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Livres sur le sujet « Fibroblast Growth Factor 2 »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 18 février 2022

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1

Lyn-Cook, Richard X. Cortical development in fibroblast growth factor 2 knockout mice. [New Haven, Conn : s.n.], 1999.

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2

Smith, Conrad. Developmental changes in the injury induced expression of fibroblast growth factor-2 and fibroblast growth factor receptor 1 in the rat brain. Birmingham : University of Birmingham, 1998.

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3

Thompson, Stuart David. Fibroblast growth factor 2 and its receptor, FGFR 1 in the normal thyroid and multinodular goitre. Birmingham : University of Birmingham, 2000.

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4

Wang, David I. Kuo. The effects of fibroblast growth factor 2 on the early stages on in vitro endothelial wound repair. Ottawa : National Library of Canada, 1998.

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5

Clarke, Wendy Elizabeth. Intracellular compartmentalisation of fibroblast growth factor-2 and associated high and low affinity receptors after cerebral injury to the adult rat brain. Birmingham : University of Birmingham, 1999.

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6

Burgar, Helen Rachel. Fibroblast growth factor receptor signalling. Birmingham : University of Birmingham, 2002.

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7

Walters, Jean Elizabeth. Immunochemical studies on fibroblast growth factor-1 and fibroblast growth factor receptor 1. Oxford : Oxford Brookes University, 1998.

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8

Cocks, Helen Catherine. Fibroblast growth factor in the thyroid. Birmingham : University of Birmingham, 2003.

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9

Daley, Sandra J. Basic fibroblast growth factor mediates neointimal formation in porcine aortic explants. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1997.

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10

Plowright, Elizabeth Emma. Expression of fibroblast growth factor receptor 3 in multiple myeloma causes II-6-independence and enhanced survival. Ottawa : National Library of Canada, 1999.

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11

Onwuazor, Obiageli Nneka. Mutation, SNP and isoform analysis of fibroblast growth factor receptor 3 (FGFR3) in 150 newly diagnosed multiple myeloma patients. Ottawa : National Library of Canada, 2003.

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12

Hellweg, Rainer. Der Nerve Growth Factor bei neuropsychiatrischen Erkrankungen. Heidelberg : Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-96006-2.

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13

Tsai, Anne Chun-Hui. Characterization of the trophic properties of GLP-2, a novel intestinal growth factor. Ottawa : National Library of Canada, 1996.

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14

Perlikowski, Sandra Michelle. Replication timing of insulin-like growth factor-2 (IFG2) in Beckwith-Wiedemann syndrome. Ottawa : National Library of Canada = Bibliothèque nationale du Canada, 1999.

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15

1945-, Lippman Marc E., Ortho Pharmaceutical Corporation et University of California, Los Angeles., dir. Growth regulation of cancer : Proceedings of an Ortho-UCLA Symposium on Growth Regulation of Cancer, held at Park City, Utah, January 17-23, 1987. New York : Liss, 1988.

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16

Jakowlew, Sonia B. Transforming Growth Factor-β in Cancer Therapy, Volume I. Totowa, NJ : Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-292-2.

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17

Dworkin, Chaim R. The use of growth factors in cancer therapy. [Bethesda, Md.?] : U.S. DHHS, PHS, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1993.

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18

Battaglini, Michelina. Determination of the transforming growth factor-B (TGF-B) receptor on the surface of interleukin-2 activated natural killer (IANK) cells. Sudbury, Ont : Laurentian University, 1992.

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19

International Symposium on Molecular and Cellular Biology of Insulin and IGFs (3rd 1990 Gainesville, Fla.). Molecular biology and physiology of insulin and insulin-like growth factors. New York : Plenum Press, 1991.

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20

C, Baxter R., Gluckman Peter D et Rosenfeld Ron G, dir. The insulin-like growth factors and their regulatory proteins : Proceedings of the Third International Symposium on Insulin-Like Growth Factors, Sydney, 6-10 February 1994. Amsterdam : Excerpta Medica, 1994.

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21

Steinfeld, R. Modulation of the Interaction Between Fibroblast Growth Factor-2 and Fibroblast Growth Factor Receptor-1 by Cell Surface Heparan Sulfate Proteoglycans. Leuven University Press, 1996.

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22

Wang, Zhouguang, Xiaokun Li, Li Lin, Saverio Bellusci et Jin-San Zhang, dir. The Fibroblast Growth Factor Signaling Pathway in Metabolic Regulation, Development, Disease and Repair After Injury. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-128-2.

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23

Photochemical Systematic Evolution of Ligands by Exponential Enrichment (Photoselex) Employing the 5-BROMO-2'-Deoxyuridine Chromophore for the Basic Fibroblast Growth Factor Target. Storming Media, 1999.

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24

White, Kenneth, Christian Faul et Orlando Gutierrez. Fibroblast Growth Factor 23. Elsevier, 2021.

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25

Fibroblast Growth Factor 23. Elsevier, 2021. http://dx.doi.org/10.1016/c2018-0-03274-0.

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26

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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27

Baird, Andrew, 1954 July 27-, Klagsbrun Michael et New York Academy of Sciences., dir. The Fibroblast growth factor family. New York, N.Y : New York Academy of Sciences, 1991.

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28

Pedro, Cuevas, dir. Fibroblast growth factor in the cardiovascular system. Munich : I. Holzapfel, 2002.

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29

Padela, Sanna. Hepatocyte growth factor and fibroblast growth factor-7 in neonatal lung development and injury. 2006.

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30

Fibroblast Growth Factor Receptor (FGFR) Signaling Pathway in Tumor. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03936-785-6.

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31

Ashton, Anthony. Fibroblast Growth Factor : Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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32

Zhang, Zhe. Cell Surface Heparan Sulfate Proteoglycans As Co-Receptors for Fibroblast Growth Factor. Leuven Univ Pr, 2002.

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33

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.

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34

Endocrine Fgfs and Klothos Advances in Experimental Medicine and Biology. Springer, 2012.

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35

Carroll, Camilla Ma. The effects of the angiogenic growth factors, platelet derived growth factor and basic fibroblast growth factor, on the survival,perfusion and function of the latissmus dorsi muscle flap. 1997.

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36

Bardin, Thomas, et Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

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37

The catabolism of glucagon-like peptidea 2 : A novel intestinal growth factor. Ottawa : National Library of Canada, 1998.

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38

Growth regulation of cancer : Proceedings of an Ortho-UCLA Symposium on Growth Regulation of Cancer, held at Park City, Utah, January 17-23, 1987 (UCLA symposia on molecular and cellular biology). Liss, 1988.

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39

Hoeflich, Andreas, John Pintar et Briony Forbes, dir. Current Perspectives on Insulin-like Growth Factor Binding Protein (IGFBP) Research. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-718-2.

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40

Hirschberg, Raimund. Transforming Growth Factor-B in the Kidney & Renal Diseases (Mineral & Electrolyte Metabolism Ser. 2-3). S Karger Pub, 1998.

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41

Bothwell, M. Neuronal Growth Factors (Current Topics in Microbiology & Immunology). Sous la direction de M. Bothwell. Springer, 1991.

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42

Kjell, Fuxe, et Wenner-Grenska samfundet, dir. Trophic regulation of the basal ganglia : Focus on dopamine neurons. Oxford, OX, UK : Pergamon, 1994.

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43

Tsai, Eve Chung. Mechanisms of locomotor recovery after spinal cord repair with peripheral nerves, fibroblast growth factor 1, and fibrin glue after complete spinal cord transection in the adult mammal. 2004.

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44

Cimpean, Anca Maria, Andreea Adriana Jitariu et Marius Raica. Growth Factors and Their Corresponding Receptors as Targets for Ovarian Cancer Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0011.

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Ovarian cancer remains one of the most aggressive and difficult to manage malignancies regarding evaluation and therapeutic options. The high mortality persists despite extensive research in the field. Current conventional chemotherapy does not improve disease-free survival and does not decrease recurrences amongst patients. This calls for a stringent reconsideration of the drugs selection, focused on the most targeted strategies and personalization of the therapy. Targeted agents against growth factors and their corresponding receptors are already approved as first- or second-line neoadjuvant therapy with controversial results. This chapter critically discusses the role of growth factors as vascular endothelial growth factor, fibroblast growth factors, or platelet-derived growth factors and their corresponding receptors in the pathogenesis, progression, and selection of therapeutic strategies. Other growth factors, such as nerve growth factor or endocrine gland derived growth factor, seem to have a strong involvement in ovarian carcinogenesis but their actual impact is not fully understood.

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45

Yoshii, Akira, Martha Constantine-Paton et Nancy Y. Ip, dir. Cell and molecular signaling, and transport pathways involved in growth factor control of synaptic development and function. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-643-2.

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46

Voinescu, Alexandra, Nadia Wasi Iqbal et Kevin J. Martin. Pathophysiology of chronic kidney disease-mineral and bone disorder. Sous la direction de David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0117.

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Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.

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47

Dryzek, John S. 2. Looming Tragedy : Limits, Boundaries, Survival. Oxford University Press, 2017. http://dx.doi.org/10.1093/hepl/9780199696000.003.0002.

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This chapter focuses on the environmental discourse of limits and survival and how it set the apocalyptic horizon of environmentalism. Population biologists and ecologists use the concept of ‘carrying capacity’ — the maximum population of a species that an ecosystem can support in perpetuity. When the population of a species grows to the point where carrying capacity is exceeded, the ecosystem is degraded and the population crashes, recovering only if and when natural processes restore the ecosystem to its previous capacity. One complicating factor when it comes to applying population biology to human societies is the possibility of economic growth. The chapter first considers the origins of survivalism before discussing the political philosophy of survival, discourse analysis of limits and survival, and limits and survival in practice. It also examines the challenges confronting the limits discourse, including the lack of international action on climate change.

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48

(Editor), Derek LeRoith, et Mohan K. Raizada (Editor), dir. Molecular Biology and Physiology of Insulin and Insulin-Like Growth Factors (Advances in Experimental Medicine and Biology). Springer, 1991.

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49

Baxter, R. C., et Peter D. Gluckman. The Insulin-Like Growth Factors and Their Regulatory Proteins : Proceedings of the Third International Symposium on Insulin-Like Growth Factors, Sydn (International Congress Series). Elsevier Science Pub Co, 1994.

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50

Meier, Petra M., et Thomas O. Erb. Craniosynostosis and Apert Syndrome. Sous la direction de Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi et Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0021.

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Apert syndrome is a complex, progressive multisystem condition of the craniosynostosis spectrum originating from a fibroblast growth factor receptor disorder. Multidisciplinary treatment teams may include craniofacial surgery, neurosurgery, otolaryngology, ophthalmology, oro-maxillofacial surgery, and pediatric intensive care. Secondary to midface hypoplasia, children often present with a compromised airway and have a high incidence of sleep disorders. Anesthetic considerations include difficult airway assessment, the presence of obstructive sleep apnea syndrome, and increased intracranial pressure. Extensive remodeling procedures can be associated with massive hemorrhage (e.g., venous sinus bleeding) and venous air embolism. Transfusion-related complications include coagulopathy, metabolic derangements, and primarily noninfectious hazards such as transfusion-related acute lung injury and transfusion-related immunomodulation. Multimodal blood management should focus on a combination of appropriate surgical techniques and blood conservation, along with guidance from point-of-care testing (including coagulation).

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