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Bibliografias temáticas / Cellular Proliferation / Livros

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Livros sobre o tema "Cellular Proliferation"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 20 de fevereiro de 2023

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1

Guest, Simon Sean. Strathmin is an intracellular regulator of cellular proliferation. Birmingham: University of Birmingham, 1996.

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2

Renato, Baserga, ed. Biological regulation of cell proliferation. New York: Raven Press, 1986.

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3

Jones, Neil Austin. The role of a major cytosolic protein in cellular proliferation. Birmingham: University of Birmingham, 1992.

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4

L, Boynton Alton, e Leffert H. L, eds. Control of animal cell proliferation. Orlando: Academic Press, 1985.

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5

M, Veneziale Carlo, ed. Control of cell growth and proliferation. New York, N.Y: Van Nostrand Reinhold, 1985.

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6

riazi, Sheila. Pathophysiological links between impaired elastogenesis and increased cellular proliferation in development of cardiovascular disorders. Ottawa: National Library of Canada, 2002.

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7

Burton, Jean. A study of cellular proliferation rates in squamous cell carcinomas of the lung, with relation to p53 status. [S.l: The Author], 1994.

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8

Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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9

International Conference on Gene Regulation, Oncogenesis, and AIDS (1st 1989 Loutráki, Greece). Oncogenesis: Oncogenes in signal transduction and cell proliferation : papers delivered at the First International Conference on Gene Regulation, Oncogenesis, and AIDS, Loutraki, Greece, September 15-21, 1989. Editado por Papas Takis S. Woodlands, Tex: Portfolio Pub. Co., 1990.

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10

Wei, Dai, ed. Checkpoint responses in cancer therapy. Totowa, NJ: Humana Press, 2008.

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11

Heath, John K. Principles of Cell Proliferation. New York: John Wiley & Sons, Ltd., 2008.

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12

Principles of cell proliferation. Malden, MA: Blackwell Science, 2001.

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13

Postans, Richard James. Regional cellular proliferative activity in the second trimester human foetal brain. Birmingham: University of Birmingham, 1994.

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14

Biology of normal proliferating cells in vitro: Relevance for in vivo aging. Basel: Karger, 1988.

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15

Whitfield, James F. Calcium: The grand-master cell signaler. Ottawa: NRC Research Press, 2001.

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16

Whitfield, James F. Calcium: Cell cycle driver, differentiator, and killer. New York: Chapman and Hall, 1997.

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17

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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18

1943-, Ford Richard J., Maizel Abby L e M.D. Anderson Hospital and Tumor Institute., eds. Mediators in cell growth and differentiation. New York: Published for the University of Texas M.D. Anderson Hospital and Tumor Institute at Houston, Houston, Tex., by Raven Press, 1985.

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19

Macken, C. A. Stem cell proliferation and differentiation: A multitype branching process model. Berlin: Springer-Verlag, 1988.

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20

Lutje, Vittoria. Proliferative and antibody responses induced by pokeweed mitogen, sheep erythrocytes and ovalbumin in bovine leukocyte populations, and the cellular interactions involved. Uxbridge: Brunel University, 1989.

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21

David, Evered, Nugent Jonathan e Whelan Julie, eds. Growth factors in biology and medicine. London: Pitman, 1985.

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22

Thrasher, Jack D., e Ivan L. Cameron. Cellular and Molecular Renewal in the Mammalian Body. Elsevier Science & Technology Books, 2013.

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23

L, Boynton Alton, e Leffert Hyam L, eds. Control of animal cell proliferation. Academic, 1987.

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24

(Editor), B. P. Gloor, ed. Visual Field in Glaucoma Cellular Proliferation (Developments in Ophthalmology). S. Karger AG (Switzerland), 1985.

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25

Chakravarthy, Usha. The effect of gamma radiation on intraocular cellular proliferation. 1987.

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26

Nichols, Warren. Regulation of Cell Proliferation and Differentiation. Springer London, Limited, 2012.

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27

Nichols, Warren. Regulation of Cell Proliferation and Differentiation. Springer, 2012.

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28

Morshead, Cindi M. Cellular proliferation in the adult brain: Implications for neural regeneration. 1994.

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29

S, Stein Gary, e Lian Jane B, eds. Molecular and cellular approaches to the control of proliferation and differentiation. San Diego: Academic Press, 1992.

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30

Dijke, Peter, e Carl-Henrik Heldin. Smad Signal Transduction: Smads in Proliferation, Differentiation and Disease. Springer, 2010.

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31

Dijke, Peter, e Carl-Henrik Heldin. Smad Signal Transduction: Smads in Proliferation, Differentiation and Disease. Springer, 2007.

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32

Stein, Gary. Molecular and Cellular Approaches to the Control of Proliferation and Differentiation. Elsevier Science & Technology Books, 2012.

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33

Molecular and Cellular Approaches to the Control of Proliferation and Differentiation. Elsevier, 1992. http://dx.doi.org/10.1016/b978-0-126-64745-7.x5001-x.

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34

P, Cronkite Eugene, Bond Victor P, Chandra Pradeep, Rai Kanti R, United States. Dept. of Energy., Brookhaven National Laboratory e Associated Universities Inc, eds. Hematopoietic cellular proliferation: An international conference in honor of Eugene P. Cronkite. New York, N.Y: New York Academy of Sciences, 1985.

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35

Schmandt, Rosemarie Elizabeth. Characterization of TTK, a unique dual specificity kinase associated with cellular proliferation. 1996.

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36

Lang, F. P. Ion Transport in the Regulation of Cell Proliferation in Cellular Physiology and Biochemistry: Journal: Cellular Physiology and Biochemistry, Vol. 2 (Cellular Physiology & Biochemistry). S. Karger AG (Switzerland), 1992.

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37

The Enzymes, Volume 25: Molecular Machines involved in Protein Transport across Cellular Membranes (The Enzymes) (The Enzymes). Academic Press, 2007.

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38

(Editor), Fuyuhiko Tamanoi, Ross Dalbey (Editor) e Carla Koehler (Editor), eds. The Enzymes, Volume 25: Molecular Machines involved in Protein Transport across Cellular Membranes (The Enzymes) (The Enzymes). Academic Press, 2007.

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39

Growth, Cancer, and the Cell Cycle: The Molecular, Cellular, and Developmental Biology. Humana Press, 2011.

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40

Skehan, Philip, e Susan J. Friedman. Growth, Cancer, and the Cell Cycle: The Molecular, Cellular, and Developmental Biology. Humana Press, 2012.

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41

Jimi, Shiro, Satoshi Takagi e Arman Saparov, eds. Cellular and Molecular Mechanisms at the Proliferation Stage in Wound Healing: From Scarring to Tissue Regeneration. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-637-9.

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42

Lories, Rik. Mechanisms of bone destruction and proliferation in psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0008.

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Psoriatic arthritis is a chronic inflammatory joint disease that can affect both the peripheral and axial skeleton. The clinical presentation of psoriatic arthritis is very heterogeneous and different subforms have been described. Structural damage to the joint is a feared complication of psoriatic arthritis. The severity of joint inflammation and subsequent damage can range from mild to extreme. Over the last decade, insights into the molecular and cellular mechanisms that underlie the skeletal changes in psoriatic arthritis have gradually increased although translational validation of concepts using patient-derived materials still lags behind. Current treatment strategies directed against key mediators of inflammation appear to have good effects on joint destruction, but their short and long-term impact on new bone formation and ankylosis is still unclear. The identification of the role that key growth factors play in the latter process identifies new opportunities for therapeutic interventions.

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43

(Editor), Peter ten Dijke, e Carl-Henrik Heldin (Editor), eds. Smad Signal Transduction: Smads in Proliferation, Differentiation and Disease (Proteins and Cell Regulation). Springer, 2006.

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44

Tsilfidis, Cathy *. "In vivo" and "in vitro" effects of nerves on cellular proliferation in the post-metamorphic '"Xenopus laevis" forelimb regenerate. 1990.

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45

Bunch, Chris. Normal blood function. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0277.

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This chapter reviews normal blood function and disorders of haemopoiesis. Blood consists of cells of three main types, suspended in plasma. The cellular component comprises about 40%–50% of the total volume and consists of red cells (erythrocytes), white cells (leucocytes), and platelets. Blood cells are formed from progenitor cells in the bone marrow by haemopoiesis, a process of proliferation and differentiation. Failure of haemopoiesis usually results from damage to proliferating marrow cells by cytotoxic drugs or radiation, haemopoietic malignancy, or a combination of the two.

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46

Bond, Victor P. Hematopoietic Cellular Proliferation: An International Conference in Honor of Eugene P. Cronkite (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1985.

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47

Whitfield, James F., Elisabeth R. Lefebvre e Balu Chakravarthy. Calcium: The Grand-Master Cell Signaler. NRC Research Press, 2001.

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48

Meridith, Alan T. Handbook of Prostate Cancer Cell Research: Growth, Signalling and Surviva. Nova Science Publishers, Incorporated, 2009.

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49

Bertolaso, Marta, e John Dupré. A Processual Perspective on Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198779636.003.0016.

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This chapter attempts to illuminate the dynamic stability of the organism and the robustness of its developmental pathway by considering the biology of cancer. Healthy development and stable functioning of a multicellular organism require an exquisitely regulated balance between processes of cell division, differentiation, and death (apoptosis). Cancer involves a disruption of this balance, which results in unregulated cell proliferation. The thesis defended in this chapter is that the coupling between proliferation and differentiation, whether normal or pathological (as in cancer), is best understood within a process-ontological framework. This framework emphasizes the interactions and mutual stabilizations between processes at different levels and this, in turn, explains the difficulty in allocating the neoplastic process to any particular level (genetic, epigenetic, cellular, or histological). Understanding these interactions is likely to be a precondition of a proper understanding of how these mutual regulations are disrupted in the processes we call cancerous.

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50

Cell Proliferation Lymphomas. Blackwell Science, 1993.

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