30 resultados para Bollinger, Lee C., 1946-


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We provide the quantum-mechanical description of the excitation of surface plasmon polaritons on metal surfaces by single photons. An attenuated-reflection setup is described for the quantum excitation process in which we find remarkably efficient photon-to-surface plasmon wave-packet transfer. Using a fully quantized treatment of the fields, we introduce the Hamiltonian for their interaction and study the quantum statistics during transfer with and without losses in the metal.

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We analyse the process of rapid positron annihilation in large polyatomic molecules due to positron capture into vibrational Feshbach resonances. Resonant annihilation occurs in molecules which can bind positrons, and we analyse positron binding to alkanes using zero-range potentials. Related questions of spectra of annihilation gamma quanta and molecular fragmentation following annihilation, are discussed briefly.

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Positrons can attach to molecules via vibrational Feshbach resonances, leading to very large annihilation rates. The predictions of a recent theory for this process are validated for deuterated methyl halides where all modes are dipole coupled to the incident positron. Data and analysis are presented for methanol and ethylene, demonstrating the importance of combination and overtone resonances and the ability of the theory to account for these features. The mechanism for these resonances and criteria for their occurrence as well as outstanding questions are discussed.

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In this paper we use a zero-range potential (ZRP) method to model positron interaction with molecules. This allows us to investigate the e?ect of molecular vibrations on positron–molecule annihilation using the van der Waals dimer Kr2 as an example. We also use the ZRP to explore positron binding to polyatomics and examine the dependence of the binding energy on the size of the molecule for alkanes. We ?nd that a second bound state appears for a molecule with ten carbons, similar to recent experimental evidence for such a state emerging in alkanes with twelve carbons.

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Gastrointestinal endocrine cell tumors are a heterogeneous population of lesions believed to arise from neuroendocrine cells of the gastrointestinal mucosa. The current classification of these tumors is based on tumor size, microscopic features and clinical evidence of metastasis. Although diagnostic categories generally correlate with prognosis, molecular prognostic markers will be clinically useful adjuncts. Cofilin has been implicated in tumor invasion, and its immunolocalisation was studied in gastrointestinal endocrine cell tumors. The immunolocalisation of cofilin was studied by immunohistochemistry in 34 formalin-fixed, paraffin wax-embedded gastrointestinal endocrine cell tumors using a tissue microarray platform. A significant correlation was found between high cofilin immunolabelling and the depth of invasion (p

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In intestinal epithelial cells, inactivation of APC, a key regulator of the Wnt pathway, activates beta-catenin to initiate tumorigenesis. However, other alterations may be involved in intestinal tumorigenesis. Here we found that RUNX3, a gastric tumor suppressor, forms a ternary complex with beta-catenin/7CF4 and attenuates Wnt signaling activity. A significant fraction of human sporadic colorectal adenomas and Runx3(+/-) mouse intestinal adenomas showed inactivation of RUNX3 without apparent beta-catenin accumulation, indicating that RUNX3 inactivation independently induces intestinal adenomas. In human colon cancers, RUNX3 is frequently inactivated with concomitant beta-catenin accumulation, suggesting that adenomas induced by inactivation of RUNX3 may progress to malignancy. Taken together, these data demonstrate that RUNX3 functions as a tumor suppressor by attenuating Wnt signaling.

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Background/Aims: Hepatocellular carcinoma is a leading cause of global cancer mortality, with standard chemotherapy being minimally effective in prolonging survival. We investigated if combined targeting of vascular endothelial growth factor protein and expression might affect hepatocellular carcinoma growth and angiogenesis.

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This study aimed to test these hypotheses: cystathionine gamma-lyase (CSE) is expressed in a human artery, it generates hydrogen sulfide (H2S), and H2S relaxes a human artery. H2S is produced endogenously in rat arteries from cysteine by CSE. Endogenously produced H2S dilates rat resistance arteries. Although CSE is expressed in rat arteries, its presence in human blood vessels has not been described. In this study, we showed that both CSE mRNA, determined by reverse transcription-polymerase chain reaction, and CSE protein, determined by Western blotting, apparently occur in the human internal mammary artery (internal thoracic artery). Artery homogenates converted cysteine to H2S, and the H2S production was inhibited by DL-propargylglycine, an inhibitor of CSE. We also showed that H2S relaxes phenylephrine-precontracted human internal mammary artery at higher concentrations but produces contraction at low concentrations. The latter contractions are stronger in acetylcholine-prerelaxed arteries, suggesting inhibition of nitric oxide action. The relaxation is partially blocked by glibenclamide, an inhibitor of K-ATP channels. The present results indicate that CSE protein is expressed in human arteries, that human arteries synthesize H2S, and that higher concentrations of H2S relax human arteries, in part by opening K-ATP channels. Low concentrations of H2S contract the human internal mammary artery, possibly by reacting with nitric oxide to form an inactive nitrosothiol. The possibility that CSE, and the H2S it generates, together play a physiological role in regulating the diameter of arteries in humans, as has been demonstrated in rats, should be considered.

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A tissue microarray analysis of 22 proteins in gastrointestinal stromal tumours ( GIST), followed by an unsupervised, hierarchical monothetic cluster statistical analysis of the results, allowed us to detect a vascular endothelial growth factor ( VEGF) protein overexpression signature discriminator of prognosis in GIST, and discover novel VEGF-A DNA variants that may have functional significance.

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Histone deacetylases ( HDACs) 1 and 2 share a high degree of homology and coexist within the same protein complexes. Despite their close association, each possesses unique functions. We show that the upregulation of HDAC2 in colorectal cancer occurred early at the polyp stage, was more robust and occurred more frequently than HDAC1. Similarly, while the expression of HDACs1 and 2 were increased in cervical dysplasia and invasive carcinoma, HDAC2 expression showed a clear demarcation of high-intensity staining at the transition region of dysplasia compared to HDAC1. Upon HDAC2 knockdown, cells displayed an increased number of cellular extensions reminiscent of cell differentiation. There was also an increase in apoptosis, associated with increased p21(Cip1/WAF1) expression that was independent of p53. These results suggest that HDACs, especially HDAC2, are important enzymes involved in the early events of carcinogenesis, making them candidate markers for tumor progression and targets for cancer therapy.

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.The design of a 6T SRAM cell with 20 nm junctionless (JL) MOSFETs is reported. It is shown that a 6T SRAM cell designed with JL MOSFETs achieves a high static noise margin (SNM) of 185 mV, retention noise or hold margin (RNM) of 381 mV and writability current (IWR) of 33 mA along with a low leakage current of 2 pA at a supply voltage (VDD) of 0.9 V for cell and pullup ratios of 1. Results offer a new opportunity to design future SRAM cells with nanoscale JL MOSFETs.