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Books on the topic 'Differential modulator'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Bailey, Nicola Ann. Modulated differential scanning colorimetry. Birmingham: University of Birmingham, 1998.

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2

Reading, Mike, and Douglas J. Hourston, eds. Modulated Temperature Differential Scanning Calorimetry. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-3750-3.

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3

Moose, Paul H. A progress report on communications digital signal processing: Theory and performance of frequency domain differentially encoded multi-frequency modulation. Monterey, Calif: Naval Postgraduate School, 1990.

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4

Pereira, Nuno, and Nuno Paulino. Design and Implementation of Sigma Delta Modulators (ΣΔM) for Class D Audio Amplifiers using Differential Pairs. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11638-9.

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5

Topological modular forms. Providence, Rhode Island: American Mathematical Society, 2014.

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6

Kipps, Mark Rew. A modular approach to modeling an isolated power system on a finite voltage bus using a differential algebraic equation solving routine. Monterey, Calif: Naval Postgraduate School, 1994.

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7

Hogendoorn, R. A. Data compression in computational fluid dynamics. Amsterdam: National Aerospace Laboratory, 1986.

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8

Farkas, Hershel M. Theta constants, Riemann surfaces, and the modular group: An introduction with applications to uniformization theorems, partition identities, and combinatorial number theory. Providence, R.I: American Mathematical Society, 2001.

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9

Trends in number theory: Fifth Spanish meeting on number theory, July 8-12, 2013, Universidad de Sevilla, Sevilla, Spain. Providence, Rhode Island: American Mathematical Society, 2015.

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10

Topology and geometry in dimension three: Triangulations, invariants, and geometric structures : conference in honor of William Jaco's 70th birthday, June 4-6, 2010, Oklahoma State University, Stillwater, OK. Providence, R.I: American Mathematical Society, 2011.

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11

Cox, William. Ordinary Differential Equations (Modular Mathematics Series). Butterworth-Heinemann, 1995.

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12

Reading, Mike, and Douglas J. Hourston. Modulated Temperature Differential Scanning Calorimetry: Theoretical and Practical Applications in Polymer Characterisation. Springer, 2010.

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13

Mike, Reading, and Hourston Douglas J, eds. Modulated temperature differential scanning calorimetry: Theoretical and practical applications in polymer characterisation. Dordrecht: Springer, 2006.

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14

Analysis and Performance Comparison of Adaptive Differential Pulse Code Modulation Data Compression Systems. Storming Media, 1996.

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15

Paulino, Nuno, and Nuno Pereira. Design and Implementation of Sigma Delta Modulators for Class D Audio Amplifiers using Differential Pairs. Springer, 2014.

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16

Center, Goddard Space Flight, ed. Differential absorption lidar measurements of atmospheric water vapor using a pseudonoise code modulated AIGaAs laser. Greenbelt, Md: National Aeronautics and Space Administration, Goddard Space Flight Center, 1994.

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17

Lam, Andrew C. C. Differential receiver design for the Offset-QPSK modulation scheme: ISI-free and non-ISI-free receiver algorithms. 2004.

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18

Zuccon, Johnny Francais. High-frequency differential piezoelectric photothermal wave investigation of ion-implanted (100) silicon wafers via beam position modulation. 1986.

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19

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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20

Theta Constants, Riemann Surfaces and the Modular Group. American Mathematical Society, 2001.

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21

(Editor), Mike Reading, and Douglas J. Hourston (Editor), eds. Modulated Temperature Differential Scanning Calorimetry: Theoretical and Practical Applications in Polymer Characterisation (Hot Topics in Thermal Analysis and Calorimetry). Springer, 2006.

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22

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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23

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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24

Rees, Gayla, Benjamin Shapiro, and Matthew Torrington. Integrative Approach to Sedative-Hypnotic Use Disorder. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0005.

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Sedatives, hypnotics, and anxiolytics are CNS depressants with GABAergic activity that are potentially habit-forming due to their activity in brain reward pathways. They are central in the drug overdose epidemic with benzodiazepines (BZD) being involved in approximately 31% of all fatal overdoses. There are 4 withdrawal syndromes: High dose minor and major withdrawal, low dose withdrawal, and protracted withdrawal. Benzodiazepines are chemically related positive allosteric modulators of the GABA at the GABA-A receptor. In differential expression 5 different receptor subunits play a role in acute and prolonged withdrawal syndromes. Benzodiazepines have supplanted barbiturates for treatment of anxiety and insomnia due to their wider therapeutic index. Barbiturates can be helpful managing opiate and benazodiazapeine withdrawal. Traditional Chinese Medicine can improve hypnotics-dependent insomnia. Mindfulness-based relapse prevention and yoga may offer benefits but are poorly studied.

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25

Perova, Tatiana. Differential modulation of intracellular calcium responses in B lymphoblasts by mood stabilizers: Relevance to the molecular therapeutics of bipolar disorder. 2006.

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26

United States. National Aeronautics and Space Administration., ed. Parameter identification for nonlinear aerodynamic systems: First annual (second semiannual) technical report to the Aircraft Guidance and Controls Branch/489, Guidance and Control Division, National Aeronautics and Space Administration, Langley Research Center ... period covered, October 23, 1989 to October 22, 1990. [Washington, DC]: The Administration, 1990.

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27

Parameter identification for nonlinear aerodynamic systems. [Washington, DC: National Aeronautics and Space Administration, 1992.

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28

Parameter identification for nonlinear aerodynamic systems: Final technical report to the Aircraft Guidance and Controls Branch/489, Guidance and Control Division, National Aeronautics and Space Administration, Langley Research Center ... period covered, October 23, 1989 to February 28, 1993. [Washington, DC]: The Administration, 1993.

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29

Dourish, Paul. Protocols, Packets, and Proximity. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252039362.003.0008.

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This chapter analyzes the materialities of Internet protocols, focusing on the relationship between content and conduit, which involves both the compression and modulation of signals. Network protocols are shaped by material constraints. Similarly, the centrality of routing to the Internet can be understood materially in terms of the arrangement of network nodes, the cost of routing, the structure of networks, the size of routing tables, and the dynamics of connectivity. Critically, this materiality cuts across apparently different domains of concern—from the practice of network operations to the rhetoric of democratic access. The chapter then contrasts two different protocols, the Routing Information Protocol and the Exterior Gateway Protocol, which emerged in different historical moments and cultural conditions. Examining the social construction of these network protocols can help differentiate the actual Internet from a possible or imagined Internet.

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30

Colvin, Lesley A., and Marie T. Fallon. Pain physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0009.

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The International Association for the Study of Pain defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’. A good understanding of the physiology of pain processing is important, with recent advances in basic science, functional neuroimaging, and clinical pain syndromes contributing to our understanding. It is also important to differentiate between nociception, the process of detecting noxious stimuli, and pain perception, which is a much more complex process, integrating biological, psychological, and social factors. The somatosensory nervous system, from peripheral nociceptors, to sensory nerves and spinal cord synapses has many potential sites for modulation, with ascending pathways to the brain, balanced by ‘top-down’ control from higher centres. Under certain circumstances, for example, after tissue injury from trauma or surgery, there will be continued nociceptive input, with resultant changes in the whole somatosensory nervous system that lead to development of chronic pain syndromes. In such cases, even when the original injury has healed, the pathophysiological changes in the nervous system itself lead to ongoing pain, with peripheral or central sensitization, or both. Additionally, in some chronic pain syndromes, for example, chronic widespread pain, it has been postulated that abnormalities in central processing may be the initiating factor, with some evidence for this from neuroimaging studies. Further work is needed to fully understand pain neurobiology in order to advance our management.

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