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Dynamic and steady-state models of metabolic pathways a theoretical evaluation /Ehlde, Magnus. January 1995 (has links)
Thesis (Ph. D.)--University of Lund, 1995. / Published dissertation.
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Dynamic and steady-state models of metabolic pathways a theoretical evaluation /Ehlde, Magnus. January 1995 (has links)
Thesis (Ph. D.)--University of Lund, 1995. / Published dissertation.
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Die Abhängigkeit des Stoffwechsels von der Körperoberfläche Inaugural-Dissertation /Fackler, Karl, January 1934 (has links)
Thesis (doctoral)--Ludwig-Maximilians-Universität zu München, 1934.
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Die Abhängigkeit des Stoffwechsels von der Körperoberfläche Inaugural-Dissertation /Fackler, Karl, January 1934 (has links)
Thesis (doctoral)--Ludwig-Maximilians-Universität zu München, 1934.
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The energy requirement of normal three- and four-year-old children under standard basal metabolism conditions and during periods of quiet playRobb, Elda Iantha, January 1934 (has links)
Thesis (Ph. D.)--Columbia University, 1934. / Vita. Published also as Child development monographs, Monograph no. 16. Bibliography: p. 55-56.
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Effects of metabolic alteration on apparent covalent binding of carcinogens to rat hepatocyte macromolecules in primary monolayer cultureLoretz, Linda Joanne. January 1983 (has links)
Thesis (M.S.)--University of Wisconsin--Madison, 1983. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.
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Treatment factors and neuropsychological outcome in phenylketonuriaGriffiths, Peter V. January 1997 (has links)
Phenylketonuria (PKU) is an inherited metabolic disease that affects about one in 10,000 of the population worldwide. In the classical form of the condition, the hepatic enzyme phenylalanine hydroxlase is absent or much reduced. If untreated, severe or profound mental handicap customarily results due to the accumulation of dietary phenylalanine (phe) which is neurotoxic. The mechanism by which phe impairs growth in the immature nervous system is little understood, but myelin metabolism appears to be disturbed. Treatment is by reduction of phe in daily food intake. Treatment should ideally begin in the neonatal period if intellectual loss is to be avoided. However, the safe range of phe concentrations during treatment and the age at which treatment can be discontinued without further damage being inflicted are uncertain. The studies reported in this volume investigated neuropsychological outcomes of treatment control and cessation factors. In addition, the question of whether executive functions are especially vulnerable to elevated phe concentrations during treatment was addressed. Patient samples conformed to the practice adopted in the West of Scotland regional centre for the management of PKU of maintaining dietary treatment until age 10 or beyond. Almost exclusively, negative findings emerged. These suggested that, if control of phe intake conforms to current UK recommendations for the preschool and primary years, neither global nor specific intellectual deficit result. Furthermore, the data supported the view that cessation of treatment at 10 years of age does not have harmful consequences. These findings have direct implications for the formulation of clinical policy on the treatment of PKU, but it must be recognized that the history of the successful treatment of PKU and mass screening for the disease spans a mere three decades. Thus, treatment outcome research to date is based only on children and young adults. In future investigations, a life-span approach will be required before the issues raised in this thesis can be finally settled.
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I. The specific metabolic principle of the pituitary II. Thermostable oxidations in tumor tissue /Feinstein, Robert N., January 1940 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1940. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 180-182).
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