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Books on the topic 'Cellular respiration'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Sarangarajan, Rangaprasad, and Shireesh Apte, eds. Cellular Respiration and Carcinogenesis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-435-3.

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2

NATO Advanced Research Workshop on Thiol Metabolism and Redox Regulation of Cellular Functions (2002 Pisa, Italy). Thiol metabolism and redox regulation of cellular functions. Amsterdam: IOS Press, 2002.

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3

Harris, S., J. Harris, and P. Narini. Cellular Respiration. Permacharts Inc., 1999.

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4

P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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5

Apte, Shireesh, and Rangaprasad Sarangarajan. Cellular Respiration and Carcinogenesis. Humana, 2014.

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6

P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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7

Apte, Shireesh, and Rangaprasad Sarangarajan. Cellular Respiration and Carcinogenesis. Springer, 2009.

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8

P, Apte Shireesh, and Sarangarajan Rangaprasad, eds. Cellular respiration and carcinogenesis. New York: Springer, 2008.

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9

Gijsbert, Osterhoudt, and Barhydt Jos, eds. Cell respiration and cell survival: Processes, types and effects. Hauppauge, N.Y: Nova Science Publishers, 2009.

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10

Thomson, Robert G., and Peter Abramoff. Cellular Respiration: Separate from Laboratory Outlines in Biology VI. W. H. Freeman, 1995.

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11

(Editor), Chi-Sang Poon, and Homayoun Kazemi (Editor), eds. Frontiers in Modeling and Control of Breathing: Integration at Molecular, Cellular, and Systems Levels. Springer, 2001.

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12

Poon, Chi-Sang, and Homayoun Kazemi. Frontiers in Modeling and Control of Breathing: Integration at Molecular, Cellular, and Systems Levels. Springer, 2012.

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13

Sukhamay, Lahiri, and Comroe Julius H. 1911-, eds. Chemoreceptors and reflexes in breathing: Cellular and molecular aspects. Oxford: Oxford University Press, 1989.

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14

1942-, Cutz Ernest, ed. Cellular and molecular biology of airway chemoreceptors. Austin: Landes Bioscience, 1997.

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15

Italy) NATO Advanced Research Workshop on Thiol Metabolism and Redox Regulation of Cellular Functions (2002 : Pisa. Thiol Metabolism and Redox Regulation of Cellular Functions. Ios Pr Inc, 2002.

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16

(Editor), Sukhamay Lahiri, Robert E. Foster (Editor), Richard Davis (Editor), and Allan Pack (Editor), eds. Chemoreceptors and Reflexes in Breathing: Cellular and Molecular Aspects The Julius M. Comroe Memorial Volume. Oxford University Press, USA, 1989.

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17

Sukhamay, Lahiri, and Comroe Julius H. 1911-, eds. Chemoreceptors and reflexes in breathing: Cellular and molecular aspects : the Julius H. Comroe Memorial volume. New York: Oxford University Press, 1989.

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18

Aliev, Gjumrakch. Role of Oxidative Stress, Mitochondria Failure, and Cellular Hypoperfusion in the Context of Alzheimer Disease: Past, Present and Future. Nova Science Publishers, Incorporated, 2013.

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19

Cianni, Juliana. Uma aventura pela respiração celular. Brazil Publishing, 2021. http://dx.doi.org/10.31012/978-65-5861-454-8.

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The story contained in this book is the result of my inquiries as a teacher and as a student looking for an easier and more fun way to learn dense content from the disciplines contained in the so beautiful universe of Sciences. I believe that pleasurable and consistent learning is possible, if we have a little bit of imagination and a powder of pimpimpimpim, allowing the student to be enchanted with the mysteries of life, a life that pulsates in the macro and microcosm. So, one fine day, watching Professor Rita's Biotechnology class at USP in Lorena / SP, I asked myself: why not facilitate the high school content that is charged in entrance exams and turn them into something playful and made it easier for students to have more effective access to deeper knowledge of science? It was with this objective that this little book was born that, in addition to offering a new experience about cellular respiration, also offers some excerpts from books that have always enchanted my eyes and touched my heart. Thus, more than an adventure through cellular respiration, this book proposes an adventure for the human spirit itself, that everything can and is capable, reminding us that the material world is intrinsically linked to the world of ideas, the first being nothing more it is more than an adventure of the human spirit itself.

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20

Gray, Doug, Carole Proctor, and Tom Kirkwood. Biological aspects of human ageing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0001.

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At the molecular and cellular levels human ageing is characterized by the accumulation of unrepaired random damage, and an accompanying loss of function. A major source of damage is oxidative stress caused by the generation of reactive oxygen species as a by-product of respiration. DNA and proteins are both susceptible to damage but whereas DNA damage repair systems exist, faulty proteins are generally removed by protein degradation systems. During ageing these systems become less efficient and the subsequent accumulation of damaged protein promotes protein aggregation, a process which is especially problematic in the ageing brain. Other aspects of ageing include genetic and epigenetic changes, mitochondrial dysfunction, telomere shortening, and cellular senescence, all subject to stochasticity. The complexity of the biology of ageing has led to an increase in the use of systems biology approaches whereby the use of mathematical modelling and bioinformatic tools complement the more traditional experimental approaches.

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21

Raju, Raghavan, and 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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22

Tissue respiration in the light of recent research. [Canada?: s.n., 1995.

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23

Seyfried, Thomas N., and Laura M. Shelton. Metabolism-Based Treatments to Counter Cancer. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0012.

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Accumulating evidence indicates that cancer is a type of mitochondrial metabolic disease. Chronic damage to mitochondria causes a gradual shift in cellular energy metabolism from respiration to fermentation. Consequently, fermentable metabolites become the drivers of cancer. Mitochondrial injury can explain the long-standing “oncogenic paradox,” and all major hallmarks of cancer including genomic instability. Restriction of fermentable fuels therefore becomes a viable therapeutic strategy for cancer management. The ketogenic diet (KD) is a metabolic therapy that lowers blood glucose and elevates blood ketone bodies. Ketone bodies are a “super fuel” for functional mitochondria, but cannot be metabolized efficiently by tumor mitochondria. The efficacy of KDs for cancer management can be enhanced when used together with drugs and procedures (such as hyperbaric oxygen therapy) (that further target fermentation. Therapeutic ketosis can represent an alternative, nontoxic strategy for managing and preventing a broad range of cancers while reducing healthcare costs.

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24

Fullerton, James N., and Mervyn Singer. Oxygen in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0032.

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Oxygen therapy is primarily administered to alleviate arterial hypoxaemia and tissue hypoxia, and to facilitate aerobic cellular respiration. Hypoxaemia (PaO2 < 8 kPa [60 mmHg], SaO2 <92%) is associated with end-organ damage and adverse clinical outcomes, serving as a proxy measure for reduced intracellular PO2. Increasing the fraction of inspired oxygen should form part of an overall strategy to maximize tissue oxygen delivery. Permissive hypoxaemia represents a valid treatment strategy in a selected patient cohort. Oxygen is a drug and oxygen therapy is not benign, and oxygen administration at high, sustained doses (FiO2 >0.5, >12 hours) may cause oxygen toxicity. Observational studies in both mechanically-ventilated patients and survivors of non-traumatic cardiac arrest indicate an independent association between increasing hyperoxaemia and mortality. Oxygen therapy may additionally precipitate hypercapnic ventilatory failure in those at risk and oxygen should be administered to achieve a prescribed target SaO2 or PaO2 range, via adjustment of dose and delivery device. If no monitoring is available, hypoxaemia should be avoided by giving high-flow oxygen to achieve a FiO2 of near 1.0 with subsequent titration once oxygenation status is established.

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25

Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.

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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.

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26

Hill, Geoffrey E. Mitonuclear Ecology. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198818250.001.0001.

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Eukaryotes were born of a chimeric union of two prokaryotes. The legacy of this fusion is organisms with both a nuclear and mitochondrial genome that must work in a coordinated fashion to enable cellular respiration. The coexistence of two genomes in a single organism requires tight coadaptation to enable function. The need for coadaptation, the challenge of co-transmission, and the possibility of genomic conflict between mitochondrial and nuclear genes have profound consequences for the ecology and evolution of eukaryotic life. This book defines mitonuclear ecology as an emerging field that reassesses core concepts in evolutionary ecology in light of the necessity of mitonuclear coadaptation. I discuss and summarize research that tests new mitonuclear-based theories for the evolution of sex, two sexes, senescence, a sequestered germ line, speciation, sexual selection, and adaptation. The ideas presented in this book represent a paradigm shift for evolutionary ecology. Through the twentieth century, mitochondrial genomes were dismissed as unimportant to the evolution of complex life because variation within mitochondrial genomes was proposed to be functionally neutral. These conceptions about mitochondrial genomes and mitonuclear genomic interactions have been changing rapidly, and a growing literature in top journals is making it increasingly clear that the interactions of the mitochondrial and nuclear genomes over the past 2 billion years have played a major role in shaping the evolution of eukaryotes. These new hypotheses for the evolution of quintessential characteristics of complex life hold the potential to fundamentally reshape the field of evolutionary ecology and to inform the emerging fields of mitochondrial medicine and mitochondrial-based reproductive therapies.

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27

Kirchman, David L. The nitrogen cycle. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0012.

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Nitrogen is required for the biosynthesis of many cellular components and can take on many oxidation states, ranging from −3 to +5. Consequently, nitrogen compounds can act as either electron donors (chemolithotrophy) or electron acceptors (anaerobic respiration). The nitrogen cycle starts with nitrogen fixation, the reduction of nitrogen gas to ammonium. Nitrogen fixation is carried out only by prokaryotes, mainly some cyanobacteria and heterotrophic bacteria. The ammonium resulting from nitrogen fixation is quickly used by many organisms for biosynthesis, being preferred over nitrate as a nitrogen source. It is also oxidized aerobically by chemolithoautotrophic bacteria and archaea during the first step of nitrification. The second step, nitrite oxidation, is carried out by other bacteria not involved in ammonia oxidation, resulting in the formation of nitrate. Some bacteria are capable of carrying out both steps (“comammox”). This nitrate can then be reduced to nitrogen gas or nitrous oxide during denitrification. It can be reduced to ammonium, a process called “dissimilatory nitrate reduction to ammonium.” Nitrogen gas is also released by anaerobic oxidation of ammonium (“anammox”) which is carried out by bacteria in the Planctomycetes phylum. The theoretical contribution of anammox to total nitrogen gas release is 29%, but the actual contribution varies greatly. Another gas in the nitrogen cycle, nitrous oxide, is a greenhouse gas produced by ammonia-oxidizing bacteria and archaea. The available data indicate that the global nitrogen cycle is in balance, with losses from nitrogen gas production equaling gains via nitrogen fixation. But excess nitrogen from fertilizers is contributing to local imbalances and several environmental problems in drinking waters, reservoirs, lakes, and coastal oceans.

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28

Myocardial and Skeletal Muscle Bioenergetics. Springer, 1986.

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29

G, O'Regan R., and International Symposium on Arterial Chemoreceptors (12th : 1993 : Dublin, Ireland), eds. Arterial chemoreceptors: Cell to system. New York: Plenum Press, 1994.

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