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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 6 lutego 2022

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Sprawdź 18 najlepszych książek naukowych na temat „Oxygen (O2)”.

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1

Swift, Kerry. Microwave excitation of oxygen O2(super 1 delta) for an oxygen-iodine laser. Koln: DFVLR, 1989.

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2

Hitch, B. D. Reduced H2-O2 mechanisms for use in reacting flow simulation. New York: AIAA, 1988.

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3

1946-, Frimer Aryeh A., red. Singlet O2. Boca Raton, Fla: CRC Press, 1985.

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4

Fawkner, Samantha G., i Neil Armstrong. Oxygen uptake kinetics. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0022.

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The two main purposes of Chapter 22 are to (i) explore the methodological issues involved in assessing the O2 kinetic response to exercise in children, and (ii) explain the O2 kinetic response to exercise in children and review the literature regarding changes with age and sex and with respect to conventional markers of aerobic fitness.
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5

Kato, Masato. Oxygen Potentials and Defect Chemistry in Nonstoichiometric (U, Pu)O2. INTECH Open Access Publisher, 2012.

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6

Temperature dependence of the collisional removal of O2(A(sup 3)Sigma(sup +)(sub u), upsilon=9) with O2 and N2. [Washington, DC: National Aeronautics and Space Administration, 1997.

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7

A, Copeland Richard, i United States. National Aeronautics and Space Administration., red. Temperature dependence of the collisional removal of O2(A(sup 3)Sigma(sup +)(sub u), upsilon=9) with O2 and N2. [Washington, DC: National Aeronautics and Space Administration, 1997.

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8

A, Copeland Richard, i United States. National Aeronautics and Space Administration., red. Temperature dependence of the collisional removal of O2(A(sup 3)Sigma(sup +)(sub u), upsilon=9) with O2 and N2. [Washington, DC: National Aeronautics and Space Administration, 1997.

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9

Zhang, Wensheng. SO 2/O2 as an oxidant in hydrometallurgy. Murdoch University, 2000.

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10

Kreit, John W. Gas Exchange. Redaktor John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0002.

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Gas Exchange explains how four processes—delivery of oxygen, excretion of carbon dioxide, matching of ventilation and perfusion, and diffusion—allow the respiratory system to maintain normal partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Partial pressure is important because O2 and CO2 molecules diffuse between alveolar gas and pulmonary capillary blood and between systemic capillary blood and the tissues along their partial pressure gradients, and diffusion continues until the partial pressures are equal. Ventilation is an essential part of gas exchange because it delivers O2, eliminates CO2, and determines ventilation–perfusion ratios. This chapter also explains how and why abnormalities in each of these processes may reduce PaO2, increase PaCO2, or both.
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11

Glasper, Edward Alan, Gillian McEwing i Jim Richardson, red. Respiratory problems. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780198569572.003.0010.

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Anatomy and physiology 274Apnoea 276Asthma 278Recognition of respiratory distress 282Bronchiolitis 284Croup syndromes 286Epiglottitis 288Pneumonia 290Respiratory syncytial virus 292Related skillsPulse oximetry 294Nasopharyngeal aspirate 296Administration of oxygen (O2) 298Clinical skillsTracheostomy, changing tapes, and cleaning stoma site ...
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12

J, Jachimowski Casimir, Rogers R. Clayton i United States. National Aeronautics and Space Administration. Scientific and Technical Information Branch., red. Ignition of mixtures of SiH4, CH4, O2, and Ar or N2 behind reflected shock waves. [Washington, D.C.]: National Aeronautics and Space Administration, Scientific and Technical Information Branch, 1985.

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13

Lei, Yuan. Special Ventilation Functions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784975.003.0010.

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‘Special Ventilation Functions’ examines those hard-to-classify features such as standby; sigh; temporary oxygen enrichment or 100% O2; apnoea backup or apnoea ventilation; and tube resistance compensation, also known as tube compensation or automatic tube compensation. It describes each function in depth, including indications for use and details on typical implementations, providing examples from popular ventilators.
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14

Armstrong, Neil, i Joanne R. Welsman. Aerobic fitness. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0008.

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Maximal oxygen uptake ( V O 2 · max), the highest rate at which an individual can consume O2 during exercise, is widely recognized as the best single measure of adults’ aerobic fitness.1,2 Maximal V O 2 · ultimately limits an individual’s capacity to perform aerobic exercise but it does not describe fully all aspects of aerobic fitness. The transient kinetics of V O 2 · best reflect the integrated response of the O2 delivery system and the metabolic requirements of the exercising muscle to rapid changes in exercise intensity. Furthermore, V O 2 · max is not the best index of an individual’s ability to sustain submaximal aerobic exercise and despite its derivation from anaerobic metabolism, measures of blood lactate accumulation during submaximal exercise provide useful indicators of aerobic fitness.As the assessment of V O 2 · kinetics is addressed in Chapter 22, in this chapter, we will focus on the assessment of V O 2 · max and blood lactate accumulation.
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15

Gattinon, Luciano, i Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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16

Gattinon, Luciano, i Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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17

Warburton, Darren E. R., Lindsay Nettlefold, K. Ashlee McGuire i Shannon S. D. Bredin. Cardiovascular function. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0007.

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The physiological adaptations to exercise training have been evaluated extensively in children and youth. In particular, considerable research has examined the changes in cardiovascular function that occur with aerobic exercise training. Various indicators of cardiovascular function have been assessed at rest and during exercise. Many of these measures have important implications from performance and health-related perspectives. Owing to the importance of oxygen (O2) transport for human performance and health, this chapter reviews comprehensively the varied non-invasive and invasive methods of assessing cardiac function including an in-depth evaluation of the limitations and strengths of each methodology. Specific reference is given to the applicability and ease of usage of each technology with young people. This chapter also deals extensively with the evaluation of cardiovascular regulation and vascular function owing to their role in optimal exercise performance and health.
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18

Nakamura, Tomohiro, i Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.
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