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A possible explanation for the superiority of the amino donor, L-aspartic add, has come from studies carried out on mutants of E. coli, in which only one of the three transaminases that are found in E. coli are present. It is believed that a branched chain transaminase, an aromatic amino add transaminase and an aspartate phenylalanine aspartase can be present in E. coli. The reaction of each of these mutants with different amino donors gave results which indicated that branched chain transminase and aromatic amino add transminase containing mutants were not able to proceed to high levels of conversion of phenylpyruvic add to L-phenylalanine. However, aspartate phenylalanine transaminase containing mutants were able to yield 98% conversion on 100 mmol l 1 phenylpyruvic acid. The explanation for this is probably that both branched chain transaminase and aromatic amino acid transminase are feedback inhibited by L-phenylalanine, whereas aspartate phenylalanine transaminase is not inhibited by L-phenylalanine. In addition, since oxaloacetate, which is produced when aspartic add is used as the amino donor, is readily converted to pyruvic add, no feedback inhibition involving oxaloacetate occurs. The reason for low conversion yield of some E. coli strains might be that these E. cdi strains are defident in the aspartate phenylalanine transaminase. [Pg.268]

Figure 2.14 Relation between the EEG recorded from an epileptic focus on the surface of the cerebral cortex (EEG) and the activity of a single cortical neuron recorded extracellularly (e.c.) and intracellularly (i.c.) during an experimental epilepsy induced by topical application of penicillin. Note that the large EEG excursions correspond to the large (synchronised) depolarisations of the neuron, not to action potential discharges. (Adapted from Brain Res. 52 Ayala, GF et al. Genesis of Epileptic Interictal Spikes. New Knowledge of Cortical Feedback systems suggests a Neurophysiological Explanation of Brief Paroxysms, 1-17 (1973) with permission from Elsevier Science)... Figure 2.14 Relation between the EEG recorded from an epileptic focus on the surface of the cerebral cortex (EEG) and the activity of a single cortical neuron recorded extracellularly (e.c.) and intracellularly (i.c.) during an experimental epilepsy induced by topical application of penicillin. Note that the large EEG excursions correspond to the large (synchronised) depolarisations of the neuron, not to action potential discharges. (Adapted from Brain Res. 52 Ayala, GF et al. Genesis of Epileptic Interictal Spikes. New Knowledge of Cortical Feedback systems suggests a Neurophysiological Explanation of Brief Paroxysms, 1-17 (1973) with permission from Elsevier Science)...
A rather satisfactory explanation of the irreversibility of amino acid accumulation in yeast cells is that it might result from specific regulatory mechanisms capable of immobilizing the transporters in a closed position. Uptake of amino acids by a number of permeases does indeed appear to be regulated by specific, and possibly allosteric, feedback inhibition. This idea is based on the fact that a number of transport systems seem to be specifically inhibited by their internally accumulated... [Pg.232]

The limitation of transfer function representation becomes plain obvious as we tackle more complex problems. For complex systems with multiple inputs and outputs, transfer function matrices can become very clumsy. In the so-called modem control, the method of choice is state space or state variables in time domain—essentially a matrix representation of the model equations. The formulation allows us to make use of theories in linear algebra and differential equations. It is always a mistake to tackle modem control without a firm background in these mathematical topics. For this reason, we will not overreach by doing both the mathematical background and the control together. Without a formal mathematical framework, we will put the explanation in examples as much as possible. The actual state space control has to be delayed until after tackling classical transfer function feedback systems. [Pg.64]

Ayala, G. F., Dichter, M., Gumnit, R. L, Matsumoto, H. and Spencer, W. A. Genesis of epileptic interictal spikes. New knowledge of cortical feedback systems suggests a neurophysiological explanation of brief paroxysms. Brain Res. 52 1-17,1973. [Pg.638]

Finally, a feedback mechanism has often been used to explain observed (negative and positive) deviations from the Scatchard type plots or nonunity slopes of the nonsaturated portion of the logarithmic Michaelis-Menten plots (e.g. [209]). When no artifacts are present (cf. [197,198]), deviations can indeed be interpreted to indicate that the intrinsic stability or dissociation rate constants vary with the number of occupied transport sites. Nonetheless, several other physical explanations, including multiple carriers, non 1 1 binding, carrier aggregation, etc. must also be considered. [Pg.496]

This, of course, is a very important part of the program. We are developing it on an as-needed basis in response to feedback from users. In particular, we still have not implemented a complete explanation facility. The user interface currently provides online help and a menu based selection of valid responses whenever applicable. [Pg.295]

Biochemistry provides the explanation for Porter s observations a decrease in the plasma concentration of testosterone could account for the inability to perform whilst die reduced extent of feedback inhibition on die pituitary would lead to an increased rate of secretion and hence an increase in die blood concentration of luteinising hormone, which has been claimed to increase the degree of sexual arousal in men. [Pg.328]

The explanation for this phenomenon is that in the prepubertal phase the amount of testosterone that is secreted is not sufficient to cause development of the male genitalia, which is normally stimulated by dihydrotestosterone. However, at puberty the secretion of testosterone increases. The increase is large in this syndrome, because lack of dihydrotestosterone decreases the extent of the feedback inhibition of the hormone secretions by the pituitary so that more gonadotrophins are released which stimulate, markedly, the rate of testosterone secretion and hence its concentration in the blood. At these high levels, testosterone has sufficient androgenic effects to stimulate development of the external genitalia. [Pg.439]

Why weeds reduce crop yields cannot be adequately answered. Considerable data have accumulated which relate duration of weed presence and weed density to crop yield. However, such data provide little explanation for why crop yields are reduced. The objectives of this paper are to 1) provide an overview of the time relationship of competition for growth factors and of allelopathy as factors in crop yield reduction and 2) suggest a direct feedback effect on reproduction in response to light as a possible third direct factor in explaining effects of weeds on crop yield. [Pg.300]

The remainder of this discussion examines the possibility of a direct feedback mechanism in response to light as an explanation for crop yield reduction from early weed presence. Three types of data will be examined 1) results of our research on velvetleaf interference with light in soybeans 2) a comparison of observed and estimated soybean yield reductions for weed presence versus leaf removal and 3) the poor correlation between weed control and crop yields. [Pg.306]

As indicated in the explanation, there is a compounding of effects. Earliest reduction in crop yield potential may be due to only one factor, e.g. direct feedback. The effect of this factor is visualized as persisting for the remainder of the crop growth cycle... [Pg.311]

Table 4 summarizes these HPA findings in PTSD and the explanations compatible with these findings. This table demonstrates that the model of enhanced negative feedback is compatible with 15/21 observations of HPA alterations in PTSD, whereas reduced adrenal capacity is consistent with 9/21 observations. [Pg.394]

Finally, our thanks to you, the reader. It is the honest desire of the authors to hear from you. We would like to receive your feedback. It is impossible to produce a text like this that satisfies everyone, their expectations and needs. Many things were left out of the book, but if you feel that some more explanations, reviews or information are required, please do not hesitate to contact us. If a new version comes with the winds of the future, your suggestions will be greatly appreciated and, as far as possible, included (and publicly acknowledged, of course). [Pg.325]

For approximately two decades, the lapse hypothesis was the dominant theoretical explanation for the effects of sleep loss on cognitive performance. In their seminal monograph, Williams, Lubin, and Goodnow (43) reported that performance lapses on experimenter-paced RT tasks increased with increasing hours of wakefulness, and that while poorest performance worsened, subjects were still able to perform at almost optimum levels between lapse periods. Thus, the longer subjects remained awake, the more variable their performance became. Importantly, this was observed regardless of the type (simple vs. choice) or duration (10 vs. 30 min) of RT task, and whether or not subjects were provided with performance feedback. [Pg.47]


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