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Books on the topic 'PCV2'

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Published: 4 June 2021
Last updated: 9 March 2023

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1

Association, American Bankers, ed. Pricing consumer credit: PC2 sourcebook. Washington, D.C. (1120 Connecticut Ave., N.W., Washington 20036): American Bankers Association, 1986.

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2

Roberts, Todd F. Microencapsulation of PC12 cells in a HEMA/MMA copolymer. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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3

Vallbacka, Jennifer Jane. Microencapsulation of PC12 cells and delivery in a hemiparkinsoian rat model. Ottawa: National Library of Canada, 1998.

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4

Moore, Heidi Maria. Modulation of pH homeostasis by extracellular ATP in pheochromocytoma (PC12) cells. Ottawa: National Library of Canada, 1995.

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5

Nguyẽ̂n, Văn Linh. Nguyen Van Linh, secrétaire général du CC du PCV répond. Hanoi: Editions en Langues étrangères, 1989.

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6

Hill, Mary Catherine. Preconditioned Conjugate-Gradient 2 (PCG2), a computer program for solving ground-water flow equations. Denver, Colo: Dept. of the Interior, U.S. Geological Survey, 1990.

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7

Hill, Mary Catherine. Preconditioned Conjugate-Gradient 2 (PCG2), a computer program for solving ground-water flow equations. Denver, Colo: Dept. of the Interior, U.S. Geological Survey, 1990.

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8

Hill, Mary Catherine. Preconditioned Conjugate-Gradient 2 (PCG2), a computer program for solving ground-water flow equations. Denver, Colo: Dept. of the Interior, U.S. Geological Survey, 1990.

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9

Hill, Mary Catherine. Preconditioned Conjugate-Gradient 2 (PCG2), a computer program for solving ground-water flow equations. Denver, Colo: Dept. of the Interior, U.S. Geological Survey, 1990.

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10

Hill, Mary Catherine. Preconditioned Conjugate-Gradient 2 (PCG2), a computer program for solving ground-water flow equations. Denver, Colo: Dept. of the Interior, U.S. Geological Survey, 1990.

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11

Welsh, Philip. The bus & coach driving manual: Including the officially recommended syllabus for the PCV driving test. London: HMSO, 1995.

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12

Wadia, Jehangir S. R(-)-deprenyl treatment blocks apoptosis in PC12 cells by affecting mitochondrial membrane potential, mitochondrial calcium and superoxide radical generation. Ottawa: National Library of Canada, 1996.

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13

Sirk, Daniel. The effects of sub-lethal A[Beta](25-25) on mitochondrial protein import and degradation in differentiated PC12 cells. Ottawa: National Library of Canada, 2002.

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14

Gatti, Andrea. Involvement of protein kinase C (PKC) in the short- and long-term action of nerve growth factor in PC12 cells. Uxbridge: Brunel University, 1993.

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15

Campioni, Elly G. A qualitative and quantitative assessment of HEMA/MMA microencapsulated PC12 cells stereotaxically implanted in the denervated striatum of hemiparkinsonian rats. Ottawa: National Library of Canada, 1996.

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16

Souza, Rose Evelyn De. The involvement of Ecto-ATPase activity in the phosphorylation of intracellular proteins by extra-cellular [32P] ATP in PC12 cells. Ottawa: National Library of Canada, 1990.

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17

Ideológico, Partido Comunista de Venezuela Taller Nacional. Contribución al debate sobre el socialismo en Venezuela: Conclusiones del Taller Nacional Ideológico del Partido Comunista de Venezuela (PCV) : 1-5 febrero 2008. Caracas, Venezuela: Instituto de Estudios Políticos y Sociales Bolivar-Marx, 2008.

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18

Contribución al debate sobre el socialismo en Venezuela: Conclusiones del Taller Nacional Ideológico del Partido Comunista de Venezuela (PCV) : 1-5 febrero 2008. Caracas, Venezuela: Instituto de Estudios Políticos y Sociales Bolivar-Marx, 2008.

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19

Batistatou, Anna. Studies on the mechanism(s) of neuronal survival/death using cultures of PC12 cells and sympathetic neurons. 1993.

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20

Inc, Bergwall Productions. PC12 Communicate/Workplace Activity Sheets. Delmar Pub, 1997.

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21

Ruby Bridges: Through My Eyes. Scholastic, 2005.

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22

Sheldon, Nathan D., Ria L. Mitchell, and Rebecca M. Dzombak. Reconstructing Precambrian PCO2 and PO2 Using Paleosols. Cambridge University Press, 2021.

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23

Sheldon, Nathan D., Ria L. Mitchell, and Rebecca M. Dzombak. Reconstructing Precambrian PCO2 and PO2 Using Paleosols. Cambridge University Press, 2021.

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24

Sheldon, Nathan D., Ria L. Mitchell, and Rebecca M. Dzombak. Reconstructing Precambrian PCO2 and PO2 Using Paleosols. Cambridge University Press, 2021.

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25

Rach PC2 Marche Slave CD. HarperCollins Publishers Ltd, 1991.

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26

Souza, Rose Evelyn De. Nucleotide-evoked cellular responses in pheochromocytoma (PC12) cells. 1995.

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27

Raha, Sandeep. Characterization of the P2u purinoceptor in pheochromocytoma (PC12) cells. 1996.

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28

250 Theory Test Questions for PCVs: Highway Code Questions and Answers. Independently Published, 2022.

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29

Sobeih, Magdi Maged. Expression and regulation of the Thy-1 gene in PC12 cells. [New York], 1993.

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30

Teng, Kenneth Kien-Feng. Studies on NGF-promoted neuritogenesis in PC12 cells: Experimental dissection of the underlying mechanism. 1994.

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31

Vietnam, un an après le VIIe Congrès national du PCV. Hanoi: The Gioi, 1992.

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32

Arunachalam, Lakshmanan. Functional importance of Munc18-1 and its interaction with syntaxin1 in PC12 cells. 2005.

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33

The 1991 Post Census Survey of Vacant Property (Pcvs) (Statistical Bulletin: Housing Series). Stationery Office Books, 1993.

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34

Ischemia in neuronal PC12 cells: Role of free radical generation and cellular damage. Ottawa: National Library of Canada, 2001.

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35

Muders, Thomas, and Christian Putensen. Pressure-controlled mechanical ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0096.

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Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.
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36

Phan, Nam. Stress induced modulation of mitochondrial protein import in differentiated PC12 cells: The role of Tom20. 2006.

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37

Van, Linh M. Signaling mechanism involved in L1-[alpha]v[beta]3-mediated neurite outgrowth from PC12 cells. 2004.

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38

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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39

The role of f G[alpha]o and G[alpha]s isoforms in neuronal development: Studies in PC12 cells. Ottawa: National Library of Canada, 1994.

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40

The 2006-2011 World Outlook for New Gasoline Engine Positive Crankcase Ventilation (PCV) Valves for Motor Vehicles. Icon Group International, Inc., 2005.

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41

Parker, Philip M. The 2007-2012 World Outlook for New Gasoline Engine Positive Crankcase Ventilation (PCV) Valves for Motor Vehicles. ICON Group International, Inc., 2006.

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42

WORLD OCEAN DATABASE 2001, VOLUME 6: TEMPORAL DISTRIBUTION OF PH, ALKALINITY, PCO2 AND TCO2 PROFILES... NOAA ATLAS NESDIS 47... U.S. DEPARTM. [S.l: s.n., 2002.

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43

Gattinoni, Luciano, and Alfredo Lissoni. Pathophysiology and therapeutic strategy of respiratory acidosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0113.

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Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.
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44

Byrne, Maria, Pauline M. Ross, Symon A. Dworjanyn, and Laura Parker, eds. Larval Ecology in the Face of Changing Climate—Impacts of Ocean Warming and Ocean Acidification. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198786962.003.0017.

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Ocean warming and acidification are major climate change stressors for marine invertebrate larvae, and their impacts differ between habitats and regions. In many regions species with pelagic propagules are on the move, exhibiting poleward trends as temperatures rise and ocean currents change. Larval sensitivity to warming varies among species, influencing their invasive potential. Broadly distributed species with wide developmental thermotolerances appear best able to avail of the new opportunities provided by warming. Ocean acidification is a multi-stressor in itself and the impacts of its covarying stressors differ among taxa. Increased pCO2 is the key stressor impairing calcification in echinoid larvae while decreased mineral saturation is more important for calcification in bivalve larvae. Non-feeding, non-calcifying larvae appear more resilient to warming and acidification. Some species may be able to persist through acclimatization/adaptation to produce resilient offspring. Understanding the capacity for adaptation/acclimatization across generations is important to predicting the future species composition of marine communities.
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45

Halperin, Mitchell L., and Kamel S. Kamel. Approach to the patient with metabolic acidosis or alkalosis. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0035_update_001.

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The pathophysiology, clinical approach, and management of the common causes of metabolic acidosis and alkalosis are discussed. In metabolic acidosis, a quantitative estimate of the extracellular volume (ECFV) is required to determine its content of bicarbonate in a patient with ECFV contraction. Buffering of H+ must occur by the bicarbonate buffer system in muscle to avoid binding to intracellular proteins, this requires low muscle capillary PCO2; acid gain type of metabolic acidosis is detected by the finding of new anions in blood and/or urine. The urine osmolal gap is the best indirect test to assess [NH4+] in urine. In metabolic alkalosis, Cl− depletion alkalosis is misleading. Deficits must be defined as HCl, KCl, and/or NaCl. A quantitative assessment of ECFV helps determine the contribution of individual deficits of Cl− salts. There is no tubular maximum for HCO3− reabsorption. Angiotensin II and the usual pH in proximal convoluted tubule cells, the two major stimuli for NaHCO3 reabsorption, must be removed/ changed for NaHCO3 to be excreted.
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