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The secondary laticifer differentiation in rubber tree is induced by trichostatin A, an inhibitor of histone acetylation

Shixin ZHANG,Shaohua WU,Weimin TIAN

《农业科学与工程前沿(英文)》 2016年 第3卷 第4期   页码 357-362 doi: 10.15302/J-FASE-2016125

摘要: The secondary laticifer, a specific tissue in the secondary phloem of rubber tree, is differentiated from the vascular cambia. The number of the secondary laticifer in the trunk bark of rubber tree is positively correlated with rubber yield. Although jasmonates have been demonstrated to be crucial in the regulation of secondary laticifer differentiation, the mechanism for the jasmonate-induced secondary laticifer differentiation remains to be elucidated. By using an experimental morphological technique, the present study revealed that trichostatin A (TSA), an inhibitor of histone deacetylation, could induce the secondary laticifer differentiation in a concentration-dependent manner. The results suggest that histone acetylation is essential for the secondary laticifer differentiation in rubber tree.

关键词: Hevea brasiliensis     histone acetylation     laticifer differentiation     trichostatin     vascular cambia    

Emerging roles of podoplanin in vascular development and homeostasis

null

《医学前沿(英文)》 2015年 第9卷 第4期   页码 421-430 doi: 10.1007/s11684-015-0424-9

摘要:

Podoplanin (PDPN) is a mucin-type O-glycoprotein expressed in diverse cell types, such as lymphatic endothelial cells (LECs) in the vascular system and fibroblastic reticular cells (FRCs) in lymph nodes. PDPN on LECs or FRCs activates CLEC-2 in platelets, triggering platelet activation and/or aggregation through downstream signaling events, including activation of Syk kinase. This mechanism is required to initiate and maintain separation of blood and lymphatic vessels and to stabilize high endothelial venule integrity within lymph nodes. In the vascular system, normal expression of PDPN at the LEC surface requires transcriptional activation of Pdpn by Prox1 and modification of PDPN with core 1-derived O-glycans. This review provides a comprehensive overview of the roles of PDPN in vascular development and lymphoid organ maintenance and discusses the mechanisms that regulate PDPN expression related to its function.

关键词: podoplanin     CLEC-2     Prox1     O-glycosylation     lymphatic vascular development and maintenance     lymphoid organ homeostasis    

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    

Crk-associated substrate, vascular smooth muscle and hypertension

TANG Dale

《医学前沿(英文)》 2008年 第2卷 第4期   页码 323-331 doi: 10.1007/s11684-008-0062-6

摘要: Hypertension is characterized by vascular smooth muscle constriction and vascular remodeling involving cell migration, hypertrophy and growth. Crk-associated substrate (CAS), the first discovered member of the adapter protein CAS family, has been shown to be a critical cellular component that regulates various smooth muscle functions. In this review, the molecular structure and protein interactions of the CAS family members are summarized. Evidence for the role of CAS in the regulation of vascular smooth muscle contractility is presented. Contraction stimulation induces CAS phosphorylation on Tyr-410 in arterial smooth muscle, creating the binding site for the Src homology (SH) 2/SH3 protein CrkII, which activates neuronal Wiskott-Aldrich syndrome protein (N-WASP)-mediated actin assembly and force development. The functions of CAS in cell migration, hypertrophy and growth are also summarized. Abelson tyrosine kinase (Abl), c-Src, focal adhesion kinase (FAK), proline-rich tyrosine kinase 2 (PYK2), protein tyrosine phosphatase-proline, glutamate, serine and threonine sequence protein (PTP-PEST) and SHP-2 have been documented to coordinate the phosphorylation and dephosphorylation of CAS. The downstream signaling partners of CAS in the context of cell motility, hypertrophy, survival and growth are also discussed. These new findings establish the important role of CAS in the modulation of vascular smooth muscle functions. Furthermore, the upstream regulators of CAS may be new biologic targets for the development of more effective and specific treatment of cardiovascular diseases such as hypertension.

关键词: Contraction stimulation     phosphatase-proline     molecular structure     discovered     hypertension    

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    

Progress in tumor vascular normalization for anticancer therapy: challenges and perspectives

null

《医学前沿(英文)》 2012年 第6卷 第1期   页码 67-78 doi: 10.1007/s11684-012-0176-8

摘要:

Antitumor angiogenic therapy has been shown promising in the treatment of several advanced cancers since the approval of the first antiangiogenic drug Avastin in 2004. Although the current antiangiogenic drugs reduce the density of tumor blood vessels and result in tumor shrinkage at the early stage of treatment, recent studies have shown that antiangiogenic therapy has transient and insufficient efficacy, resulting in tumor recurrence in patients after several months of treatment. Blockage of blood and oxygen supplies creates a hypoxic and acidic microenvironment in the tumor tissues, which fosters tumor cells to become more aggressive and metastatic. In 2001, Jain proposed tumor vascular normalization as an alternative approach to treating cancers based on the pioneering work on tumor blood vessels by several other researchers. At present, normalizing the disorganized tumor vasculature, rather than disrupting or blocking them, has emerged as a new option for anticancer therapy. Preclinical and clinical data have shown that tumor vascular normalization using monoclonal antibodies, proteins, peptides, small molecules, and pericytes resulted in decreased tumor size and reduced metastasis. However, current tumor vascular normalizing drugs display moderate anticancer efficacy. Accumulated data have shown that a variety of vasculogenic/angiogenic tumor cells and genes play important roles in tumor neovascularization, growth, and metastasis. Therefore, multiple-targeting of vasculogenic tumor cells and genes may improve the efficacy of tumor vascular normalization. To this end, the combination of antiangiogenic drugs with tumor vascular normalizing therapeutics, as well as the integration of Western medicine with traditional Chinese medicine, may provide a good opportunity for discovering novel tumor vascular normalizing drugs for an effective anticancer therapy.

关键词: angiogenesis     vasculogenesis     neovascularization     tumor     vasculature     normalization     traditional Chinese medicine    

sulfate promotes the formation of atherosclerotic lesions and induces plaque instability by targeting vascular

null

《医学前沿(英文)》 2016年 第10卷 第3期   页码 320-329 doi: 10.1007/s11684-016-0463-x

摘要:

Coronary atherosclerosis is a major complication of chronic kidney disease. This condition contributes to the increased mortality in dialysis patients. p-Cresyl sulfate (PCS) is a prototype of protein-bound uremic toxins that cannot be efficiently removed through routine dialysis procedures. In the present study, ApoE−/− mice that underwent 5/6 nephrectomy were randomly divided into two groups, namely, vehicle-treated group (n = 20) and PCS-treated group (n = 20). Mice were sacrificed for en face and immunohistological analyses after 8 or 24 weeks of high-fat diet. Rat aortic vascular smooth muscle cells (VSMCs) were treated with phosphate buffer solution or 500 µmol/L PCS for in vitro evaluation. PCS-treated mice were observed to suffer increased atherosclerotic lesions after eight weeks of PCS administration. Moreover, 24 weeks of PCS administration also markedly increased the vulnerability index of aortic plaques. PCS was also observed to facilitate the migration and proliferation of VSMCs during the progression of the disease. Moreover, PCS disturbed the balance between matrix metalloproteinases and tissue inhibitor of metalloproteinases within the plaques. Thus, PCS played a vital role in promoting atherogenesis and disturbing the stability of formed plaques probably by targeting VSMCs.

关键词: p-cresyl sulfate     atherosclerosis     plaque stability     vascular smooth muscle cell    

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

《医学前沿(英文)》 2017年 第11卷 第3期   页码 403-409 doi: 10.1007/s11684-017-0522-y

摘要:

Tissue factor pathway inhibitor (TFPI) is the main inhibitor of tissue factor-mediated coagulation. TFPI is expressed by endothelial and smooth muscle cells in the vasculature. Endothelium-derived TFPI has been reported to play a regulatory role in arterial thrombosis. However, the role of endogenous TFPI in vascular smooth muscle cells (VSMCs) in thrombosis and vascular disease development has yet to be elucidated. In this TFPIFlox mice crossbred with Sma–Cre mice were utilized to establish TFPI conditional knockout mice and to examine the effects of VSMC-directed TFPI deletion on development, hemostasis, and thrombosis. The mice with deleted TFPI in VSMCs (TFPISma) reproduced viable offspring. Plasma TFPI concentration was reduced 7.2% in the TFPISma mice compared with TFPIFlox littermate controls. Plasma TFPI concentration was also detected in the TFPITie2 (mice deleted TFPI in endothelial cells and cells of hematopoietic origin) mice. Plasma TFPI concentration of the TFPITie2 mice was 80.4% lower (P<0.001) than that of the TFPIFlox mice. No difference in hemostatic measures (PT, APTT, and tail bleeding) was observed between TFPISma and TFPIFlox mice. However, TFPISma mice had increased ferric chloride–induced arterial thrombosis compared with TFPIFlox littermate controls. Taken together, these data indicated that endogenous TFPI from VSMCs inhibited ferric chloride–induced arterial thrombosis without causing hemostatic effects.

关键词: arterial thrombosis     conditional knockout mice     tissue factor pathway inhibitor     vascular smooth muscle cells    

Alteration of heat shock protein 20 expression in preeclamptic patients and its effect in vascular and

Fanfan Li, Mengzhou He, Meitao Yang, Yao Fan, Yun Chen, Xi Xia, Yin Xie, Dongrui Deng

《医学前沿(英文)》 2018年 第12卷 第5期   页码 542-549 doi: 10.1007/s11684-017-0576-x

摘要:

Preeclampsia (PE) is a pregnancy-specific, multi-system disorder and the leading cause of maternal and perinatal morbidity and mortality in obstetrics worldwide. Excessive vasoconstriction and dysregulated coagulation function are closely associated with PE. Heat shock protein 20 (HSP20) is ubiquitously expressed under normal physiological conditions and has important roles in vascular dilatation and suppression of platelet aggregation. However, the role of HSP20 in the pathogenesis of PE remains unclear. In this study, we collected chorionic plate resistance arteries (CPAs) and serum from 118 healthy pregnant women and 80 women with PE and detected the levels of HSP20 and its phosphorylated form. Both HSP20 and phosphorylated HSP20 were downregulated in CPAs from women with PE. Comparison of the vasodilative ability of CPAs from the two groups showed impaired relaxation responses to acetyl choline in preeclamptic vessels. In addition to the reduced HSP20 in serum from women with PE, the platelet distribution width and mean platelet volume were also decreased, and the activated partial thromboplastin time and thromboplastin time were elevated. With regard to the vital roles of HSP20 in mediating vasorelaxation and coagulation function, the decreased HSP20 might contribute to the pathogenesis of PE.

关键词: preeclampsia     heat shock protein 20     vascular relaxation     coagulation-fibrinolytic system    

Visualization of vascular ultrastructure during osteogenesis by tissue engineering technique

ZHANG Kaigang, ZENG Bingfang, ZHANG Changqing

《医学前沿(英文)》 2007年 第1卷 第2期   页码 181-184 doi: 10.1007/s11684-007-0034-2

摘要: The aim of this paper was to observe and visualize the changes in osteoblasts by electron microscopy during osteogenesis using tissue engineering technique. We also studied the feasibility of improving tissue vascularization of th

关键词: feasibility     engineering     osteogenesis     vascularization     microscopy    

Effect of bradykinin on bradykinin-B2 receptor in rat aortic vascular smooth muscle cells and the involved

Wen YAN MD, Min FENG MD, Pei-Hua WANG MD, Dao-Wen WANG MD,

《医学前沿(英文)》 2010年 第4卷 第2期   页码 225-228 doi: 10.1007/s11684-010-0003-z

摘要: The aim of this paper is to study the effect of bradykinin (BK) on bradykinin-B2 receptor as well as the possible involved signal transduction pathways in cultured rat aortic vascular smooth muscle cells (VSMCs). Rat aortic VSMCs were cultured. Cells after 4–6 passages were used in the experiment. VSMCs were incubated with BK, BK+ B2 receptor inhibitor (HOE-140), BK+ MEK inhibitor (PD98059), BK+ mitogen-activated protein kinase (MAPK) inhibitor (apigenin), BK+ phosphoinositide 3-kinase (PI3K) inhibitor (LY294002), and BK+ Akt inhibitor to evaluate the expression of B2 receptor and phosphorylation of signaling molecules MAPK, Akt, and PI3K by Western blot. (1) BK markedly up-regulated the expression of B2 receptor in VSMC. (2) Apigenin, PD98059, Akt inhibitor, and LY294002 inhibited up-regulation of B2 receptor induced by BK. (3) Signal transduction pathways of MAPK and PI3K were involved in the up-regulation of B2 receptor by BK mediation. Results suggest that bradykinin can up-regulate the expression of B2 receptor in VSMCs.

关键词: bradykinin     vascular smooth muscle cells     signal transduction pathways    

The second short-term warm ischemia after vascular anastomosis did not affect early renal function recovery

null

《医学前沿(英文)》 2012年 第6卷 第3期   页码 329-331 doi: 10.1007/s11684-012-0211-9

摘要:

Ischemic postconditioning was defined as rapid intermittent interruptions of blood ?ow in the early phase of reperfusion, which has been found to be protective against renal ischemia-reperfusion injury (IRI) in animal models but not in clinical trials. We describe a case that the allograft renal vein was twisted because of the surgeon’s mistake, which caused the warm ischemia of allograft after reperfusion. The allograft restored blood flow without second reperfusion and cold preservation after 9 min of warm ischemia. The patient was followed up for 3 months and the allograft worked well without complications.

关键词: renal transplantation     vein twist     ischemia-reperfusion injury    

Stroke prevention: an update

null

《医学前沿(英文)》 2012年 第6卷 第1期   页码 22-34 doi: 10.1007/s11684-012-0178-6

摘要:

Stroke is a personal, familial, and social disaster. It is the third cause of death worldwide, the first cause of acquired disability, the second cause of dementia, and its cost is astronomic. The burden of stroke is likely to increase given the aging of the population and the growing incidence of many vascular risk factors. Prevention of stroke includes—as for all other diseases—a “mass approach” aiming at decreasing the risk at the society level and an individual approach, aiming at reducing the risk in a given subject. The mass approach is primarily based on the identification and treatment of vascular risk factors and, if possible, in the implementation of protective factors. These measures are the basis of primary prevention but most of them have now been shown to be also effective in secondary prevention. The individual approach combines a vascular risk factor modification and various treatments addressing the specific subtypes of stroke, such as antiplatelet drugs for the prevention of cerebral infarction in large and small artery diseases of the brain, carotid endarterectomy or stenting for tight carotid artery stenosis, and oral anticoagulants for the prevention of cardiac emboli. There is a growing awareness of the huge evidence-to-practice gap that exists in stroke prevention largely due to socio-economic factors. Recent approaches include low cost intervention packages to reduce blood pressure and cheap “polypills” combining in a single tablet aspirin and several drugs to lower blood pressure and cholesterol. Polypill intake should however not lead to abandon the healthy life-style measures which remain the mainstay of stroke prevention.

关键词: stroke     prevention     vascular risk factors     cerebral infarction     cerebral hemorrhage     anti-thrombotic drugs     carotid endarterectomy    

Beneficial effect of arginine vasopressin on hemorrhagic shock through improving the vascular reactivity

LI Tao, YANG Guangming, XU Jing, LIU Jiancang, LIU Liangming

《医学前沿(英文)》 2008年 第2卷 第3期   页码 248-254 doi: 10.1007/s11684-008-0047-5

摘要: The vascular reactivity and calcium sensitivity were decreased following hemorrhagic shock. Arginine vasopressin (AVP) was beneficial to endotoxic, infectious/septic and hemorrhagic shock. Our previous studies found that Rho kinase played an important role in the occurrence of calcium desensitization following shock. It was reported that AVP was with stimulation effect of Rho kinase. So we hypothesized that AVP might have beneficial effect on shock via activation of Rho kinase to regulate the calcium sensitivity and vascular reactivity. Hemorrhagic shock (40 mmHg for 2 h) Wistar rats were adopted to observe the effects of small dose of AVP on hemodynamics, 24-h survival rate, the pressor effect of norepinephrine (NE) and the contractility of superior mesenteric artery (SMA). Isolated SMAs from hemorrhagic shock rats were adopted to observe the effects of AVP on vascular reactivity and calcium sensitivity and its relationship to Rho kinase with an isolated organ perfusion system. The results show that AVP at the concentration of 0.1 U/kg and 0.4 U/kg significantly improved the hemodynamic parameters and the 24-h survival rate of hemorrhagic shock rats. Meanwhile, these dosages of AVP significantly increased the pressor effect of NE and the contractile response of SMA to NE. Y-27632 (3 ?g/kg), a Rho kinase specific inhibitor, abolished the beneficial effects of AVP. , the calcium sensitivity and vascular reactivity of SMA to calcium and NE were significantly decreased following hemorrhagic shock. AVP at the concentration of 0.5 nmol/L and 5 nmol/L significantly increased the calcium sensitivity and vascular reactivity. These effects of AVP were abolished by Y-27632 (10 ?mol/L). Taken together, the results suggest that AVP at 0.1 U/kg and 0.4 U/kg is beneficial to hemorrhagic shock by improving the vascular reactivity, which involves activation of Rho kinase.

Vein of Galen malformations - report of 2 cases and literature review

CAI Chunquan, ZHANG Qingjiang, SHEN Changhong

《医学前沿(英文)》 2008年 第2卷 第3期   页码 317-322 doi: 10.1007/s11684-008-0061-7

摘要: Vein of Galen malformations (VGMs) are rare, consisting approximately 1% of intracranial vascular malformations, but nearly one third of pediatric vascular malformations, which can cause severe morbidity and mortality in infants and older children, but more particularly in neonates. We presented 2 patients with VGMs which were confirmed by characteristic clinical symptoms and neuroradiological findings (including CT, MRI and/or angiography). One patient underwent embolization followed by CT, MRI and conventional angiography. The patient’s neurological and cognitive status was normal at present. The other neonate died of congestive heart failure 36 h after birth.

关键词: underwent embolization     angiography     pediatric vascular     cognitive     characteristic    

标题 作者 时间 类型 操作

The secondary laticifer differentiation in rubber tree is induced by trichostatin A, an inhibitor of histone acetylation

Shixin ZHANG,Shaohua WU,Weimin TIAN

期刊论文

Emerging roles of podoplanin in vascular development and homeostasis

null

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

Crk-associated substrate, vascular smooth muscle and hypertension

TANG Dale

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

Progress in tumor vascular normalization for anticancer therapy: challenges and perspectives

null

期刊论文

sulfate promotes the formation of atherosclerotic lesions and induces plaque instability by targeting vascular

null

期刊论文

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

期刊论文

Alteration of heat shock protein 20 expression in preeclamptic patients and its effect in vascular and

Fanfan Li, Mengzhou He, Meitao Yang, Yao Fan, Yun Chen, Xi Xia, Yin Xie, Dongrui Deng

期刊论文

Visualization of vascular ultrastructure during osteogenesis by tissue engineering technique

ZHANG Kaigang, ZENG Bingfang, ZHANG Changqing

期刊论文

Effect of bradykinin on bradykinin-B2 receptor in rat aortic vascular smooth muscle cells and the involved

Wen YAN MD, Min FENG MD, Pei-Hua WANG MD, Dao-Wen WANG MD,

期刊论文

The second short-term warm ischemia after vascular anastomosis did not affect early renal function recovery

null

期刊论文

Stroke prevention: an update

null

期刊论文

Beneficial effect of arginine vasopressin on hemorrhagic shock through improving the vascular reactivity

LI Tao, YANG Guangming, XU Jing, LIU Jiancang, LIU Liangming

期刊论文

Vein of Galen malformations - report of 2 cases and literature review

CAI Chunquan, ZHANG Qingjiang, SHEN Changhong

期刊论文