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Книги з теми "Capillaire laser"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Capillaire laser.

Автор: Grafiati

Опубліковано: 7 липня 2024

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Ознайомтеся з топ-15 книг для дослідження на тему "Capillaire laser".

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1

H, Sørensen, and Royal Society of Chemistry (Great Britain), eds. Chromatography and capillary electrophoresis in food analysis. Cambridge: Royal Society of Chemistry, 1999.

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2

1934-, Cazes Jack, ed. Encyclopedia of chromatography. New York, NY: M. Dekker, 2004.

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3

Todd, David A. A study of nitrogen emission from a capillary laser and a supersonic expansion of a discharge plasma. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1991.

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4

1934-, Cazes Jack, ed. Encyclopedia of chromatography. New York: Marcel Dekker, 2001.

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5

1934-, Cazes Jack, ed. Encyclopedia of chromatography. 3rd ed. Boca Raton: Taylor & Francis, 2010.

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6

1934-, Cazes Jack, ed. Encyclopedia of chromatography. 3rd ed. Boca Raton: Taylor & Francis, 2010.

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7

1934-, Cazes Jack, ed. Encyclopedia of chromatography. 3rd ed. Boca Raton: Taylor & Francis, 2010.

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8

Schultz, Nicole M. Rapid immunoassays by capillary zone electrophoresis with laser- induced fluorescence detection. 1994.

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9

Wronski, Matthew M. F2 and ultrafast laser microfabrication of an optofluidic capillary electrophoresis biochip. 2005.

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10

Lee, Yuan-Hsiang. Detection of a single molecule in a capillary by laser-induced fluorescence. 1994.

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11

Lehotay, Steven John. Approaching single molecule detection by laser-induced fluorescence of flowing dye solutions in a capillary. 1992.

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12

van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

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This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.

13

Rodriguez-Iturbe, Bernardo, and Mark Haas. Immunoglobulin A-dominant post-infectious glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0078_update_001.

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Immunoglobulin A (IgA)-dominant post-infectious glomerulonephritis is usually associated with infections with Staphylococcus aureus. It is most commonly seen in patients over 60, and particularly in men. The renal lesion is acute and severe, and commonly includes crescent formation, although the described histological features vary widely. IgA is the dominant immunoglobulin and in later phases when capillary deposits are resolving it may be impossible to distinguish the condition from IgA nephropathy without the use of electron microscopy. Diabetes appears to be a risk factor. Complement levels are frequently low but may be normal. Clinically there is often severe nephrotic syndrome and hypertension may be less prominent.

14

Hedenstierna, Göran, and Hans Ulrich Rothen. Physiology of positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0088.

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During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).

15

Raghunathan, Karthik, and Andrew Shaw. Crystalloids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0057.

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‘Crystalloid’ refers to solutions of crystalline substances that can pass through a semipermeable membrane and are distributed widely in body fluid compartments. The conventional Starling model predicts transvascular exchange based on the net balance of opposing hydrostatic and oncotic forces. Based on this model, colloids might be considered superior resuscitative fluids. However, observations of fluid behaviour during critical illness are not consistent with such predictions. Large randomized controlled studies have consistently found that colloids offer no survival advantage relative to crystalloids in critically-ill patients. A revised Starling model describes a central role for the endothelial glycocalyx in determining fluid disposition. This model supports crystalloid utilization in most critical care settings where the endothelial surface layer is disrupted and lower capillary pressures (hypovolaemia) make volume expansion with crystalloids effective, since transvascular filtration decreases, intravascular retention increases and clearance is significantly reduced. There are important negative consequences of both inadequate and excessive crystalloid resuscitation. Precise dosing may be titrated based on functional measures of preload responsiveness like pulse pressure variation or responses to manoeuvres such as passive leg raising. Crystalloids have variable electrolyte concentrations, volumes of distribution, and, consequently variable effects on plasma pH. Choosing balanced crystalloid solutions for resuscitation may be potentially advantageous versus ‘normal’ (isotonic, 0.9%) saline solutions. When used as the primary fluid for resuscitation, saline solutions may have adverse effects in critically-ill patients secondary to a reduction in the strong ion difference and hyperchloraemic, metabolic acidosis. Significant negative effects on immune and renal function may result as well.