Integrated billing mechanisms in the Internet of Things to support information sharing and enable new business opportunities

The Internet of Things (IOT) concept and enabling technologies such as RFID offer the prospect of linking the real world of physical objects with the virtual world of information technology to improve visibility and traceability information within supply chains and across the entire lifecycles of products, as well as enabling more intuitive interactions and greater automation possibilities. There is a huge potential for savings through process optimization and profit generation within the IOT, but the sharing of financial benefits across companies remains an unsolved issue. Existing approaches towards sharing of costs and benefits have failed to scale so far. The integration of payment solutions into the IOT architecture could solve this problem. We have reviewed different possible levels of integration. Multiple payment solutions have been researched. Finally we have developed a model that meets the requirements of the IOT in relation to openness and scalability. It supports both hardware-centric and software-centric approaches to integration of payment solutions with the IOT. Different requirements concerning payment solutions within the IOT have been defined and considered in the proposed model. Possible solution providers include telcos, e-payment service providers and new players such as banks and standardization bodies. The proposed model of integrating the Internet of Things with payment solutions will lower the barrier to invoicing for the more granular visibility information generated using the IOT. Thus, it has the potential to enable recovery of the necessary investments in IOT infrastructure and accelerate adoption of the IOT, especially for projects that are only viable when multiple benefits throughout the supply chain need to be accumulated in order to achieve a Return on Investment (ROI). In a long-term perspective, it may enable IT-departments to become profit centres instead of cost centres. © 2010 - IOS Press and the authors. All rights reserved.

Isolating and recognizing crudeoiklegrading [sic] bacteria of Queshm Island shores for biodegradation of crude oil pollutions

This research was carried out for recognizing Natural Flora Bacteria of oil pollution in the coasts of Queshm island. In The First steps, The coasts of this Island were scrutinized as a Field of research and For knowing whether oil stains exist or not. It gets obvious That southern coasts of Queshm have got oil pollution which is created by oil tankers which carry oil of Iran continental shelf. Them oil stains were sampled from to certain stations. In The First step, primary isolation of exisiting bacteria in every oil sample was done and then purification of each bacterium was carried out. Then each purified bacterium that has got strong, recognized, typic growth was enriched oil sample of T5 station. And Bacterium C4 (gram—negative coccobacillus) was chosen as the second priority From oil sample of TA station and Bacterium B1 (gram—positive coccus) was chosen as The third priority From oil sample of TI station. All The above mentioned bacteria were biochemically, physiologically and morphologically experimented For specking The species. According To The tests done and comparing with The tests done and comparing with the reference Berge y' s, bacterium A5 Pelongs to the species pseudomonas sp and becterium C4 belongs to the species Aeromonas sp and bacterium BI belongs to The species micrococcus sp. In The Last stage, bacterium with The First priority (TA5 pseudomonas sp) was used in the planned microcosm. The sake of optimum and adapting to Laboratory conditions Each enriched and purified bacterium was given a code for station and a code For itself . Then This bacterium was studied and it was proved that it has potentiality For using oil as a source of carbon. From oil samples of 10 stations, 30 various Colonies of bacterium were Isolated, of which 20 bacteria had the highest potentiality of growth. And the other bacteria that has no typic growth were omitted From being studied. Since all of These 20 bacterium are able to use oil, a bacterium with maximum rate of growth in the presence of crude oil and Lack of other hydrocarbonic sources and with The code A5 ( gram — negative Bacillus ) was chosen as First priority From The mentioned microcosm contains sea water , suspension oil degrading bacterium , crude oil, azote and various concentrations of carbon and Incubated in 30°` and shook 150 PRA1 According to the results , index oil degrading bacterium (pseudomonas sp) belongs oil sample of T5 stations (east of sheeb draz Gulf) which growth best and have the potentiality of degrading oil in 25 glli malas and 50 glli cheese water and with 5 gill urea .

Glucocorticoid receptor and protein/RNA synthesis-dependent mechanisms underlie the control of synaptic plasticity by stress

Learning and memory are exquisitely sensitive to behavioral stress, but the underlying mechanisms are still poorly understood. Because activity-dependent persistent changes in synaptic strength are believed to mediate memory processes in brain areas such as the hippocampus we have examined the means by which stress affects synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats, Inescapable behavioral stress (placement on an elevated platform for 30 min) switched the direction of plasticity, favoring low frequency stimulation-induced decreases in synaptic transmission (long-term depression, LTD), and opposing the induction of long-term potentiation by high frequency stimulation, We have discovered that glucocorticoid receptor activation mediates these effects of stress on LTD and longterm potentiation in a protein synthesis-dependent manner because they were prevented by the glucocorticoid receptor antagonist RU 38486 and the protein synthesis inhibitor emetine. Consistent with this, the ability of exogenously applied corticosterone in non-stressed rats to mimic the effects of stress on synaptic plasticity was also blocked by these agents, The enablement of low frequency stimulation-induced LTD by both stress and exogenous corticosterone was also blocked by the transcription inhibitor actinomycin D, Thus, naturally occurring synaptic plasticity is liable to be reversed in stressful situations via glucocorticoid receptor activation and mechanisms dependent on the synthesis of new protein and RNA, This indicates that the modulation of hippocampus-mediated learning by acute inescapable stress requires glucocorticoid receptor-dependent initiation of transcription and translation.

Mechanisms of H+ modulation of glycinergic response in rat sacral dorsal commissural neurons

Many ionotropic receptors are modulated by extracellular H+. So far, few studies have directly addressed the role of such modulation at synapses. In the present study, we investigated the effects of changes in extracellular pH on glycinergic miniature inhibitory postsynaptic currents (mIPSCs) as well as glycine-evoked currents (I-Gly) in mechanically dissociated spinal neurons with native synaptic boutons preserved. H+ modulated both the mIPSCs and I-Gly, biphasically, although it activated an amiloride-sensitive inward current by itself. Decreasing extracellular pH reversibly inhibited the amplitude of the mIPSCs and I-Gly, while increasing external pH reversibly potentiated these parameters. Blockade of acid-sensing ion channels (ASICs) with amiloride, the selective antagonist of ASICs, or decreasing intracellular pH did not alter the modulatory effect of H+ on either mIPSCs or I-Gly, H+ shifted the EC50 of the glycine concentration-response curve from 49.3 +/- 5.7 muM at external pH 7.4 to 131.5 +/- 8.1 muM at pH 5.5, without altering the Cl- selectivity of the glycine receptor (GlyR), the Hill coefficient and the maximal I-Gly, suggesting a competitive inhibition of I-Gly by H+. Both Zn2+ and H+ inhibited I-Gly. However, H+ induced no further inhibition of I-Gly in the presence of a saturating concentration of Zn2+. In addition, H+ significantly affected the kinetics of glycinergic mIPSCs and I-Gly. It is proposed that H+ and/or Zn2+ compete with glycine binding and inhibit the amplitude of glycinergic mIPSCs and I-Gly. Moreover, binding of H+ induces a global conformational change in GlyR, which closes the GlyR Cl- channel and results in the acceleration of the seeming desensitization of IGly as well as speeding up the decay time constant of glycinergic mIPSCs. However, the deprotonation rate is faster than the unbinding rate of glycine from the GlyR, leading to reactivation of the undesensitized GlyR after washout of agonist and the appearance of a rebound I-Gly. H+ also modulated the glycine cotransmitter, GABA-activated current (I-GABA). Taken together, the results support a 'conformational coupling' model for H+ modulation of the GlyR and suggest that W may act as a novel modulator for inhibitory neurotransmission in the mammalian spinal cord.

Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction

The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation ( similar to 20%) to synaptic depression ( similar to 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction.

Computational mechanisms of sensorimotor control.

In order to generate skilled and efficient actions, the motor system must find solutions to several problems inherent in sensorimotor control, including nonlinearity, nonstationarity, delays, redundancy, uncertainty, and noise. We review these problems and five computational mechanisms that the brain may use to limit their deleterious effects: optimal feedback control, impedance control, predictive control, Bayesian decision theory, and sensorimotor learning. Together, these computational mechanisms allow skilled and fluent sensorimotor behavior.