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Books on the topic 'Plasma deposits'

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Published: 1 June 2024

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1

J, Mort, and Jansen Frank, eds. Plasma deposited thin films. Boca Raton, Florida: CRC, 1986.

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2

J, Mort, and Jansen F. Ph D, eds. Plasma deposited thin films. Boca Raton, Fla: CRC Press, 1986.

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3

Zimcik, D. G. Plasma-deposited protective coatings for spacecraft applications. [S.l.]: [s.n.], 1991.

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4

Tennyson, Roderick C. Evaluation of plasma-deposited protective coatings for spacecraft applications. Washington, D. C: American Institute of Aeronautics and Astronautics, 1992.

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5

Miyoshi, Kazuhisa. Plasma-deposited amorphous hydrogenated carbon films and their tribological properties. Cleveland, Ohio: Lewis Research Center, 1989.

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6

Miyoshi, Kazuhisa. Plasma-deposited amorphous hydrogenated carbon films and their tribological properties. Cleveland, Ohio: Lewis Research Center, 1989.

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7

Miyoshi, Kazuhisa. Plasma-deposited amorphous hydrogenated carbon films and their tribological properties. Cleveland, Ohio: Lewis Research Center, 1989.

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8

Miyoshi, Kazuhisa. Plasma-deposited amorphous hydrogenated carbon films and their tribological properties. Cleveland, Ohio: Lewis Research Center, 1989.

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9

Flückiger, Roger Sylvain. Microcrystalline silicon thin films deposited by VHF plasmas for solar cell applications. Konstanz: Hartung-Gorre Verlag, 1995.

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10

Kim, Danny. Dry passivation studies of GaAs(110) surfaces by gallium oxide thin films deposited by electron cyclotron resonance plasma reactive molecular beam epitaxy for optoelectronic device applications. Ottawa: National Library of Canada, 2001.

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11

L, Smith Donald. Thin-film deposition: Principles and practice. New York: McGraw-Hill, 1995.

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12

Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-chain amyloidosis), or granular precipitates (in monoclonal immunoglobulin deposition disease). They may disrupt organ structure and function, inducing life-threatening complications. All of the pathologic entities related to immunoglobulin deposition principally involve the kidney, which is not only explained by the high levels of renal plasma flow and glomerular filtration rate, but also by the sieving properties of the glomerular capillary wall and by the prominent role of the renal tubule in LC handling and catabolism.The different renal (and other) manifestations are related to the unique physicochemical characteristics of each paraprotein or immunoglobulin fragment, and the rate of their production.
13

Mort. Plasma Deposited Thin Films. Edited by J. Mort and F. Jansen. CRC Press, 2018. http://dx.doi.org/10.1201/9781351075817.

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14

Mort. Plasma Deposited Thin Films. Taylor & Francis Group, 2018.

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15

Mort. Plasma Deposited Thin Films. Taylor & Francis Group, 2018.

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16

Mort. Plasma Deposited Thin Films. Taylor & Francis Group, 2018.

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17

Mort. Plasma Deposited Thin Films. Taylor & Francis Group, 2018.

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18

Mort. Plasma Deposited Thin Films. Taylor & Francis Group, 2017.

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19

Lachmann, Helen J., and Giampaolo Merlini. The patient with amyloidosis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0152.

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Amyloidosis is a disorder of protein folding in which normally soluble plasma proteins are deposited in the extracellular space in an abnormal insoluble fibrillar form. The process of amyloid formation and deposition causes cytotoxicity and progressive organ dysfunction. Amyloid is remarkably diverse and can be hereditary or acquired, localized or systemic, and lethal or merely an incidental finding. The most important numerically are AL amyloidosis, in which the fibrils are composed of monoclonal immunoglobulin light chains, and AA amyloidosis, in which the acute phase reactant Serum Amyloid A component forms the fibrils.The kidney is involved in 75% of patients with systemic amyloidosis. Heavy proteinuria or nephrotic syndrome is characteristic of most amyloid variants.Without treatment, systemic disease is usually fatal but measures that reduce the supply of amyloid fibril precursor proteins can result in regression of amyloid deposits, prevention of organ failure, and improved quality of life and survival. Early diagnosis, before irreversible organ damage has occurred, is the key to effective treatment. Recent advances in diagnosis and therapy have much improved the outlook of patients with AL amyloidosis, but agents with broader promise are under investigation.
20

Friction and wear of plasma-deposited diamond films. [Washington, D.C.]: NASA, 1993.

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21

Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0337.

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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide, which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic.Key clinical signs are angiokeratoma found by close examination of skin; characteristic eye lesions may be seen; lipid deposits may be seen in urine. Renal biopsy appearances are characteristic and this is commonly where the diagnosis is first made. Increasingly, cardiologists are suspecting the condition in adults with echocardiographic appearances of left ventricular hypertrophy. Diagnosis in men is usually made by measurement of alpha-galactosidase in either white cells or plasma (or using blood spots). Unfortunately, many female patients can have normal enzyme levels so that genetic testing is the only way to confirm a diagnosis. Non-selective screening strategies (e.g. males on renal replacement therapy with uncertain renal diagnoses) have had low yields.
22

Unger, Wolfgang E. S. Surface Chemical Analysis: Characterization Techniques for Plasma-deposited Organic Films. Wiley & Sons, Incorporated, John, 2009.

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23

Semi-annual progress report on a study of reactive plasma deposited thin films. Greensboro, N.C: North Carolina Agricultural and Technical State University, Dept. of Physics, 1986.

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24

Semi-annual progress report on a study of reactive plasma deposited thin films. Greensboro, N.C: North Carolina Agricultural and Technical State University, Dept. of Physics, 1986.

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25

Adhesion, friction, and wear of plasma-deposited thin silicon nitride films at temperatures to 700⁰C. Cleveland, Ohio: Lewis Research Center, NASA, 1989.

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26

Medjeral-Thomas, Nicholas, Anna Richards, and Matthew C. Pickering. Molecular basis of complement-mediated renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0333.

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Abnormal regulation of complement is intimately associated with C3 glomerulopathy and atypical haemolytic uraemic syndrome. Atypical haemolytic uraemic syndrome is characterized by renal thrombotic microangiopathy due to an inability to regulate complement activation along the renal endothelium. The development of thrombosis is critically dependent on the ability to activate C5. Eculizumab, a monoclonal anti-C5 antibody, is an effective therapy for this condition. C3 glomerulopathy refers to glomerular lesions characterized by accumulation of C3 in the absence of immunoglobulin. The prototypic example is dense deposit disease. This condition is associated with impaired regulation of the alternative pathway in plasma. In other subtypes of C3 glomerulopathy, familial studies have identified mutations within the complement factor H-related protein family. Polymorphic variation within this protein family also influences susceptibility to IgA nephropathy. The mechanism underlying these associations remains unknown and is the subject of ongoing research efforts.
27

Yue, Liu. Remote quantitative temperature and thickness measurements of plasma-deposited titanium nitride thin coatings on steel using a laser interferometric thermoreflectance optical thermometer. 2005.

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28

National Aeronautics and Space Administration (NASA) Staff. Friction and Wear Properties of Selected Solid Lubricating Films. Part 3; Magnetron-Sputtered and Plasma-Assisted, Chemical-Vapor-Deposited Diamondlike Carbon Films. Independently Published, 2018.

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29

National Aeronautics and Space Administration (NASA) Staff. Friction and Wear Properties of Selected Solid Lubricating Films. Part 3; Magnetron-Sputtered and Plasma-Assisted, Chemical-Vapor-Deposited Diamondlike Carbon Films. Independently Published, 2018.

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30

Abhishek, Abhishek, and Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.
31

Cockrem, Jeremy Maurice. Investigation of plasma nitriding and titanium nitride coating by physical vapour deposition of titanium 6A14V alloy to improve the wear resistance of inner bores V2:Final test results of plasma nitrided and physical vapour deposited titanium nitride coated titanium 6A1-4V samples and compared with samples coated using the established techniquesof electroless nickel phosphorous plating. 1995.

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