1,465 research outputs found

    Online support vector machine application for model based fault detection and isolation of HVAC system

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    Abstract—Preventive maintenance plays an important role in Heating, Ventilation and Air Conditioning (HVAC) system. One cost effective strategy is the development of analytic fault detection and isolation (FDI) module by online monitoring the key variables of HAVC systems. This paper investigates realtime FDI for HAVC system by using online Support Vector Machine (SVM), by which we are able to train a FDI system with manageable complexity under real time working conditions. It is also proposed a new approach which allows us to detect unknown faults and updating the classifier by using these previously unknown faults. Based on the proposed approach, a semi unsupervised fault detection methodology has been developed for HVAC system

    Performance analysis of the generalised projection identification for time-varying systems

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    © The Institution of Engineering and Technology 2016. The least mean square methods include two typical parameter estimation algorithms, which are the projection algorithm and the stochastic gradient algorithm, the former is sensitive to noise and the latter is not capable of tracking the timevarying parameters. On the basis of these two typical algorithms, this study presents a generalised projection identification algorithm (or a finite data window stochastic gradient identification algorithm) for time-varying systems and studies its convergence by using the stochastic process theory. The analysis indicates that the generalised projection algorithm can track the time-varying parameters and requires less computational effort compared with the forgetting factor recursive least squares algorithm. The way of choosing the data window length is stated so that the minimum parameter estimation error upper bound can be obtained. The numerical examples are provided

    Soft X-ray resonant scattering study of single-crystal LaSr2_2Mn2_2O7_7

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    Soft X-ray resonant scattering studies at the Mn LII, IIIL_{\texttt{II, III}}- and the La MIV, VM_{\texttt{IV, V}}- edges of single-crystal LaSr2_2Mn2_2O7_7 are reported. At low temperatures, below TN160T_\texttt{N} \approx 160 K, energy scans with a fixed momentum transfer at the \emph{A}-type antiferromagnetic (0 0 1) reflection around the Mn LII, IIIL_{\texttt{II, III}}-edges with incident linear σ\sigma and π\pi polarizations show strong resonant enhancements. The splitting of the energy spectra around the Mn LII, IIIL_{\texttt{II, III}}-edges may indicate the presence of a mixed valence state, e.g., Mn3+^{3+}/Mn4+^{4+}. The relative intensities of the resonance and the clear shoulder-feature as well as the strong incident σ\sigma and π\pi polarization dependences strongly indicate its complex electronic origin. Unexpected enhancement of the charge Bragg (0 0 2) reflection at the La MIV, VM_{\texttt{IV, V}}-edges with σ\sigma polarization has been observed up to 300 K, with an anomaly appearing around the orbital-ordering transition temperature, TOO220T_{\texttt{OO}} \approx 220 K, suggesting a strong coupling (competition) between them.Comment: Accepted by European Physical Journal

    Targeting serine hydroxymethyltransferases 1 and 2 for T-cell acute lymphoblastic leukemia therapy

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    Despite progress in the treatment of acute lymphoblastic leukemia (ALL), T-cell ALL (T-ALL) has limited treatment options, particularly in the setting of relapsed/refractory disease. Using an unbiased genome-scale CRISPR-Cas9 screen we sought to identify pathway dependencies for T-ALL which could be harnessed for therapy development. Disruption of the one-carbon folate, purine and pyrimidine pathways scored as the top metabolic pathways required for T-ALL proliferation. We used a recently developed inhibitor of SHMT1 and SHMT2, RZ-2994, to characterize the effect of inhibiting these enzymes of the one-carbon folate pathway in T-ALL and found that T-ALL cell lines were differentially sensitive to RZ-2994, with the drug inducing a S/G2 cell cycle arrest. The effects of SHMT1/2 inhibition were rescued by formate supplementation. Loss of both SHMT1 and SHMT2 was necessary for impaired growth and cell cycle arrest, with suppression of both SHMT1 and SHMT2 inhibiting leukemia progression in vivo. RZ-2994 also decreased leukemia burden in vivo and remained effective in the setting of methotrexate resistance in vitro. This study highlights the significance of the one-carbon folate pathway in T-ALL and supports further development of SHMT inhibitors for treatment of T-ALL and other cancers

    Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells

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    Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to by-pass chemoresistance in cancer cells. Therefore, we explored the potential of this approach in breast cancer cells. Cisplatin and paclitaxel induced apoptosis in a dose-dependent manner in MCF-7 (drug-sensitive) and MDA-MB-231 (drug-insensitive) cells. Furthermore, when we transiently silenced Bcl-2, both cisplatin and paclitaxel induced apoptosis more than parental cells. Dose dependent induction of apoptosis by drugs was enhanced by the pre-treatment of these cells with HA14-1, a Bcl-2 inhibitor. Although the effect of cisplatin was significant on both cell lines, the effect of paclitaxel was much less potent only in MDA-MB-231 cells. To further understand the distinct role of drugs in MDA-MB-231 cells pretreated with HA14-1, caspases and Bcl-2 family proteins were studied. The apoptotic effect of cisplatin with or without HA14-1 pre-treatment is shown to be caspase-dependent. Among pro-apoptotic Bcl-2 proteins, Bax and Puma were found to be up-regulated whereas Bcl-2 and Bcl-x(L) were down-regulated when cells were pretreated with HA14-1 followed by paclitaxel or cisplatin. Enforced Bcl-2 expression in MDA-MB-231 cells abrogated the sensitizing effect of HA14-1 in cisplatin induced apoptosis. These results suggest that the potentiating effect of HA14-1 is drug and cell type specific and may not only depend on the inhibition of Bcl-2. Importantly, alteration of other pro-apoptotic or anti-apoptotic Bcl-2 family members may dictate the apoptotic response when HA14-1 is combined with chemotherapeutic drugs

    Next-to-leading order QCD predictions for Z0H0+jetZ^0 H^0 + {\rm jet} production at LHC

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    We calculate the complete next-to-leading order (NLO) QCD corrections to the Z0H0Z^0H^0 production in association with a jet at the LHC. We study the impacts of the NLO QCD radiative corrections to the integrated and differential cross sections and the dependence of the cross section on the factorization/renormalization scale. We present the transverse momentum distributions of the final Z0Z^0-, Higgs-boson and leading-jet. We find that the NLO QCD corrections significantly modify the physical observables, and obviously reduce the scale uncertainty of the LO cross section. The QCD K-factors can be 1.183 and 1.180 at the s=14TeV\sqrt{s}=14 TeV and s=7TeV\sqrt{s}=7 TeV LHC respectively, when we adopt the inclusive event selection scheme with pT,jcut=50GeVp_{T,j}^{cut}=50 GeV, mH=120GeVm_H=120 GeV and μ=μr=μf=μ01/2(mZ+mH)\mu=\mu_r=\mu_f=\mu_0 \equiv 1/2(m_Z+m_H). Furthermore, we make the comparison between the two scale choices, μ=μ0\mu=\mu_0 and μ=μ1=1/2(ETZ+ETH+jETjet)\mu=\mu_1=1/2(E_{T}^{Z}+E_{T}^{H}+ \sum_{j}E_{T}^{jet}), and find the scale choice μ=μ1\mu=\mu_1 seems to be more appropriate than the fixed scale μ=μ0\mu=\mu_0.Comment: 18 pages, 7 figure

    3D-bioprinting of patient-derived cardiac tissue models for studying congenital heart disease.

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    INTRODUCTION: Congenital heart disease is the leading cause of death related to birth defects and affects 1 out of every 100 live births. Induced pluripotent stem cell technology has allowed for patient-derived cardiomyocytes to be studied in vitro. An approach to bioengineer these cells into a physiologically accurate cardiac tissue model is needed in order to study the disease and evaluate potential treatment strategies. METHODS: To accomplish this, we have developed a protocol to 3D-bioprint cardiac tissue constructs comprised of patient-derived cardiomyocytes within a hydrogel bioink based on laminin-521. RESULTS: Cardiomyocytes remained viable and demonstrated appropriate phenotype and function including spontaneous contraction. Contraction remained consistent during 30 days of culture based on displacement measurements. Furthermore, tissue constructs demonstrated progressive maturation based on sarcomere structure and gene expression analysis. Gene expression analysis also revealed enhanced maturation in 3D constructs compared to 2D cell culture. DISCUSSION: This combination of patient-derived cardiomyocytes and 3D-bioprinting represents a promising platform for studying congenital heart disease and evaluating individualized treatment strategies
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