascular smooth muscle cells was promoted, which ultimately resulted in atherogenesis, balloon damage also involved in this process, which may be one of the mechanisms of restenosis.CONCLUSION: The changes of correlated inflammatory factor and cytokine can be served as inflammatory reaction indexes;moreover, soluble CD40 ligand, C-reactive protein and matrix metalloproteinase 9 may be associated with in-stent restenosis.
8.Analysis of risk factors of contrast-induced acute kidney injury after cerebrovascular intervention
Yiming TAO ; Yuanhan CHEN ; Jialun LUO ; Zhilian LI ; Jiaqi XU ; Liyi MO ; Wei DONG ; Ruizhao LI ; Wei SHI ; Xinling LIANG
Chinese Journal of Cerebrovascular Diseases 2014;(12):624-629,672
Objective To investigate the related risk factors of contrast-induced acute kidney injury (CI-AKI)after cerebrovascular intervention. Methods The clinical data of 5423 patients performed cerebrovascular angiography and intervention at the Departments of Neurology and Neurosurgery,Guangdong People′s Hospital from January 2005 to December 2013 were analyzed retrospectively. The patients who underwent cerebrovascular angiography and intervention were evaluated and screened. A clinical history database was established. All the selected patients used iodixanol,an isotonic contrast agent. The occurrence of CI-AKI was used as an endpoint. The patients were divided into either a CI-AKI group or a non CI-AKI group. A multivariate Logistic regression model was used to analyze the risk factors associated with the occurrence of CI-AKI. Results A total of 4164 patients were finally enrolled,including 137 had CI-AKI. The incidence of CI-AKI was 3. 3%. The results of multivariate Logistic regression showed that age >60 years (OR,1. 965,95%CI 1. 244-3. 136),baseline estimated glomerular filtration rate (eGFR)<60mL/(min·1. 73 m2)(OR,4. 163,95%CI 2. 422-5. 873),diabetes (OR,3. 140,95%CI 1. 983-3. 902),and anemia (OR,1. 524,95%CI 1. 226 -3. 253)were the influencing factors for occurring CI-AKI after cerebrovascular angiography and intervention. Conclusion Chronic kidney disease (eGFR<60 mL/[min·1. 73 m2 ]),diabetes,anemia,and old age (age >60 years)are the independent risk factors for occurring CI-AKI after cerebrovascular angiography and intervention.
9.Kinetic metrics changes of FDG in key organs after chemo-immunotherapy in patients with locally advanced non-small cell lung cancer identified by total-body PET/CT dynamic imaging
Yiwen MO ; Hui LIU ; Yuan WEI ; Xinling LI ; Ruping LI ; Xu ZHANG ; Wei FAN
Chinese Journal of Nuclear Medicine and Molecular Imaging 2022;42(12):719-723
Objective:To evaluate the kinetic metrics changes of FDG in key organs after chemo-immunotherapy in patients with locally advanced non-small cell lung cancer (NSCLC) identified by total-body PET/CT dynamic imaging, and explore its potential biological significance.Methods:From August 2020 to March 2021, 16 patients (13 males, 3 females; age: 43-67 years) with locally advanced NSCLC who underwent total-body 18F-FDG PET/CT dynamic imaging in Sun Yat-sen University Cancer Center were retrospectively analyzed. ROIs of key organs were drawn at baseline and after chemo-immunotherapy to obtain the time-activity curves (TACs). The kinetic metrics, including K1, k2, k3 and metabolic rate of FDG (MR FDG), were fitted by the two-tissue compartment model. Paired t test or Wilcoxon signed rank test was used to compare the differences of FDG kinetic parameters in each organ before and after treatment. Results:Compared with baseline, SUV max of colon (3.23±1.29 vs 4.81±2.73), MR FDG ((2.77±1.96) vs 3.56(1.07, 9.89) μmol·100 g -1·min -1) of lungs, SUV max (2.16±0.27 vs 2.33±0.41), k3 ((0.008±0.002) vs (0.012±0.004) min -1) and MR FDG ((2.65±0.81) vs (3.76±1.59) μmol·100 g -1·min -1) of spleen, and SUV max (2.59±0.45 vs 4.49±2.73), k2 ((0.76±0.37) vs (1.27±0.66) min -1), k3 ((0.032±0.007) vs (0.066±0.029) min -1) and MR FDG ((5.14±1.44) vs (8.39±2.67) μmol·100 g -1·min -1) of bone marrow were increased after chemo-immunotherapy with significant differences ( t values: from -5.40 to 3.47, z=-2.02, all P<0.05). There were no significant differences of SUV max, k values and MR FDG in other organs ( t values: from -2.00 to 2.35, z values: from -1.45 to -0.05, all P>0.05). Conclusions:After chemo-immunotherapy, the activation of immune system may be manifested as the increase of FDG kinetic rate constants in spleen and bone marrow. The lung and colon may be target organs for immune-related adverse effects.
10.Chaperone-mediated Autophagy Regulates Cell Growth by Targeting SMAD3 in Glioma.
Hanqun LIU ; Yuxuan YONG ; Xingjian LI ; Panghai YE ; Kai TAO ; Guoyou PENG ; Mingshu MO ; Wenyuan GUO ; Xiang CHEN ; Yangfu LUO ; Yuwan LIN ; Jiewen QIU ; Zhiling ZHANG ; Liuyan DING ; Miaomiao ZHOU ; Xinling YANG ; Lin LU ; Qian YANG ; Pingyi XU
Neuroscience Bulletin 2022;38(6):637-651
Previous studies suggest that the reduction of SMAD3 (mothers against decapentaplegic homolog 3) has a great impact on tumor development, but its exact pathological function remains unclear. In this study, we found that the protein level of SMAD3 was greatly reduced in human-grade IV glioblastoma tissues, in which LAMP2A (lysosome-associated membrane protein type 2A) was significantly up-regulated. LAMP2A is a key rate-limiting protein of chaperone-mediated autophagy (CMA), a lysosome pathway of protein degradation that is activated in glioma. We carefully analyzed the amino-acid sequence of SMAD3 and found that it contained a pentapeptide motif biochemically related to KFERQ, which has been proposed to be a targeting sequence for CMA. In vitro, we confirmed that SMAD3 was degraded in either serum-free or KFERQ motif deleted condition, which was regulated by LAMP2A and interacted with HSC70 (heat shock cognate 71 kDa protein). Using isolated lysosomes, amino-acid residues 75 and 128 of SMAD3 were found to be of importance for this process, which affected the CMA pathway in which SMAD3 was involved. Similarly, down-regulating SMAD3 or up-regulating LAMP2A in cultured glioma cells enhanced their proliferation and invasion. Taken together, these results suggest that excessive activation of CMA regulates glioma cell growth by promoting the degradation of SMAD3. Therefore, targeting the SMAD3-LAMP2A-mediated CMA-lysosome pathway may be a promising approach in anti-cancer therapy.