7,309 research outputs found

    The Possible Interpretations of Y(4260)

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    The recently observed Y(4260) lies far above the decay threshold with a width less than 100 MeV. We argue that it's very difficult to accommodate Y(4260) as a conventional ccˉc\bar c radial excitation or a D-wave state. It can't be a hadronic molecule. Its production mechanism and special decay pattern do not favor the glueball interpretation. If Y(4260) is a scalar tetraquark, it must be produced by the I=0 component of the virtual photon. Then the I=1,Iz=0I=1, I_z=0 component of the virtual photon should have produced its isovector partner Y′(4260)Y^\prime (4260), which may be searched for in the decay channel π+π−π0J/ψ\pi^+\pi^-\pi^0 J/\psi using exactly the same database from the initial state radiation process. The observation/non-observation of Y′(4260)Y^\prime (4260) can easily confirm/reject the tetraquark hypothesis. However, a tetraquark far above threshold can fall apart into DDˉ,D∗DˉD\bar D, D^\ast\bar D very easily. Its not-so-large width and the non-observation of DDˉD\bar D mode tend to disfavor the tetraquark hypothesis. Hence the only feasible interpretation is a hybrid charmonium if Y(4260) is {\sl NOT} an experimental artifact. At present, none of the experimental information from BABAR measurement is in conflict with the hybrid charmonium picture.Comment: some references adde

    Structural design of a silicon six-wafer micro-combustor under the effect of heat transfer boundary condition at the outer walls

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    The aim of this investigation was to establish a methodology for designing highly stressed micro fabricated structures by studying the structural design issues associated with a silicon six–wafer micro combustor under the effect of heat transfer boundary condition at the outer walls. Some experimental and numerical simulation results have indicated that the flame can not be sustained in the micro combustor if the poor heat transfer coefficients at the outer wall are present. This could cause the combustor wall temperature higher than the auto ignition temperature of reactants and results in the upstream burning. Since silicon has relatively poor high temperature strength and creep resistance when the temperature is above the brittle to ductile transition temperature (BDTT), e.g. 900K, the combustion in the recirculation jacket could possibly damage the micro combustor due to the high wall temperature

    Numerical investigation of the structure of a silicon six-wafer micro-combustor under the effect of hydrogen/air ratio

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    Research reports indicate that sufficiently high equivalence ratio of the hydrogen/air mixture leads to the upstream burning in the recirculation jacket, possibly damaging the micro- combustor due to the high wall temperature. This work investigates the influences of the equivalence ratio of the mixture on the structure of a micro-combustor device. Numerical simulation approaches focused on the structural design of the micro-combustor with the flame burning in the recirculation jacket. Combustion characteristics of the combustor were first analysed based on 2D computational Fluid Dynamics (CFD), and then thermo-mechanical analysis on the combustor was carried out by means of 3D Finite Element Analysis (FEA) method. The results showed that the most dangerous locations where the critical failure could possibly occur lay at the burning areas in the recirculation jacket due to the poor bonding, the high temperature and the residual stress. The results of this study can be used for the design and improvement of the micro-combustors

    Global transcription profiling reveals differential responses to chronic nitrogen stress and putative nitrogen regulatory components in Arabidopsis

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    <p>Abstract</p> <p>Background</p> <p>A large quantity of nitrogen (N) fertilizer is used for crop production to achieve high yields at a significant economic and environmental cost. Efforts have been directed to understanding the molecular basis of plant responses to N and identifying N-responsive genes in order to manipulate their expression, thus enabling plants to use N more efficiently. No studies have yet delineated these responses at the transcriptional level when plants are grown under chronic N stress and the understanding of regulatory elements involved in N response is very limited.</p> <p>Results</p> <p>To further our understanding of the response of plants to varying N levels, a growth system was developed where N was the growth-limiting factor. An Arabidopsis whole genome microarray was used to evaluate global gene expression under different N conditions. Differentially expressed genes under mild or severe chronic N stress were identified. Mild N stress triggered only a small set of genes significantly different at the transcriptional level, which are largely involved in various stress responses. Plant responses were much more pronounced under severe N stress, involving a large number of genes in many different biological processes. Differentially expressed genes were also identified in response to short- and long-term N availability increases. Putative N regulatory elements were determined along with several previously known motifs involved in the responses to N and carbon availability as well as plant stress.</p> <p>Conclusion</p> <p>Differentially expressed genes identified provide additional insights into the coordination of the complex N responses of plants and the components of the N response mechanism. Putative N regulatory elements were identified to reveal possible new components of the regulatory network for plant N responses. A better understanding of the complex regulatory network for plant N responses will help lead to strategies to improve N use efficiency.</p

    NF-kappa B mediated Up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia

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    BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most frequently occurring malignant neoplasm in children. Despite advances in treatment and outcomes for ALL patients, the pathogenesis of the disease remains unclear. Microarray analysis of samples from 100 Chinese children with ALL revealed the up-regulation of CTCF (CCCTC binding factor). CTCF is a highly conserved 11-zinc finger protein that is involved in many human cancers; however, the biological function of CTCF in pediatric ALL is unknown. METHODS: The expression patterns of CTCF were evaluated in matched newly diagnosed (ND), complete remission (CR), and relapsed (RE) bone marrow samples from 28 patients. The potential oncogenic mechanism of CTCF and related pathways in leukemogenesis were investigated in leukemia cell lines. RESULTS: We identified significant up-regulation of CTCF in the ND samples. Importantly, the expression of CTCF returned to normal levels after CR but rebounded in the RE samples. In the pre-B ALL cell line Nalm-6, siRNA-mediated silencing of CTCF expression promoted cell apoptosis and reduced cell proliferation; accordingly, over-expression of a cDNA encoding full-length CTCF protected cells from apoptosis and enhanced cell proliferation. Furthermore, inhibition or activation of the nuclear factor-kappa B (NF-κB) pathway resulted in marked variations in the levels of CTCF mRNA and protein in leukemic cells, indicating that CTCF may be involved downstream of the NF-κB pathway. Moreover, inhibition of the NF-κB pathway increased cell apoptosis, which was partially rescued by ectopic over-expression of CTCF, suggesting that CTCF may play a significant role in the anti-apoptotic pathway mediated by NF-κB. CONCLUSIONS: Our results indicate that CTCF serves as both an anti-apoptotic factor and a proliferative factor in leukemic cells. It potentially contributes to leukemogenesis through the NF-κB pathway in pediatric ALL patients

    MiRNA-145 increases therapeutic sensibility to gemcitabine treatment of pancreatic adenocarcinoma cells.

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    Pancreatic adenocarcinoma is one of the most leading causes of cancer-related deaths worldwide. Although recent advances provide various treatment options, pancreatic adenocarcinoma has poor prognosis due to its late diagnosis and ineffective therapeutic multimodality. Gemcitabine is the effective first-line drug in pancreatic adenocarcinoma treatment. However, gemcitabine chemoresistance of pancreatic adenocarcinoma cells has been a major obstacle for limiting its treatment effect. Our study found that p70S6K1 plays an important role in gemcitabine chemoresistence. MiR-145 is a tumor suppressor which directly targets p70S6K1 for inhibiting its expression in pancreatic adenocarcinoma, providing new therapeutic scheme. Our findings revealed a new mechanism underlying gemcitabine chemoresistance in pancreatic adenocarcinoma cells
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