946 research outputs found

    Analysis of the strong vertices of ΣcND\Sigma_cND^{*} and ΣbNB\Sigma_bNB^{*} in QCD sum rules

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    The strong coupling constant is an important parameter which can help us to understand the strong decay behaviors of baryons. In our previous work, we have analyzed strong vertices ΣcND\Sigma_{c}^{*}ND, ΣbNB\Sigma_{b}^{*}NB, ΣcND\Sigma_{c}ND, ΣbNB\Sigma_{b}NB in QCD sum rules. Following these work, we further analyze the strong vertices ΣcND\Sigma_{c}ND^{*} and ΣbNB\Sigma_{b}NB^{*} using the three-point QCD sum rules under Dirac structures q ⁣ ⁣ ⁣/p ⁣ ⁣ ⁣/γαq\!\!\!/p\!\!\!/\gamma_{\alpha} and q ⁣ ⁣ ⁣/p ⁣ ⁣ ⁣/pαq\!\!\!/p\!\!\!/p_{\alpha}. In this work, we first calculate strong form factors considering contributions of the perturbative part and the condensate terms qq\langle\overline{q}q\rangle, αsπGG\langle\frac{\alpha_{s}}{\pi}GG\rangle and qgsσGq\langle\overline{q}g_{s}\sigma Gq\rangle. Then, these form factors are used to fit into analytical functions. According to these functions, we finally determine the values of the strong coupling constants for these two vertices ΣcND\Sigma_{c}ND^{*} and ΣbNB\Sigma_{b}NB^{*}.Comment: arXiv admin note: text overlap with arXiv:1705.0322

    Revisiting the Pion Leading-Twist Distribution Amplitude within the QCD Background Field Theory

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    We study the pion leading-twist distribution amplitude (DA) within the framework of SVZ sum rules under the background field theory. To improve the accuracy of the sum rules, we expand both the quark propagator and the vertex (z\cdot \tensor{D})^n of the correlator up to dimension-six operators in the background field theory. The sum rules for the pion DA moments are obtained, in which all condensates up to dimension-six have been taken into consideration. Using the sum rules, we obtain \left|_{\rm 1\;GeV} = 0.338 \pm 0.032, \left|_{\rm 1\;GeV} = 0.211 \pm 0.030 and \left|_{\rm 1\;GeV} = 0.163 \pm 0.030. It is shown that the dimension-six condensates shall provide sizable contributions to the pion DA moments. We show that the first Gegenbauer moment of the pion leading-twist DA is a2π1  GeV=0.403±0.093a^\pi_2|_{\rm 1\;GeV} = 0.403 \pm 0.093, which is consistent with those obtained in the literature within errors but prefers a larger central value as indicated by lattice QCD predictions.Comment: 13 pages, 7 figure

    Neuroprotective effects of bis(7)-tacrine against glutamate-induced retinal ganglion cells damage

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    <p>Abstract</p> <p>Background</p> <p>Glutamate-mediated excitotoxicity, primarily through N-methyl-D-aspartate (NMDA) receptors, may be an important cause of retinal ganglion cells (RGCs) death in glaucoma and several other retinal diseases. Bis(7)-tacrine is a noncompetitive NMDA receptors antagonist that can prevent glutamate-induced hippocampal neurons damage. We tested the effects of bis(7)-tacrine against glutamate-induced rat RGCs damage in vitro and in vivo.</p> <p>Results</p> <p>In cultured neonatal rats RGCs, the MTT assay showed that glutamate induced a concentration- and time-dependent toxicity. Bis(7)-tacrine and memantine prevented glutamate-induced cell death in a concentration-dependent manner with IC50 values of 0.028 μM and 0.834 μM, respectively. The anti-apoptosis effects of bis(7)-tacrine were confirmed by annexin V-FITC/PI staining. In vivo, TUNEL analysis and retrograde labeling analysis found that pretreatment with bis(7)-tacrine(0.2 mg/kg) induced a significant neuroprotective effect against glutamate-induced RGCs damage.</p> <p>Conclusions</p> <p>Our results showed that bis(7)-tacrine had neuroprotective effects against glutamate-induced RGCs damage in vitro and in vivo, possibly through the drug's anti-NMDA receptor effects. These findings make bis(7)-tacrine potentially useful for treating a variety of ischemic or traumatic retinopathies inclusive of glaucoma.</p

    Optimal Location through Distributed Algorithm to Avoid Energy Hole in Mobile Sink WSNs

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    In multihop data collection sensor network, nodes near the sink need to relay on remote data and, thus, have much faster energy dissipation rate and suffer from premature death. This phenomenon causes energy hole near the sink, seriously damaging the network performance. In this paper, we first compute energy consumption of each node when sink is set at any point in the network through theoretical analysis; then we propose an online distributed algorithm, which can adjust sink position based on the actual energy consumption of each node adaptively to get the actual maximum lifetime. Theoretical analysis and experimental results show that the proposed algorithms significantly improve the lifetime of wireless sensor network. It lowers the network residual energy by more than 30% when it is dead. Moreover, the cost for moving the sink is relatively smaller

    Differentiation between tuberculosis and leukemia in abdominal and pelvic lymph nodes: evaluation with contrast-enhanced multidetector computed tomography

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    PURPOSE: To compare the characteristics of tubercular vs. leukemic involvement of abdominopelvic lymph nodes using multidetector computed tomography (CT). MATERIALS AND METHODS: We retrospectively reviewed multidetector computed tomography features including lymph node size, shape, enhancement patterns, and anatomical distribution, in 106 consecutive patients with newly diagnosed, untreated tuberculosis (55 patients; 52%) or leukemia (51 patients; 48%). In patients with leukemia, 32 (62.7%) had chronic lymphocytic leukemia, and 19 (37.3%) had acute leukemias; of these, 10 (19.6%) had acute myeloid leukemia, and 9 (17.6%) had acute lymphocytic leukemia. RESULTS: The lower para-aortic (30.9% for tuberculosis, 63.2% for acute leukemias and 87.5% for chronic lymphocytic leukemia) and inguinal (9.1% for tuberculosis, 57.9% for acute leukemias and 53.1% for chronic lymphocytic leukemia) lymph nodes were involved more frequently in the three types of leukemia than in tuberculosis (both with

    (Z)-2-(2-Chloro-3,3,3-trifluoro­prop-1-en­yl)-6-methoxy­phenyl acetate

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    The crystal structure of the title compound, C12H10ClF3O3, was determined in order to establish the configuration of the C=double bond. The compound was found to be the Z isomer. The crystal structure is dominated by Cl⋯O halogen bonds [Cl⋯O = 3.111 (3) Å], as well as C—H⋯O and C—H⋯F hydrogen-bonding inter­actions, that connect neighboring mol­ecules into a three-dimensional supra­molecular network

    1-[Bicyclo[4.2.0]octa-1(6),2,4-trien-3-yl]-3-[bicyclo[4.2.0]octa-1(6),2,4-trien-3-yl­methyl]imidazolium hexa­fluoro­phos­phate

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    In the title compound, C20H19N2 +·PF6 −, the two benzocyclo­butene units are essentially planar and they form dihedral angles of 38.0 (2) and 72.7 (2)°, with the central imidazolium ring. In the crystal structure, weak C—H⋯π and π-–π stacking inter­actions [centroid–centroid distance = 3.742 (2) Å] contribute to the stability of the crystal structure. The PF6 − ion is disordered over two positions with site occupancies of 0.869 (9) and 0.131 (9)

    catena-Poly[diammonium [diaqua­bis(pyridine-2,4-dicarboxyl­ato-κ2 N,O 2)cuprate(II)] [[diaqua­copper(II)]-μ-pyridine-2,4-dicarboxyl­ato-κ3 N,O 2:O 2′-[tetra­aqua­cadmium(II)]-μ-pyridine-2,4-dicarboxyl­ato-κ3 O 2:N,O 2′] hexa­hydrate]

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    The title mixed-metal complex, {(NH4)2[Cu(C7H3NO4)2(H2O)2][CdCu(C7H3NO4)2(H2O)6]·6H2O}n, contains one octa­hedrally coordinated CdII center and two octa­hedrally coordinated CuII centers, each lying on an inversion center. The two CuII atoms are each coordinated by two O atoms and two N atoms from two 2,4-pydc (2,4-H2pydc = pyridine-2,4-dicarboxylic acid) ligands in the equatorial plane and two water mol­ecules at the axial sites, thus producing two crystallographically independent [Cu(2,4-pydc)2(H2O)2]2− metalloligands. One metalloligand exists as a discrete anion and the other connects the Cd(H2O)4 units, forming a neutral chain. O—H⋯O and N—H⋯O hydrogen bonds connects the polymeric chains, complex anions, ammonium cations and uncoordinated water mol­ecules into a three-dimensional supra­molecular network

    Refined mapping of loss of heterozygosity in Chinese sporadic gastric carcinoma

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    The aim of this study is to explore precise deleted regions where the candidate tumor suppressor genes might be located in Chinese sporadic gastric carcinoma. By searching in Genothon, NCBI and GDB databases, 145 polymorphic microsatellite markers were chosen, at a mean density of approximately one marker every 2 - 4 cM, covering 15 chromosomes. These polymorphic microsatellite markers in gastric carcinoma and adjacent tissue were analyzed via PCR. PCR products were submitted to electrophoresis on an ABI 3730 DNA sequencer. Genemapper3.2 software was used for LOH (Loss of Heterozygosity) scanning and analysis. Comparison between LOH frequency and clinicopathological factors was performed by Fisher’s exact test. 26 refined regions were mapped as candidate regions for TSGs (Tumor suppression genes) in Chinese sporadic gastric cancer. Associations between LOH and clinical information indicated that 6 loci was associated with pTNM stage, 5 with Lauren's type, 4 with lymph nodes metastasis and another 2 with distant metastasis. Through refined deletion mapping, 26 candidate regions, where TSGs may be located, were found and 17 loci were proposed to be used as clinical markers in Chinese sporadic gastric cancer.Keywords: Gastric carcinoma, refined mapping, loss of heterozygosity (LOH), tumor suppressor genes (TSGs), tumor markersAfrican Journal of Biotechnology Vol. 9(35), pp. 5754-5761, 30 August, 201

    Maintenance of Sorafenib following combined therapy of three-dimensional conformal radiation therapy/intensity-modulated radiation therapy and transcatheter arterial chemoembolization in patients with locally advanced hepatocellular carcinoma: a phase I/II study

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    BACKGROUND: Three-dimensional conformal radiation therapy (3DCRT)/intensity-modulated radiation therapy (IMRT) combined with or without transcatheter arterial chemoembolization (TACE) for locally advanced hepatocellular carcinoma (HCC) has shown favorable outcomes in local control and survival of locally advanced HCC. However, intra-hepatic spreading and metastasis are still the predominant treatment failure patterns. Sorafenib is a multikinase inhibitor with effects against tumor proliferation and angiogenesis. Maintenance Sorafenib would probably prevent or delay the intrahepatic and extrahepatic spread of HCC after radiotherapy, which provides the rationale for the combination of these treatment modalities. METHODS AND DESIGN: Patients with solitary lesion (bigger than 5 cm in diameter) histologically or cytologically confirmed HCC receive TACE (1-3 cycles) plus 3DCRT/IMRT 4-6 weeks later. Maintenance Sorafenib will be administered only for the patients with non-progression disease 4 to 6 weeks after the completion of radiotherapy. The dose will be 400 mg, p.o., twice a day. Sorafenib will be continuously given for 12 months unless intolerable toxicities and/or tumor progression. If no more than 3 patients discontinue Sorafenib treatment who experience dose-limiting toxicity after necessary dose modification and delay and/or radiation-induced liver disease in the first 15 enrolled patients, the study will recruit second fifteen patients for further evaluating safety and efficacy of treatment. Hypothesis of the current study is that Sorafenib as a maintenance therapy after combined therapy of 3DCRT/IMRT and TACE is safe and superior to radiotherapy combined with TACE alone in terms of time to progression (TTP), progression-free survival (PFS) and overall survival (OS) in comparison to historical data. DISCUSSION: A recent meta-analysis showed TACE in combination with radiotherapy, improved the survival and the tumor response of patients, and was thus more therapeutically beneficial. In this study, local therapy for HCC is the combination of TACE and radiotherapy. Radiation exposure as a kind of stress might induce the compensatory activations of multiple intracellular signaling pathway mediators, such as PI3K, MAPK, JNK and NF-kB. Vascular endothelial growth factor (VEGF) was identified as one factor that was increased in a time- and dose-dependent manner after sublethal irradiation of HCC cells in vitro, translating to enhanced intratumor angiogenesis in vivo. Therefore, Sorafenib-mediated blockade of the Raf/MAPK and VEGFR pathways might enhance the efficacy of radiation, when Sorafenib is followed sequentially as a maintenance modality. (ClinicalTrials.gov number, NCT00999843.
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