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Vascular endothelial growth factor


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Evaluation of recombinant human vascular endothelial growth factor VEGF121-loaded poly-l-lactide microparticles as a controlled release delivery system

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Vascular endothelial growth factor (VEGF) or vascular permeability factor (VPF) (Senger et al., 1983. Nowak et al., 2010). VEGF is a heparin-binding growth factor (Leung et al., 1989) and an effective mitogen for endothelial cells (Walsh et al., 2002). Taktak-Ben Amar et al., 2017), among which 2 cysteine residues contribute to. homodimer structure and the other six generate three- loop structures (Muller et al., 1997.

Hepatocellular Carcinoma: Targeted Therapy and Multidisciplinary P43

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Vascular anatomy of HCC, 288–290 arteriolar/venular angiogenesis, 288 coronal T1- weighted, contrast-enhanced. vascular endothelial cells, 288 vascular supply of HCC, 289f Vascular control during complex HCC. Vascular endothelial growth factor (VEGF f t–373t, 374 Vascular endothelial growth factor receptor. VEGF, see Vascular endothelial growth factor (VEGF).

Hepatocellular Carcinoma: Targeted Therapy and Multidisciplinary P39

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The epidermal growth factor receptor (EGFR) is frequently expressed in human HCC cell cultures and EGF may be one of the mitogens that are needed for cellu- lar proliferation. HER, human epidermal growth factor receptor. VEGF, vascular endothelial growth factor receptor. EGFR, epithelial growth factor receptor. HCC, hepatocellular carcinoma. PDGF, platelet-derived growth factor. EGFR/HER1 expression was detected in 88% of the patients in a Phase II study of erlotinib [20].

Hepatocellular Carcinoma: Targeted Therapy and Multidisciplinary P5

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El-Assal ON, Yamanoi A, Soda Y, Yamaguchi M, Igarashi M, Yamamoto A, Nabika T, et al (1998) Clinical significance of microvessel density and vascular endothelial growth factor expression in hepatocellular carcinoma and surrounding liver: possible involvement of vascular endothelial growth factor in the angiogenesis of cirrhotic liver.

A modular analysis of microglia gene expression, insights into the aged phenotype

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acute inflammatory response. negative regulation of cellular response to insulin stimulus response to interleukin-1 regulation of acute. negative regulation of phosphorus metabolic process. regulation of vascular endothelial growth factor production. adiponectin secretion regulation of adiponectin secretion negative regulation of. extrinsic apoptotic signaling pathway regulation of calcidiol 1-monooxygenase activity muscle cell proliferation. positive regulation of NF-kappaB transcription factor.

Chapter 007. Medical Disorders during Pregnancy (Part 1)

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Although the precise placental factors that cause preeclampsia are unknown, the end result is vasospasm and endothelial injury in multiple organs.. Excessive placental secretion of a soluble fms-like tyrosine kinase 1, a naturally occurring vascular endothelial growth factor antagonist, and decreased secretion of placental growth factor may contribute to the endothelial dysfunction, hypertension, and proteinuria observed in preeclampsia..

Chapter 106. Plasma Cell Disorders (Part 3)

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(Table 106-1) Multiple myeloma (MM) cells bind via cell-surface adhesion molecules to bone marrow stromal cells (BMSCs) and extracellular matrix (ECM), which triggers MM cell growth, survival, drug resistance, and migration in the bone marrow milieu (Fig. These effects are due both to direct MM cell–. BMSC binding and to induction of various cytokines including IL-6, insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), and stromal cell–derived growth factor (SDF)-1α.

Effects of propofol/remifentanil-based total intravenous anesthesia versus sevoflurane-based inhalational anesthesia on the release of VEGF-C and TGF-β and prognosis after breast cancer surgery: A prospective, randomized and controlled study

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TGF: Transforming growth factor;. TIVA: Total intravenous anesthesia. VEGF: Vascular endothelial growth factor. Effect of anesthetic technique on serum vascular endothelial growth factor C and transforming growth factor β in women undergoing anesthesia and surgery for breast cancer.. Cancer recurrence after surgery: direct and indirect effects of anesthetic agents. Effects of sevoflurane on breast cancer cell function in vitro.

Anti-PD-1 combined sorafenib versus antiPD-1 alone in the treatment of advanced hepatocellular cell carcinoma: A propensity score-matching study

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Recently, vascular endothelial growth factor (VEGF) was found to play a role in the tumor microenvironment.. Based on these data, this regimen become the first recommended combination therapy in the first line setting of advanced HCC.. When combined with anti-PD-1, sorafenib inhibited tumor growth by inducing effective natural killer cells [12].. These data suggested that sorafenib may be a potential candidate to combine with anti-PD-1..

Hepatocellular Carcinoma: Targeted Therapy and Multidisciplinary P38

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EGF, epidermal growth factor. VEGF, vascular endothelial growth factor. IGF-I, insulin-like growth factor-I. c-met, hepatocyte growth factor receptor. The impact of liver function and the etiology of liver failure, whose etiologic spectrum comprises entities as diverse as viral, toxic, and metabolic origins, has been extensively studied as part of the development of sorafenib and related targeted agents.

Comparative analysis of the effects of opioids in angiogenesis

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In conclusion, our work on the comparative analysis of four opioids in endothelial cells demonstrates that opioids have differential effects on angiogenesis and there is no common mechanism for their action. HUVEC: Human umbilical vein endothelial cell. VEGF: Vascular endothelial growth factor. EGFR: Epithelial growth factor receptor. endothelial growth factor receptor. Isolation of human umbilical vein endothelial cells (HUVEC).

Chapter 090. Bladder and Renal Cell Carcinomas (Part 5)

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VHL encodes a tumor-suppressor protein that is involved in regulating the transcription of vascular endothelial growth factor (VEGF), platelet- derived growth factor (PDGF), and a number of other hypoxia-inducible proteins.. Inactivation of VHL leads to overexpression of these agonists of the VEGF and PDGF receptors, which promote tumor angiogenesis and tumor growth. Agents that inhibit proangiogenic growth factor activity show antitumor effects.

CLINICAL USE OF PLATELET-RICH PLASMA IN ORTHOPAEDICS

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The following growth factors can be found in the environment of a blood clot:. Transforming growth factor beta (TGF-b. Platelet-derived growth factor (PDGF. Insulin-like growth factor (IGF). Vascular endothelial growth factors (VEGF. Epidermal growth factor (EGF). Fibroblast growth factor-2 (FGF-2).

Thông Tim, Mổ Tim và Làm Mọc Nhánh Mới

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Người ta dùng thuốc lọai kích thích tăng trưởng (growth factor), thí dụ như vascular endothelial growth factor (gọi tắt là VEGF), chích thẳng vào bắp thịt tim, hoặc là truyền thuốc vào máu để động mạch vành được kích thích mọc ra những nhánh mới để nuôi tim.

Chapter 103. Polycythemia Vera and Other Myeloproliferative Diseases (Part 5)

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Fibrosis in this disorder is associated with overproduction of transforming growth factor βand tissue inhibitors of metalloproteinases, while osteosclerosis is associated with overproduction of osteoprotegerin, an osteoclast inhibitor. Marrow angiogenesis occurs due to increased production of vascular endothelial growth factor (VEGF). Importantly, fibroblasts in chronic IMF are polyclonal and not part of the neoplastic clone.. No signs or symptoms are specific for chronic IMF.

Neurochemical Mechanisms in Disease P19

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Zhang Z, Chopp M (2002) Vascular endothelial growth factor and angiopoietins in focal cerebral ischemia. Zhang ZG, Zhang L, Jiang Q, Zhang R, Davies K, Powers C, Bruggen N, Chopp M (2000) VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain.

Chapter 061. Disorders of Granulocytes and Monocytes (Part 4)

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The endothelial responses (increased blood flow from increased vasodilation and permeability) are mediated by anaphylatoxins (e.g., C3a and C5a) as well as vasodilators such as histamine, bradykinin, serotonin, nitric oxide, vascular endothelial growth factor (VEGF), and prostaglandins E and I. In the healthy adult, most neutrophils leave the body by migration through the mucous membrane of the gastrointestinal tract.

Chapter 035. Hypoxia and Cyanosis (Part 1)

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The adaptations to hypoxia are mediated, in part, by the upregulation of genes encoding a variety of proteins, including glycolytic enzymes such as phosphoglycerate kinase and phosphofructokinase, as well as the glucose transporters Glut-1 and Glut-2. and by growth factors, such as vascular endothelial growth factor (VEGF) and erythropoietin, which enhance erythrocyte production..

Association of cerebrovascular dysfunction with the development of Alzheimer’s disease-like pathology in OXYS rats

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, vascular process in circulatory system, vasoconstriction, smooth muscle contraction, regulation of blood pressure, positive regulation of smooth muscle cell proliferation, regulation of angiogenesis, regulation of endothelial cell proliferation, regulation of vasoconstriction, positive regula- tion of endothelial cell proliferation, vascular endothelial growth factor receptor signaling pathway, regulation of smooth muscle cell proliferation according to DAVID and pathways: vascular smooth muscle

Prognostic value of endothelial biomarkers in refractory cardiogenic shock with ECLS: A prospective monocentric study

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Keywords: Extracorporeal membrane oxygenation, Angiopoietin, Vascular endothelial growth factor, Endothelial biomarker. Extracorporeal membrane oxygenation (ECMO) is often used in critical patients with severe myocardial failure (e.g., cardiogenic shock or myocarditis). However, despite the rapid advances in the ECMO tech- nique and post-operative care in recent decades, the mortality rate of patients on ECMO remains high [1 – 4].. prediction for patients on ECMO [1, 5, 6].