52 research outputs found

    Transport Properties of Doped t-J Ladders

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    Conductivity and Hall coefficient for various types of t-J ladders are calculated as a function of temperature and frequency by numerical diagonalization. A crossover from an incoherent to a coherent charge dynamics is found at a temperature T_{coh}. There exists another crossover at T_{PG} below which a pseudogap opens in the optical spectra, induced by the opening of a spin gap. In the absence of the spin gap, T_{coh} and the coherent weight are suppressed especially with increasing dimensionality. On the contrary, T_{coh} is strongly enhanced by the pseudogap formation below T_{PG}, where the coherent Drude weight decreases with increasing dimensionality. The Hall coefficient shows a strong crossover at T_{PG} below which it has large amplitude for small doping concentration.Comment: 4 pages, RevTeX, 5 PostScript figure

    Charge-Spin Separation in 2D Fermi Systems: Singular Interactions as Modified Commutators, and Solution of 2D Hubbard Model in Bosonized Approximation

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    The general 2-dimensional fermion system with repulsive interactions (typified by the Hubbard Model) is bosonized, taking into account the finite on-shell forward scattering phase shift derived in earlier papers. By taking this phase shift into account in the bosonic commutation relations a consistent picture emerges showing the charge-spin separation and anomalous exponents of the Luttinger liquid.Comment: Latex file 14 pages. email: [email protected]

    Marginal Fermi liquid analysis of 300 K reflectance of Bi2Sr2CaCu2O8+x

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    We use 300 K reflectance data to investigate the normal-state electrodynamics of the high temperature superconductor Bi2_{2}Sr2_{2}CaCu2_{2}O8+Ξ΄_{8+\delta} over a wide range of doping levels. The data show that at this temperature the free carriers are coupled to a continuous spectrum of fluctuations. Assuming the Marginal Fermi Liquid (MFL) form as a first approximation for the fluctuation spectrum, the doping-dependent coupling constant Ξ»(p)\lambda (p) can be estimated directly from the slope of the reflectance spectrum. We find that Ξ»(p)\lambda (p) decreases smoothly with the hole doping level, from underdoped samples with p=0.103 p=0.103 (Tc=67T_c = 67 K) where Ξ»(p)=0.93\lambda (p)= 0.93 to overdoped samples with p=0.226p=0.226, (Tc=60T_c= 60 K) where Ξ»(p)=0.53\lambda(p)= 0.53. An analysis of the intercept and curvature of the reflectance spectrum shows deviations from the MFL spectrum symmetrically placed at the optimal doping point p=0.16p=0.16. The Kubo formula for the conductivity gives a better fit to the experiments with the MFL spectrum up to 2000 cmβˆ’1^{-1} and with an additional Drude component or an additional Lorentz component up to 7000 cmβˆ’1^{-1}. By comparing three different model fits we conclude that the MFL channel is necessary for a good fit to the reflectance data. Finally, we note that the monotonic variation of the reflectance slope with doping provides us with an independent measure of the doping level for the Bi-2212 system.Comment: 11 pages, 11 figure

    Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition

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    <p>Abstract</p> <p>Background</p> <p>Prostate cancer is a leading cause of cancer-related death in men worldwide. Survivin is a member of the inhibitor of apoptosis (IAP) protein family that is expressed in the majority of human tumors including prostate cancer, but is barely detectable in terminally differentiated normal cells. Downregulation of survivin could sensitize prostate cancer cells to chemotherapeutic agents <it>in vitro </it>and <it>in vivo</it>. Selenium is an essential trace element. Several studies have shown that selenium compounds inhibit the growth of prostate cancer cells. The objective of this study is to investigate whether survivin gene silencing in conjunction with selenium treatment could enhance the therapeutic efficacy for prostate cancer and to elucidate the underlying mechanisms.</p> <p>Methods</p> <p>Expression of survivin was analyzed in a collection of normal and malignant prostatic tissues by immunohistochemical staining. <it>In vitro </it>studies were conducted in PC-3M, C4-2B, and 22Rv1 prostate cancer cells. The effect of selenium on survivin expression was analyzed by Western blotting and semi-quantitative RT-PCR. Survivin gene knockdown was carried out by transfecting cells with a short hairpin RNA (shRNA) designed against survivin. Cell proliferation was quantitated by the 3-(4,5-Dimethylthiazol-2-yl)- 2,5-Diphenyltetrazolium Bromide (MTT) assay and apoptosis by propidium iodide staining followed by flow cytometry analysis. Finally, <it>in vivo </it>tumor growth assay was performed by establishing PC-3M xenograft in nude mice and monitoring tumor growth following transfection and treatment.</p> <p>Results</p> <p>We found that survivin was undetectable in normal prostatic tissues but was highly expressed in prostate cancers. Survivin knockdown or selenium treatment inhibited the growth of prostate cancer cells, but the selenium effect was modest. In contrast to what have been observed in other cell lines, selenium treatment had little or no effect on survivin expression in several androgen-independent prostate cancer cell lines. Survivin knockdown sensitized these cells to selenium growth inhibition and apoptosis induction. In nude mice bearing PC-3M xenografts, survivin knockdown synergizes with selenium in inhibiting tumor growth.</p> <p>Conclusions</p> <p>Selenium could inhibit the growth of hormone-refractory prostate cancer cells both <it>in vitro </it>and <it>in vivo</it>, but the effects were modest. The growth inhibition was not mediated by downregulating survivin expression. Survivin silencing greatly enhanced the growth inhibitory effects of selenium.</p

    Non-Fermi liquid regime of a doped Mott insulator

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    We study the doping of a Mott insulator in the presence of quenched frustrating disorder in the magnetic exchange. A low doping regime Ξ΄<J/t\delta<J/t is found, in which the quasiparticle coherent scale is low : Ο΅Fβˆ—=J(Ξ΄/Ξ΄βˆ—)2\epsilon_F^* = J (\delta/\delta^*)^2 with Ξ΄βˆ—=J/t\delta^*=J/t (the ratio of typical exchange to hopping). In the ``quantum critical regime'' Ο΅Fβˆ—<T<J\epsilon_F^*<T<J, several physical quantities display Marginal Fermi Liquid behaviour : NMR relaxation time 1/T1∼const.1/T_1\sim const., resistivity ρdc(T)∝T\rho_{dc}(T) \propto T, optical lifetime \tau_{opt}^{-1}\propto \omega/\ln(\omega/\epstar) and response functions obey Ο‰/T\omega/T scaling, e.g. Jβˆ‘qΟ‡β€²β€²(q,Ο‰)∝tanh⁑(Ο‰/2T)J\sum_q \chi''(q,\omega) \propto \tanh (\omega/2T). In contrast, single-electron properties display stronger deviations from Fermi liquid theory in this regime with a Ο‰\sqrt{\omega} dependence of the inverse single-particle lifetime and a 1/Ο‰1/\sqrt{\omega} decay of the photoemission intensity. On the basis of this model and of various experimental evidence, it is argued that the proximity of a quantum critical point separating a glassy Mott-Anderson insulator from a metallic ground-state is an important ingredient in the physics of the normal state of cuprate superconductors (particularly the Zn-doped materials). In this picture the corresponding quantum critical regime is a ``slushy'' state of spins and holes with slow spin and charge dynamics responsible for the anomalous properties of the normal state.Comment: 40 pages, RevTeX, including 13 figures in EPS. v2 : minor changes, some references adde

    Low-Frequency Crossover of the Fractional Power-Law Conductivity in SrRuO

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    We combine the results of terahertz time-domain spectroscopy with far-infrared transmission and reflectivity to obtain the conductivity of SrRuO{sub 3} over an unprecedented continuous range in frequency, allowing us to characterize the approach to zero frequency as a function of temperature. We show that the conductivity follows a simple phenomenological form, with an analytic structure fundamentally different from that predicted by the standard theory of metals

    A phase II study of biweekly dose-intensified oral capecitabine plus irinotecan (bXELIRI) for patients with advanced or metastatic gastric cancer

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    Capecitabine, a prodrug of 5-FU, has been reported to generate maximal tumour activity at tumour sites and/or to improve drug tolerability as compared with 5-FU infusion, and it has also been demonstrated to act synergistically with irinotecan against some solid cancers. A previous study concluded that dose-intensified biweekly capecitabine seems to be more effective at increasing both response rate and progression-free survival time than conventional dose and schedule of capecitabine in colon cancer. We conducted this study to ascertain the efficacy and toxicity of dose-intensified biweekly capecitabine and irinotecan combination chemotherapy in chemotherapy-naΓ―ve advanced or metastatic gastric cancer patients. Patients were treated with irinotecan 130 mg mβˆ’2 intravenously for 90 min on days 1 and 15. Capecitabine at 3500 mg mβˆ’2 dayβˆ’1, divided into two sessions per day, was administered for seven consecutive days from days 1 and 15, and followed by a 7-day drug-free period, respectively. Fifty-five eligible patients were enrolled in this study from November 2003 to April 2006. There were 22 women and 33 men: median patient age was 54 years (range: 27–81). A total of 200 treatment cycles were administered at a median number of four per patient (range: 1–9). Intent-to-treatment analysis showed that one patient achieved complete response (1.8%), 23 partial response (41.8%), 15 stable disease (27.3%), 10 progressive disease (18.2%) and 6 were non-evaluable (10.9%). The overall response rate was 43.6% (95% confidence interval: 30.2–56.9). The common grade 3–4 toxicities were neutropenia in 12 (21.8%), nausea/vomiting in 3 (5.4%) and diarrhea in 4 (7.2%) patients. Median time to progression was 5 months (range: 0.5–11 months), median survival duration was 11 months (range: 0.5–45 months) and median response duration was 6 months (range: 0.5–9 months). Biweekly dose-intensified capecitabine and irinotecan combination chemotherapy was active for the treatment of advanced or metastatic gastric cancers with a tolerable safety profile

    Selenium and Lung Cancer: A Systematic Review and Meta Analysis

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    Selenium is a natural health product widely used in the treatment and prevention of lung cancers, but large chemoprevention trials have yielded conflicting results. We conducted a systematic review of selenium for lung cancers, and assessed potential interactions with conventional therapies.Two independent reviewers searched six databases from inception to March 2009 for evidence pertaining to the safety and efficacy of selenium for lung cancers. Pubmed and EMBASE were searched to October 2009 for evidence on interactions with chemo- or radiation-therapy. In the efficacy analysis there were nine reports of five RCTs and two biomarker-based studies, 29 reports of 26 observational studies, and 41 preclinical studies. Fifteen human studies, one case report, and 36 preclinical studies were included in the interactions analysis. Based on available evidence, there appears to be a different chemopreventive effect dependent on baseline selenium status, such that selenium supplementation may reduce risk of lung cancers in populations with lower baseline selenium status (serum<106 ng/mL), but increase risk of lung cancers in those with higher selenium (β‰₯ 121.6 ng/mL). Pooling data from two trials yielded no impact to odds of lung cancer, OR 0.93 (95% confidence interval 0.61-1.43); other cancers that were the primary endpoints of these trials, OR 1.51 (95%CI 0.70-3.24); and all-cause-death, OR 0.93 (95%CI 0.79-1.10). In the treatment of lung cancers, selenium may reduce cisplatin-induced nephrotoxicity and side effects associated with radiation therapy.Selenium may be effective for lung cancer prevention among individuals with lower selenium status, but at present should not be used as a general strategy for lung cancer prevention. Although promising, more evidence on the ability of selenium to reduce cisplatin and radiation therapy toxicity is required to ensure that therapeutic efficacy is maintained before any broad clinical recommendations can be made in this context
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