Tesi sul tema "Vascular endothelial growth factor-receptor 2"
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Ruch, Claudia. "Structure / function analysis of the extracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2) /". Zürich : ETH/PSI, 2007. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17030.
Testo completoJellbauer, Stefan. "Tumorvakzinierung gegen den "Vascular Endothelial Growth Factor Receptor 2" (VEGFR2)mittels heterologem Antigentransport durch rekombinante Salmonellen". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-120905.
Testo completoIizuka, Takumi. "Vascular endothelial growth factor receptor 3 (VEGFR3) expression in the mouse uterus during decidualization /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1650512501&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.
Testo completoHiggins, Kelly Jean. "Regulation of vascular endothelial growth factor receptor-2 in pancreatic and breast cancer cells by Sp proteins". Texas A&M University, 2003. http://hdl.handle.net/1969.1/6010.
Testo completoDeshpande, Abhishek. "Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) and blood vessel density changes in an experimental model of Chronic Hydrocephalus". Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1279288736.
Testo completoKwan, Joanne. "Induction of tumor proliferation and metastasis by expression of vascular endothelial growth factor receptor 2 in prostate carcinomas". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12462.
Testo completoVascular endothelial growth factor receptor 2 (VEGFR2) was first discovered on the cells of blood vessels, and has thus been referred to as an endothelial receptor. However, recent evidence suggests that some tumor cells may express VEGFR2 as well. We examine the function of the lowly metastatic human prostate cancer cell line PC3M and its highly metastatic lymph node variant PC3M-LN4. We discovered that PC3M-LN4 cells express high levels of VEGFR2. In vivo, PC3M-LN4 tumors are larger, more metastatic, and more vascularized than PC3M tumors. To further demonstrate the function of VEGFR2, PC3M cells were transfected with a VEGFR2 plasmid and G418 resistant cells were selected then grown as clones. PC3M-VEGFR2 cells were analyzed by Western blot analysis, a migration assay, and a proliferation assay. Cells expressing high levels of VEGFR2 were selected through Western blotting. A Transwell migration assay examining PC3M-VEGFR2.28 revealed greater cell migration towards VEGF-treated media as compared to VEGF-untreated media. A proliferation assay for this same clone showed greater cell proliferation with increasing concentrations of VEGF in both SF and 1% FBS media. These data suggest a direct relationship between VEGFR2 expression and tumor proliferation and metastasis. Furthermore, we noticed that an elongated cell morphology may be a characteristic of metastatic cells. Immunohistochemical analysis of prostate cancer patient biopsies reveals VEGFR2 expression on both tumor cells and endothelial cells. Interestingly, we noticed that this expression is heterogeneous between different patients and even varies within the same biopsy. Our data suggests that anti-VEGFR2 therapies may target both the tumor and blood vessels to inhibit prostate cancer disease progression in those patients that express the receptor.
王, 英泰. "Hypoxia and vascular endothelial growth factor selectively upregulate angiopoietin-2 in bovine microvascular endothelial cells". Kyoto University, 2001. http://hdl.handle.net/2433/150200.
Testo completoMagnusson, Peetra. "Fibroblast Growth Factor Receptor-1 Function in Vasculo- and Angiogenesis". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5824.
Testo completoCheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Testo completoCheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Testo completoOwing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life
Ward, Stephen. "Small Interfering RNA Decreases VEGF mRNA Expression and Proliferation of Colorectal Cancer Cells". Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-151558/.
Testo completoShao, Esther Szu-Chia. "Study of the role of activin receptor like kinase-1 signaling in control of vascular endothelial growth factor expression and atherosclerosis". Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=2026896091&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Testo completoLas, Heras Alonso Hortensia Paula. "Implicaciones de la sobreexpresión de la ciclooxigenasa-2 (COX-2) en la carcinogénesis colónica experimental". Doctoral thesis, Universitat de Lleida, 2011. http://hdl.handle.net/10803/52097.
Testo completoINTRODUCCIÓN La angiogénesis es esencial para el crecimiento de los tumores sólidos y participa en el proceso metastático. El VEGF-C, un potente factor angiogénico, se encuentra elevado en pacientes con cáncer colorrectal (CCR).Hay muchas evidencias que sugieren que la COX-2 es un factor importante en el proceso de carcinogénesis colorrectal. El objetivo principal del estudio es investigar el efecto que un inhibidor selectivo de la ciclooxigenasa-2, comparándolo con otros no selectivos, pueda tener, en un modelo de carcinógesis colónica experimental, sobre la superficie tumoral del colon y su traducción en los niveles séricos de VEGF-C y en la expresión de ciclooxigenasa-2 (COX-2). MATERIAL Y MÉTODOS Se utilizaron 100 ratas Sprague-Dawley no consanguíneas distribuidas en cinco grupos: grupo control, grupo con CCR inducido con DMH, grupo de ratas tratadas con celecoxib, grupo de ratas tratadas con ácido acetilsalicílico y grupo de ratas tratadas con indometacina. Tras el sacrificio, se tomaron muestras de sangre para determinar el VEGF-C sérico mediante ELISA y muestras de los segmentos del colon y de aquellos sugestivos de contener neoplasia para estudiar la expresión de COX-2 en los tumores y en la mucosa normal del colon descendente mediante inmunohistoquímica. Se utilizó la prueba estadística más idónea en cada supuesto de estudio y se consideró significativo cuando la p£ 0,05. RESULTADOS Encontramos expresión positiva de COX-2 en el 57,14 - 66,67% de los tumores de colon. El 72% de tumores carcinomas mucinosos presentaron un score de tinción de COX-2 positivo, vs. un 48,46% de los adenocarcinomas (p<0,05). Se encontraron diferencias significativas entre los grupos que recibieron fármacos cuando se comparó el valor sérico de VEGF-C (p=0,008). El grupo que tomó ácido acetilsalicílico presentó unos niveles séricos menores a los del grupo que recibió celecoxib (63,67 vs. 92,58 pg/ml) (p=0,003). No se apreciaron diferencias significativas entre el grupo que recibió celecoxib y el grupo control con inducción tumoral (92,58 vs. 89,89 pg/ml.) (p=0,698). No se encontraron diferencias estadísticamente significativas entre los valores de VEGF-C sérico y la expresión tumoral de COX-2 en ninguno de los grupos de estudio (p>0,05). Se encontraron diferencias significativas entre el valor sérico medio de VEGF-C y la extensión de la expresión de COX-2 en el tumor (p=0,035). También se halló correlación estadísticamente significativa entre el valor circulante de VEGF-C sérico y la suma de superficie tumoral (p=0,045). Se encontraron diferencias estadísticamente significativas en el valor sérico de VEGF-C según los animales presentasen o no metástasis a distancia o hematógenas (p=0,015). CONCLUSIONES La mayoría de tumores de colon inducidos experimentalmente en la rata expresaron COX-2. La expresión de COX-2 en el CCR se asocia de forma significativa al tipo de tumor, incrementándose conforme aumentaba la malignidad de la histología del tumor. El VEGF-C sérico se relaciona con la progresión de la enfermedad. Valores elevados se correlacionaron con sumas de superficies tumorales elevadas de un modo estadísticamente significativo. Celecoxib no redujo de un modo significativo la expresión de COX-2 en los tumores respecto de los grupos tratados con fármacos no selectivos, ni disminuyó de forma significativa los valores séricos de VEGF-C, ni la suma de superficie tumoral en el colon. El ácido acetilsalicílico induce una disminución en los niveles séricos circulantes de VEGF-C cercanos a los niveles control. Sin embargo, no existieron cambios en la expresión de COX-2 en los tumores, ni en la suma de superficie tumoral al comparar este grupo con los demás.
INTRODUCTION Angiogenesis is essential for the growth of solid tumours and takes part in the metastatic process. VEGF-C, a strong angiogenic factor, is increased in patients with colorectal cancer (CRC). There are evidences suggesting that COX-2 is an important factor in the colorectal carcinogenesis process. The main aim of the study is to investigate the effect that a selective COX-2 inhibitor, comparing it with non-selective ones, could have on experimental colon carcinogenesis, on the colorectal tumour area, and its results in the serum VEGF-C levels and in the cyclooxigenase-2 (COX-2) expression. MATERIAL AND METHODS 100 Sprague-Dawley rats without consanguinity were used. They were divided into five groups: control group, group with DMH induced CRC, group that was treated with celecoxib, group that was treated with aspirin and group that was treated with indomethacin. Blood samples were taken after slaughter of rats, in order to determine serum VEGF-C with ELISA technique. Colon segments samples and specimens from the areas that were suggested to contain neoplasms were taken too, in order to study COX-2 expression in colon tumors and in the normal mucosa with immunohistochemistry technique. The most appropriate statistical test was used in each case of the study and it was considered significant when p£ 0.05. RESULTS We found positive COX-2 expression in 57.14-66.67% of colon tumours. 72% of mucinous carcinomas presented a positive score for COX-2 expression, vs. 48.46% of adenocarcinomas (p<0.05). We found significant differences between groups that received drugs when we compared the serum VEGF-C level (p=0.008). The AAS group presented lower serum VEGF-C levels than the celecoxib group (63.67 vs. 92.58 pg/ml) (p=0.003). We didn’t appreciate significant differences between the celecoxib group and the control group with tumor induction (92.58 vs. 89.89 pg/ml) (p=0.698). There were no statistically significant differences between the serum VEGF-C levels and tumor expression of COX-2 in any of the groups of the study (p>0.05). We found significant differences between the serum VEGF-C level and the extension of COX-2 expression in the tumor (p=0.035). We also found statistically significant correlation between the value of serum VEGF-C and the sum of tumor area (p = 0.045). Statistically significant differences were found in the serum VEGF-C level between animals having or not hematogenous metastasis (p=0.015). CONCLUSIONS Most experimentally induced colon tumors in rats expressed COX-2. The expression of COX-2 in CRC is significantly associated with the type of tumor, and increases according to the increases of malignancy of the tumor histology. Serum VEGF-C is related to disease progression. High values were correlated with high sum of tumor surfaces in a statistically significant manner. Celecoxib didn’t reduce significantly the expression of COX-2 in tumors regarding groups treated with non-selective drugs, nor significantly decreased serum VEGF-C, or the sum of tumor area in the colon. Aspirin decreases serum VEGF-C levels which were similar to control levels. However, there were no changes in the expression of COX-2 in tumors, or the sum of tumor area by comparing this group with other treated groups.
Sköld, Mattias. "On VEGF and related factors in neurotrauma /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-986-2/.
Testo completoFerraro, Bernadette. "Intradermal Delivery of Plasmids Encoding Angiogenic Growth Factors by Electroporation Promotes Wound Healing and Neovascularization". [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002823.
Testo completoSarkar, Nondita. "Myocardial angiogenesis induced by plasmid VEGF-A165 gene transfer : experimental and clinical studies /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-196-2/.
Testo completoStar, Gregory. "The effects of bone morphogenic proteins and transforming growth factor [beta] on in-vitro endothelin-1 production by human pulmonary microvascular endothelial cells /". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111942.
Testo completoRecently mutations in the bone morphogenic protein receptor type II (BMPRII) have been linked to the disease. Interestingly mutations in activin-like kinase-1 (ALK-1) and endoglin have been linked to hereditary haemorrhagic telangiectasia (HHT), a disease that results in PAH clinically indistinguishable from IPAH. All of these proteins are either receptors or co-receptors to members of the TGFbeta superfamily. The connection of these mutations to the disease still remains largely a mystery to researchers and the effects of either bone morphogenic proteins 2, 4, 7 or TGFbeta levels on endothelin-1(ET-1) production in human microvascular endothelial cells cultured from normal lungs (HMVEC-LBI) are unknown.
Methods: HMVEC-LBI cells were cultured in the presence of various concentrations of BMP 2,4,7 and TGFbeta, in complete media or serum starved conditions. After allotted time points the media was collected and assayed by ELISA, meanwhile the cells were lysed and protein content assayed for normalization purposes. Small Mothers against Decapentaplegic (SMAD) 1/5 phosphorylation was also measured.
Results and Conclusions: Despite evidence that all BMPs used were biologically active, namely through SMAD phosphorylation studies, only BMP7 at very high dosages increased ET-1 production levels. TGFbeta had a more pronounced effect at earlier time points with lower concentrations. The results provide insights on the effects of an important group of proteins, the BMPs and TGFbeta, on lung microvascular ECs and which are likely the key cellular player In IPAH development. These findings may have clinical relevance in terms of control of the disease and understanding the normal response of these cells BMPs and TGFbeta.
Dreilich, Martin. "Predictive Factors in Esophageal Carcinoma". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6831.
Testo completoRennel, Emma. "Molecular Mechanisms in Endothelial Cell Differentiation". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4059.
Testo completoGomes, Luana Pimenta. "Avaliação dos fatores de crescimento endotelial vascular VEGF e de seus principais receptores VEGFR-1 e -2 no processo de cicatrização com influência da radioterapia em ratos da linhagem Wistar". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-05112013-125011/.
Testo completoTissue damages of any nature unchain a series of events that will promote regeneration or healing of the injured tissue. This repair is a complex process that involves the interaction of various cells types. These cells are activated by a vast gamma of chemical mediators of the extracellular matrix, microorganisms and chemical and physical alterations in the injury microenvironment and adjacent areas. The participation of vascular endothelial growth factors (VEGF) and their two main receptors (VEGFR-1 and -2) has great importance in the healing process considering neovascularization. After a detailed analysis of the literature about radiotherapy effect in neovascularization and its relation with the expression of VEGF and VEGFR-1 and -2 in the healing, it was observed that there are many questions to be investigated. The objective of this study was to evaluate the immunohistochemical expression of VEGF and VEGFR-1 and -2 and sanguineous vessel density (DVS) after incision and cutaneous repairing in animals under influence of the radiotherapy at three and six months. This study used 60 Wistar rats randomly distributed in six groups: control, preoperative radiotherapy and postoperative radiotherapy, of 3 and 6 month each. The specimens evaluated macro/microscopically were removed after animal\'s sacrifice, in accordance to clinical ethics principles. The immunohistochemistry study of VEGFs were conducted using above-mentioned specific antibodies in manufacturer specified dilutions, while the study of the DVS was performed with the Von Willebrand Factor antibody (VWF) which was used to mark endothelial cells specifically. In both periods studied, surgical wound and radiation damages are similar in most cases. The primarily irradiated cases presented bizarre cellularity, multinucleated giant cells, stromal hyalinization structures, moderate to strong necrosis, overexpression of VEGF receptors in the endothelium and blood vessels in consequence of radiotherapy. These findings are in accordance to the literature, since the strong relationship between VEGFR-2 receptor and its persistence in neovascularization and granulation tissue formation were seen. Our results have shown that VEGF expression is constantly expressed in different times of wound healing and scar formation
Bermudez, Yira. "Growth Factor-Mediated Telomerase Activity in Ovarian Cancer Cells". [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0002028.
Testo completoGonçalves, Silvana Beltrami. "Efeito do VEGF na angiogênese pulpar e na apoptose". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/25/25138/tde-22062007-094740/.
Testo completoThe Vascular endothelial growth factor (VEGF) plays na important role in angiogenesis by inducing endothelial cell proliferation, migration, and survival. To promote new vessel formation and improve collateral circulation, VEGF has been used to treat ischemic heart areas in cardiovascular disease. Maintenance of pulp vitality with VEGF may improve the outcomes of avulsed teeth, preventing premature tooth loss. The purpose of this study was to develop a model system to study the process of dental pulp revascularization, and assess the effect of VEGF-165 in the human pulp angiogenesis and apoptosis. Human tooth slices were maintained in vitro for 7 days +/- VEGF (50ng/mL). Immunohistochemistry staining for Von Willebrand?s factor (Factor VIII) was used to quantify the number of vessels in pulp tissues. There was a significantly higher number of blood vessels in the VEGF group (67.8 Mean) compared to the control group (46.2 Mean, p<0.05). Tunel Assay was used to determine the number of apoptotic cells in +/- VEGF groups. RTPCR analyses of VEGFR-2 transcripts were used on human dermal microvascular endothelial cells (HDMECs), undifferentiated pulp cells (OD-21), mouse odontoblast-like cells (MDPC-23), and macrophages. VEGFR-2 expression was detected in HDMECs but not in the other 3 cell lines. Four tooth slices per mouse were subcutaneously implanted in the dorsal region for 7 days. Pulp vitality was determined by histological and immunohistochemical analysis. Also, Tunel Assay was used to determine the number of apoptotic cells. SCID mouse model of pulp angiogenesis demonstrated to be a good model system to study revascularization of human dental pulps. Taking into account the findings of this study, it is suggested that VEGF could have a positive effect in the revascularization of avulsed teeth. It is hoped that this pulp angiogenesis model be useful to answer a number of new experimental questions in the area of Endodontics.
Meade, Eliza. "Hypoxic Regulation of VEGF and PAI-1 Expression by HIF-1[alpha] and HIF-2[alpha] in First Trimester Trophoblasts". Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-115727/.
Testo completoAlves, Brunna Eulálio 1979. "Avaliação de moduladores do aumento da permeabilidade microvascular e sua correlação com a evolução clínica na sepse em pacientes onco-hematológicos neutropênicos febris". [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309168.
Testo completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Pacientes portadores de neoplasia hematológica e neutropenia febril representam um grupo de risco elevado de sepse e choque séptico. Nas últimas décadas, estratégias terapêuticas alvo-específicas para a sepse não modificaram de forma significativa a sobrevida dos pacientes e o tratamento permanece baseado em antibioticoterapia e cuidados de suporte, com altas taxas de mortalidade. A quebra da barreira endotelial é um evento fundamental na fisiopatologia do choque séptico e a compreensão dos mecanismos envolvidos neste evento tem o potencial de auxiliar na identificação de novos biomarcadores de gravidade e de novos alvos terapêuticos para estes pacientes. Estudos recentes demonstraram a participação do fator de crescimento do endotélio vascular (VEGF-A), do seu receptor solúvel (sFlt-1) e das angiopoietinas 1 e 2, proteínas envolvidas na angiogênese e na regulação da integridade da barreira endotelial na fisiopatogenia do choque séptico em pacientes não oncológicos internados em unidade de terapia intensiva. Neste trabalho, avaliamos prospectivamente a cinética do VEGF-A, do sFlt-1 e das angiopoietinas 1 e 2 durante as 48 horas inicias da neutropenia febril em 41 pacientes portadores de neoplasia hematológica submetidos a quimioterapia intensiva ou a regime de condicionamento para transplante de células progenitoras hematopoiéticas, através da dosagem dos mesmos por ensaio imuno-enzimático. Exploramos também a associação dos níveis séricos destes biomarcadores com a gravidade da sepse através da correlação com o MASCC, um índice desenvolvido para identificar pacientes com neutropenia febril de baixo risco, e com o SOFA, um escore de avaliação de disfunção orgânica em pacientes com sepse, ambos amplamente aceitos. A evolução para choque séptico foi associada a níveis significativamente maiores de VEGF-A, sFlt-1 e angiopoietina-2 48 horas após o início da neutropenia febril quando comparado aos valores em pacientes com sepse não complicada e a estimativa da acurácia diagnóstica sugere a capacidade de discriminar os pacientes que evoluíram com choque séptico. Estes biomarcadores também apresentaram correlação com os escores gravidade, sugerindo a relevância biológica da associação. Em conclusão, nossos achados sugerem que a avaliação destes biomarcadores em pacientes com neutropenia febril deve ser avaliada em estudos com maior número de pacientes, quanto ao seu potencial de incorporação na prática clínica. Além disso, os resultados reforçam o potencial terapêutico da intervenção nestas vias para o tratamento da sepse
Abstract: Patients with hematologic malignancy and neutropenia represent a group at high risk of sepsis and septic shock. In recent decades, target-specific therapeutic strategies for sepsis did not change significantly the survival of patients and treatment is still based on antibiotic therapy and supportive care, with high mortality rates. The breakdown of the endothelial barrier is a key event in the pathophysiology of septic shock and understanding of the mechanisms involved in this event has the potential to assist in the identification of new biomarkers and severity of new therapeutic targets for these patients. Recent studies have demonstrated the involvement of endothelial growth factor (VEGF-A), its soluble receptor (sFlt-1) and angiopoietins 1 and 2, proteins involved in angiogenesis and in regulation of endothelial barrier integrity in the pathogenesis of shock septic patients without cancer admitted to the intensive care unit. In this study, we prospectively evaluated the kinetics of VEGF-A, sFlt-1 and angiopoietins 1 and 2 during the initial 48 hours of febrile neutropenia in 41 patients with hematological malignancy undergoing intensive chemotherapy or conditioning regimen for stem cell transplantation hematopoietic cells by the same dosage by enzyme immunoassay. We also explored the association of serum levels of these biomarkers with the severity of sepsis through correlation with the MASCC, an index developed to identify patients with febrile neutropenia at low risk, and the SOFA score for assessment of organ dysfunction in patients with sepsis, both widely accepted. Progression to septic shock was associated with significantly higher levels of VEGF-A, sFlt-1 and angiopoietin-2 48 hours after the onset of febrile neutropenia when compared to values in patients with uncomplicated sepsis and the estimation of diagnostic accuracy suggests the ability to discriminate among patients who developed septic shock. These biomarkers also correlated with the severity scores, suggesting the biological relevance of the association
Doutorado
Clinica Medica
Doutor em Clínica Médica
Agra, Ivan Marcelo Gonçalves. "Recidiva local de carcinomas epidermóides da boca e orofaringe: estudo de variáveis anatomopatológicas e de marcadores biológicos associados ao prognóstico em pacientes submetidos à cirurgia de resgate". Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-24012008-140634/.
Testo completoINTRODUCTION: Local and regional relapses are the main sites of treatment failure in patients with oral and oropharyngeal squamous cell carcinoma. In these instances, salvage surgery is the most widely used treatment approach. The aim of this study is to analyze the prognostic effect of the expression of EGFR, MMP-2, MMP-9 and VEGF in patients with recurrent cancer sumitted to salvage surgery. METHODS: The charts of 111 patients with local recurrence of oral or oropharyngeal squamous cell carcinomas were retrospectively analyzed. The tumor sites were: the lip in 11 cases (9%), the oral cavity in 68 (61%) and the oropharynx in 33 (30%). The previous treatment was: Surgery in 33 patients (30%), radiotherapy with or without cisplatin based chemotherapy in 46 (41%) and surgery with adjuvant radiotherapy in 32 (29%). EGFR, MMP-2, MMP-9 and VEGF expressions were analyzed with tissue microarray immunohistochemical technique. RESULTS: The disease-free interval ranged from 0.89 to 140.9 months with a median of 6.87 months. The patients were categorized into two groups: Those with recurrence in less than 1 year (69 patients - 62.2%) and those with recurrence after 1 year (42 - 37.8%). The group with the shorter disease-free interval presented a worse prognosis (p=0.01). The clinical stage of recurrence (rCS) was I/II in 31 cases (27.9%) and III/IV in 80 cases (72.1%). Patients with more advanced diseases (rCS III/IV) had worse rates of cancer specific survival (CSS) than patients with rCS I/II (p=0.04). An over-expression of EGFR was associated with worse treatment results. Positive EGFR cases had a 3 year CSS of 27.2%, while EGFR negative patients had 64.3% (p=0.001). The MMP-2 and MMP-9 over-expression were also associated with a worse prognosis but without statistical significance (p=0.83 and p=0.15). VEGF expression did not show prognostic significance in this group of patients. In a multivariate analysis only the disease-free interval and over-expression of EGFR were associated with a higher risk of death. CONCLUSION: Local recurrence in oral and oropharyngeal squamous cell carcinomas usually indicates an unfavorable prognosis. A disease-free interval greater than 1 year and a negative EGFR expression are the main prognostic factors which indicate a better cancer specific survival rate in patients submitted to salvage surgery.
Arantes, Ricardo Vinicius Nunes. "Estudo da angiogênese e da expressão temporal do VEGF e dos seus receptores VEGFR-1/Flt-1 e VEGFR-2/Flk-1 durante o reparo ósseo alveolar normal e com uso terapêutico de um antiinflamatório não esteroidal seletivo para COX-2 em ratos". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-12062012-151744/.
Testo completoObjective: To evaluate the effect of Meloxicam on the expression of VEGF and its receptors during the post-extraction alveolar healing in rats. Material and Methods: The extraction of the right upper incisor was made in 180 male Wistar rats, aged 60 days old. The sample was divided in: 1) Control group (n=90) - the rats received intraperitoneal injection of 0.1 ml of 0.9% NaCl daily for 7 days, and 2) experimental group (n=90) - the rats received intraperitoneally 3mg/kg body weight of Meloxicam in 0.9% NaCl solution daily for 7 days. At 3, 7, 10, 14, 21 and 30 days later, the alveolar samples were collected, fixed in 10% formaldehyde in phosphate buffer, radiographed and histologically processed. For RT-PCR, the samples were placed in Trizol and stored at -80° and for Western blotting stored at -80°. Transversal semi-serial histological sections (with 250 um interval) of the whole alveolus were obtained and stained with hematoxylin and eosin. In these sections the volume density of bone tissue (% TO), connetive tissue (% CT), blood clot (Coa%) and blood vessel (% VS) was evaluated by point counting volumetry morphometric method. The obtained data were compared between groups for period by \"t\" test and between periods within each group by ANOVA and Tukey test, with a p<0.05 significance level. Results: a) The radiographic analysis showed changes in the contour of the cortical alveolar bone , reduction in size of the alveolus, and a small increase in radiodensity in their central region ; b) Morphologically the experimental group showed, in all periods, a delay in the repair process as compared to control, displaying greater amount of blood clot with slow replacement by connective tissue and lower cortical alveolar bone resorption and bone formation / remodeling c) In morphometric analysis the %TO in the control group were 0.817, 0.255, 0.368, 0.409 and 0.453 times higher than the experimental group during periods of 3, 7, 10, 14 and 21 days , respectively. The %Coa, the values in the control group were 0,097, 0,611, 1,189 and 1.497 times lower than in the experimental group on days 7, 10, 14 and 21 days respectively. The %VS in the control group showed 0.328 and 0.439 times higher than in the experimental group on days 10 and 14 days respectively. The% CT showed no statistical difference between groups. d) The imumunostaining for VEGF and VEGFR-1 were observed in osteoblasts and osteocytes in the cortical alveolar, and fibroblasts within the alveolus, which was statistically significant only for VEGFR-1, where the immunostaining in the control group was 0,544; 0,325 and 0,325 times higher than the experimental group during periods of 3, 7 and 10 days respectively e) The RT-PCR analysis for VEGF in the control group was 1.274 times higher within 10 days compared to the experimental group. In the expression of mRNA for VEGFR-1, the control group was 1,431; 0,951 and 0,845times higher in periods of 3, 10 and 30 days, respectively, compared to the experimental group and VEGFR-2 was 4.64 and 0.79 times higher in periods of 3 and 7 days, respectively, and f) The protein expression of VEGF in the control group was 0,365; 1,056; 2,187 and 0,350 times higher in periods of 3, 7, 10, 14 and 21 days compared to the experimental group. Conclusions: Based on the present results it was concluded that the use of Meloxicam, antiinflammatory administered daily for 7 days, alters the expression of mRNA and protein of VEGF and its receptors VEGFR, and slows the process of repair and remodeling post extraction alveolar
Rotter, Anita. "Avaliação dos níveis plasmáticos e urinários do fator de crescimento do endotélio vascular e dos níveis urinários das metaloproteinases 2 e 9 em pacientes com hemangioma infantil antes e durante o tratamento com betabloqueador sistêmico e tópico". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-16022018-083833/.
Testo completoINTRODUCTION: Angiogenic factors have been studied in regard to their role in the pathogenesis of infantile hemangioma (IH). During ß-blocker treatment, patients were monitored through physical examination and comparisons by photography and ultrasonography. In addition, plasma and urinary levels of vascular endothelial growth factor (VEGF) and urinary levels of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9) can be non-invasive tools to monitor the evolution of IH and its therapeutic follow-up. OBJECTIVES: To study plasma and urinary levels of VEGF and urinary levels of MMP-2 and MMP-9 in patients with IH, in order to evaluate their potential relation to the IH angiogenesis. METHODS: 68 IH patients and 25 controls were included, matched by age and gender. Systemic treatment with propranolol was administered to 45 patients, while topical timolol was administered to 23 patients. Patients were monitored for up to 12 months of treatment with measurements of IH volume through ultrasonography, plasma and urinary levels of VEGF and urinary levels of MMP-2 and MMP-9 (Luminex assays). RESULTS: MMP-2 levels were not detectable in over 50% of the samples. Before treatment, there was no difference in plasma and urinary levels of VEGF and urinary levels of MMP-9 between IH patients and control group. There was no significant difference in plasma and urinary levels for the biomarkers in accordance to the proliferative phase (12-month-old children or younger, in relation to children over 12 months of age). There was no correlation between IH size and biomarkers levels. There was a significant correlation between urinary levels of VEGF and MMP-9. In the propranolol group, a significant reduction of the IH volume with treatment was observed; this was not observed in the group treated with timolol. The variation of the biomarkers values obtained before, up to six months and from seven to twelve months of treatment indicated significant decrease in plasma levels of VEGF and urinary levels of MMP-9 in children treated with propranolol. It was not observed a significant variation of the biomarkers levels during timolol treatment. CONCLUSIONS: Plasma and urinary levels of VEGF and urinary levels of MMP-9 were not good markers of increased angiogenesis in patients with IH, nor reflected the increase in angiogenesis characteristic of the proliferative phase of IH. During therapeutic monitoring of IH treated with propranolol, a significant decrease in plasma VEGF and urinary MMP-9 levels was observed. The reduction in volume associated to the decrease in biomarkers in patients treated with propranolol suggested that its mechanism of action in IH occurs also through the inhibition of the angiogenesis. Thus, measurements of plasma levels of VEGF and urinary levels of MMP-9 may be useful to monitor the effectiveness of treatment
Roberts, Selene Karen. "Signalling via vascular endothelial growth factor receptor complexes". Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29705.
Testo completoSuzuma, Izumi. "Stretch-induced retinal vascular endothelial growth factor expression is mediated by phosphatidylinositol 3-kinase and protein kinase c (PKC)-ζ but not by stretch-induced ERK1/2, Akt, Ras, or classical/novel PKC pathways". Kyoto University, 2004. http://hdl.handle.net/2433/147489.
Testo completoKrishnan, Jaya. "The role of vascular endothelial growth factor receptor 3, and its ligands vascular endothelial growth factor C and vascular endothelial growth factor D in tumour metastasis and haematopoeisis". Thesis, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270576.
Testo completoGroot, Marcel. "Die Rolle des Tyrosinkinase-Rezeptors VEGFR-2 im neuronalen Kontext". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1166623362738-03904.
Testo completoGarvin, Stina. "Effects of sex steroids and tamoxifen on VEGF in the breast". Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7230.
Testo completoMahlman, M. (Mari). "Genetic background and antenatal risk factors of bronchopulmonary dysplasia". Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526219530.
Testo completoTiivistelmä Ennenaikaisen syntymän ja keskoslasten hoidon kehittymisen myötä yhä useammat huomattavan epäkypsinä syntyneet lapset jäävät henkiin. Samalla erityisesti juuri näitä lapsia uhkaavien sairauksien esiintyvyys on pysynyt korkeana. Bronkopulmonaalinen dysplasia (BPD, keskosen krooninen keuhkosairaus) on yksi näistä sairauksista. BPD:n molekyylitasoinen tautimekanismi on vielä osin tuntematon, eikä BPD:tä tehokkaasti estävää tai siitä parantavaa hoitoa ole. Myös BPD riskin arvioiminen vastasyntyneen keskoslapsen kohdalla on vaikeaa. BPD on huomattavan perinnöllinen tauti. BPD:lle altistavista geeneistä on kuitenkin vasta vähän tietoa. Tämän tutkimuksen tavoitteena oli lisätä tietoa BPD:n tautimekanismista tutkimalla BPD:lle altistavia geenejä. Lisäksi tutkimuksessa tarkasteltiin BPD:n esiintyvyyttä ja syntymää edeltäviä riskitekijöitä erityisesti kaksosten osalta. Ehdokasgeenitutkimuksessa verisuonten endoteelikasvutekijää koodaava geeni ei assosioitunut toistuvasti BPD:hen. Kit ligandia koodaava geeni sen sijaan assosioitui. Koko genomin assosiaatiotutkimuksessa C-reaktiivista proteiinia (CRP) koodaavan geenin lähistöltä löydettiin BPD:hen mahdollisesti assosioituva alue. Lisäksi ensimmäisen viikon CRP-arvojen osoitettiin ennakoivan myöhemmin kehittyvää BPD:tä. BPD-riskin todettiin olevan matalampi kaksi- kuin yksisikiöisistä raskauksista syntyneillä lapsilla. Tutkimuksen tulokset lisäävät tietoa BPD:n perinnöllisyydestä ja sitä kautta BPD:n tautimekanismista. Tutkimus toi myös uutta tietoa BPD:n riskitekijöistä parantaen vastasyntyneen keskoslapsen BPD-riskin arviota
Wendt, Astrid [Verfasser]. "Korrelation von placental growth factor, vascular endothelial growth factor und soluble vascular endothelial growth factor receptor-1 im Serum mit Tumorstadien und Prognose des hepatozellulären Karzinoms / Astrid Wendt". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1212435109/34.
Testo completoMcKeeman, G. C. "The measurement of circulation soluble vascular endothelial growth factor receptor-1 (sFlt-1)". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273085.
Testo completoLuque, Yosu. "Rôle de l'épithélium et de l'endothélium rénal au cours des glomérulopathies expérimentales. Etude des glomérulonéphrites inflammatoires et des glomérulopathies toxique et hypertensive". Electronic Thesis or Diss., Paris 6, 2016. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2016PA066394.pdf.
Testo completoGlomerular diseases are a leading cause of kidney failure and represent a public health problem. Classically, systemic effectors such as the immune system, drug toxicity or hypertension are thought to be the main drivers of glomerular diseases. The hypothesis developed in this manuscript is that epithelium and endothelium, the two main components of the renal parenchyma, are major players in the formation of glomerular lesions. Three experimental models of glomerular disease (inflammatory, toxic and hypertensive) in mice allowed us to study epithelial γC / JAK / STAT signaling classically described in immune cells and the endothelial hypoxia inducible system in order to support this hypothesis. After discussing the main role traditionally assigned to T cells in the anti- glomerular basement membrane model, an animal model of inflammatory glomerulonephritis, we demonstrated the protective role of the glomerular interleukin common γ chain (γC) receptor and its dependent podocyte-specific STAT5 during the anti-GBM model and adriamycin nephropathy. We then showed the protective role of endothelial EPAS1 (HIF-2α), a regulatory subunit of HIF complex in focal segmental glomerulosclerosis (FSGS) induced by angiotensin II. In total, this work highlights the important role of the closely linked renal epithelium and endothelium in the formation of glomerular lesions using three experimental models of glomerular diseases. The renal parenchyma is a full player in the pathophysiology of these lesions as shown by the works studying γC / JAK / STAT and HIF systems
Johansson, Anders. "Search for biomarkers in ALS and Parkinson's Disease positron emission tomography and cerebrospinal fluid studies /". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univeritetsbiblioteket [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102040.
Testo completoGhosh, Rajarshi. "Transcriptional Regulation of VEGFA by Unfolded Protein Response Signaling Pathway". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/469.
Testo completoIsmail, Hodan. "Vascular endothelial growth factor and angiopoietin-1 regulate leukocyte adhesion to endothelial cells through the nuclear receptor Nur77". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107844.
Testo completoLes facteurs de croissance endothélials vasculaires (VEGF) et l'angiopoïétine 1 (Ang-1) sont de régulateurs essentiels de l'angiogénèse. En outre, tous les deux ont été découverts pour leur participation dans le processus d'inflammation: VEGF comme pro-infammatoire et Ang-1 comme médiateur anti-inflammatoire. Nur77 est un membre de la famille des récepteurs orphelins (NR4A) qui comprend Nurr1 and Nor1 et jouent un rôle dans la régulation de l'inflammation vasculaire; toutefois cela n'est pas encore totalement compris. Le but de cette étude était d'évaluer si l'expression de Nur77 dans les cellules endothéliales (ECs) sert de mécanisme de rétroaction négatif conçu pour inhiber l'induction de NFκB en réduisant l'expression de la E-selectin et de VCAM1 induite par VEGF, ainsi que l'adhésion des leucocytes aux ECs, et pour agir en médiateur de la suppression de l'activation des ECs induite par le traitement avec Ang-1. Le traitement des cellules endothéliales humaines de la veine ombilicale (HUVECs) soit avec VEGF ou Ang-1 induit de façon significative et transitoire l'expression de Nur77 et augmente la Phosphorylation de HDAC7 PKD dépendante et la mobilisation du noyau vers le cytosol. Les HUVECs transduits avec les adénovirus exprimant HDAC7 muté ou un dominant négatif PKD1 inhibent VEGF, mais pas l'expression de Nur77 induit par Ang-1. L'inhibition de la PI3K et de ERK1/2 aboutit à la suppression de l'expression de Nur77 induit par Ang-1 alors que l'inhibition de JNK résulte de façon significative en une plus grande induction de Nur77 par Ang-1. L'essai d'activité de liaison de NFκB ainsi que celui du gel de retardation révèlent que Nur77 inhibe l'activité de NFκB induit par VEGF. La surexpression de Nur77 a montré une sur-régulation dépendante de la titration de l'ARNm et de l'expression protéique de IκBα, pas évidente avec les HUVECs transduites avec les virus exprimant la forme dominante négative de Nur77 (Ad-dnNur77). J'ai trouvé que Nur77 réprimait l'ARNm et l'expression protéique de E-selectin and VCAM1 induit par VEGF. De façon importante, le rôle de Nur77 dans l'adhésion des leucocytes aux ECs induits par les cytokines a été examiné. L'adhérence des cellules U937 aux HUVECs activées par VEGF était réprimée par la surexpression de Nur77 alors que la perte de Nur77 par l'ARNsi d'interférence résulte dans une augmentation de l'adhésion. De manière intéressante, Ang-1 était capable d'amortir l'adhésion aux monocouches de HUVECs induite par VEGF. Je conclus que Nur77 joue un rôle important en fournissant un mécanisme de rétroaction négatif conçu pour atténuer la réponse pro-infammatoire induite par VEGF à travers l'inhibition sélective de l'activation de NFκB. Par ailleurs Nur77 en partie, peut être vital pour les réponses anti-inflammatoires d'Ang-1.
Vuorela, Piia. "Vascular endothelial growth factor, its receptors, and the Tie receptor in normal and complicated pregnancy". Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/vuorela/.
Testo completoNourse, Marilyn Brower. "Control of endothelial cell differentiation and proliferation for vascular tissue engineering /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/7998.
Testo completoCardoso, Camila Lopes. "Análise morfométrica e molecular da alveolite induzida em ratos com diferentes modalidades de tratamento". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/25/25132/tde-27052009-102252/.
Testo completoDry socket is an inflammatory postoperative complication that undertakes sockets of recently extracted teeth. The incidence of such complication varies from 1 to 4% and might reach up to 30%. The objective of this study was to analyze the biological mechanisms involved in the repair process of intentionally infected sockets in mice; compare different treatment conditions and correlate the results of two different analysis (microscopic and molecular). 84 mice were used in this study, divided according the following groups: I: uninfected socket; II: infected socket without any treatment; III: infected socket treated with irrigation of 2% sodium iodide and 3% hydrogen peroxide solution at 1:1 proportion; and IV: infected socket submitted to curettage, physiological saline solution irrigation and fulfillment with metronidazole base paste. The animals were killed at a postoperative period of 6, 15 and 28 days. A quantitative analysis was performed using a RealTimePCR to evaluate the genes expression involved [Collagen Type I (COL-I), vascular endothelial growth factor (VEGF), osteocalcin (OCN), alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX2) and tumor necrosis factor-alpha (TNF-\'alpha\')], in the repair process, correlating its expression with the microscopic characteristics observed in both qualitative and quantitative manner. Based in the results of the microscopic and molecular analysis, it can be concluded that the RUNX2, OCN and TNF-\'alpha\' markers can be used as indicators to evaluate the dry socket bone neoformation and inflammatory infiltrate quantity. The ALP and VEGF markers did not represented appropriately what was observed microscopically. Although the dry socket treatment with metronidazole base paste promotes an increase in the bone neoformation density at 28 days, no difference was found among the treatments.
Inoue, Mayumi. "Oxidized LDL regulates vascular endothelial growth factor expression in human macrophages and endothelial cells through activation of peroxisome proliferator-activated receptor-γ". Kyoto University, 2003. http://hdl.handle.net/2433/148671.
Testo completoLi, Xiaobo. "PHYSICAL INTERACTIONS BETWEEN NEUROPILIN AND VEGFRS, INTEGRINS IN REGULATING ENDOTHELIAL CELL FUNCTIONS". UKnowledge, 2015. http://uknowledge.uky.edu/biochem_etds/23.
Testo completoZabihi, Sheller. "Fetal Outcome in Experimental Diabetic Pregnancy". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8739.
Testo completoWomen with pregestational diabetes have a 2-5 fold increased risk of giving birth to malformed babies compared with non-diabetic women. Diabetes-induced oxidative stress in maternal and embryonic tissues has been implicated in the teratogenic process. The malformations are likely to be induced before the seventh week of pregnancy, when the yolk sac is partly responsible for the transfer of metabolites to the embryo, and the uterine blood flow to the implantation site determines the net amount of nutrients available to the conceptus. We aimed to evaluate the effect on embryogenesis caused by a diabetes-induced disturbance in yolk sac morphology, uterine blood flow or altered maternal antioxidative status in conjunction with a varied severity of the maternal diabetic state.
We investigated to which extent maternal diabetes with or without folic acid (FA) supplementation affects mRNA levels and protein distribution of ROS scavenging enzymes (SOD, CAT, GPX), vascular endothelial growth factor-A (Vegf-A), folate binding protein-1 (Folbp-1), and apoptosis associated proteins (Bax, Bcl-2, Caspase-3) in the yolk sacs of rat embryos on gestational days 10 and 11. We found that maternal diabetes impairs, and that FA supplementation restores, yolk sac vessel morphology, and that maternal diabetes is associated with increased apoptotic rate in embryos and yolk sacs, as well as impaired SOD gene expression. We assessed uterine blood flow with a laser-Doppler-flow-meter and found increased blood flow to implantation sites of diabetic rats compared with controls. Furthermore, resorbed and malformed offspring showed increased and decreased blood flow to their implantation sites, respectively. In mice with genetically altered CuZnSOD levels, maternal diabetes increased embryonic dysmorphogenesis irrespective of CuZnSOD expression. We thus found the maternal diabetic state to be a major determinant of diabetic embryopathy and that the CuZnSOD status exerts a partial protection for the embryo in diabetic pregnancy.
Chan, Gallant Kar Lun. "Molecular studies of the vascular endothelial growth factor (Vegf-A) and VEGF-receptor (Flk-1) genes of grass carp /". access full-text access abstract and table of contents, 2005. http://libweb.cityu.edu.hk/cgi-bin/ezdb/thesis.pl?mphil-bch-b19887668a.pdf.
Testo completo"Submitted to Department of Biology and Chemistry in partial fulfillment of the requirements for the degree of Master of Philosophy" Includes bibliographical references (leaves 124-141)
Kubo, Hajime. "Involvement of Vascular Endothelial Growth Factor Receptor-3 in maintenance of integrity of entothelial cell lining during tumor angiogenesis". Kyoto University, 2000. http://hdl.handle.net/2433/151420.
Testo completoWang, Shiyang. "The role of TRKB receptors in regulation of coronary microvascular endothelial cell angiogenesis /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1543605071&sid=5&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Testo completoWang, Amanda Cyphers. "Common Signaling Elements in Response Pathways Activated by the Endothelial Survival Factors VEGF and Insulin". Thesis, Virginia Tech, 2008. http://hdl.handle.net/10919/36205.
Testo completoMaster of Science
Roos, Kelly. "The effect of sunitinib on neuroblastoma and glioblastoma cell growth". University of the Western Cape, 2020. http://hdl.handle.net/11394/7952.
Testo completoCancer is a global health catastrophe, with neuroblastoma, the most common solid childhood tumor, and glioblastoma, a deadly brain tumor, being aggressive and unresponsive to current treatment modalities. These tumors are known to utilize uncontrollable cell proliferative capabilities as a mechanism for tumor survival. Therefore, malignant cell growth can be mitigated by targeting the essential proteins that regulate cell growth, such as receptor tyrosine kinases (RTKs). Under normal physiological conditions, RTKs bind with varying affinity to mitogenic stimuli such as growth factors such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) which, in turn, leads to receptor phosphorylation and activation.