1.Study on right ventricular function in patients with acute inferior wall myocardial infarction
Guanxue XU ; Bei SHI ; Changyin SHEN ; Ranzun ZHAO ; Gehong PENG
Chinese Journal of Geriatrics 2010;29(5):359-362
Objective To evaluate the right ventricular (RV) function in patients with acute inferior wall myocardial infarction ( AIMI ) with tissue Doppler imaging and M-mode echocardiography. Methods There were 50 cases of AIMI, 34 males and 16 females. And 50 healthy persons were as control group, 30 males and 20 males. From the echocardiographic apical 4- chamber views, the systolic, early and late diastolic motion (SD, DED, DAD) of the tricuspid annulus were recorded at the RV free wall with the use of two-dimentional guided M-mode recordings. Peak systolic, early and late diastolic velocities (Sm, Em, Am) of the tricuspid annulus were also recorded at the same site by tissue Doppler imaging. The ratios of DAD/DAD and Em/Am were calculated. Results SD, DED, Sm and Em of the tricuspid annulus at the RV free wall, as well as the ratios of DED/DAD and Em/Am, were reduced significantly in patients with AIMI as compared with health control [SD: (18.7±5.5) mmvs. (24.9±2.8) mm; DED: (10.9±3.4) mmvs. (16.6±3.4) mm;Sm: (12.9±2.8) cm/s vs. (15.9±2.7) cm/s; Em: (12.3±3.4) cm/s vs. (16.7±4.7) cm/s;DED/DAD: (1.5±0.6) vs. (2.3±0.9); Em/Am: (0.9±0.4) vs. (1.1±0.3); t=18.711,19. 055, 11. 851, 14. 781, 6.068, 2. 127; P<0. 01 or 0. 05, respectively]. There were no statistically significant differences in DAD and Am between two groups [DAD: (8. 8±1.9) mm vs. (7.7±2.1)mm; Am: (17.5±4.8) cm/s vs. (16.6±5.2) cm/s; t=0.414, 0.649; both P>0.05].Conclusions The systolic and diastolic functions of RV are impaired in patients with AIMI.
2.Effects of transplantation of peripheral blood mesenchymal stem cells with hypoxia preconditioning on postangioplasty restenosis in rabbits
Bei SHI ; Yan GUO ; Zhenglong WANG ; Dongmei WANG ; Changyin SHEN
Chinese Journal of Pathophysiology 1999;0(09):-
AIM: To investigate the function and the mechanism of transplanting bone marrow derived peripheral blood mesenchymal stem cells(PBMSCs) on restenosis after carotid balloon angioplasty in the model of carotid atherosclerosis rabbits,and to determine if the functions of PBMSCs are enhanced after hypoxia preconditioning.METHODS: Bone marrow cells were mobilized by granulocyte colony-stimulating factor(G-CSF),and PBMSCs were collected through density gradient centrifugation and adherent culture,labeled with enhancement type green fluorescent protein(EGFP) genes.All animals with carotid atherosclerosis stenosis were randomly divided into three groups: hypoxia preconditioning group(n=24,received intravenous transplantation of PBMSCs with hypoxia preconditioning),non-hypoxia preconditioning group(n=24,received normal culture of PBMSCs) and control group(n=24,only received equal-volume of culture medium).Vascular endothelial growth factor(VEGF) was determined by enzyme linked immunosorbent assay(ELISA) at 7 d,14 d and 28 d post-angioplasty,respectively.The vessel morphology,the homing of MSCs and the reendothelialization were analyzed with Weigert staining and immunohistochemistry.RESULTS: Compared to control group,the level of VEGF significantly increased in both hypoxia preconditioning group and non-hypoxia preconditioning group at all time points(P
3.Determination of Hesperidin in Jinshuiliujun Decoction by RP-HPLC
Shuhao GUO ; Xiaogang HU ; Yan BAI ; Yingshen SHEN ; Jie JIANG ; Changyin ZHAO ;
Chinese Traditional Patent Medicine 1992;0(12):-
Objective: The content of hesperidin in Jinshuiliujun Decoction (JSLJD) was determined by RP HPLC. Methods: The chromatographic column was Hyperisl BDS C 8(10?). The mobile phase was acetonitrile water containing 8% acetic acid (17∶83). The flow rate was 1.0 mL/min. The column temperature was 40 ?C and the detection wavelength was 284nm. The external standard and peak area method were used to determine hesperidin content. Results: There was a very good linear relationship between hesperidin and peak area when the sample injection was from 0.02 to 2.00?g. The average recovery of adding sample was 100.5% and RSD was 1.85%. Conclusions: This method is simple and believable. It can be effectively used for the quality control of JSLJD.
4.Experiment of effects of HMGB-1 combined with MSCs transplantation on cardiac function in rats with acute myocardial infarction
Yifeng TANG ; Bei SHI ; Dongmei WANG ; Changyin SHEN
Chongqing Medicine 2018;47(12):1583-1588
Objective To investigate the effects and mechanisms of HMGB-1 combined with MSCs transplantation on the heart function in rat with acute myocardial infarction.Methods A total of 144 male SD rats were divided into the healthy control group,model control group,MSCs transplantation group,HMGB-1 injection group,HMGB-1 injection+ MSCs transplantation group,HMGB-1 BoxA injection+MSCs transplantation group.On the 28th day after surgery,the heart function,myocardial pathological section,myocardial infarction area and new vessel density in infarction area were detected.Andthe level of related serum cytokines were measured on the 3rd,7th and 28th days after surgery.Results On the 28th day after surgery,left ventricular end diastolic dimension (LVDd) and left ventricular iiaternal diameter at end-systole (LVDs) in the HMGB-1 injection+ MSCs transplantation group were significantly decreased and the fractional shortening (FS) and ejection fraction (EF) value were significantly increased compared with the other five groups (P<0.05);the infarction area in the HMGB-1 injection+MSCs transplantation group was significantly decreased and the new vessels number in the infarction area was significantly increased compared with the other model groups (P<0.05).On the 3rd and 7th days after surgery,serum TLR4 and VEGF levels in the HMGB-1 injection+MSCs transplantation group were the highest (P<0.05).On the 7th and 28th days after surgery,the levels of serum IL-6,NF-κB and TNF-α in the HMGB-1 injection+MSCs transplantation group were the lowest among all groups (P<0,05).Conclusion HMGB-1 injection combined with MSCs transplantation treatment can effectively improve the prognosis of myocardial infarction.
5.Long-term follow-up of stage 1-2 neuroblastoma
Ci PAN ; Anan ZHANG ; Qidong YE ; Min ZHOU ; Huiliang XUE ; Jing CHEN ; Changyin LUO ; Shuhong SHEN ; Jiangmin WANG ; Yanjing TANG ; Jingyan TANG
Journal of Clinical Pediatrics 2014;(5):410-412
Objectives To evaluate the clinical features, treatment scheme and long-term outcomes of stage 1、2 childhood neuroblastoma (NB). Methods The retrospective study included 49 newly diagnosed NB stage 1、2 patients from June 1998 to December 2010. Clinical data and long-term outcomes were analyzed. Results Twenty-four patients with stage 1 NB and twenty patients with stage 2 NB were found among all 237 patients with NB enrolled in this study. The median age at diagnosis was 25 months( 2 week to 9 year old),29 males and 20 females. Thirty-one patients (63.6%) without symptoms were discovered with tumor by physical or imaging examination. Thorax and abdomen were the most common sites of primary tumor (21 and 22 cases, accounting for 42.9% and 44.9% of all patients, respectively). Forty (81.6%) NB patients had favorable pathology classification. One patient was of MYCN amplification status. Urine vanilla mandelic acid was normal in 32 (91.4%) patients, and serum lactate dehydrogenase was less than five times of the normal value in all patients. Ten NB patients were treated ac-cording to the low-risk protocol who received surgery alone.Thirty-nine patients were treated according to intermediate-risk protocol who received both surgery and chemotherapy. All the patients achieved very good partial remission (100%).The medi-an follow-up period was 60 months(22 months to148months). Nine patients were lost after a follow up of 3 months in medi-an. The 2-、3-、5-year event free survival and overall survial of all 49 patients was 100%. Conclusions The prognosis for neu-roblastoma of stage 1、2 in this study was with 100%survival, which provides opportunity for further reduction of dosage and/or duration of episodes in chemotherapy.
6. Optical coherence tomographic analysis of in-stent neoatherosclerosis in lesions with restenosis after drug-eluting stent implantation
Zhijiang LIU ; Bei SHI ; Chancui DENG ; Guanxue XU ; Ranzun ZHAO ; Changyin SHEN ; Zhenglong WANG ; Hanlin LIU
Chinese Journal of Cardiology 2018;46(1):44-49
Objective:
To explore the imaging characteristics and related influencing factors of in-stent neoatherosclerosis (ISNA) in patients with restenosis after drug-eluting stent(DES) implantation with optical coherence tomography(OCT).
Methods:
A total of 25 cases of coronary heart disease patients(DES placement time ≥8 months) with coronary artery angiography showing DES in-stent restenosis (ISR) in Zunyi medical college affiliated hospital from July 2013 to December 2015 were included in this study and patient's data were retrospectively analyzed.In these patients with ISR, OCT images were acquired before percutaneous coronary intervention. Patients were divided into the ISNA group (12 patients and 12 lesions) and non-ISNA group(13 patients and 13 lesions) according to the result of OCT. ISNA on OCT was defined as neointima formation with the presence of lipids or calcification.
Results:
(1) The incidence of chronic kidney disease and increased low-density lipoprotein cholesterol level in ISNA group were significant higher than that in non-ISNA group(all
7.Mechanisms by which Mettl3 regulates pericyte-myofibroblast transdifferentiation through PI3K/AKT signaling pathway
Yi DENG ; Yan WANG ; Pingping HE ; Jiao LI ; Weiwei LIU ; Jinsong YUAN ; Hongyan ZHAO ; Zhijiang LIU ; Changyin SHEN ; Bei SHI
Chinese Journal of Cardiology 2024;52(7):814-826
Objective:To investigate the role and underlying mechanisms of methyltransferase (Mettl) 3 in the process of angiotensin Ⅱ (Ang Ⅱ)-induced pericyte-to-myofibroblast transdifferentiation and renal fibrosis.Methods:C57BL/6J mice were used, in cell experiments, mouse renal pericytes were isolated and cultured using magnetic bead sorting. These pericytes were then induced to transdifferentiate into myofibroblasts with 1×10 6 mmol/L Ang Ⅱ, which was the Ang Ⅱ group, while pericytes cultured in normal conditions served as the control group. Successful transdifferentiation was verified by immunofluorescence staining, Western blotting, and real-time reverse transcription PCR (RT-qPCR) for α-smooth muscle actin (α-SMA). The levels of m6A modifications and related enzymes (Mettl3, Mettl14), Wilms tumor 1-associated protein (WTAP), fat mass and obesity protein (FTO), ALKBH5, YTHDF1, YTHDF2, YTHDC1, YTHDC2, YTHDC3 were assessed by Dot blot, RT-qPCR and Western blot. Mettl3 expression was inhibited in cells using lentivirus-mediated Mettl3-shRNA transfection, creating sh-Mettl3 and Ang Ⅱ+sh-Mettl3 groups, while lentivirus empty vector transfection served as the negative control (Ang Ⅱ+sh-NC group). The impact of Ang Ⅱ on pericyte transdifferentiation was observed, and the expression of downstream phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway proteins, including PI3K, AKT, phosphorylated AKT at serine 473 (p-AKT (S473)), and phosphorylated AKT at threonine 308 (p-AKT (T308)), were examined. PI3K gene transcription was inhibited by co-culturing cells with actinomycin D, and the half-life of PI3K mRNA was calculated by measuring residual PI3K mRNA expression over different co-culture time. The reversibility of Mettl3 inhibition on Ang Ⅱ-induced pericyte-to-myofibroblast transdifferentiation was assessed by adding the AKT activator SC79 to the Ang Ⅱ+sh-Mettl3 group. In animal experiments, mice were divided into these groups: sham group (administered 0.9% sterile saline), Ang Ⅱ group (infused with Ang Ⅱ solution), sh-Mettl3 group (injected with Mettl3 shRNA lentivirus solution), Ang Ⅱ+sh-Mettl3 group (infused with Ang Ⅱ solution and injected with Mettl3 shRNA lentivirus solution), and Ang Ⅱ+sh-Mettl3+SC79 group (administered Ang Ⅱ solution and Mettl3 shRNA lentivirus, with an additional injection of SC79). Each group consisted of six subject mice. Blood pressure was measured using the tail-cuff method before and after surgery, and serum creatinine, urea, and urinary albumin levels were determined 4 weeks post-surgery. Kidney tissues were collected at 28 days and stained using hematoxylin-eosin (HE) and Masson′s trichrome to assess the extent of renal fibrosis. Results:Primary renal pericytes were successfully obtained by magnetic bead sorting, and intervened with 1×10 6 mmol/L Ang Ⅱ for 48 hours to induce pericyte-to-myofibroblast transdifferentiation. Dot blot results indicated higher m6A modification levels in the Ang Ⅱ group compared to the control group ( P<0.05). RT-qPCR and Western blot results showed upregulation of Mettl3 mRNA and protein levels in the Ang Ⅱ group compared to the control group (both P<0.05). In the Ang Ⅱ+sh-Mettl3 group, Mettl3 protein expression was lower than that in the Ang Ⅱ group, with reduced expression levels of α-SMA, vimentin, desmin, fibroblast agonist protein (FAPa) and type Ⅰ collagen (all P<0.05). Compared to the control group, PI3K mRNA expression level was elevated in the Ang Ⅱ group, along with increased p-AKT (S473) and p-AKT (T308) expressions. In the Ang Ⅱ+sh-Mettl3 group, PI3K mRNA expression and p-AKT (S473) and p-AKT (T308) levels were decreased (all P<0.05). The half-life of PI3K mRNA was shorter in the Ang Ⅱ+sh-Mettl3 group than that in the Ang Ⅱ+sh-NC group (2.34 h vs. 3.42 h). The ameliorative effect of Mettl3 inhibition on Ang Ⅱ-induced pericyte-to-myofibroblast transdifferentiation was reversible by SC79. Animal experiments showed higher blood pressure, serum creatinine, urea, and 24-hour urinary protein levels, and a larger fibrosis area in the Ang Ⅱ group compared to the sham group (all P<0.05). The fibrosis area was smaller in the Ang Ⅱ+sh-Mettl3 group than that in the Ang Ⅱ group ( P<0.05), but increased again upon addition of SC79. Conclusion:Mettl3-mediated RNA m6A epigenetic regulation is involved in Ang Ⅱ-induced pericyte-to-myofibroblast transdifferentiation and renal fibrosis, potentially by affecting PI3K stability and regulating the PI3K/AKT signaling pathway.