111 research outputs found

    Developing an online predictor to predict product sulfur concentration for HDS unit

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    Hydrodesulfurization (HDS) is an important process in refining industries. Advanced control system (e.g. model predictive controller) requires on-line measurement of the product sulfur at the reactor outlet. However, most HDS processes do not have a sulfur analyzer at the reactor outlet. In order to predict product sulfur concentration usually a data based sulfur predictor is developed. Performance of data based predictor is usually poor since some of the input parameters (e.g. feed sulfur concentration) are unknown. The objective of this thesis is to overcome these limitations of data based predictors and develop an online product sulfur predictor for HDS unit. In this thesis, a hybrid model is proposed, developed and validated (using industrial data), which could predict product sulfur concentration for online HDS system. The proposed hybrid structure is a combination of a reaction kinetics based HDS reactor model and an empirical model based on support vector regression (SVR). The mechanistic model runs in off-line mode to estimate the feed sulfur concentration while the data based model uses the estimated feed sulfur concentration and other process variables to predict the product sulfur concentration. The predicted sulfur concentration can be compared with the lab measurements or sulfur analyzer located further downstream of the process at the tankage. In case there is a large discrepancy, the predictor goes to a calibration mode and uses the mechanistic model to re-estimate the feed sulfur concentration. The detailed logic for the online prediction is also developed. Finally a Matlab based Graphical User Interface (GUI) has been developed for the hybrid sulfur predictor for easy implementation to any HDS process

    Stented ureterovesical anastomosis in renal transplantation: does it influence the rate of urinary tract infections?

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    <p>Abstract</p> <p>Objective</p> <p>Our objective was to evaluate the impact of routine use of double-J stents on the incidence of urinary tract infection after renal transplantation.</p> <p>Methods</p> <p>We conducted a retrospective-comparative single-centre study in 310 consecutive adult deceased donor kidney recipients transplanted from 2002 to 2006. Patients were divided in two groups, with or without urinary stent implantation. To evaluate the predictive factors for UTI, donor and recipients pre- and post-transplantation data were analysed. Early urological complications and renal function within 12 months of transplantation were included as well.</p> <p>Results</p> <p>A total of 157 patients were enrolled to a stent (ST) and 153 patients to a no-stent (NST) group. The rate of urinary tract infection at three months was similar between the two groups (43.3% ST vs. 40.1% NST, p = 0.65). Of the identified pathogens Enterococcus and Escherichia coli were the most common species. In multivariate analysis neither age nor immunosuppressive agents, BMI or diabetes seemed to have influence on the rate of UTI. When compared to males, females had a significantly higher risk for UTI (54.0% vs. 33.5%).</p> <p>Conclusion</p> <p>Prophylactic stenting of the ureterovesical anastomosis does not increase the risk of urinary tract infection in the early postoperative period.</p

    N-3 PUFA Supplementation Triggers PPAR-α Activation and PPAR-α/NF-κB Interaction: Anti-Inflammatory Implications in Liver Ischemia-Reperfusion Injury

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    Dietary supplementation with the n-3 polyunsaturated fatty acids (n-3 PUFA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) to rats preconditions the liver against ischemia-reperfusion (IR) injury, with reduction of the enhanced nuclear factor-κB (NF-κB) functionality occurring in the early phase of IR injury, and recovery of IR-induced pro-inflammatory cytokine response. The aim of the present study was to test the hypothesis that liver preconditioning by n-3 PUFA is exerted through peroxisone proliferator-activated receptor α (PPAR-α) activation and interference with NF-κB activation. For this purpose we evaluated the formation of PPAR-α/NF-κBp65 complexes in relation to changes in PPAR-α activation, IκB-α phosphorylation and serum levels and expression of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in a model of hepatic IR-injury (1 h of ischemia and 20 h of reperfusion) or sham laparotomy (controls) in male Sprague Dawley rats. Animals were previously supplemented for 7 days with encapsulated fish oil (General Nutrition Corp., Pittsburg, PA) or isovolumetric amounts of saline (controls). Normalization of IR-altered parameters of liver injury (serum transaminases and liver morphology) was achieved by dietary n-3 PUFA supplementation. EPA and DHA suppression of the early IR-induced NF-κB activation was paralleled by generation of PPAR-α/NF-κBp65 complexes, in concomitance with normalization of the IR-induced IκB-α phosphorylation. PPAR-α activation by n-3 PUFA was evidenced by enhancement in the expression of the PPAR-α-regulated Acyl-CoA oxidase (Acox) and Carnitine-Palmitoyl-CoA transferase I (CPT-I) genes. Consistent with these findings, normalization of IR-induced expression and serum levels of NF-κB-controlled cytokines IL-lβ and TNF-α was observed at 20 h of reperfusion. Taken together, these findings point to an antagonistic effect of PPAR-α on NF-κB-controlled transcription of pro-inflammatory mediators. This effect is associated with the formation of PPAR-α/NF-κBp65 complexes and enhanced cytosolic IκB-α stability, as major preconditioning mechanisms induced by n-3 PUFA supplementation against IR liver injury

    Barrier Tissue Macrophages: Functional Adaptation to Environmental Challenges

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    Macrophages are found throughout the body, where they have crucial roles in tissue development, homeostasis and remodeling, as well as being sentinels of the innate immune system that can contribute to protective immunity and inflammation. Barrier tissues, such as the intestine, lung, skin and liver, are exposed constantly to the outside world, which places special demands on resident cell populations such as macrophages. Here we review the mounting evidence that although macrophages in different barrier tissues may be derived from distinct progenitors, their highly specific properties are shaped by the local environment, which allows them to adapt precisely to the needs of their anatomical niche. We discuss the properties of macrophages in steady-state barrier tissues, outline the factors that shape their differentiation and behavior and describe how macrophages change during protective immunity and inflammation

    Precise measurement of the Ds+D^+_s lifetime at Belle II

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    We measure the lifetime of the Ds+D_s^+ meson using a data sample of 207 fb1^{-1} collected by the Belle II experiment running at the SuperKEKB asymmetric-energy e+ee^+ e^- collider. The lifetime is determined by fitting the decay-time distribution of a sample of 116×103116\times 10^3 Ds+ϕπ+D_s^+\rightarrow\phi\pi^+ decays. Our result is \tau^{}_{D^+_s} = (498.7\pm 1.7\,^{+1.1}_{-0.8}) fs, where the first uncertainty is statistical and the second is systematic. This result is significantly more precise than previous measurements.Comment: 7 pages, 4 figures, to be submitted to Physical Review Letter

    Measurement of CPCP asymmetries in B0ϕKS0B^0\to \phi K^0_S decays with Belle II

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    We present a measurement of time-dependent rate asymmetries in B0ϕKS0B^0\to \phi K^0_S decays to search for non-standard-model physics in bqqsb\to q \overline{q}s transitions. The data sample is collected with the Belle II detector at the SuperKEKB asymmetric-energy e+ee^{+}e^{-} collider in 2019-2022 and contains (387±6)×106(387\pm 6)\times 10^6 bottom-antibottom mesons from Υ(4S)\Upsilon(4S) resonance decays. We reconstruct 162±17162\pm17 signal events and extract the charge-parity (CPCP) violating parameters from a fit to the distribution of the proper-decay-time difference of the two BB mesons. The measured direct and mixing-induced CPCP asymmetries are A=0.31±0.20±0.05A=0.31\pm0.20\pm0.05 and S=0.54±0.260.08+0.06S=0.54\pm0.26^{+0.06}_{-0.08}, respectively, where the first uncertainties are statistical and the second are systematic. The results are compatible with the CPCP asymmetries observed in bccsb\to c\overline{c} s transitions

    Tests of light-lepton universality in angular asymmetries of B0DνB^0 \to D^{*-} \ell \nu decays

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    We present the first comprehensive tests of light-lepton universality in the angular distributions of semileptonic \Bz-meson decays to charged spin-1 charmed mesons. We measure five angular-asymmetry observables as functions of the decay recoil that are sensitive to lepton-universality-violating contributions. We use events where one neutral \B is fully reconstructed in \PUpsilonFourS{} \to\B\overline{B} decays in data corresponding to \lumion integrated luminosity from electron-positron collisions collected with the \belletwo detector. We find no significant deviation from the standard model expectations

    Measurement of branching fractions and direct CPCP asymmetries for BKπB \to K\pi and BππB\to\pi\pi decays at Belle II

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    We report measurements of the branching fractions and direct CP\it{CP} asymmetries of the decays B0K+πB^0 \to K^+ \pi^-, B+K+π0B^+ \to K^+ \pi^0, B+K0π+B^+ \to K^0 \pi^+, and B0K0π0B^0 \to K^0 \pi^0, and use these for testing the standard model through an isospin-based sum rule. In addition, we measure the branching fraction and direct CP\it{CP} asymmetry of the decay B+π+π0B^+ \to \pi^+\pi^0 and the branching fraction of the decay B0π+πB^0 \to \pi^+\pi^-. The data are collected with the Belle II detector from e+ee^+e^- collisions at the Υ(4S)\Upsilon(4S) resonance produced by the SuperKEKB asymmetric-energy collider and contain 387×106387\times 10^6 bottom-antibottom meson pairs. Signal yields are determined in two-dimensional fits to background-discriminating variables, and range from 500 to 3900 decays, depending on the channel. We obtain 0.03±0.13±0.04-0.03 \pm 0.13 \pm 0.04 for the sum rule, in agreement with the standard model expectation of zero and with a precision comparable to the best existing determinations
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