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Livres sur le sujet « Vegfc »

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Auteur : Grafiati

Publié le 6 juillet 2024

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1

Fiedler, Lorna R., et Caroline Pellet-Many, dir. VEGF Signaling. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2217-9.

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Fiedler, Lorna, dir. VEGF Signaling. New York, NY : Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2917-7.

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3

Bandello, F. Anti-VEGF. Basel : Karger, 2010.

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4

Anti-VEGF. Basel : Karger, 2010.

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5

Harmey, Judith H. VEGF and Cancer. Boston, MA : Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9148-5.

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6

Harmey, Judith H. VEGF and cancer. Georgetown, Tex : Landes Bioscience/Eurekah.com, 2004.

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7

Christiana, Ruhrberg, dir. VEGF in development. Austin, Tex : Landes Bioscience/Eurekah.com, 2008.

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8

H, Harmey Judith, dir. VEGF and cancer. Georgetown, Tex : Landes Bioscience/Eurekah.com ; New York, N.Y. : Kluwer Academic/Plenum Publishers, 2004.

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9

Duker, Jay, et Michelle Liang. Anti-VEGF Use in Ophthalmology. Boca Raton : CRC Press, 2024. http://dx.doi.org/10.1201/9781003522577.

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10

Hastie, Rohan Ferguson. A study of VEGF gene regulation and assessment of the VEGF promoter as a tumour specific promoter in gene therapy. Birmingham : University of Birmingham, 1999.

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11

Chiarotto, James Anthony. Hypoxia-induced upregulation of VEGF mRNA in cervical cancer cell lines. Ottawa : National Library of Canada, 1998.

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12

Fuchs, Johanna. Photodynamische - und anti - VEGF-Therapie als Kombinationstherapie bei der exsudativen altersabhängigen Makuladegeneration. Regensburg : Universitätsbibliothek Regensburg, 2017.

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13

Volz, Yvonne. The molecular function of CD44v6 for the receptor tyrosine kinases Met and VEGFR-2. [S.l : s.n.], 2013.

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14

Muhr, Johanna. Therapieansprechen im Fall eines Rezidivis während der Anti-VEGF-Therapie mit Ranibizumab bei feuchter altersabhängiger Makuladegeneration. [S.I : s.n.], 2013.

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15

Processing Of Vegfc And Vegfd By The Pcs And Tumorigenesis. Biota Publishing, 2013.

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16

Karaman, Sinem, Aleksanteri Aspelund, Michael Detmar et Kari Alitalo. The lymphatic system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0009.

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The lymphatic vascular system is an integral component of the circulatory system; it forms a one-way conduit that transports tissue interstitial components back to the venous circulation through lymph nodes. Lymphatic vessels extend to most tissues and contribute to the regulation of interstitial fluid homeostasis, trafficking of immune cells, and absorption of dietary fats from the gut. Developmentally, lymphatic vessels originate from embryonic veins and specialized angioblasts. A number of molecules have been identified in the commitment of endothelial cells to the lymphatic lineage, and the sprouting, expansion and maturation of the lymphatic vascular tree. Importantly, the vascular endothelial growth factor (VEGF) family members VEGFC and VEGFD, together with their receptors VEGFR2 and VEGFR3 have been implicated as critical regulators of lymphangiogenesis. Lymphatic vessels are involved in several human diseases, including cancer, where they contribute to tumour metastasis, the leading cause of cancer-related deaths. Lymphatic vessels regulate immune responses against foreign pathogens by transporting leucocytes to lymph nodes, but are also in involved in the regulation of self-tolerance. Defects in the lymphatic vascular system are causal for the development of lymphoedema.

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Bandello, F., M. Battaglia Parodi, A. J. Augustin, P. Iacono, R. O. Schlingemann, U. Schmidt-Erfurth et F. D. Verbraak, dir. Anti-VEGF. S. Karger AG, 2010. http://dx.doi.org/10.1159/isbn.978-3-8055-9530-8.

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VEGF in Development. New York, NY : Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-78632-2.

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19

Ruhrberg, Christiana, et Christiana Ruhrberg. VEGF in Development. Springer, 2010.

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20

Harmey, Judith H. VEGF and Cancer. Springer, 2004.

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21

Ruhrberg, Christiana. VEGF in Development. Springer, 2009.

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22

Harmey, Judith H. VEGF and Cancer. Springer, 2012.

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23

Ruhrberg, Christiana. VEGF in Development. Springer London, Limited, 2008.

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24

The role of VEGF abd VEGF receptors in bone development and homeostasis. 2010.

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25

VEGF Signaling : Methods and Protocols. Springer, 2022.

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26

VEGF Signaling : Methods and Protocols. Springer New York, 2015.

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27

Anti-VEGF Use in Ophthalmology. SLACK, Incorporated, 2017.

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28

Fiedler, Lorna. VEGF Signaling : Methods and Protocols. Springer New York, 2016.

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29

of, American Academy. Anti-VEGF Treatment for AMD. American Academy of Ophthalmology, 2014.

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30

Gee, Matthew Frederick William. Studies of autocrine VEGF signalling in rhabdomyosarcoma. 2004.

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31

Vallbacka, Jennifer Jane. Microencapsulation of VEGF-secreting cells : Vascularization for tissue-engineering. 2006.

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32

Ford, Knatokie Marie. Role of VEGF in the Adult : A Tale of Two Epithelia. 2011.

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33

Actualización de Terapia Anti-VEGF en Enfermedades de la Retina y Coroides. Elsevier, 2010. http://dx.doi.org/10.1016/c2011-0-08638-6.

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34

Viloria-Petit, Alicia. The role of VEGF in tumor angiogenesis induced by EGFR-type oncogenic tyrosine kinases. 2003.

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35

Ormiston, Mark L. The effect of VEGF-induced angiogenesis on the viability of microencapsulated cells in vivo. 2005.

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36

Ormiston, Mark L. The effect of VEGF-induced angiogenesis on the viability of microencapsulated cells in vivo. 2005.

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37

Hodgkiss, Andrew. Psychiatric consequences of cancer treatments : ‘small molecule’ molecularly targeted agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0008.

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The psychiatric consequences of a range of small-molecule, molecularly targeted systemic treatments for cancer are reviewed. Psychopathology may arise from the endocrine complications of VEGFR/multiple TK inhibitors. The mechanisms by which PI3K/AKT inhibition and proteasome inhibition can provoke anxiety and depressive phenomena in animals and humans are discussed. PARP-1 inhibition impairs memory acquisition in animal models and is neuroprotective. PARP-2 inhibitors display anti-neuroinflammatory properties in mice. The cognitive enhancing, mood stabilizing, and neuroprotective effects of HDAC inhibitors are considered.

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38

(Editor), Eduardo Diaz-Rubio, et Hans-Joachim Schmoll Halle (Editor), dir. Critical Role of Anti-angiogenesis And Vegf Inhibition in Colorectal Cancer (Supplement Issue : Oncology 2005). Not Avail, 2005.

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39

Anderson, Erin Michelle. Endothelial Progenitor Cell Recruitment for Therapeutic Neovascularization using Alginate Hydrogels for VEGF and SDF Delivery. 2014.

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40

Khatib, Abdel-Majid, A.-Majid Khatib et Geraldine Siegfried. Processing of VEGF-C and -D by the Proprotein Convertases : Importance in Angiogenesis, Lymphangiogenesis, and Tumorigenesis. Morgan & Claypool Life Science Publishers, 2013.

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41

Patil, Bheema, et Pankaj Puri. Medical retina. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199237593.003.0004.

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The chapter begins by discussing key clinical skills, namely fundus fluorescein angiography, abnormal fluorescein angiography, indocyanine green angiography, and electrophysiology. The following areas of clinical knowledge are then discussed: diabetic retinopathy, hypertensive retinopathy, retinal vein occlusion, retinal artery occlusions, age-related macular degeneration, intravitreal anti-VEGF injections, central serous chorioretinopathy, retinal vascular anomalies, retinal dystrophies, and choroidal dystrophies. The chapter concludes with eight case-based discussions, on gradual visual loss, central visual loss, visual loss in a hypertensive patient, sudden, painless visual loss, diabetic retinopathy, difficult night vision, visual loss in child, and macular lesion.

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42

Sundaram, Venki, et Michel Michaelides. Medical retina. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199672516.003.0006.

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This chapter starts off with a discussion of fundus fluorescein angiography and the causes of abnormal fluorescein angiography. It then discusses indocyanine green angiography, including the main indications for this technique. It goes on to cover fundus autofluorescence imaging and electrophysiology. It also includes clinical knowledge areas of diabetic retinopathy, hypertensive retinopathy, retinal vein occlusion, retinal artery occlusions, age-related macular degeneration, central serous chorioretinopathy, retinal vascular anomalies, inherited retinal disorders, macular dystrophies, and choroidal dystrophies. It also discusses a number of important clinical trial studies and contains a section on the use of intravitreal injections of agents against vascular endothelial growth factor (known as VEGF).

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43

Remesal, Ana. Effects of Oxidative Stress and Antenatal Corticosteroids on the Pulmonary Expression of Vascular Endothelial Growth Factor (VEGF) and Alveolarization. INTECH Open Access Publisher, 2012.

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44

Beverungen, Mirjam. Überprüfung der Wirkung von gefäßinduzierenden Wachstumsfaktoren (VEGF=Vascular Endothelial Growth Factor) auf die Vaskularisierung und Osteogenese in festen Knochenersatzstoffen. 2010.

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45

Levy, David. Management of microvascular and associated complications. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0007.

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While end-stage microvascular complications are now relatively uncommon, the burden of microvascular disease is still heavy. National diabetic retinopathy screening programmes have contributed to reducing advanced retinal disease, as has improved laser technology and vitreoretinal surgery. More recently intravitreal anti-VEGF agents (bevacizumab, ranibizumab, and aflibercept) have been effective in reducing visual loss from macular oedema. Diabetic nephropathy has a variable phenotype, and high rates of natural regression from microalbuminuria to normoalbuminuria mandate careful and regular review with regular urinary albumin-creatinine ratio (ACR) measurements. Up to one-quarter of patients with renal impairment have never had microalbuminuria. Long-term glycaemic control is the most important treatment for early diabetic nephropathy; angiotensin blockade treatment (ACE-inhibitors, angiotensin receptor blockers) are less important. In established diabetic nephropathy, intensive multimodal treatment is needed. Neuropathic complications are usually plantar ulceration, Charcot neuroarthropathy, and autonomic, especially gastroparesis and erectile dysfunction.

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46

Duman, Ronald S. Neurotrophic Mechanisms of Depression. Sous la direction de Dennis S. Charney, Eric J. Nestler, Pamela Sklar et Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.

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47

Eremina, Vera. Role of vascular endothelial growth factor A in the glomerulus : Analysis of phenotypes with glomerular-specific alterations of VEGF-A expression in murine transgenic lines. 2006.

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48

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff et Madhumita Bhattacharyya. Gynaecological cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0020_update_001.

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Genitourinary cancers examines the malignancies arising in the kidney, ureter, bladder, prostate, testis, and penis. Renal cancer has high propensity for systemic spread, largely mediated by overexpression of vascular endothelial growth factor (VEGF). Treatments include surgery, immunotherapy, and targeted therapy. Wilms tumour, a childhood malignancy of the kidney, warrants specialist paediatric oncology management to provide expertise in its unique pathology, staging, and treatment, often with surgery and chemotherapy. Cancer of the bladder and ureters, another tobacco related cancer, may present as either superficial or invasive disease. The former is managed by transurethral resection and intravesical therapy. The latter may require radical surgery, preoperative chemotherapy, or radiotherapy. Prostate cancer, the commonest male cancer, is an androgen dependent malignancy. It has attracted controversy with regards to PSA screening, and potential over treatment with radical prostatectomy. Division into low, intermediate, and high risk disease according to tumour grade, stage, and PSA helps in deciding best treatment, antiandrogen therapy for metastatic disease, radiotherapy and adjuvant hormone therapy for locally advanced disease, either surgery or radiotherapy for early intermediate risk disease, and active monitoring for low risk cases. Testicular cancer divides according to pathology into seminoma, nonseminomatous germ cell tumours (NSGCT), and mixed tumours, the latter two frequently producing tumour markers, alpha-fetoprotein (AFP) and/or human chorionic gonadotrophin (HCG). Stage I disease is managed by inguinal orchidectomy and surveillance or adjuvant chemotherapy. More advanced disease is managed by chemotherapy, with high probability of cure in the majority. Penile cancer, often HPV related, can be excised when it presents early, but delay in presentation may lead to regional and systemic spread with poor prognosis.

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