565 research outputs found
Regulation of Mouse Small Heat Shock Protein αb-Crystallin Gene by Aryl Hydrocarbon Receptor
The stress-inducible small heat shock protein (shsp)/αB-crystallin gene is expressed highly in the lens and moderately in other tissues. Here we provide evidence that it is a target gene of the aryl hydrocarbon receptor (AhR) transcription factor. A sequence (â329/â323, CATGCGA) similar to the consensus xenobiotic responsive element (XRE), called here XRE-like, is present in the αBE2 region of αB-crystallin enhancer and can bind AhR in vitro and in vivo. αB-crystallin protein levels were reduced in retina, lens, cornea, heart, skeletal muscle and cultured muscle fibroblasts of AhRâ/â mice; αB-crystallin mRNA levels were reduced in the eye, heart and skeletal muscle of AhRâ/â mice. Increased AhR stimulated αB-crystallin expression in transfection experiments conducted in conjunction with the aryl hydrocarbon receptor nuclear translocator (ARNT) and decreased AhR reduced αB-crystallin expression. AhR effect on aB-crystallin promoter activity was cell-dependent in transfection experiments. AhR up-regulated αB-crystallin promoter activity in transfected HeLa, NIH3T3 and COS-7 cells in the absence of exogenously added ligand (TCDD), but had no effect on the αB-crystallin promoter in C2C12, CV-1 or Hepa-1 cells with or without TCDD. TCDD enhanced AhR-stimulated αB-crystallin promoter activity in transfected αTN4 cells. AhR could bind to an XRE-like site in the αB-crystallin enhancer in vitro and in vivo. Finally, site-specific mutagenesis experiments showed that the XRE-like motif was necessary for both basal and maximal AhR-induction of αB-crystallin promoter activity. Our data strongly suggest that AhR is a regulator of αB-crystallin gene expression and provide new avenues of research for the mechanism of tissue-specific αB-crystallin gene regulation under normal and physiologically stressed conditions
Nanoparticles in cigarette smoke; real-time undiluted measurements by a scanning mobility particle sizer
Cigarette smoke is a complex mixture of smoke constituents, often characterised by size-resolved particle distributions. Since descriptions of ultrafine particles <50 nm are absent, our aim was to explore the existence of these nanoparticles in fresh and undiluted cigarette smoke. We measured undiluted smoke particles real-time by a scanning mobility particle sizer with Faraday cup electrometer, integrated in our custom-made smoking machine. Cigarettes were smoked by 2 s puffs, 30 s puff intervals and 50 ml puff volume. We tested six different cigarettes (1â10 mg tar per cigarette) at ten particle size-ranges between 6 and 50 nm, and repeated measurements five times. The formation of nanoparticles in fresh cigarette smoke was observed over the entire range between 6 and 50 nm, and reproduced in all cigarettes. The highest mean yield was 8.8âĂâ109 (SDâ=â1.1âĂâ109) particles per cigarette at the largest particle size range by high-tar cigarettes. Nanoparticle counts appear to increase with particle size, claimed tar values and blocking of filter ventilation holes, and inversely with butt length. Fresh undiluted cigarette smoke contains large amounts of potentially toxic nanoparticles <50 nm. We recommend to further study nanoparticles in the characterisation of cigarette smoke
Measurement of the branching fraction and CP content for the decay B(0) -> D(*+)D(*-)
This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APS.We report a measurement of the branching fraction of the decay B0âD*+D*- and of the CP-odd component of its final state using the BABAR detector. With data corresponding to an integrated luminosity of 20.4ââfb-1 collected at the ΄(4S) resonance during 1999â2000, we have reconstructed 38 candidate signal events in the mode B0âD*+D*- with an estimated background of 6.2±0.5 events. From these events, we determine the branching fraction to be B(B0âD*+D*-)=[8.3±1.6(stat)±1.2(syst)]Ă10-4. The measured CP-odd fraction of the final state is 0.22±0.18(stat)±0.03(syst).This work is supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the A.P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation
Measurement of D-s(+) and D-s(*+) production in B meson decays and from continuum e(+)e(-) annihilation at âs=10.6 GeV
This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APSNew measurements of Ds+ and Ds*+ meson production rates from B decays and from qqÌ
continuum events near the ΄(4S) resonance are presented. Using 20.8 fb-1 of data on the ΄(4S) resonance and 2.6 fb-1 off-resonance, we find the inclusive branching fractions B(BâDs+X)=(10.93±0.19±0.58±2.73)% and B(BâDs*+X)=(7.9±0.8±0.7±2.0)%, where the first error is statistical, the second is systematic, and the third is due to the Ds+âÏÏ+ branching fraction uncertainty. The production cross sections Ï(e+e-âDs+X)ĂB(Ds+âÏÏ+)=7.55±0.20±0.34pb and Ï(e+e-âDs*±X)ĂB(Ds+âÏÏ+)=5.8±0.7±0.5pb are measured at center-of-mass energies about 40 MeV below the ΄(4S) mass. The branching fractions ÎŁB(BâDs(*)+D(*))=(5.07±0.14±0.30±1.27)% and ÎŁB(BâDs*+D(*))=(4.1±0.2±0.4±1.0)% are determined from the Ds(*)+ momentum spectra. The mass difference m(Ds+)-m(D+)=98.4±0.1±0.3MeV/c2 is also measured.This work was supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the Swiss NSF, A. P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation
Search for rare quark-annihilation decays, B --> Ds(*) Phi
We report on searches for B- --> Ds- Phi and B- --> Ds*- Phi. In the context
of the Standard Model, these decays are expected to be highly suppressed since
they proceed through annihilation of the b and u-bar quarks in the B- meson.
Our results are based on 234 million Upsilon(4S) --> B Bbar decays collected
with the BABAR detector at SLAC. We find no evidence for these decays, and we
set Bayesian 90% confidence level upper limits on the branching fractions BF(B-
--> Ds- Phi) Ds*- Phi)<1.2x10^(-5). These results
are consistent with Standard Model expectations.Comment: 8 pages, 3 postscript figues, submitted to Phys. Rev. D (Rapid
Communications
Soil chemical factors and grassland species density in Emas National Park (central Brazil)
Semaphorin 3A Suppresses Tumor Growth and Metastasis in Mice Melanoma Model
<div><h3>Background</h3><p>Recent understanding on cancer therapy indicated that targeting metastatic signature or angiogenic switch could be a promising and rational approach to combat cancer. Advancement in cancer research has demonstrated the potential role of various tumor suppressor proteins in inhibition of cancer progression. Current studies have shown that axonal sprouting inhibitor, semaphorin 3A (Sema 3A) acts as a potent suppressor of tumor angiogenesis in various cancer models. However, the function of Sema 3A in regulation of melanoma progression is not well studied, and yet to be the subject of intense investigation.</p> <h3>Methodology/Principal Findings</h3><p>In this study, using multiple <em>in vitro</em> and <em>in vivo</em> approaches we have demonstrated that Sema 3A acts as a potent tumor suppressor <em>in vitro</em> and <em>in vivo</em> mice (C57BL/6) models. Mouse melanoma (B16F10) cells overexpressed with Sema 3A resulted in significant inhibition of cell motility, invasiveness and proliferation as well as suppression of <em>in vivo</em> tumor growth, angiogenesis and metastasis in mice models. Moreover, we have observed that Sema 3A overexpressed melanoma clone showed increased sensitivity towards curcumin and Dacarbazine, anti-cancer agents.</p> <h3>Conclusions</h3><p>Our results demonstrate, at least in part, the functional approach underlying Sema 3A mediated inhibition of tumorigenesis and angiogenesis and a clear understanding of such a process may facilitate the development of novel therapeutic strategy for the treatment of cancer.</p> </div
Measurement of the branching fraction for
We present a measurement of the branching fraction for the decay B- --> D0 K*- using a sample of approximately 86 million BBbar pairs collected by the BaBar detector from e+e- collisions near the Y(4S) resonance. The D0 is detected through its decays to K- pi+, K- pi+ pi0 and K- pi+ pi- pi+, and the K*- through its decay to K0S pi-. We measure the branching fraction to be B.F.(B- --> D0 K*-)= (6.3 +/- 0.7(stat.) +/- 0.5(syst.)) x 10^{-4}
Observation of a significant excess of events in B meson decays
We present an observation of the decay based on a sample of 124 million pairs recorded by the BABAR detector at the PEP-II asymmetric-energy Factory at SLAC. We observe events, where the first error is statistical and the second is systematic, corresponding to a significance of 4.2 standard deviations including systematic uncertainties. We measure the branching fraction \BR(B^{0} \to \pi^{0} \pi^{0}) = (2.1 \pm 0.6 \pm 0.3) \times 10^{-6}, averaged over and decays
Observation of the Decay B=> J/psi eta K and Search for X(3872)=> J/psi eta
We report the observation of the meson decay
and evidence for the decay , using {90} million
events collected at the \ensuremath{\Upsilon{(4S)}}\xspace resonance
with the detector at the PEP-II asymmetric-energy storage
ring. We obtain branching fractions of )= and
)=. We search for the new narrow mass state, the
X(3872), recently reported by the Belle Collaboration, in the decay B^\pm\to
X(3872)K^\pm, X(3872)\to \jpsi \eta and determine an upper limit of
(B^\pm \to X(3872) K^\pm \to \jpsi \eta K^\pm)
at 90% C.L.Comment: 7 pages and two figures, submitted to Phys. Rev. Lett
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