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Filename: drivers/Session_files_driver.php
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Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/helpers/my_audit_helper.php
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Function: str_replace
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Objective: Mitomycin C (MMc) is an antibiotic that exerts a potent antiproliferative effect in tumor cells. Because the proliferation of vascular smooth muscle cells (VSMCs) plays a prominent role in the development of restenosis after percutaneous coronary interventions, the present study examined the effect of MMc on VSMC proliferation and on neointima formation after arterial balloon injury.
Methods And Results: Treatment of cultured rat aortic VSMCs with MMc (1 nmol to 30 micromol/L) inhibited VSMC proliferation in a concentration-dependent manner. Whereas high concentrations of MMc (1 to 30 micromol/L) induced VSMC apoptosis, as reflected by DNA laddering and caspase-3 activation, lower concentrations of MMc (1 to 300 nmol/L) directly inhibited VSMC growth by arresting cells in the G2/M phase of the cell cycle. The antiproliferative action of MMc was associated with a selective increase in the expression of the cyclin-dependent kinase inhibitor p21, and with a decrease in cyclin B1-cyclin-dependent kinase-1 complex activity. Finally, the local perivascular delivery of MMc immediately after balloon injury of rat carotid arteries induced p21 expression and markedly attenuated neointima formation.
Conclusions: These studies demonstrate that MMc exerts a potent inhibitory effect on VSMC proliferation and neointima formation after arterial injury. MMc represents a potentially new therapeutic agent in treating and preventing vasculoproliferative disease.
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http://dx.doi.org/10.1161/01.ATV.0000184779.01822.9d | DOI Listing |
J Surg Res
December 2024
Department of Vascular and Endovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Introduction: Neointimal hyperplasia is one of the persistent complications after vascular interventions, and is the major cause of treatment failure. Interleukin-33 (IL-33) emerges as a crucial factor in many biological processes and plays an important role in vascular diseases. Adventitial injection is catching attention for its effectiveness and fewer side effects.
View Article and Find Full Text PDFActa Pharmacol Sin
December 2024
Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, School of Food and Biological Engineering, Hefei University of Technology, Hefei, 230601, China.
Vascular smooth muscle cell (VSMC) phenotype transformation significantly contributes to vascular intimal hyperplasia. However, effective preventive and therapeutic measures are lacking. Colchicine, a binary alkaloid derived from Colchicum autumnale, is traditionally used for treating inflammatory diseases.
View Article and Find Full Text PDFClin Transl Med
December 2024
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Front Bioeng Biotechnol
November 2024
Division of Cardiovascular Surgery, Cardiac and Vascular Center, The University of Hong Kong-Shenzhen Hospital, Shenzhen, Guangdong, China.
Introduction: This study evaluates the efficacy of uncrosslinked porcine collagen coated vascular grafts (UPCCVG) in facilitating neointima formation and endothelialization.
Methods: Prior to coating, the uncrosslinked porcine collagen underwent comprehensive characterization employing SDS-PAGE, image analysis, circular dichroism and immunogenicity. The PET substrate of the vascular graft was coated with collagen solution utilizing the dip-coating method.
Biochem Biophys Res Commun
January 2025
Department of Cardiology, The First Hospital of Hebei Medical University, Shijiazhuang, 050031, Hebei, China; Hebei Key Laboratory of Heart and Metabolism, Shijiazhuang, 050031, Hebei, China. Electronic address:
We aim to explore the impact of Proprotein convertase subtilisin-kexin type 9 (PCSK9) and its inhibitor evolocumab on neointimal hyperplasia. Wild type and PCSK9 knockout (PCSK9) mice were subjected to ligation of the common carotid artery, with or without subcutaneous injection of evolocumab. Mouse aortic vascular smooth muscle (MOVAS) cells were pretreated with evolocumab or under siRNA-mediated suppression of PCSK9, and then exposed to platelet-derived growth factor type BB(PDGF-BB), a major promoter of MOVAS transformation to a proliferative phenotype.
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