Energy metabolism model

JaJri, M.J., Dudycha, J., O Rourke, B. (2001). Cardiac energy metabolism models of cellular respiration. Annu. Rev. Biomed. Eng. 3 57-81. 

Models for batch culture can be constructed by assuming mechanisms for each phase of the cycle. These mechanisms must be reasonably comph-cated to account for a lag phase and for a prolonged stationary phase. Unstructured models treat the cells as a chemical entity that reacts with its environment. Structured models include some representation of the internal cell chemistry. Metabolic models focus on the energy-producing mechanisms within the cells. 

Figure 11.1. A flow-model scheme for treating the protein routing question. Labels refer to flow rates of carbon. The total carbon flux, into and out of the body, is 1, divided into F (for protein) and 1 - F for the remainder. The significant relevant internal fluxes are between the amino acid pool (coupled to the body protein pool), and the energy metabolism pool . The extent to which protein routing is observable in the body protein composition depends on the value ofX (See Fig. 11.2). Numbers in refer to suggested isotopic fractionations associated with a metabolic path, which are consistent with the data of the Ambrose and Norr (1993) and Tieszen and Fagre (1993) data set (see Section 4.1).

Nehlig, A. Age-dependent pathways of brain energy metabolism the suckling rat, a natural model of the ketogenic diet. Epilepsy Res. 37 211-221,1999. 

At the point where amphiphiles were recruited to provide the precursors to cell membranes, stable lipid vesicles could have evolved [141] to enclose autocatalytic chiral hypercycles. Credible models for the subsequent evolution of vesicles containing self-replicating chiral molecules have appeared in the literature. [193,194] These vesicles could then emerge from the feldspar spaces [134,192] as micron-sized self-reproducing, energy-metabolizing vesicular systems protobacteria ready to face the hydrothermal world on their own terms. 

An index of the phospho anhydride (i.e.,P—O—P) bond content of the adenine nucleotides of a cell, based on a hypothetical modeP that attempts to explain the metabolic basis for control of ATP utilization and regeneration. Later studies demonstrated that the energy charge model is overly simplistic and that its principles are unlikely to constitute a useful model for the control of energy metabolism within biological systems. 

Shugaev, B.S. (1989). A mathematical model of selection, entailing energy metabolism of organisms as a tool for studying the evolutionary process (In Russian). Zhumal Obshchey Biologii 50,199-206. 

Especially in models of transient cerebral ischemia, apoptotic cell death has been observed after 3-7 days post insult in selected brain regions in which basal energy metabolism has been preserved (Chen et al. 1997 Du et al. 1996). In the meantime, molecular switches have been identified that gate different populations of neurons with regard to the type of cell death they eventually undergo (Nicotera 2003). However, there is little doubt that in animal stroke the vast majority of cells would die from necrosis or, alternatively, secondary energy failure even in the presence of a pro-apop-totic genetic balance. The concept of thresholds of cerebral blood flow (CBF) for various functions of brain parenchyma (see below) explains why the infarct core suffers from pan-necrosis whereas the peri-infarct border in which function is suppressed, but structure initially preserved (the so-called ischemic penumbra), may show apoptotic cell death or a combination of both. 

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