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1

service), ScienceDirect (Online, ed. RNA turnover in eukaryotes: Nucleases, pathways and analysis of mRNA decay. San Diego, Calif: Academic, 2008.

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2

Bacterial Cellular Metabolic Systems Metabolic Regulation Of A Cell System With 13cmetabolic Flux Analysis. Woodhead Publishing, 2012.

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3

Systems Biology: Constraint-Based Reconstruction and Analysis. Cambridge University Press, 2015.

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4

Palsson, Bernhard O. Systems Biology: Constraint-Based Reconstruction and Analysis. Cambridge University Press, 2015.

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5

Lamari, Foudil, and Jean-Marie Saudubray. Disorders of Complex Lipids Synthesis and Remodeling. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0066.

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Defective lipid catabolic pathways are involved in numerous inherited metabolic diseases such as lysosomal storage diseases and peroxisome biogenesis disorders. We recently described a new classification of a rapidly growing group of inherited metabolic disorders involving biosynthesis and remodeling of complex lipids including phospholipids and sphingolipids. The remarkable progress achieved over the last decade in high throughput gene sequencing and in lipid analysis technologies have enabled the description of more than 40 diseases linked to defects in enzymes involved in these pathways. Some of these defects present in infancy or childhood but most of them are diagnosed in adolescence or adulthood. In this review we focus on those with adult presentation.
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Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2002.

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7

Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2004.

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8

Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2002.

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9

Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2002.

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10

Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2002.

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11

Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2011.

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12

Voit, Eberhard O., and Néstor V. Torres. Pathway Analysis and Optimization in Metabolic Engineering. Cambridge University Press, 2009.

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13

Challacombe, Jean F. Metabolic Pathway Engineering: Analysis and Applications in the Life Sciences. Jenny Stanford Publishing, 2021.

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14

Challacombe, Jean F. Metabolic Pathway Engineering: Analysis and Applications in the Life Sciences. Jenny Stanford Publishing, 2021.

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15

Metabolic Pathway Engineering: Analysis and Applications in the Life Sciences. Jenny Stanford Publishing, 2021.

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16

Challacombe, Jean F. Metabolic Pathway Engineering: Analysis and Applications in the Life Sciences. Jenny Stanford Publishing, 2021.

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17

Kiledjian, Megerditch, and Lynne E. Maquat. RNA Turnover in Eukaryotes: Analysis of Specialized and Quality Control RNA Decay Pathways. Elsevier Science & Technology Books, 2011.

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18

von Caemmerer, S. Biochemical Models of Leaf Photosynthesis. CSIRO Publishing, 2000. http://dx.doi.org/10.1071/9780643103405.

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Increasing concerns of global climate change have stimulated research interests in all aspects of carbon exchange. This has restored interest in leaf photosynthetic models to predict and assess changes in photosynthetic CO2 assimilation in different environments. This is a comprehensive presentation of the most widely used models of steady-state photosynthesis by an author who is a world authority. Treatments of CO3, CO4 and intermediate pathways of photosynthesis in relation to environment have been update to include work on antisense transgenic plants. It will be a standard reference for the formal analysis of photosynthetic metabolism in vivo by advanced students and researchers.
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19

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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