827 research outputs found
J/Psi and Psi' total cross sections and formation times from data for charmonium suppression in collisions
The recent data for E866 experiment on the x_F dependence for charmonium
suppression in pA collisions at 800 GeV are analyzed using a time- and
energy-dependent preformed charmonium absorption cross section
\sigma_{abs}^\psi(\tau,\sqrt{s}). For \sqrt{s}=10 GeV the initially (\tau=0)
produced premeson has an absorption cross section of \sigma_{pr}~3mb. At the
same energy but for \tau -> \infty one deduces for the total cross sections
\sigma_{tot}^{J/Psi N}=(2.8\pm 0.3)mb, \sigma_{tot}^{J/Psi N}= (10.5\pm 3.6)mb.
The date are compatible with a formation time \tau_{1/2}=0.6 fm/c.Comment: 13 pages of Latex including 2 figures; typos in the abstract are
correcte
Neutrino masses from new generations
We reconsider the possibility that Majorana masses for the three known
neutrinos are generated radiatively by the presence of a fourth generation and
one right-handed neutrino with Yukawa couplings and a Majorana mass term. We
find that the observed light neutrino mass hierarchy is not compatible with low
energy universality bounds in this minimal scenario, but all present data can
be accommodated with five generations and two right-handed neutrinos. Within
this framework, we explore the parameter space regions which are currently
allowed and could lead to observable effects in neutrinoless double beta decay,
conversion in nuclei and experiments. We
also discuss the detection prospects at LHC.Comment: 28 pages, 4 figures. Version to be published. Some typos corrected.
Improved figures 3 and
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
Effective Rheology of Bubbles Moving in a Capillary Tube
We calculate the average volumetric flux versus pressure drop of bubbles
moving in a single capillary tube with varying diameter, finding a square-root
relation from mapping the flow equations onto that of a driven overdamped
pendulum. The calculation is based on a derivation of the equation of motion of
a bubble train from considering the capillary forces and the entropy production
associated with the viscous flow. We also calculate the configurational
probability of the positions of the bubbles.Comment: 4 pages, 1 figur
Opposing effects of cancer-type-specific SPOP mutants on BET protein degradation and sensitivity to BET inhibitors.
It is generally assumed that recurrent mutations within a given cancer driver gene elicit similar drug responses. Cancer genome studies have identified recurrent but divergent missense mutations affecting the substrate-recognition domain of the ubiquitin ligase adaptor SPOP in endometrial and prostate cancers. The therapeutic implications of these mutations remain incompletely understood. Here we analyzed changes in the ubiquitin landscape induced by endometrial cancer-associated SPOP mutations and identified BRD2, BRD3 and BRD4 proteins (BETs) as SPOP-CUL3 substrates that are preferentially degraded by endometrial cancer-associated SPOP mutants. The resulting reduction of BET protein levels sensitized cancer cells to BET inhibitors. Conversely, prostate cancer-specific SPOP mutations resulted in impaired degradation of BETs, promoting their resistance to pharmacologic inhibition. These results uncover an oncogenomics paradox, whereby mutations mapping to the same domain evoke opposing drug susceptibilities. Specifically, we provide a molecular rationale for the use of BET inhibitors to treat patients with endometrial but not prostate cancer who harbor SPOP mutations
The Role of Research in Viral Disease Eradication and Elimination Programs: Lessons for Malaria Eradication
Using their experiences from, and analysis of, global campaigns to eradicate smallpox, poliomyelitis, and measles, Myron Levine and colleagues derive lessons for malaria eradication
Control of the induction of type I interferon by Peste des petits ruminants virus.
Peste des petits ruminants virus (PPRV) is a morbillivirus that produces clinical disease in goats and sheep. We have studied the induction of interferon-β (IFN-β) following infection of cultured cells with wild-type and vaccine strains of PPRV, and the effects of such infection with PPRV on the induction of IFN-β through both MDA-5 and RIG-I mediated pathways. Using both reporter assays and direct measurement of IFN-β mRNA, we have found that PPRV infection induces IFN-β only weakly and transiently, and the virus can actively block the induction of IFN-β. We have also generated mutant PPRV that lack expression of either of the viral accessory proteins (V&C) to characterize the role of these proteins in IFN-β induction during virus infection. Both PPRV_ΔV and PPRV_ΔC were defective in growth in cell culture, although in different ways. While the PPRV V protein bound to MDA-5 and, to a lesser extent, RIG-I, and over-expression of the V protein inhibited both IFN-β induction pathways, PPRV lacking V protein expression can still block IFN-β induction. In contrast, PPRV C bound to neither MDA-5 nor RIG-I, but PPRV lacking C protein expression lost the ability to block both MDA-5 and RIG-I mediated activation of IFN-β. These results shed new light on the inhibition of the induction of IFN-β by PPRV
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