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Books on the topic 'Q00'

Author: Grafiati

Published: 10 September 2021

Last updated: 14 February 2022

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1

All about coenzyme Q10. Garden City Park, N.Y: Avery, 1998.

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2

Sinatra, Stephen T. The coenzyme Q10 phenomenon. Los Angeles: Lowell House, 1998.

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3

International Telegraph and Telephone Consultative Committee. Plenary Assembly. Blue book.: Recommendations Q.251-Q300. Geneva: International Telecommunications Union, 1989.

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4

Cottman, Ronald J. A guidebook to ISO 9000 and ANSI/ASQC Q90. Milwaukee, Wis: ASQC Quality Press, 1993.

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5

Lee, William H. Coenzyme Q10: Is it our new fountain of youth?. New Canaan,Conn: Keats Publishing, 1987.

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6

Parker, Philip M., and James N. Parker. Coenzyme Q10: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

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7

Sinatra, Stephen T. The coenzyme Q10 and the heart: A miracle nutrient for the prevention and successful treatment of heart disease. New Canaan, Conn: Keats Pub., 1998.

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8

Lee, William C. Y. Coenzyme Q10. McGraw-Hill, 1998.

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9

Rahman, Shamima, and Mirian C. H. Janssen. Coenzyme Q10 Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0011.

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Primary CoQ10 deficiencies are usually diagnosed in childhood, but late-onset forms are recognized. The expression of all clinical symptoms is extremely variable, but six major phenotypes are recognized: (1) encephalomyopathy, seizures, and ataxia; (2) infantile-onset multisystem disease; (3) cerebellar ataxia; (4) isolated myopathy; (5) Leigh syndrome; and (6) isolated nephrotic syndrome. Early treatment with exogenous CoQ10 supplementation may result in a good outcome.

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10

Flytlie, Dr Knut. UBIQUINONE Q10 BODY FUEL. Forlaget Ny Videnskab, 1994.

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11

Kachelriess, Michael. Hadrons, partons and QCD. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198802877.003.0018.

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This chapter first discusses the breaking of scale invariance of QCD with massless quarks by quantum corrections and explains that this effect is responsible for the bulk of hadron masses. Then the parton picture is introduced, where one replaces a hadron which is probed in a hard process by free quarks and gluons. Perturbative QCD describes via the DGLAP equations the evolution of parton distribution functions f(x,Q2) as functions of Q2, requires however as as input f(x,Q20) from measurements at a fixed scale Q0 »QCD. The total annihilation cross section e+e →hadrons is calculated and it is shown that infrared singularities due to massless gluons and quarks cancel.

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12

GeraldL, Hunt, ed. The miracle nutrient coenzyme Q10. Thorsons, 1988.

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13

(Editor), Shirley Linde, ed. Coenzyme Q10: Nature's Heart Energizer. Impakt Communications Inc, 1998.

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14

Co-Enzym Q10 (German Edition). Books On Demand, 2009.

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15

Bliznakov, Emile. The Miracle Nutrient: Coenzyme Q10. Bantam, 1986.

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16

Hargreaves, Iain P. Coenzyme Q10: From Fact to Fiction. Nova Science Publishers, Incorporated, 2015.

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17

Group, Ltd Marcom. Q30 First Aid Video-Industrial Shop. Delmar Learning, 1991.

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18

ANSI/ASQC [Q90-94-1987]: American national standard. Milwaukee, Wis: The Society, 1987.

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19

Challem, Jack, and Ray Sahelian. FAQs All about Coenzyme Q10 (Freqently Asked Questions). Avery, 1998.

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20

Wexler, Barbara. Coenzyme Q10: The Essence of Energy (Woodland Health). Woodland Publishing, 2007.

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21

Littarru, G. P. The Fourth Conference of the International Coenzyme Q10 Association. IOS Press, 2006.

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22

Grigoryeva, Sabine. Coenzyme Q10: Uses, Health Effects and Role in Disease. Nova Science Publishers, Incorporated, 2018.

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23

Group, Ltd Marcom. Q40 Hand, Wrist, & Finger Safety Video-Shop (Safety Meeting Kits). Delmar Learning, 1994.

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24

Judy, Dr William V. The Substance that Powers Life: Coenzyme Q10 - an Insider's Guide. Forlaget Ny Videnskab, 2018.

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25

Zucker, Martin. User's Guide to Coenzyme Q10: Don't Be a Dummy. Become an Expert on What Coenzyme Q10 Can Do for Your Health (Basic Health Publications User's Guide). Basic Health Publications, 2002.

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26

Publications, ICON Health. Coenzyme Q10 - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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27

Energy and Defense : Facts and Perspectives on Coenzyme Q10 in Biology and Medicine. Casa Editrice Scientifica, 1995.

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28

American Society for Quality Control. Chemical Interest Committee. Ansi/Asqc Q90/Iso 9000: Guidelines for Use by the Chemical and Process Industries. Amer Society for Quality, 1992.

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29

American Society for Quality Control. Chemical Interest Committee., ed. ANSI/ASQC Q90/ISO 9000: Guidelines for use by the chemical and process industries. Milwaukee, Wis: ASQC Quality Press, 1992.

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30

United States. Agency for Healthcare Research and Quality. and Southern California Evidence-Based Practice Center/RAND., eds. Effect of supplemental antioxidants vitamin C, vitamin E, and coenzyme Q10 for the prevention and treatment of cardiovascular disease. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Healthcare Research and Quality, 2003.

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31

Coenzyme Q10: All-Around Nutrient for All-Around Health! Latest Research As a Heart Strengthener, Energy Promoter, Aging Fighter and Much More. Bl Publications, 1999.

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32

Shekelle, Paul G. Effect of the Supplemental Use of Antioxidants Vitamin C, Vitamin E, and Coenzyme Q10 for the Prevention and Treatment of Cancer (Evidence Report/Technology Assessment). Dept., 2003.

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33

Clarke, Andrew. Temperature, growth and size. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0013.

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Growth involves two flows of energy. The first is chemical potential energy in the monomers used to construct the proteins, lipids, polysaccharides and nucleic acids forming the new tissue. The second is the metabolic energy (ATP or GTP) used to construct the new tissue; this is the metabolic cost of growth and can be expressed as a dimensionless fraction of the energy retained in the new tissue. Its value is ~0.33. Typical temperature sensitivities for growth in the wild lie in the range Q10 1.5 – 3. Within species there may be evolutionary adjustments to growth rate to offset the effects of temperature, though these involve trade-offs with other physiological factors affecting fitness. Outside the tropics, many mammals and birds exhibit a cline in size, with larger species at higher latitudes (Bergmann’s rule). Carl Bergmann predicted such a cline from biophysical arguments based on endotherm thermoregulatory costs; Bergmann’s rule thus applies only to mammals and birds. Many ectotherms grow more slowly but attain a larger adult size when grown at lower temperatures (the temperature-size rule). The large size of some aquatic invertebrates at lower temperatures (notably in the polar regions and the deep sea) is associated with a higher oxygen content of the water.

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34

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.

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