Gotowe bibliografie tematyczne / Angiogenesis

Gotowa bibliografia na temat „Angiogenesis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 lipca 2024

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Artykuły w czasopismach na temat "Angiogenesis"

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Budhraja, Mridula, Rashmi Wardhan i Keerti Jain Behera. "Continuous Models of Tumor Induced Angiogenesis and Anti-Angiogenesis Strategy". Mathematical Journal of Interdisciplinary Sciences 2, nr 1 (2.09.2013): 57–75. http://dx.doi.org/10.15415/mjis.2013.21005.

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Lee, Hyun Ji, Yong Jun Hong i Miri Kim. "Angiogenesis in Chronic Inflammatory Skin Disorders". International Journal of Molecular Sciences 22, nr 21 (7.11.2021): 12035. http://dx.doi.org/10.3390/ijms222112035.

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Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.
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Tang, Jen-Yang, Yuan-Bin Cheng, Ya-Ting Chuang, Kun-Han Yang, Fang-Rong Chang, Wangta Liu i Hsueh-Wei Chang. "Oxidative Stress and AKT-Associated Angiogenesis in a Zebrafish Model and Its Potential Application for Withanolides". Cells 11, nr 6 (11.03.2022): 961. http://dx.doi.org/10.3390/cells11060961.

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Oxidative stress and the AKT serine/threonine kinase (AKT) signaling pathway are essential regulators in cellular migration, metastasis, and angiogenesis. More than 300 withanolides were discovered from the plant family Solanaceae, exhibiting diverse functions. Notably, the relationship between oxidative stress, AKT signaling, and angiogenesis in withanolide treatments lacks comprehensive understanding. Here, we summarize connecting evidence related to oxidative stress, AKT signaling, and angiogenesis in the zebrafish model. A convenient vertebrate model monitored the in vivo effects of developmental and tumor xenograft angiogenesis using zebrafish embryos. The oxidative stress and AKT-signaling-modulating abilities of withanolides were highlighted in cancer treatments, which indicated that further assessments of their angiogenesis-modulating potential are necessary in the future. Moreover, targeting AKT for inhibiting AKT and its AKT signaling shows the potential for anti-migration and anti-angiogenesis purposes for future application to withanolides. This particularly holds for investigating the anti-angiogenetic effects mediated by the oxidative stress and AKT signaling pathways in withanolide-based cancer therapy in the future.
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Zhu, Dandan, Ruth Muljadi, Siow Teng Chan, Patricia Vosdoganes, Camden Lo, Joanne C. Mockler, Euan M. Wallace i Rebecca Lim. "Evaluating the Impact of Human Amnion Epithelial Cells on Angiogenesis". Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4565612.

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The effects of human amnion epithelial cells (hAECs) on angiogenesis remain controversial. It is yet unknown if the presence of inflammation and/or gestational age of hAEC donors have an impact on angiogenesis. In this study, we examined the differences between term and preterm hAECs on angiogenesisin vitroandin vivo. Conditioned media from term hAECs induced the formation of longer huVEC tubules on Matrigel. Both term and preterm hAECs expressedVEGFA,PDGFB, ANGPT1,andFOXC1, which significantly increased after TNFαand IFNγstimulation. In the presence of TNFαand IFNγ, coculture with term hAECs reduced gene transcription ofTie-2andFoxc1in huVECs, while coculture with preterm hAECs increased gene transcription ofPDGFRαandPDGFRβand reduced gene transcription ofFOXC1in huVECs.In vivoassessment of angiogenesis using vWF immunostaining revealed that hAEC treatment decreased angiogenesis in a bleomycin model of lung fibrosis but increased angiogenesis in a neonatal model of hyperoxia-induced lung injury. In summary, our findings suggested that the impact of hAECs on angiogenesis may be influenced by the presence of inflammation and underlying pathology.
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Lazarov, Nikolai, i Faisal Saghir. "AN INSIGHT INTO ENDOMETRIOSIS: ROLE AND INFLUENCE OF THE PROCESS OF ANGIOGENESISS". Journal of IMAB - Annual Proceeding (Scientific Papers) 30, nr 1 (23.01.2024): 5323–27. http://dx.doi.org/10.5272/jimab.2024301.5323.

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Introduction: Endometriosis is one of the most common gynaecological disorders present in females. According to the implantation of ectopic endometrial tissue outside of the uterine cavity, angiogenesis is an essential prerequisite for the progression of the disease. The purpose is to provide insight and a better understanding of the role that angiogenetic factors play within endometriosis and how this can translate into more effective diagnostic and therapeutic approaches taken by medical specialists when treating this disease. Materials and methods: We conducted a review of the available scientific literature on PubMed, Google Scholar and Science Direct, which included randomized controlled trials, observational studies, prospective controlled studies and case reports. Results and Discussion: Our review of the scientific literature showed that the role of angiogenesis upon the development of endometrial ectopic tissue is very significant, and a positive relationship is established with an increase in neo-angiogenesis and a quicker rate of development of ectopic endometrial tissue. We also found data indicating that there are a multitude of angiogenetic and anti-angiogenetic factors functioning in a homeostatic manner to provide an optimal environment for the endometrial tissue to proliferate and for translocation for the implantation of the ectopic tissue within different locations both within the uterine cavity and distant anatomical locations and regions located outside of the uterine cavity. Conclusion: Recently, the research surrounding the process of angiogenesis is positive and positive correlations have been established between the role of angiogenesis and the extent to which the ectopic endometrial tissue proliferates.
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Aziz, Shiekh Aejaz. "Angiogenesis and Cancer". JMS SKIMS 12, nr 2 (13.12.2009): 32–33. http://dx.doi.org/10.33883/jms.v12i2.11.

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Tumors measuring 1-2 (mm)3 lack blood supply and neovascularization is a major process orchestrated by over-production and release of pro-angiogenic growth factors causing sequential step-wise formation of blood vessel capillaries in tumors.Moleculars mediators of tumors angiogenesis include VEGF family, IL-8, EGF receptor ligands, basic and acidic FGF, PDGF etc. There are natural endogenenous inhibitors of tumorigenesis (TSP-1,Vasostatin).Negative feedback mechanisms do exist to control/regulate tumor angiogenesis. Angiogeneis is detrimental to tumor progression favouring transition from hyperplasia to a neoplastic state, influencing cancer cell dissemination besides exerting an independent negative prognosis. Tumor vasculature is dysfunctional, heterogeneous in the tumor mass interms of density leading to a limited/retarded diffusion of drugs especially certain antibodies,gene therapy vectors, immune-effector cells through interstitium of these tumors. The hypoxic zones in tumors are the areas of resistance to the chemotherapy. Angiogenesis is upregulated in tumorigenesis leading to over-production of proangiogenic growth factors that have become targets for anticancer drug development. J Med Sci.2009;12(2):32-33
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Gammone, Maria A., Antonella Danese i Nicolantonio D’Orazio. "Anti-Angiogenetic Agents from the Sea: A New Potential Preventive and Therapeutic Wave?" Anti-Cancer Agents in Medicinal Chemistry 20, nr 17 (12.11.2020): 2005–11. http://dx.doi.org/10.2174/1871520620666200705215226.

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: Angiogenesis, generation of novel blood vessels from pre-existing ones, is a prerequisite for the physiological expansion, reparation, and functioning of body tissues and systems. However, it is also involved in some pathological inflammatory situations, such as oncologic and chronic degenerative disorders. The correct angiogenesis and neo-vascular response also accompanies wound healing, interaction with biocompatible materials, and tissue regeneration. : In this respect, natural products deriving from terrestrial and marine plants/organisms may prevent and even cure various angiogenesis-dependent disorders. : Bioactive natural compounds with antioxidant and anti-inflammatory activities could concur to maintain adequate vascularization and endothelial functions and inhibit angiogenesis, thus controlling tumor development. : This review aims to illustrate the role of some marine-derived compounds as anti-angiogenetic agents.
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Zhu, Jianlin, Lu Wang, Fan Liu, Jinghua Pan, Zhimeng Yao, Yusheng Lin, Yabing Yang i in. "Targeting PELP1 Attenuates Angiogenesis and Enhances Chemotherapy Efficiency in Colorectal Cancer". Cancers 14, nr 2 (13.01.2022): 383. http://dx.doi.org/10.3390/cancers14020383.

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Abnormal angiogenesis is one of the important hallmarks of colorectal cancer as well as other solid tumors. Optimally, anti-angiogenesis therapy could restrain malignant angiogenesis to control tumor expansion. PELP1 is as a scaffolding oncogenic protein in a variety of cancer types, but its involvement in angiogenesis is unknown. In this study, PELP1 was found to be abnormally upregulated and highly coincidental with increased MVD in CRC. Further, treatment with conditioned medium (CM) from PELP1 knockdown CRC cells remarkably arrested the function of human umbilical vein endothelial cells (HUVECs) compared to those treated with CM from wildtype cells. Mechanistically, the STAT3/VEGFA axis was found to mediate PELP1-induced angiogenetic phenotypes of HUVECs. Moreover, suppression of PELP1 reduced tumor growth and angiogenesis in vivo accompanied by inactivation of STAT3/VEGFA pathway. Notably, in vivo, PELP1 suppression could enhance the efficacy of chemotherapy, which is caused by the normalization of vessels. Collectively, our findings provide a preclinical proof of concept that targeting PELP1 to decrease STAT3/VEGFA-mediated angiogenesis and improve responses to chemotherapy due to normalization of vessels. Given the newly defined contribution to angiogenesis of PELP1, targeting PELP1 may be a potentially ideal therapeutic strategy for CRC as well as other solid tumors.
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Hansen, Torben Frøstrup, Camilla Qvortrup i Per Pfeiffer. "Angiogenesis Inhibitors for Colorectal Cancer. A Review of the Clinical Data". Cancers 13, nr 5 (1.03.2021): 1031. http://dx.doi.org/10.3390/cancers13051031.

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Since the late 1990s, therapy for metastatic colorectal cancer (mCRC) has changed considerably, and the combination of doublet or triplet chemotherapy and a targeted agent are now routinely used. The targeting of angiogenesis, the development of new blood vessels, represents a key element in the overall treatment strategy. Since the approval in 2004 of the first anti-angiogenetic drug, multiple agents have been approved and others are currently under investigation. We present an overview of the recent literature on approved systemic treatment of mCRC, with a focus on anti-angiogenic drugs, and current treatment approaches, and elaborate on the future role of angiogenesis in colorectal cancer as seen from a clinical perspective. The treatment of mCRC, in general, has changed from “one strategy fits all” to a more personalized approach. This is, however, not entirely the case for anti-angiogenetic treatments, partly due to a lack of validated biomarkers. The anti-angiogenetic standard treatment at the present primarily includes monoclonal antibodies. The therapeutic field of angiogenesis, however, has received increased interest after the introduction of newer combinations. These approaches will likely change the current treatment strategy, once again, to the overall benefit of patients.
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Miyazawa, Teruo, i Akira Shibata. "Angiogenesis". Nippon Shokuhin Kagaku Kogaku Kaishi 56, nr 8 (2009): 467. http://dx.doi.org/10.3136/nskkk.56.467.

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Rozprawy doktorskie na temat "Angiogenesis"

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PARMA, LAURA. "INTRAPLAQUE ANGIOGENESIS AND THERAPEUTIC TARGETING OF ANGIOGENESIS". Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/777113.

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In this thesis we have investigated different approaches to block intraplaque angiogenesis in atherosclerosis. Intraplaque angiogenesis is a physiological response to the increased oxygen demand in the plaque but also has adverse effects by facilitating intraplaque hemorrhage and influx of inflammatory mediators, resulting in plaque instability and consequent rupture. To study this phenomenon we used in vitro assays as well as the accelerated atherosclerosis vein graft model in ApoE3*Leiden mice, a unique model in which the formed plaque shows characteristics that highly resemble human atherosclerotic lesions, including intraplaque angiogenesis and hemorrhage and a high inflammatory cell content. We focused on different approaches to restore plaque stability via improving intraplaque oxygen levels as well as via blocking different growth factors signaling. Moreover we studied the effects of our treatments on the interaction between angiogenesis and inflammation both in vitro and in vivo.
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Small, Gary R. "Glucocorticoids and angiogenesis". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29367.

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It was hypothesised that generation of endogenous glucocorticoids by 11βHSD1 within the vessel wall regulates angiogenesis. In vitro mouse aortic ring cultures established that physiologically-relevant concentrations of glucocorticoids inhibit angiogenesis in a glucocorticoid receptor-dependent manner.  In addition 11βHSD1 was found to modulate glucocorticoid-induced angiostasis, for 11dehydrocorticosterone (a substrate for 11βHSD1) although angiostatic in C57B16 aortae did not inhibit angiogenesis in llβHSD1 deficient animals. In vivo using subcutaneous sponge implants in mice, endogenous glucocorticoids were found to inhibit angiogenesis: sponges in adrenalectomised mice grew more vessels compared to sponges from sham-operated animals. 11βHSD1 regulated the angiostatic effects of glucocorticoids, for cortisone (the human equivalent of 11dehydrocorticosterone), although angiostatic in controls did not inhibit angiogenesis in 11βHSD1 deficient mice. In pathology in cutaneous wounds and infracted myocardium endogenous glucocorticoids were found to inhibit angiogenesis. RU38486, (a glucocorticoids receptor antagonist) in comparison to placebo enhanced angiogenesis in both tissues. In similar studies in C57B16 or llβHSD1 deficient mice, 11βHSD1 was found to tonically repress angiogenesis and impair left ventricular remodelling post infarction. Thus 11βHSD1 deficient mice had increased myocardial revascularisation and preserved left ventricular function. In conclusion, by using in vitro, in vivo, and pathological models, endogenous glucocorticoids were seen to inhibit angiogenesis. In addition, 11βHSD1 regeneration of glucocorticoids tonically repressed angiogenesis and influenced left ventricular remodelling post myocardial infarction. Thus 11βHSD1 appears to be an attractive therapeutic target for the management of tissue revascularisation.
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Cunha, Filipa. "Controlling angiogenesis electrically?" Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=232613.

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Physiological electrical fields (EFs) can direct some important angiogenic responses of endothelial cells such as directional migration, orientation and proliferation. It has been reported that human umbilical vein endothelial cells (HUVEC) and human microvasculature endothelial cells (HMEC) migrate in opposite directions; to anode and cathode, respectively. Although, in the present study both cell types migrated toward the cathode, HUVEC directedness started at 50mV/mm while HMEC directedness started at 100mV/mm. These results suggest that EFs can promote wound healing by directing endothelial cells to the wound site since EFs of 40 to 100 mV/mm are present in normal healing wounds. EFs also increased cell proliferation and orientated the cleavage plane of dividing cells perpendicular to the EF vector in both endothelial cell lines. The present study showed for the first the time that EFs upregulated the expression of the chemokine receptors CXCR4 and CXCR2 as well as upregulating the levels of phosphorylation of both chemokines in HUVEC and HMEC. It also showed differences of chemokine receptors used by HUVEC and HMEC cells in the early stages of electrotaxis. Ionizing radiation has been shown to directly phosphorylate VEGF receptors in the absence of its ligand VEGF. A question was raised: in the absence of the ligands are EFs able to directly phosphorylate the chemokine receptors? Results showed that in starved HUVEC cells EFs had no effect on the phosphorylation levels of CXCR4 and CXCR2 however in starved HMEC cells an EF may have a direct effect on the phosphorylation levels of CXCR4 and CXCR2. Therefore, EFs represent a physical stimulus that could directly phosphorylate proteins in the absence of its ligand. This work substantiate the importance of endogenous EFs in directing endothelial cells and suggests that EFs might be developed as a component in the clinic to control angiogenesis.
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Järvenpää, J. (Jouko). "Placental angiogenesis and angiogenesis related risk factors in severe pre-eclampsia". Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514288760.

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Abstract The incidence of pre-eclampsia (PE) is 2–7% in different populations and in the worst cases PE may threaten the survival of both mother and newborn; its pathogenesis is not resolved. Field literature today considers PE an angiogenic disorder. Coordinated vascularization is essential for placental development. We wanted to find novel factors in the etiology of PE, and focused our attention on angiogenesis, inherited thrombophilia and folate-homocysteine metabolism. Homocysteine inhibits endothelial cell proliferation, which is closely related to angiogenesis. We performed gene expression profiling of placental tissue using microarray chips, studied the prevalence of factor V Leiden (FVL), prothrombin (F5) G20210A and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism in patients with severe pregnancy complications and normal controls, compared the expression of the placental adiponectin, leptin and their receptor genes and the relationship of each to trophoblast apoptosis and further, studied the effect of folic acid fortified mineral water on plasma homocysteine concentration during pregnancy. Gene expression profiling revealed downregulation of nine and upregulation of four genes. Interestingly, in one PE patient with cord compression during delivery the profile resembled that observed in normals. The expression level of the leptin and the adiponectin receptor 1 (ADIPOR1) genes was significantly higher in PE. No other significant expression changes were observed. The rate of apoptosis was higher in patients with PE. The FVL prevalence was 9.5%, in PE cases and 1.8% in the controls; a difference of 7.7%, (95% CI 2.0–13.4%). No statistical difference was found in other polymorphisms.. Maternal serum folate concentration increased in our intervention group, but decreased in the control group (p < 0.05). The plasma homocysteine concentrations decreased more in the intervention group (p < 0.001). The expression of angiogenesis-related placental genes can be altered in PE and cord compression cases. The activity of adipocytokine genes in PE may mean that they have a role in placental angiogenesis and apoptosis. Women with FVL may have an increased risk of PE. Fortified mineral water will help us to ensure that especially pregnant women achieve adequate folate intake.
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Sköldenberg, Erik. "Angiogenesis in childhood malignancies". Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3481.

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Angiogenesis is necessary for the growth and spread of solid tumors. In these studies angiogenesis was measured in childhood malignancies in general and in Wilms’ tumor in particular, and cutting needle biopsy (CNB) specimens were evaluated for diagnosis in childhood renal tumors.

In 33 patients with Wilms’ tumor, tumor capillaries were quantified, expression of angiogenic growth factors in tumor tissue investigated, and concentrations of angiogenic growth factors in serum measured. Reference values for angiogenic growth factors were obtained in 80 healthy adults (fibroblast growth factor 2 [FGF-2], vascular endothelial growth factor A [VEGF-A]) and 94 healthy children (angiogenin [ANG], epidermal growth factor [EGF], FGF-2, hepatocyte growth factor [HGF], tumor necrosis factor alpha [TNFA] and VEGF-A) aged 0.5-18 years. These reference values were compared with values in sera taken at diagnosis in 268 children with tumors and leukemias. CNB specimens were evaluated in 25 children with renal tumors.

A large number of capillaries was an independent prognostic factor for a poor outcome in Wilms’ tumor. Angiogenic growth factors were expressed in Wilms’ tumor tissue, and elevated concentrations of HGF and VEGF-A were found in both benign and malignant tumors. HGF was increased in leukemia, and TNFA was increased in leukemia, lymphoma and neuroblastoma. CNB, which proved to be a safe procedure, had a sensitivity of 76%.

These studies have demonstrated that quantification of capillaries is a prognostic factor in Wilms’ tumor and that HGF, TNFA and VEGF-A are frequently elevated in sera from children with cancer. Quantification of capillaries in tumor tissue and of circulating angiogenic growth factors would therefore seem to be of clinical relevance in managing children with cancer.

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Mellberg, Sofie. "Molecular Regulation of Angiogenesis". Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9418.

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Angiogenesis, de novo formation of blood vessels from the pre-existing vasculature, is crucial in embryo development, and in processes in the adult such as wound healing and ovulation. Angiogenesis is also involved in pathological conditions such as cancer and chronic inflammatory diseases, which are propagated by dysregulated, excess angiogenesis. On the other hand, lack of functional vessels and poor blood flow is a major problem in myocardial and peripheral ischemia. A detailed understanding of the molecular mechanisms underlying angiogenesis is of vital importance for the development of drugs to regulate angiogenesis. The aim of this thesis has been to identify genes involved in regulation of angiogenesis. We have investigated gene expression over time in endothelial cells (ECs), using different in vitro models. We show that the proteoglycan endocan is upregulated in ECs invading a fibrin matrix in response to vascular endothelial growth factor (VEGF)-A. There was increased expression of endocan in renal tumour cells and tumour vessels compared to normal renal tissues, indicating that endocan might have a role in tumour growth and tumour angiogenesis. We also show that vascular endothelial protein tyrosine phosphatase (VE-PTP) is induced in ECs during differentiation into vessel structures in a three dimensional collagen matrix. Silencing of VE-PTP disrupts vessel formation and increases the activity of VEGF receptor-2 (VEGFR-2) and downstream signalling, leading to increased EC proliferation. This presents a possible mechanism for the failure of vessel formation, as EC morphogenesis requires growth arrest of the cells. We also show that VE-PTP and VEGFR-2 are closely associated in resting ECs. VEGF-A stimulation leads to rapid loss of association, coinciding with increased phosphorylation of VEGFR-2. The function of VE-PTP in vivo was investigated using the zebrafish model. We demonstrate specific expression of a zebrafish VE-PTP orthologue (zVE-PTP) in the developing vasculature. Silencing of zVE-PTP leads to defective vessel sprouting and branching, indicating a critical role for zVE-PTP in development of the zebrafish vasculature. In conclusion, this thesis presents gene regulation during endothelial cell morphogenesis and details the expression pattern of endocan and the function of VE-PTP in regulation of VEGFR-2-driven angiogenesis.
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Zetterberg, Eva. "Angiogenesis in myeloproliferative disorders /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-383-3/.

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Sköldenberg, Erik. "Angiogenesis in childhood malignancies /". Uppsala : Institutionen för kirurgiska vetenskaper, Uppsala universitet, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3481.

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O'Brien, Timothy Stephen. "Angiogenesis in bladder cancer". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388846.

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Chan, Hock Yee. "Studies on tumour angiogenesis". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299162.

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Książki na temat "Angiogenesis"

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Benest, Andrew V., red. Angiogenesis. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2059-5.

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Figg, William D., i Judah Folkman, red. Angiogenesis. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6.

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Maragoudakis, Michael E., red. Angiogenesis. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4221-6.

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Maragoudakis, Michael E., red. Angiogenesis. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9185-3.

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Maragoudakis, Michael E., Pietro M. Gullino i Peter I. Lelkes, red. Angiogenesis. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9188-4.

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Steiner, Rudolf, Paul B. Weisz i Robert Langer, red. Angiogenesis. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7001-6.

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G, Mikos Antonios, i Johnson Peter C, red. Angiogenesis. New Rochelle, NY: Mary Ann Liebert, 2010.

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Ribatti, Domenico. Angiogenesis and Anti-Angiogenesis in Hematological Malignancies. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8035-3.

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Murray, J. Clifford. Angiogenesis Protocols. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591434.

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Staton, Carolyn A., Claire Lewis i Roy Bicknell, red. Angiogenesis Assays. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470029350.

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Części książek na temat "Angiogenesis"

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Folkman, Judah. "History of Angiogenesis". W Angiogenesis, 1–14. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_1.

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Saharinen, Pipsa, Lauri Eklund i Kari Alitalo. "Angiopoietins and Tie Receptors". W Angiogenesis, 113–20. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_10.

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Duncan, Michael B., i Raghu Kalluri. "Basement Membrane Derived Inhibitors of Angiogenesis". W Angiogenesis, 121–27. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_11.

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Folkman, Judah. "Angiostatin and Endostatin: Angiogenesis Inhibitors in Blood and Stroma". W Angiogenesis, 129–46. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_12.

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Bornstein, Paul. "Thrombospondins: Endogenous Inhibitors of Angiogenesis". W Angiogenesis, 147–58. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_13.

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Ribatti, Domenico, i Angelo Vacca. "Overview of Angiogenesis During Tumor Growth". W Angiogenesis, 161–68. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_14.

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Charlesworth, Philip J. S., i Adrian L. Harris. "Hypoxic Regulation of Angiogenesis by HIF-1". W Angiogenesis, 169–79. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_15.

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Bottaro, Donald P., Nelly Tan i W. Marston Linehan. "Regulation of Angiogenesis by von Hippel Lindau Protein and HIF2". W Angiogenesis, 181–91. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_16.

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Morbidelli, L., S. Donnini i M. Ziche. "Nitric Oxide in Tumor Angiogenesis". W Angiogenesis, 193–204. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_17.

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Kawamura, Harukiyo, Xiujuan Li, Michael Welsh i Lena Claesson-Welsh. "VEGF Signal Tranduction in Angiogenesis". W Angiogenesis, 205–16. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71518-6_18.

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Streszczenia konferencji na temat "Angiogenesis"

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Miles, K. A. "Imaging tumor angiogenesis". W Research Workshop on Automated Medical Image Analysis, redaktorzy Binh Pham, Michael Braun, Anthony J. Maeder i Michael P. Eckert. SPIE, 1999. http://dx.doi.org/10.1117/12.351624.

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Gounis, Matthew J., Baruch B. Lieber, Keith A. Webster, Bernard J. Wasserlauf, Howard M. Prentice i Ajay K. Wakhloo. "Angiographic Quantification of Angiogenesis". W ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43196.

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Therapeutic angiogenesis is the attempt to increase vascular density by means of an exogenously administered proangiogenic agent and offers a potential treatment for diseases associated with tissue ischemia. Vascular endothelial growth factor (VEGF) expressed by gene therapy has been shown to be a potent stimulator of angiogenesis and to improve the function of ischemic tissues in patients [Isner, 1998]. Unregulated gene therapy is disconcerting since there is no assurance that the treatment will target the ischemic territory. A new regulated adeno-associated viral vector expressing VEGF165 that is conditionally silenced has been developed by one of the authors (KAW). The transgene expression is regulated by silencing the genes in the absence of the disease and at the same time having strong and local activation in the presence of the disease. The purpose of this work is to establish protocols and techniques to quantify the efficacy of therapeutic angiogenesis. The initial phase of this research involves assessment of angiogenesis using an unregulated, adenoviral vector that is encoded to express VEGF165. Using the rabbit hind limb ischemia model, angiography was performed on animals that were given the proangiogenic treatment and on a sham group, in which phosphate buffered saline (PBS) was injected. Angiographic contrast intensity curves were obtained, modeled, and the optimized model parameters provided insight into flow characteristics within the targeted vascular bed. In the second phase of the project the conditionally silent vector will be employed using the developed protocols and methods of the first phase to afford comparisons with the previous groups.
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Tas, S. "SP0048 Targeting of angiogenesis". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7153.

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Dyson, Mary. "How phototherapy affects angiogenesis". W Biomedical Optics (BiOS) 2007, redaktorzy Michael R. Hamblin, Ronald W. Waynant i Juanita Anders. SPIE, 2007. http://dx.doi.org/10.1117/12.713180.

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Mathew, Justin G., i Alisa Morss Clyne. "Glycated Collagen Decreases Urokinase Plasminogen Activator (uPA) Activity in Endothelial Cells". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80807.

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Angiogenesis is the growth of new blood vessels from pre-existing vessels. Reduced angiogenesis contributes to morbidity and mortality in diabetic patients, since it leads to improper wound healing and reduced blood flow to vital organs (Martin, 2003). Extracellular matrix (ECM) degradation is an initial step in angiogenesis, and the plasminogen system is a driving force behind this degradation.
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Sibole, Scott C., Clayton J. Underwood, James E. Guilkey i Jeffrey A. Weiss. "A Continuous-Discrete Mathematical Model Simulates In Vitro Angiogenesis". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206516.

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Angiogenesis plays a pivotal role in formative life stages such as embryogenesis, tissue remodeling such as wound healing, and in pathological conditions such as excessive proliferation of blood vessels in tumorigenesis. In all cases, angiogenesis consistently follows a sequence beginning with detachment and migration of endothelial cells from existing vasculature and ending with formation of a new vessel network. This process is influenced by chemical and mechanical factors. While the chemical processes governing angiogenesis have been studied extensively and are still an active topic for research, the mechanical aspects have received less attention [1].
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Andken, K. L., C. Sheng i I. J. Bigio. "Optical monitoring of tumor angiogenesis". W 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967837.

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Juan Samper, Gustavo, Cristina Sabater Abad, Susana Torres Martinez, Estrella Fernández-Fabrellas, Vanessa Jaimes Diaz, Esther Verdejo Mengual i Silvia Calabuig Fariñas. "Angiogenesis in idiopathic pulmonary fibrosis". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.828.

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Kolkman, Roy G. M., Kiran K. Thumma, Gerbert A. ten Brinke, Ronald I. Siphanto, Han van Neck, Wiendelt Steenbergen i Ton G. van Leeuwen. "Photoacoustic imaging of tumor angiogenesis". W Biomedical Optics (BiOS) 2008, redaktorzy Alexander A. Oraevsky i Lihong V. Wang. SPIE, 2008. http://dx.doi.org/10.1117/12.761214.

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Mahadevan, Vijay, James A. Tyrell, Ricky T. Tong, Edward B. Brown, Rakesh K. Jain i Badrinath Roysam. "Complexity analysis of angiogenesis vasculature". W Medical Imaging, redaktorzy J. Michael Fitzpatrick i Joseph M. Reinhardt. SPIE, 2005. http://dx.doi.org/10.1117/12.596016.

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Raporty organizacyjne na temat "Angiogenesis"

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DeLisser, Horace. PECAM-1 and Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2009. http://dx.doi.org/10.21236/ada567787.

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Luque, Alfonso, i Luisa Iruela-Arispe. Angiogenesis Inhibitors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2005. http://dx.doi.org/10.21236/ada436920.

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McLeskey, Sandra W. Fibrinolysis in Tumor Associated Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2005. http://dx.doi.org/10.21236/ada444235.

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Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, marzec 2001. http://dx.doi.org/10.21236/ada398034.

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McLeskey, Sandra W. Fibrinolysis in Tumor Associated Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada435364.

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McLeskey, Sandra W. Fibrinolysis in Tumor Associated Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2002. http://dx.doi.org/10.21236/ada410455.

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Ingber, Donald, Mark Puder i Joyce Bischoff. Angiogenesis and Tissue Engineering Research. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2010. http://dx.doi.org/10.21236/ada524972.

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Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1999. http://dx.doi.org/10.21236/ada378066.

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Lu, Junxuan. Angiogenesis and Cancer Prevention by Selenium. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2001. http://dx.doi.org/10.21236/ada395671.

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Chen, Xiaoyuan. Molecular Imaging of Ovarian Carcinoma Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, marzec 2007. http://dx.doi.org/10.21236/ada489876.

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