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Książki na temat „CELLULAR AND SYSTEMIC RESPONSES”

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Data publikacji: 11 września 2023

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1

King, William James. Autoimmune cellular responses towards neutrophil granule enzymes in systemic vasculitis. Birmingham: University of Birmingham, 1998.

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

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3

Feige, U., I. Yahara, R. I. Morimoto i B. S. Polla, red. Stress-Inducible Cellular Responses. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9088-5.

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Dr, Feige U., red. Stress-inducible cellular responses. Basel: Birkhäuser Verlag, 1996.

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Peter, Downes C., Wolf C. Roland i Lane David 1952-, red. Cellular responses to stress. London: Portland, 1999.

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Peter, Downes C., Wolf C. Roland i Lane David 1952-, red. Cellular responses to stress. Princeton, N.J: Princeton University Press, 1999.

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Davies, Stuart Matthew. Cellular responses to potential biomaterials. Birmingham: Aston University. Department of Chemical Engineering and Applied Chemistry, 1991.

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Galli, Corrado L., Marina Marinovich i Alan M. Goldberg, red. Modulation of Cellular Responses in Toxicity. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79872-6.

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9

L, Galli C., Marinovich Marina, Goldberg Alan M, North Atlantic Treaty Organization. Scientific Affairs Division. i NATO Advanced Study Institute on the Modulation of Cellular Responses in Toxicity (1994 : Ponte di Legno, Italy), red. Modulation of cellular responses in toxicity. Berlin: Springer, 1995.

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10

Vitor, Cohen Ricardo, red. Metabolic and systemic responses following interventional laparoscopy. Austin: R.G. Landes, 1994.

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11

Nikolaas, Akkerman Jan Willem, red. Energetics of secretion responses. Boca Raton, Fla: CRC Press, 1988.

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12

Mian, Rubina Saghir. Acute systemic hypoxia and responses in muscle microcirculation. Birmingham: University of Birmingham, 1991.

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13

B, Storey K., i Storey J, red. Environmental stressors and gene responses. Amsterdam: Elsevier, 2000.

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14

Porritt, Helen Elizabeth. Cellular interactions in the thymus regulating thymocyte signalling responses. Birmingham: University of Birmingham, 1999.

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15

Le, X. Chris. Cellular responses to arsenic: DNA damage and defense mechanisms. Denver, CO: AWWA Research Foundation, 2004.

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16

Brasier, Allan R., Adolfo García-Sastre i Stanley M. Lemon, red. Cellular Signaling and Innate Immune Responses to RNA Virus Infections. Washington, DC, USA: ASM Press, 2008. http://dx.doi.org/10.1128/9781555815561.

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17

R, Brasier Allan, García-Sastre Adolfo i Lemon Stanley M, red. Cellular signaling and innate immune responses to RNA virus infections. Washington, D.C: ASM Press, 2009.

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18

1949-, Lee R. C., Despa Florin, Hamann Kimm Jon i New York Academy of Sciences., red. Cell injury: Mechanisms, responses, and repair. New York, N.Y: New York Academy of Sciences, 2005.

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19

Davies, Marie Louise. Autoantigen specific T cell responses in relation to systemic lupus erythematosus. Birmingham: University of Birmingham, 2000.

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20

1936-, McCarthy F. Desmond, International Bank for Reconstruction and Development. Europe and Central Asia Region. Country Dept. IV. Country Operations Division 2. i International Bank for Reconstruction and Development. Office of the Vice President, Development Economics., red. External shocks and performance responses during systemic transition: The case of Ukraine. Washington, DC: World Bank, Europe and Central Asia, Country Dept. IV, Country Operations Division 2, and Office of the Vice President, Development Economics, 1994.

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21

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

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22

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

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23

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

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24

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

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25

Cooper, E. L., G. Beck, P. B. Armstrong i C. Franceschi. Invertebrate Immune Responses: Cell Activities and the Environment. Springer London, Limited, 2013.

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26

Cooper, E. L., G. Beck, P. B. Armstrong i C. Franceschi. Invertebrate Immune Responses: Cell Activities and the Environment. Springer London, Limited, 2011.

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27

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

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28

Cooper, Edwin L., red. Invertebrate Immune Responses: CELLS AND MOLECULAR PRODUCTS (DISCONTINUED (Advances in Comparative and Environmental Physiology)). SPRINGER-VERLAG, 1996.

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29

Cooper, E. L. Invertebrate Immune Responses: Cell Activities and the Environment (Advances in Comparative and Environmental Physiology). Springer-Verlag Telos, 1996.

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30

Eljaafari, Assia, i Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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31

(Editor), Nancy Rothwell, i Sarah Loddick (Editor), red. Immune and Inflammatory Responses in the Nervous System (The Molecular and Cellular Neurobiology Series (Bios Scientific Publishers).). Oxford University Press, USA, 2002.

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32

Stoddard, Frederick J., i Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.

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Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound healing is increased cortisol secretion secondary to depression and/or stress, and impaired immune response, in addition or together with the other factors such as genetic or epigenetic risk for depression. Cellular models relate both to wound healing and to depression include cytokines, the inflammatory response (Miller et al, 2008), and cellular aging (Telgenhoff and Shroot, 2005) reflected in shorter leukocyte telomere length (LTL) (Verhoeven et al, 2016). Another model of stress impacting wound healing investigated genetic correlates—immediate early gene expression or IEG from the medial prefrontal cortex, and locomotion, in isolation-reared juvenile rats. Levine et al (2008) compared isolation reared to group reared samples, and found that, immediate gene expression in the medial prefrontal cortex (mPFC) was reduced, and behavioral hyperactivity increased, in juvenile rats with 20% burn injuries. Wound healing in the isolation reared rats was significantly impaired. They concluded that these results provide candidates for behavioral biomarkers of isolation rearing during physical injury, i.e. reduced immediate mPFC gene expression and hyperactivity. They suggested that a biomarker such as IEGs might aid in demarcating patients with resilient and adaptive responses to physical illness from those with maladaptive responses
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Downes, C. P., C. R. Wolf i D. P. Lane, red. Cellular Responses to Stress. Princeton University Press, 1999. http://dx.doi.org/10.1515/9781400865048.

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Downes, C. P., C. R. Wolf i D. P. Lane. Cellular Responses to Stress. Princeton University Press, 2016.

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35

Downes, C. P., C. R. Wolf i D. P. Lane. Cellular Responses to Stress. Princeton University Press, 2014.

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36

Feige, U., R. I. Morimoto i Barbara Polla. Stress-Inducible Cellular Responses. Birkhäuser, 2011.

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Downes, C. P., C. R. Wolf i D. P. Lane. Cellular Responses to Stress. Princeton University Press, 2014.

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38

Downes, C. P., C. R. Wolf i D. P. Lane. Cellular Responses to Stress. Princeton University Press, 2014.

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39

Raju, Raghavan, i Irshad H. Chaudry. The host response to hypoxia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0305.

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The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal macrophages, hypoxaemia and initiation of endoplasmic reticulum stress. In response, the protein level of the oxygen-sensing transcription factor, hypoxia inducible factor (HIF)-1 increases; this leads to the regulation of expression of a number of genes resulting in decreased mitochondrial ATP production, but enhanced glycolytic processes, thus shifting the energy balance. In addition, sustained tissue hypoxia leads to increased free radical production and cellular apoptosis. Though the initial host response to hypoxia may be protective, sustained hypoxia becomes detrimental to the tissues and the organism as a whole.
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40

Mozes, Lee. Cellular Responses to Molecular Modulators. Elsevier Science & Technology Books, 2012.

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41

Galli, Corrado L., Alan M. Goldberg i Marina Marinovich. Modulation of Cellular Responses in Toxicity. Springer London, Limited, 2013.

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42

Razzaque, M. S., i T. Taguchi, red. Cellular Stress Responses in Renal Diseases. S. Karger AG, 2005. http://dx.doi.org/10.1159/isbn.978-3-318-01170-8.

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43

Modulation Of Cellular Responses In Toxicity. Springer, 2012.

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Galli, Corrado L., Alan M. Goldberg i Marina Marinovich. Modulation of Cellular Responses in Toxicity. Springer, 2011.

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45

Cellular Stress Responses In Renal Diseases. Muenchen: Karger, 2006.

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46

Environmental stressors and gene responses. Amsterdam: Elsevier, 2000.

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Storey, K. B., i J. M. Storey. Environmental Stressors and Gene Responses. Elsevier Science & Technology Books, 2000.

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48

Baudouin, Simon, i Steve Ball. Normal physiology of the endocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0249.

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The endocrine system describes an array of chemical signals (hormones). Working in concert with the nervous system, the endocrine system forms a complex neurohumoral network, communicating changes in the environment to facilitate adaptive responses and serving to integrate those responses in a coherent, coordinated manner. The endocrine system has inherent rhythmicity, which has important implications for the integration and coordination of metabolism, and how we measure endocrine signals in clinical settings. At a cellular level, hormone action is mediated through a series of discrete, but interacting signal transduction pathways. This chapter outlines a functional design approach to endocrinology; providing a framework covering the principles of hormone regulation and hormone action—critical for understanding the role of the endocrine system in physiology and pathophysiology.
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Shimizu, Tadamichi, i Takashi Kondo. Cellular Response to Physical Stress and Therapeutic Application. Nova Science Publishers, Incorporated, 2013.

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Baluška, František. Long-Distance Systemic Signaling and Communication in Plants. Springer, 2013.

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