178 research outputs found

    Modelling Dynamic Traffic Loads in Multiserver Queues using G/G/k Queue

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    Operations research and marketing management have benefited greatly from the important science of queuing optimisation. We take into account a multiserver single input G/G/k queue for study. This type of queue formation occurs in factories, production facilities, logistics centres, airports, and hospitals where the inter-arrival and service times are frequently not exponentially distributed. Knowing the precise number of service providers needed to avoid congestion at the lowest possible cost would therefore be the main concern. When there are more jobs than servers in a G/G/k queue, the cost incurred by the number of jobs per unit time becomes complex, making it challenging to determine the average cost. As a result, this paper obtains the bound for the ideal number of servers that would reduce the overall cost. Interpolation technique is used to determine the precise number of servers. When there are more servers (k) than job arrivals, the G/G/k queue’s optimal cost per unit time during an execution cycle is obtained. The proposed system is made up of a G/G/k queue that begins operating as soon as the first job enters the system. Due to the general distribution of job arrivals, the time interval between subsequent job arrivals is not always the same. Therefore, the study of an arrival that causes a state transition in the system is taken into account. When there are fewer servers available than job arrivals, an expression is derived to determine the optimal server count. When the number of available servers exceeds the number of jobs in the system, the optimal number of jobs that minimises the average processing cost per unit time for one job is also determined. The simulation results are obtained by simulating this system with MATLAB’s SimEvents toolbox

    Evidence that there are only two tRNA<SUP>Phe</SUP> genes in Escherichia coli

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    pheV, one of the genes that code for tRNAPhe, was deleted from the chromosome of a strain of Escherichia coli K-12. As a consequence of this mutation, expression of pheA, the gene for chorismate mutase P-prephenate dehydratase, the first enzyme in the terminal pathway of phenylalanine biosynthesis, was derepressed. Similar derepression of pheA has been reported in pheR mutants of E. coli K-12 (J. Gowrishankar and J. Pittard, J. Bacteriol. 150:1130-1137, 1982). Attempts to introduce a pheR mutation into the &#916; pheV strain failed under circumstances suggesting that this combination of mutations is lethal. Southern blot analysis of pheV+ and &#916; pheV strains indicated that there are only two tRNAPhe genes in E. coli. It is recommended that the names pheU and pheV be retained for these genes

    Evidence that there are only two tRNA<SUP>Phe</SUP> genes in Escherichia coli

    No full text
    pheV, one of the genes that code for tRNAPhe, was deleted from the chromosome of a strain of Escherichia coli K-12. As a consequence of this mutation, expression of pheA, the gene for chorismate mutase P-prephenate dehydratase, the first enzyme in the terminal pathway of phenylalanine biosynthesis, was derepressed. Similar derepression of pheA has been reported in pheR mutants of E. coli K-12 (J. Gowrishankar and J. Pittard, J. Bacteriol. 150:1130-1137, 1982). Attempts to introduce a pheR mutation into the &#916; pheV strain failed under circumstances suggesting that this combination of mutations is lethal. Southern blot analysis of pheV+ and &#916; pheV strains indicated that there are only two tRNAPhe genes in E. coli. It is recommended that the names pheU and pheV be retained for these genes

    In silico estimates of cell electroporation by electrical incapacitation waveforms

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    We use a system model of a cell and approximate magnitudes of electrical incapacitation (EI) device waveforms to estimate conditions that lead to responses with or without electroporation (EP) of cell membranes near electrodes. Single pulse waveforms of Taser X26 and Aegis MK63 devices were measured using a resistive load. For the present estimates the digitized waveforms were scaled in magnitude according to the inverse square radial distance from two tissue-penetrating electrodes, approximated as hemispheres. The corresponding tissue level electric fields were then used as inputs to the cell system model. A dynamic pore model for membrane electroporation (EP) was assigned to many different sites on the cell plasma membrane (PM). EI devices generate sufficiently large transmembrane voltage, U[subscript m](t), such that pores were created, evolving into a heterogeneous and time-dependent pore population. These approximate responses suggest that both waveforms can cause PM EP. Peripheral nerve damage by EP is a candidate side effect. More extensive EP is expected from the Taser X26 than the Aegis MK63, mainly due to the approximately eight-fold difference in the peak magnitudes. In silico examination of EI waveforms by multiscale modeling is warranted, and can involve whole body, tissue and cell level models that now exist and are rapidly being improved.National Institutes of Health (Grant RO1-GM63857)Aegis Industries, Inc

    Improvement in K<sup>+</sup>-limited growth rate associated with expression of the N-terminal fragment of one subunit (kdpA) of the multisubunit kdp transporter in Escherichia coli

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    Mutations in any one of three genes, kdpA, -B, or -C, in Escherichia coli abolish the activity of Kdp, a multisubunit K+-ATPase that belongs to the P-type ATPase family of cation transporters. We found in this study that expression in vivo of a 135-amino-acid-long N-terminal fragment (KdpA'), less than one-quarter the length of native KdpA, was able to mediate an improvement in K+-limited growth rates in two different contexts, even in the absence of both KdpC and the ATPase subunit KdpB. The first context was when KdpA' was overexpressed in cells from a heterologous inducible promoter, and the second was when KdpA' was provided with a C-terminally altered extension (following a spontaneous genetic rearrangement). Our results suggest that KdpA' provides an incipient pathway for K+ translocation which can serve to transport K+ into the cells in response to the cytoplasmic membrane potential

    Regulation of phenylalanine biosynthesis in Escherichia coli K-12: control of transcription of the pheA operon

    No full text
    Bacteriophage lambda ppheA-lac was used to obtain strains of Escherichia coli K-12 in which pheA and lacZ are each transcribed from a separate pheA promoter. Mutants in which both beta-galactosidase and chorismate mutase P-prephenate dehydratase (the pheA gene product) were derepressed were isolated, and a transacting gene (pheR) was identified. pheR was mapped at min 93 on the E. coli chromosome; pheR mutants acquired the wild-type phenotype when either F117 (which covers the 93-min region) or F116 (which covers min 59 to 65) was introduced into the cell. A rifampin resistance mutation, rpoB366, was found to derepress transcription of the pheA operon. pheR and rpoB366 affected two different systems for the phenylalanine-mediated control of pheA. A mutation in miaA (trpX), a gene known to be involved in attenuation in the tryptophan operon, was also shown to increase transcription of the pheA gene

    Regulation of phenylalanine biosynthesis in Escherichia coli K-12: control of transcription of the pheA operon

    No full text
    Bacteriophage lambda ppheA-lac was used to obtain strains of Escherichia coli K-12 in which pheA and lacZ are each transcribed from a separate pheA promoter. Mutants in which both beta-galactosidase and chorismate mutase P-prephenate dehydratase (the pheA gene product) were derepressed were isolated, and a transacting gene (pheR) was identified. pheR was mapped at min 93 on the E. coli chromosome; pheR mutants acquired the wild-type phenotype when either F117 (which covers the 93-min region) or F116 (which covers min 59 to 65) was introduced into the cell. A rifampin resistance mutation, rpoB366, was found to derepress transcription of the pheA operon. pheR and rpoB366 affected two different systems for the phenylalanine-mediated control of pheA. A mutation in miaA (trpX), a gene known to be involved in attenuation in the tryptophan operon, was also shown to increase transcription of the pheA gene

    The KdpD/KdpE two-component system : integrating K+ homeostasis and virulence

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    The two-component system (TCS) KdpD/KdpE, extensively studied for its regulatory role in potassium (K+) transport, has more recently been identified as an adaptive regulator involved in the virulence and intracellular survival of pathogenic bacteria, including Staphylococcus aureus, entero-haemorrhagic Escherichia coli, Salmonella typhimurium, Yersinia pestis, Francisella species, Photorhabdus asymbiotica, and mycobacteria. Key homeostasis requirements monitored by KdpD/KdpE and other TCSs such as PhoP/PhoQ are critical to survival in the stressful conditions encountered by pathogens during host interactions. It follows these TCSs may therefore acquire adaptive roles in response to selective pressures associated with adopting a pathogenic lifestyle. Given the central role of K+ in virulence, we propose that KdpD/KdpE, as a regulator of a high-affinity K+ pump, has evolved virulence-related regulatory functions. In support of this hypothesis, we review the role of KdpD/KdpE in bacterial infection and summarize evidence that (i) KdpD/KdpE production is correlated with enhanced virulence and survival, (ii) KdpE regulates a range of virulence loci through direct promoter binding, and (iii) KdpD/KdpE regulation responds to virulence-related conditions including phagocytosis, exposure to microbicides, quorum sensing signals, and host hormones. Furthermore, antimicrobial stress, osmotic stress, and oxidative stress are associated with KdpD/KdpE activity, and the system's accessory components (which allow TCS fine-tuning or crosstalk) provide links to stress response pathways. KdpD/KdpE therefore appears to be an important adaptive TCS employed during host infection, promoting bacterial virulence and survival through mechanisms both related to and distinct from its conserved role in K+ regulation

    A model for the regulation of expression of the potassium-transport operon, kdp, in Escherichia coli

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    The intracellular concentration of K+ in Escherichia coli is known to be determined by osmolarity of the growth medium, and it is believed that the expression of the potassium-transport operon, kdp, is controlled by the turgor pressure differential between the cytoplasm and the extracellular environment. Several lines of evidence, however, argue against a strict turgor-regulation model for kdp expression. Instead, it is proposed here that kdp is controlled by one fraction of intracellular [K+], and that the size of this fraction is independent of the osmolarity of the culture medium
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