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Libros sobre el tema "Membrane Modello"

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Publicado: 11 de marzo de 2023

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1

Les modèles moléculaires de biomembranes. Paris: Hermann, 1987.

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2

H, Templer Richard, Leatherbarrow Robin y Royal Society of Chemistry (Great Britain). Biophysical Chemistry Group., eds. Biophysical chemistry: Membranes and proteins. Cambridge, UK: Royal Society of Chemistry, 2002.

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3

1957-, Layton Harold Erick y Weinstein Alan M, eds. Membrane transport and renal physiology. New York: Springer, 2002.

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4

1932-, Osa Tetsuo y Atwood J. L, eds. Inclusion aspects of membrane chemistry. Dordrecht: Kluwer Academic Publishers, 1991.

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5

U, Raess B. y Tunnicliff Godfrey, eds. The Red cell membrane: A model for solute transport. Clifton, N.J: Humana Press, 1989.

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6

Gao, Fei. Proton exchange membrane fuel cells modeling. London: ISTE, 2011.

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7

Norbert, Latruffe, Federation of European Biochemical Societies. y Centre national de la recherche scientifique (France), eds. Dynamics of membrane proteins and cellular energetics. Berlin: Springer-Verlag, 1988.

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8

Frishman, Dmitrij. Structural bioinformatics of membrane proteins. Wien: Springer, 2010.

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9

1948-, Mrak Robert E., ed. Muscle membranes in diseases of muscle. Boca Raton, Fla: CRC Press, 1985.

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10

NATO Advanced Study Institute on Physical Methods on Biological Membranes and Their Model Systems (1982 Altavilla Milicia, Italy). Physical methods on biological membranes and their model systems. New York: Plenum Press, 1985.

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11

Păun, Andrei. Computability of the DNA and cells: Splicing and membrane computing. Choudrant, La: SBEB Pub., 2008.

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12

Elena, Eizenberg, ed. Membranes and other extendons (p-branes). Singapore: World Scientific, 1995.

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13

Ribatti, Domenico. The chick embryo chorioallantoic membrane in the study of angiogenesis and metastasis. Dordrecht: Springer, 2010.

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14

Ramón, Latorre, ed. Ionic channels in cells and model systems. New York: Plenum Press, 1986.

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15

sc, Müller Eberhard Dr y Dahse Ingo, eds. Vom Organismus zum Molekül: Physiologische Prozesse, ihre Modellierung und Beeinflussbarkeit auf verschiedenen Ebenen : Festschrift für Eberhard Müller zum 60. Geburtstag. Jena: Friedrich-Schiller-Universität, 1992.

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16

Lipowsky, Reinhard. The Structure and Conformation of Amphiphilic Membranes: Proceedings of the International Workshop on Amphiphilic Membranes, Jülich, Germany, September 16-18, 1991. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992.

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17

Jacob, Abraham. Nonlinear, finite strain, finite element model of the mechanics of the posterior tracheal membrane. [Downsview, Ont.]: University of Toronto, Institute for Aerospace Studies, 2003.

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18

Derek, Marsh, ed. Phospholipid bilayers: Physical principles and models. New York: Wiley, 1987.

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19

E, Vance Dennis y Vance Jean E, eds. Biochemistry of lipids, lipoproteins, and membranes. Amsterdam: Elsevier, 1991.

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20

Lockheed Martin Astronautics (Firm). Flight Systems Division. y United States. National Aeronautics and Space Administration., eds. Membrane Transport Phenomena (MTP): Semi-annual technical progress report, June 1997-October 1997 : contract number NAS8-40633. [Denver, Colo.]: Lockheed Martin, 1997.

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21

Lockheed Martin Astronautics (Firm). Flight Systems Division. y United States. National Aeronautics and Space Administration., eds. Membrane Transport Phenomena (MTP): Semi-annual technical progress report, May 1996 - November 1996, contract number: NAS8-40633. [Denver, Colo.]: Lockheed Martin, 1997.

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22

Lockheed Martin Astronautics (Firm). Flight Systems Division. y United States. National Aeronautics and Space Administration., eds. Membrane Transport Phenomena (MTP): Semi-annual technical progress report, May 1996 - November 1996, contract number: NAS8-40633. [Denver, Colo.]: Lockheed Martin, 1997.

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23

Lockheed Martin Astronautics (Firm). Flight Systems Division. y United States. National Aeronautics and Space Administration., eds. Membrane Transport Phenomena (MTP): Semi-annual technical progress report, November 1996 - May 1997, contract number: NAS8-40633. [Denver, Colo.]: Lockheed Martin, 1997.

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24

1941-, Beyreuther K. y Schettler Gotthard, eds. Molecular mechanisms of aging. Berlin: Springer-Verlag, 1990.

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25

Dimitrievski, Kristian. Monte Carlo simulations of supported biomembranes and protein folding. Göteborg: Göteborg University, Department of Physics, 2006.

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26

Zakrzewska-Trznadel, Grażyna. Procesy membranowe w technologiach jądrowych: Wybrane zagadnienia modelowania transportu masy oraz projektowania systemów rozdzielania. Warszawa: Instytut Chemii i Techniki Jądrowej, 2006.

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27

Zakrzewska-Trznadel, Grażyna. Procesy membranowe w technologiach jądrowych: Wybrane zagadnienia modelowania transportu masy oraz projektowania systemów rozdzielania. Warszawa: Instytut Chemii i Techniki Jądrowej, 2006.

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28

A, Gruzdkov A., Ugolev A. M y Akademii͡a︡ nauk SSSR. Otdelenie fiziologii., eds. Adaptat͡s︡ionno-kompensatornye prot͡s︡essy: Na primere membrannogo gidroliza i transporta. Leningrad: "Nauka," Leningradskoe otd-nie, 1991.

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29

National Institute of Child Health & Human Development Research Planning Workshop (1987 Bethesda, Md.). The onset of labor: Cellular and integrative mechanisms : a National Institute of Child Health & Human Development Research Planning Workshop, November 29-December 1, 1987. Ithaca, NY, U.S.A: Publisher and sole distributor, Perinatology Press, 1988.

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30

Henrik, Bohr y Brunak Søren, eds. Protein folds: A distance-based approach. Boca Raton: CRC Press, 1996.

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31

Bacterial outer membranes as model systems. New York: Wiley, 1987.

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32

Cholesterol in membrane models. Boca Raton, Fla: CRC Press, 1992.

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33

Heimburg, Thomas. Thermal Biophysics of Membranes. Wiley-VCH, 2007.

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34

Heimburg, Thomas. Thermal Biophysics of Membranes. Wiley & Sons, Incorporated, John, 2008.

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35

Heimburg, Thomas. Thermal Biophysics of Membranes. Wiley & Sons, Limited, John, 2007.

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36

von, Heijne Gunnar, ed. Membrane protein assembly. Austin: R.G. Landes, 1997.

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37

Thompson, Gary O. Flexible membrane wave barrier. 1991.

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38

Membrane Protein Models. BIOS Scientific Publ, 1996.

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39

(Editor), Harold E. Layton y Alan M. Weinstein (Editor), eds. Membrane Transport and Renal Physiology. Springer, 2002.

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40

Osa, T. y J. L. Atwood. Inclusion Aspects of Membrane Chemistry. Springer, 2012.

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41

Osa, T. y J. L. Atwood. Inclusion Aspects of Membrane Chemistry. Springer Netherlands, 2012.

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42

(Editor), B. U. Raess y G. Tunnicliff (Editor), eds. The Red Cell Membrane: A Model for Solute Transport (Contemporary Biomedicine). Humana Press, 1990.

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43

Cui, Zhao, Neil Turner y Ming-hui Zhao. Antiglomerular basement membrane disease. Editado por Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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44

(Editor), R. H. Templer y R. J. Leatherbarrow (Editor), eds. Biophysical Chemistry: Membrane and Proteins (Biotechnology Intelligence Unit, 283). Royal Society of Chemistry, 2003.

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45

Cui, Zhao, Neil Turner y Ming-hui Zhao. Antiglomerular basement membrane disease. Editado por Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.
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46

Berkowitz, Max L. Biomembrane Simulations. Taylor & Francis Group, 2019.

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47

Biomembrane Simulations: Computational Studies of Biological Membranes. Taylor & Francis Group, 2019.

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48

Berkowitz, Max L. Biomembrane Simulations: Computational Studies of Biological Membranes. Taylor & Francis Group, 2014.

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49

Berkowitz, Max L. Biomembrane Simulations. Taylor & Francis Group, 2021.

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50

Kraisuwansarn, Nichakorn. Simulation of a membrane reactor for ammonia decomposition. 1991.

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