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Books on the topic 'Growth factors – Pathophysiology'

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Published: 10 December 2022
Last updated: 28 January 2023

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1

NATO Advanced Study Institute on Advances in Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (1989 Erice, Italy). Bone regulatory factors: Morphology, biochemistry, physiology, and pharmacology. New York: Plenum Press, 1990.

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2

1947-, Cummins Peter, ed. Growth factors and the cardiovascular system. Boston: Kluwer Academic Publishers, 1993.

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3

NATO Advanced Study Institute on Advances in Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (1989 Erice, Italy). Bone regulatory factors: Morphology, biochemistry, physiology, and pharmacology. New York: Plenum Press, 1990.

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4

Nerve growth factor and pain. New York: Nova Science Publishers, 2010.

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5

Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Molecular biology and differentiation of cancer cells (oncogenes, growth factors, receptors). Budapest: Akadémiai Kiadó, 1987.

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6

Molnár, Ildikó. Nervous, immune, endocrine regulatory systems and diseases associated with nerve growth factor co-secretion. Hauppauge, N.Y: Nova Science Publishers, 2009.

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7

1952-, Dickson Robert B., and Salomon David S. 1947-, eds. Hormones and growth factors in development and neoplasia. New York: Wiley-Liss, 1998.

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8

Bengt, Westermark, Betsholtz Christer, and Hökfelt Bernt, eds. Growth factors in health and disease: Basic and clinical aspects : proceedings of the 4th Nordisk Insulin Symposium "Growth Factors in Health and Disease," Copenhagen, Denmark, 18-20 June 1990. Amsterdam: New York :Excerpta Medica, 1990.

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9

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

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10

Symposium on Biology of Growth Factors, Molecular Biology, Oncogenes, Signal Transduction, and Clinical Implications (1987 Toronto, Ont.). Biology of growth factors: Molecular biology, oncogenes, signal transduction, and clinical implications. New York: Plenum Press, 1988.

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11

service), SpringerLink (Online, ed. The Islets of Langerhans. Dordrecht: Springer Science+Business Media B.V., 2010.

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12

Symposium of the Banting and Best Diabetes Centre on Biology of Growth Factors: Molecular Biology, Oncogenes, Signal Transduction, and Clinical Implications (1987 Toronto, Ont.). Biology of growth factors: Molecular biology, oncogenes, signal transduction, and clinical implications. New York: Plenum Press, 1988.

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13

1945-, Lippman Marc E., and Dickson Robert B. 1952-, eds. Breast cancer: Cellular and molecular biology. Boston: Kluwer Academic Publishers, 1988.

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14

R, Ambruso Daniel, ed. Phagocyte production and function following burn injury. Austin: R.G. Landes, 1994.

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15

Rosen, Vicki. The cellular and molecular basis of bone formation and repair. New York: Springer, 1995.

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16

1957-, Thies Robert Scott, ed. The cellular and molecular basis of bone formation and repair. Austin: R.G. Landes, 1995.

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17

Allan, Flyvbjerg, Ørskov Hans, and Alberti George, eds. Growth hormone and insulin-like growth factor I in human and experimental diabetes. Chichester: Wiley, 1993.

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18

M, Berry, and Logan Ann, eds. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.

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19

Jr, Roberts Charles T., and Rosenfeld Ron G, eds. The IGF system: Molecular biology, physiology, and clinical applications. Totowa, N.J: Humana Press, 1999.

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20

E, Müller E., ed. IGFs in the nervous system. Berlin: Springer, 1998.

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21

1947-, Rubanyi Gabor M., ed. Angiogenesis in health and disease: Basic mechanisms and clinical applications. New York: Dekker, 2000.

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22

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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23

Nakamura, T., Wen G. Jiang, and K. Matsumoto. Growth Factors and Their Receptors in Cancer Metastasis. Springer London, Limited, 2006.

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24

Nakamura, T., Wen G. Jiang, and K. Matsumoto. Growth Factors and their Receptors in Cancer Metastasis. Springer, 2014.

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25

(Editor), W. G. Jiang, K. Matsumoto (Editor), and T. Nakamura (Editor), eds. Growth Factors and Their Receptors in Cancer Metastasis. Springer, 2001.

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26

Jiang, Wen G. Growth Factors and their Receptors in Cancer Metastasis. Springer, 2010.

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27

C, Weber Peter, and Leaf Alexander 1920-, eds. Atherosclerosis: Cellular interactions, growth factors, and lipids. New York: Raven Press, 1993.

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28

Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (Nato Science Series: A:). Springer, 1990.

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29

Weber, Peter C. Atherosclerosis: Cellular Interactions, Growth Factors, and Lipids (Atherosclerosis Reviews). Raven Pr, 1993.

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30

B, Schook Lawrence, and Laskin Debra L, eds. Xenobiotics and inflammation. San Diego: Academic Press, 1994.

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31

Nordisk Insulin Symposium Growth Factors in Health and Disease, Christer Betsholtz, and Bengt Westermark. Growth Factors in Health and Disease: Basic and Clinical Aspects : Proceedings of the 4th Nordisk Insulin Symposium 'Growth Factors in Health and Di (International Congress Series). Elsevier Science & Technology, 1991.

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32

Abhishek, Abhishek, and Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.
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33

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

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34

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

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35

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

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36

Weber, Peter C. Atherosclerosis: Its Pathogenesis and the Role of Cholesterol (Atherosclerosis Reviews). Raven Pr, 1991.

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37

Islam, Md Shahidul. Islets of Langerhans. Springer, 2015.

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38

Islam, Md Shahidul. The Islets of Langerhans. Md Shahidul Islam, 2012.

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39

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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40

Lippman, Marc E., and Robert B. Dickson. Breast Cancer: Cellular and Molecular Biology. Springer, 2012.

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41

H, Growdon John, Center for Brain Sciences and Metabolism Charitable Trust., and International Study Group on the Pharmacology of Memory Disorders Associated with Aging. Meeting, eds. Aging and Alzheimer's disease: Sensory systems neuronal growth, and neuronal metabolism. New York, N.Y: New York Academy of Sciences, 1991.

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42

Biology of Growth Factors: Molecular Biology, Oncogenes, Signal Transduction, and Clinical Implications (Advances in Experimental Medicine and Biology). Plenum Pub Corp, 1988.

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43

Growdon, John H., and Switzerland) International Study Group on the Pharmacology of Memory Disorders Associated with Aging. Meeting (6th : 1991 : Zurich. Aging and Alzheimer's Disease: Sensory Systems Neuronal Growth, and Neuronal Metabolism (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1991.

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44

Theis, R. Scott, and Vicki Rosen. Cellular & Molec Basis Bone Format (Molecular Biology Intelligence Unit). Springer, 1996.

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45

Berry, Martin, and Ann Logan. CNS Injuries: Cellular Responses and Pharmacological Strategies (Pharmacology & Toxicology (Crc Pr)). CRC, 1998.

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46

Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.

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47

Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.

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48

Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.

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49

Berry, Martin. CNS Injuries: Cellular Responses and Pharmacological Strategies. Taylor & Francis Group, 2019.

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50

Marin, Marie-France, and Mohammed R. Milad. Functional Neuroimaging of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0016.

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The merger of neuroscience and psychiatry during the last two decades has enabled psychiatric neuroscience, as a newly refined discipline, to make great advances in understanding pathophysiology of psychiatric disorders, including post-traumatic stress disorder (PTSD). The advent of neuroimaging tools and the continued exponential growth and sophistication of the methods are key factors underlying advances in the field. In this chapter, informed by neuroimaging tools and basic neuroscience, the authors paint an optimistic canvas to illustrate the current state of knowledge pertaining to the etiology and pathophysiology of PTSD. The chapter describes the state of some recent developments and what is coming on the horizon in terms of novel approaches that may be applied toward the diagnosis and treatment of PTSD.
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