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乙酰肝素酶 1

心脏代谢 1

糖尿病性心肌病 1

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Effects of resistin on insulin signaling in endothelial cells

Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 136-140 doi: 10.1007/s11684-009-0029-2

摘要： The objective of this study was to investigate the effects of resistin on insulin signaling in human umbilical vein endothelial cells (HUVECs). HUVECs were incubated with recombinant human resistin (0-100 ng/mL) for 24 h. Akt and endothelial nitric oxide synthase (eNOS) phosphorylation levels of endothelial cells under basal or insulin stimulated conditions were measured by Western blot. Nitric oxide (NO) production of HUVECs was also detected. The results showed that resistin could significantly inhibit Akt and eNOS phosphorylation and NO production in endothelial cells under insulin stimulated conditions ( < 0.05 control). But under basal conditions, treatment with resistin could result in a decrease in eNOS phosphorylation ( < 0.05 control) but had no effect on NO production and Akt phosphorylation levels. These findings suggested that resistin exerted an inhibitory effect on NO production by inhibiting insulin signaling and eNOS phosphorylation in endothelial cells.

关键词： resistin     endothelium     nitric oxide     endothelial nitric oxide synthase     Akt-binding protein     mouse    

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Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 177-180 doi: 10.1007/s11684-009-0021-x

摘要： To evaluate the mechanism of vascular endothelial growth factor (VEGF) on the prevention of restenosis after angioplasty, the recombinant adenovirus vector containing hVEGF cDNA was constructed and transfected into vascular smooth muscle cells (VSMC) . The conditioned medium containing VEGF was collected 72 h after the infection. Then, the VSMC and human umbilical vein endothelial cells (HUVEC) were divided into control group, H O -treated group and H O +VEGF-treated group to observe the proliferation and apoptosis by water soluble tetrazolium (WST-1) method, nick end labeling (TUNEL) and flow cytometry (FCM). Compared with the control and H O +VEGF-treated groups, the absorbance ( ) value of HUVEC was decreased, and apoptosis of HUVEC was significantly increased in H O -treated group. The changes of value and apoptosis of VSMC were contrary to those of HUVEC. H O could stimulate the proliferation of VSMC and induce the apoptosis of HUVEC, inhibit the proliferation of HUVEC and the apoptosis of VSMC and induce restenosis. VEGF could inhibit the effect of H O on HUVEC and VSMC and prevent restenosis. These results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.

关键词： vascular endothelial growth factors     restenosis     reactive oxygen species     endothelial cells     vascular smooth muscle cell    

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Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 284-286 doi: 10.1007/s11684-009-0062-1

摘要： To evaluate the role of nitric oxide in the biological effects of vascular endothelial growth factor (VEGF) and the possible mechanism of VEGF, the cultured vascular endothelial cells of rabbit aorta were divided into control group, VEGF-treated group and VEGF+ -nitro-L-arginine methyl ester (L-NAME)-treated group. The absorbance () value of vascular endothelial cells and the levels of prostaglandin (PGI), endothelin-1 (ET-1) and von Willebrand factor (vWF) in the supernatant were observed by water-soluble tetrazolium salt assay, radioimmunoassay and enzyme-linked immunosorbent assay. The values and PGI in VEGF-treated group and VEGF+L-NAME-treated group were higher than those in control group (<0.05 and <0.01). The ET-1 and vWF were significantly decreased in VEGF-treated group and VEGF+L-NAME-treated group compared with the control (<0.05 and <0.01). These results indicate that VEGF could promote the proliferation and secretion of PGI and inhibit the secretion of ET-1 and vWF in vascular endothelial cells and that L-NAME could inhibit the effect of VEGF partially. Nitric oxide is an important mediator in the process of stimulating proliferation and regulating secretion of vascular endothelial cells by VEGF.

关键词： vascular endothelial growth factor     nitric oxide     N-nitro-L-arginine methyl ester     vascular endothelial cells    

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Effect of hyperlipidemia on endothelial VCAM-1 expression and the protective role of fenofibrate

WU Jun, LIN Jinchao, HE Zhaochu, OU Biru, GUO Haisen

《医学前沿（英文）》 2007年 第1卷 第4期   页码 356-358 doi: 10.1007/s11684-007-0068-5

摘要： The effect of hyperlipidemia and inflammation on endothelial functions was studied. The enrolled included control (basic chow), hyperlipidemia and fenofibrate-treated groups (high fat diet). The hyperlipidemia model was set up by four-week atherogenic diet, followed by a 16-week treatment in the fenofibrate-treated group (fenofibrate 40 mg/kg every day) and without treatment in the hyperlipidemia group, respectively. In the 20th week, serum lipid level and NO levels were measured, and the expression of vascular cell adhesion molecule-1 (VCAM-1) and cell adhesiveness in aortic endothelia observed by computer-aided system. Compared with the control group, hyperlipidemia rats showed lower levels of NO and ncreases in leukocyte accumulation on the endothelial surface, also stronger and more extensive endothelial expression of VCAM-1. In fenofibrate-treated group, the expression of VCAM-1 and leukocyte accumulation on the endothelial surface was decreased, while serum levels of NO were increased as compared with hyperli pidemia group. Hyperlipidemia can inhibit the NO activity and promote the damage of VACA-1 to aortic endothelia. Fenofibrate can effectively prevent the pathogenesis of atherosclerosis by restoring NO levels and down-regulating the VCAM-1 expression.

关键词： endothelial     16-week treatment     leukocyte accumulation     mg/kg     NO    

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Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

《医学前沿（英文）》 2021年 第15卷 第4期   页码 638-643 doi: 10.1007/s11684-021-0831-z

摘要： The COVID-19 pandemic has caused numerous deaths around the world. A growing body of evidence points to the important role of overwhelming inflammatory responses in the pathogenesis of COVID-19 and the effectiveness of anti-inflammation therapy against COVID-19 is emerging. In addition to affecting the lungs, COVID-19 can be a severe systemic inflammatory disease that is related to endothelial dysfunction. We are calling for closer attention to endothelial dysfunction in COVID-19 not only for fully revealing the pathogenic mechanism of COVID-19 but also for properly adjusting the strategy of clinical intervention.

关键词： COVID-19     endothelial dysfunction     inflammation reaction     cytokine storm    

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Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

《医学前沿（英文）》 2007年 第1卷 第2期   页码 196-199 doi: 10.1007/s11684-007-0037-z

摘要： The aim of this paper was to investigate the effects of resistin on human umbilical vein endothelial cells (HUVECs), and to explore its role and mechanism of action in atherosclerosis. HUVECs were incubated with recombinant human resistin (0, 50, 100 ng/mL) for 24 h. ICAM-1, VCAM-1 and reactive oxygen species (ROS) were assayed by flow cytometer. ET-1, eNOS and iNOS mRNA expression were measured by semi-quantitative RT-PCR. Incubation of HUVECs with resistin resulted in an increase in ICAM-1 expression and ET-1 mRNA expression. However, resistin had no effect on VCAM-1 expression and ROS release. eNOS and iNOS mRNA expression were not altered by resistin stimulation. Adipokine resistin exerted a direct effect in promoting HUVEC dysfunction by promoting ICAM-1 and ET-1 expression. These data suggest that adipocyteendothelium cross-talk might play an important role in the pathogenesis of cardiovascular disease in diabetes mellitus.

关键词： endothelial     resistin stimulation     Incubation     pathogenesis     dysfunction    

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lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

《医学前沿（英文）》 2023年 第17卷 第2期   页码 317-329 doi: 10.1007/s11684-022-0931-4

摘要： Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.

关键词： lncR-GAS5     miR-193-5p     splicing factor SRSF10     autophagy     atherogenesis    

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Relationship of endothelial nitric oxide synthase gene polymorphism with blood pressure, lipid profile

TANG Zhongzhi, LI Junyao, YANG Jianhong

《医学前沿（英文）》 2008年 第2卷 第2期   页码 178-181 doi: 10.1007/s11684-008-0033-y

摘要： To study the relationship of the polymorphism of endothelial nitric oxide synthase (eNOS) gene and blood pressure, lipid profiles and blood glucose level. By using PCR-RFLP, the eNOS Glu298Asp gene polymorphism was detected in 184 patients with essential hypertension and 196 matched healthy individuals with normal blood pressure. Taking into account eNOS Glu298Asp polymorphisms, the relationship of blood pressure with triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL) and blood glucose level was analyzed. The distribution of eNOS Glu298Asp polymorphism had no significant difference between different blood pressure groups and gender groups, but there was a significant difference between different age groups, diastolic blood pressure groups or BMI groups ( < 0.05). Asp/Asp genotype significantly increased the risk of hypertension in individuals with serum TC above 5.4 mmol/L ( = 0.03, = 2.65). eNOS Glu298Asp polymorphism and serum lipid could synergistically modulate the blood pressure. eNOS Asp/Asp genotype could significantly increase the risk of hypertension in individuals with serum TC over 5.4 mmol/L. eNOS Glu298Asp in combination with serum TC could be used to predict the risk of hypertension.
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CD176 single-chain variable antibody fragment inhibits the adhesion of cancer cells to endothelial cells

null

《医学前沿（英文）》 2016年 第10卷 第2期   页码 204-211 doi: 10.1007/s11684-016-0443-1

摘要：

CD176 (Thomsen-Friedenreich antigen) is a tumor-associated carbohydrate epitope (glycotope) functionally involved in blood spread and liver metastasis of cancer cells by mediating the adhesion of cancer cells to endothelial cells and hepatocytes, respectively. CD176 could be a promising target for antitumor immunotherapy. We applied B lymphocytes obtained from mice immunized with CD176 antigen and constructed a phage display library. A positive clone of CD176 single-chain variable antibody fragment (scFv) was successfully screened from this library. The CD176 scFv was expressed in Escherichia coli and purified. The purified scFv can bind to the natural CD176 expressed on the surface of cancer cells. Furthermore, the CD176 scFv inhibits the adhesion of CD176+ cancer cells to endothelial cells and hepatocytes. This CD176 scFv provides a basis for future development of recombinant CD176-specific antibodies that can be used in therapeutic application.

关键词： CD176     Thomsen-Friedenreich antigen     scFv     cancer     therapy     adhesion     metastasis    

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Non-genetic mechanisms of diabetic nephropathy

null

《医学前沿（英文）》 2017年 第11卷 第3期   页码 319-332 doi: 10.1007/s11684-017-0569-9

摘要：

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetes mellitus patients and is characterized by thickened glomerular basement membrane, increased extracellular matrix formation, and podocyte loss. These phenomena lead to proteinuria and altered glomerular filtration rate, that is, the rate initially increases but progressively decreases. DN has become the leading cause of end-stage renal disease. Its prevalence shows a rapid growth trend and causes heavy social and economic burden in many countries. However, this disease is multifactorial, and its mechanism is poorly understood due to the complex pathogenesis of DN. In this review, we highlight the new molecular insights about the pathogenesis of DN from the aspects of immune inflammation response, epithelial–mesenchymal transition, apoptosis and mitochondrial damage, epigenetics, and podocyte–endothelial communication. This work offers groundwork for understanding the initiation and progression of DN, as well as provides ideas for developing new prevention and treatment measures.

关键词： diabetic nephropathy     immune inflammatory response     epithelial–mesenchymal transition     apoptosis     mitochondrial damage     epigenetics     podocyte–endothelial communication    

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Surface modification of biomaterials by photochemical immobilization and photograft polymerization to improve hemocompatibility

Yakai FENG, Haiyang ZHAO, Li ZHANG, Jintang GUO,

《化学科学与工程前沿（英文）》 2010年 第4卷 第3期   页码 372-381 doi: 10.1007/s11705-010-0005-z

摘要： Thrombus formation and blood coagulation are serious problems associated with blood contacting products, such as catheters, vascular grafts, artificial hearts, and heart valves. Recent progresses and strategies to improve the hemocompatibility of biomaterials by surface modification using photochemical immobilization and photograft polymerization are reviewed in this paper. Three approaches to modify biomaterial surfaces for improving the hemocompatibility, i.e., bioinert surfaces, immobilization of anticoagulative substances and biomimetic surfaces, are introduced. The biomimetic amphiphilic phosphorylcholine and Arg-Gly-Asp (RGD) sequence are the most effective and most often employed biomolecules and peptide sequence for improving hemocompatibility of material surfaces. The RGD sequence can enhance adhesion and growth of endothelial cells (ECs) on material surfaces and increase the retention of ECs under flow shear stress conditions. This surface modification is a promising strategy for biomaterials especially for cardiovascular grafts and functional tissue engineered blood vessels.

关键词： biomimetic amphiphilic     amphiphilic phosphorylcholine     endothelial     functional     biomaterial    

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Pluripotent stem cells exhibiting similar characteristics can be isolated from human fetal bone marrow, heart, liver, muscle, lung, derma, kidney, and fat

FANG Baijun, SONG Yongping, LIN Quande, ZHAO Chunhua, SHI Mingxia

《医学前沿（英文）》 2007年 第1卷 第2期   页码 185-191 doi: 10.1007/s11684-007-0035-1

摘要： Previously, we reported that a cell population derived from human fetal bone marrow (BM), termed here Flk1CD34 postembryonic pluripotent stem cells (PPSCs) that have the characteristics of mesenchymal stem cells (MSCs), could differentiate into ectodermal, endodermal and mesodermal cell types at the single cell level , and that these cells could also differentiate into the epithelium of liver, lung, gut, as well as the hematopoietic and endothelial lineages after transplantion into irradiated non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice. In this study, we further isolated pluripotent stem cells from human fetal heart, liver, muscle, lung, derma, kidney, and fat and then analyzed the characteristics and function of these stem cells. It was found that the phenotype of the culture-expanded pluripotent stem cells from different fetal tissues was similar to BM-derived Flk1CD34 PPSCs, i.e. Flk1 and CD44 positive, GlyA, CD34, CD45, class I-HLA and HLA-DR negative. Morphologically, these cells were fibroblast-like and the doubling time was about 30 h. More importantly, culture-expanded pluripotent stem cells from all these fetal tissues were able to differentiate into cells with morphologic and phenotypic characteristics of adipocytes, osteocytes, neurons, glial cells and hepatocytes. These pluripotent stem cells with characteristics similar to fetal BM-derived Flk1CD34 PPSCs can be selected and cultured from tissues other than the BM. This phenomenon may help explain the stem cell plasticity found in multiple human tissues. In addition, as fetal BM-derived Flk1CD34 PPSCs, these pluripotent stem cells from different fetal tissues had the capacity for self-renewal and multi-lineage differentiation even after being expanded for more than 40 population doublings . Thus, they may be an ideal source of stem cells for treatment of inherited or degenerative diseases.

关键词： endothelial     phenomenon     ectodermal     Flk1CD34 postembryonic     irradiated non-obese    

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糖尿病发作后心脏脂蛋白脂肪酶的变化 Review

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

《工程（英文）》 2023年 第20卷 第1期   页码 19-25 doi: 10.1016/j.eng.2022.06.013

摘要：

由于心脏持续地收缩和舒张，需要大量的能量，其中脂肪酸（FA）是其三磷酸腺苷（ATP）的主要来源。但是，心脏无法制造这种底物，而是从多种来源获得脂肪酸，包括通过脂蛋白脂肪酶（LPL）的作用。脂蛋白脂肪酶在心肌细胞中产生，随后分泌到质膜上的硫酸乙酰肝素蛋白聚糖（HSPG）结合位点。然后为了将脂蛋白脂肪酶转移到内皮细胞管腔，糖基磷脂酰肌醇锚定的高密度脂蛋白结合蛋白1（GPIHBP1）与间质性脂蛋白脂肪酶结合，并将其转移到血管管腔，在那里脂蛋白脂肪酶可将循环中的甘油三酯分解为脂肪酸。内源性-β-葡萄糖醛酸酶乙酰肝素酶（Hpa）的独特之处在于，它是唯一已知的哺乳动物酶，可以裂解硫酸乙酰肝素，从而促进上述脂蛋白脂肪酶从心肌细胞HSPG中释放。在糖尿病中，一直认为心脏产生能量方式的改变是导致糖尿病性心肌病（DCM）的原因。糖尿病发展到中度后，随着葡萄糖利用率的降低，由于Hpa 作用的增强，心脏血管腔内的脂蛋白脂肪酶活性得到增强。虽然这种适应可能有助于补偿心脏对葡萄糖的利用不足，但从长期来看，它是具有毒性的，因为有害的脂质代谢物积聚，以及脂肪酸氧化增强和因此造成的氧化应激，最终导致细胞死亡。这与一种心脏保护生长因子——血管内皮生长因子B（VEGFB）的丧失同时发生。本文探讨了乙酰肝素酶、脂蛋白脂肪酶和血管内皮生长因子B之间的相互联系及其在糖尿病性心肌病中的潜在影响。鉴于缺乏基于机制的DCM治疗，了解这种心肌病的病理，以及脂蛋白脂肪酶的作用，将有助于我们推进其临床治疗。

关键词： 心脏代谢     脂蛋白脂肪酶     乙酰肝素酶     血管内皮生长因子     糖尿病性心肌病    

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Construction of eukaryotic expression vector of human arresten gene and its secreted expression in HEK 293 cells

Wei LI PhD , Siming GUAN MM , Zifang SONG PhD , Qichang ZHENG PhD , Jun XIONG PhD , Dan SHANG PhD , Xiaogang SHU PhD ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 297-302 doi: 10.1007/s11684-009-0058-x

摘要： The eukaryotic expression vector of human arresten gene was constructed and its secretive expression human embryonic kidney (HEK 293) cells was detected. Human arresten gene was amplified from recombinant plasmid pGEM-Arr by polymerase chain reaction (PCR), and then digested with restriction endonucleases I and I. The target fragment was inserted into the I and I restriction sites of eukaryotic expression vector pSecTag2 to construct pST-AT. Restriction analysis and DNA sequencing indicated that the arresten gene was successfully inserted into pSecTag2. The recombinant plasmid was subsequently transfected into HEK 293 cells with LipofectAMINETM2000 Reagent, and the expression of the target gene was detected. RT-PCR revealed that the mRNA of the target gene was transcribed in the transfected HEK 293 cells. Western Blot analysis verified that the recombinant protein in supernatants was correct. The supernatants of transfected cells were prepared, and 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay was carried out to assess their effect on the proliferation of human umbilical vein endothelial cells, which showed that the recombinant protein could significantly suppress the proliferation of human umbilical vein endothelial cells . These results provided a solid foundation to explore the usage of arresten in tumor anti-angiogenic gene therapy.

关键词： angiogenesis inhibitor     arresten     eukaryotic expression     HEK 293 cells     endothelial cells    

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

《医学前沿（英文）》 2009年 第3卷 第2期   页码 164-170 doi: 10.1007/s11684-009-0038-1

摘要： The invasion and metastasis of breast cancer are supposed to involve several stages in which epithelial-mesenchymal transition (EMT) is regarded as the mechanistic basis for the behavior of cancer cells. A series of factors related to EMT are apparently involved in such process. The current study aimed to investigate the contributions of EMT and related factors in lymph node metastasis of breast cancer. The expressions of E-cadherin (E-Cad), N-cadherin (N-Cad), vascular endothelial cell growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and CD34 were examined in 74 cases of breast cancer, including 39 cases with lymph node metastasis and 35 cases without lymph node metastasis by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients’ prognosis. The expressions of N-Cad, VEGF, MMP-9, and COX-2 in cases with lymph node metastasis were significantly higher than those without lymph node metastasis ( <0.05), while the E-Cad level was inversely related to status of lymph node metastasis ( <0.05). The metastasis rate of lymph node in the cases with EMT (lower E-Cad expression and higher N-Cad expression) was 78.3%, while that without EMT (higher E-Cad expression and lower N-Cad expression) was 11.1%. There was a statistical difference in the expression of COX-2 protein between histological grade I and grade II or III, respectively ( <0.05). In the cases with higher grade, the expression of E-Cad was decreased, while that of N-Cad was increased. Higher microvascular density (MVD) was also found to be significantly associated with lymphatic metastasis ( <0.05), and the cases with higher MVD had shorter survival time. This study indicates that EMT and expressions of VEGF, MMP-9 and COX-2, and MVD value are strongly correlated with lymph node metastasis in breast cancer.

关键词： epithelial-mesenchymal transition     vascular endothelial cell growth factor     matrix metalloproteinase-9     cyclooxygenase-2     higher microvascular density     breast cancer    

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标题 作者 时间 类型 操作

Effects of resistin on insulin signaling in endothelial cells

Zhizhen LI, Fangping LI, Jianhong YE, Li YAN, Zuzhi FU

期刊论文

Mechanism of vascular endothelial growth factor on the prevention of restenosis after angioplasty

Qigong LIU, Honglian ZHOU, Yan ZENG, Shan YE, Jiani LIU, Zaiying LU

期刊论文

Role of nitric oxide in biological effects of vascular endothelial growth factor

Qigong LIU M D , Yan ZENG , Jiani LIU , Shan YE , Yongdong LI , Zaiying LU M D ,

期刊论文

Effect of hyperlipidemia on endothelial VCAM-1 expression and the protective role of fenofibrate

WU Jun, LIN Jinchao, HE Zhaochu, OU Biru, GUO Haisen

期刊论文

Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

期刊论文

Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

LI Zhizhen, LI Fangping, YAN Li, LI Feng, LI Yan, CHENG Hua, FU Zuzhi

期刊论文

lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

期刊论文

Relationship of endothelial nitric oxide synthase gene polymorphism with blood pressure, lipid profile

TANG Zhongzhi, LI Junyao, YANG Jianhong

期刊论文

CD176 single-chain variable antibody fragment inhibits the adhesion of cancer cells to endothelial cells

null

期刊论文

Non-genetic mechanisms of diabetic nephropathy

null

期刊论文

Surface modification of biomaterials by photochemical immobilization and photograft polymerization to improve hemocompatibility

Yakai FENG, Haiyang ZHAO, Li ZHANG, Jintang GUO,

期刊论文

Pluripotent stem cells exhibiting similar characteristics can be isolated from human fetal bone marrow, heart, liver, muscle, lung, derma, kidney, and fat

FANG Baijun, SONG Yongping, LIN Quande, ZHAO Chunhua, SHI Mingxia

期刊论文

糖尿病发作后心脏脂蛋白脂肪酶的变化

Chae Syng Lee, Yajie Zhai, Brian Rodrigues

期刊论文

Construction of eukaryotic expression vector of human arresten gene and its secreted expression in HEK 293 cells

Wei LI PhD , Siming GUAN MM , Zifang SONG PhD , Qichang ZHENG PhD , Jun XIONG PhD , Dan SHANG PhD , Xiaogang SHU PhD ,

期刊论文

Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP-9, and COX-2 in breast cancer

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

期刊论文