605 research outputs found
A pilot telephone intervention to increase uptake of breast cancer screening in socially deprived areas in Scotland (TELBRECS):study protocol for a randomised controlled trial
BACKGROUND Breast cancer accounts for almost 30% of all cancers and is the second leading cause of cancer deaths in women in Scotland. Screening is key to early detection. The Scottish Breast Screening Programme is a nationwide, free at point of delivery screening service, to which all women aged between 50 and 70 years are invited to attend every 3 years. Currently over three-quarters of invited women regularly attend screening. However, women from more deprived areas are much less likely to attend: for example in the 3 years from 2010-2012 only 63% of women in the most deprived area attended the East of Scotland Breast Screening programme versus 81% in the least deprived. Research has suggested that reminders (telephone or letter) and brief, personalised interventions addressing barriers to attendance may be helpful in increasing uptake in low-income women. METHODS/DESIGN We will employ a brief telephone reminder and support intervention, whose purpose is to elicit and address any mistaken beliefs women have about breast screening, with the aim that the perceived benefits of screening come to outweigh any perceived barriers for individuals. We will test whether this intervention, plus a simple anticipated regret manipulation, will lead to an increase in the uptake of breast cancer screening amongst low-income women who have failed to attend a first appointment, in a randomised controlled trial with 600 women. Participants will be randomly allocated to one of four treatment arms i.e. 1) Letter reminder (i.e. Treatment as usual: CONTROL); 2) Telephone reminder (TEL), 3) Telephone reminder plus telephone support (TEL-SUPP) and 4) Telephone reminder plus support plus AR (TEL-SUPP-AR). The primary outcome will be attendance at breast screening within 3 months of the reminder letter. DISCUSSION If this simple telephone support intervention (with or without AR intervention) leads to a significant increase in breast screening attendance, this would represent a rare example of a theoretically-driven, relatively simple psychological intervention that could result in earlier detection of breast cancer amongst an under-served group of lower socio-economic women. TRIAL REGISTRATION Current Controlled trials: ISRCTN06039270. Registered 16th January 2014
Design and Synthesis of a Quintessential Self-Transmissible IncX1 Plasmid, pX1.0
DNA exchange in bacteria via conjugative plasmids is believed to be among the most important contributing factors to the rapid evolution- and diversification rates observed in bacterial species. The IncX1 plasmids are particularly interesting in relation to enteric bacteria, and typically carry genetic loads like antibiotic resistance genes and virulence factors. So far, however, a “pure” version of these molecular parasites, without genetic loads, has yet to be isolated from the environment. Here we report the construction of pX1.0, a fully synthesized IncX1 plasmid capable of horizontal transfer between different enteric bacteria. The designed pX1.0 sequence was derived from the consensus gene content of five IncX1 plasmids and three other, more divergent, members of the same phylogenetic group. The pX1.0 plasmid was shown to replicate stably in E. coli with a plasmid DNA per total DNA ratio corresponding to approximately 3–9 plasmids per chromosome depending on the growth phase of the host. Through conjugation, pX1.0 was able to self-transfer horizontally into an isogenic strain of E. coli as well as into two additional species belonging to the family Enterobacteriaceae. Our results demonstrate the immediate applicability of recent advances made within the field of synthetic biology for designing and constructing DNA systems, previously existing only in silica
MSH3 polymorphisms and protein levels affect CAG repeat instability in huntington's disease mice
Expansions of trinucleotide CAG/CTG repeats in somatic tissues are thought to contribute to ongoing disease progression through an affected individual's life with Huntington's disease or myotonic dystrophy. Broad ranges of repeat instability arise between individuals with expanded repeats, suggesting the existence of modifiers of repeat instability. Mice with expanded CAG/CTG repeats show variable levels of instability depending upon mouse strain. However, to date the genetic modifiers underlying these differences have not been identified. We show that in liver and striatum the R6/1 Huntington's disease (HD) (CAG)~100 transgene, when present in a congenic C57BL/6J (B6) background, incurred expansion-biased repeat mutations, whereas the repeat was stable in a congenic BALB/cByJ (CBy) background. Reciprocal congenic mice revealed the Msh3 gene as the determinant for the differences in repeat instability. Expansion bias was observed in congenic mice homozygous for the B6 Msh3 gene on a CBy background, while the CAG tract was stabilized in congenics homozygous for the CBy Msh3 gene on a B6 background. The CAG stabilization was as dramatic as genetic deficiency of Msh2. The B6 and CBy Msh3 genes had identical promoters but differed in coding regions and showed strikingly different protein levels. B6 MSH3 variant protein is highly expressed and associated with CAG expansions, while the CBy MSH3 variant protein is expressed at barely detectable levels, associating with CAG stability. The DHFR protein, which is divergently transcribed from a promoter shared by the Msh3 gene, did not show varied levels between mouse strains. Thus, naturally occurring MSH3 protein polymorphisms are modifiers of CAG repeat instability, likely through variable MSH3 protein stability. Since evidence supports that somatic CAG instability is a modifier and predictor of disease, our data are consistent with the hypothesis that variable levels of CAG instability associated with polymorphisms of DNA repair genes may have prognostic implications for various repeat-associated diseases
Higher-order multipole amplitudes in charmonium radiative transitions
Using 24 million decays in CLEO-c, we have searched
for higher multipole admixtures in electric-dipole-dominated radiative
transitions in charmonia. We find good agreement between our data and
theoretical predictions for magnetic quadrupole (M2) amplitudes in the
transitions and ,
in striking contrast to some previous measurements. Let and
denote the normalized M2 amplitudes in the respective aforementioned decays,
where the superscript refers to the angular momentum of the . By
performing unbinned maximum likelihood fits to full five-parameter angular
distributions, we determine the ratios and , where
the theoretical predictions are independent of the charmed quark magnetic
moment and are and .Comment: 32 pages, 7 figures, acceptance updat
Dalitz Plot Analysis of Ds to K+K-pi+
We perform a Dalitz plot analysis of the decay Ds to K+K-pi+ with the CLEO-c
data set of 586/pb of e+e- collisions accumulated at sqrt(s) = 4.17 GeV. This
corresponds to about 0.57 million D_s+D_s(*)- pairs from which we select 14400
candidates with a background of roughly 15%. In contrast to previous
measurements we find good agreement with our data only by including an
additional f_0(1370)pi+ contribution. We measure the magnitude, phase, and fit
fraction of K*(892) K+, phi(1020)pi+, K0*(1430)K+, f_0(980)pi+, f_0(1710)pi+,
and f_0(1370)pi+ contributions and limit the possible contributions of other KK
and Kpi resonances that could appear in this decay.Comment: 21 Pages,available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PR
Search for D0 to p e- and D0 to pbar e+
Using data recorded by CLEO-c detector at CESR, we search for simultaneous
baryon and lepton number violating decays of the D^0 meson, specifically, D^0
--> p-bar e^+, D^0-bar --> p-bar e^+, D^0 --> p e^- and D^0-bar --> p e^-. We
set the following branching fraction upper limits: D^0 --> p-bar e^+ (D^0-bar
--> p-bar e^+) p e^- (D^0-bar --> p e^-) < 1.2 *
10^{-5}, both at 90% confidence level.Comment: 10 pages, available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PRD. Comments: changed abstract, added reference for section 1,
vertical axis in Fig.5 changed (starts from 1.5 rather than 2.0), fixed typo
Charmonium decays to gamma pi0, gamma eta, and gamma eta'
Using data acquired with the CLEO-c detector at the CESR e+e- collider, we
measure branching fractions for J/psi, psi(2S), and psi(3770) decays to gamma
pi0, gamma eta, and gamma eta'. Defining R_n = B[ psi(nS)-->gamma eta ]/B[
psi(nS)-->gamma eta' ], we obtain R_1 = (21.1 +- 0.9)% and, unexpectedly, an
order of magnitude smaller limit, R_2 < 1.8% at 90% C.L. We also use
J/psi-->gamma eta' events to determine branching fractions of improved
precision for the five most copious eta' decay modes.Comment: 14 pages, available through http://www.lns.cornell.edu/public/CLNS/,
published in Physical Review
Precision Measurement of the Mass of the h_c(1P1) State of Charmonium
A precision measurement of the mass of the h_c(1P1) state of charmonium has
been made using a sample of 24.5 million psi(2S) events produced in e+e-
annihilation at CESR. The reaction used was psi(2S) -> pi0 h_c, pi0 -> gamma
gamma, h_c -> gamma eta_c, and the reaction products were detected in the
CLEO-c detector.
Data have been analyzed both for the inclusive reaction and for the exclusive
reactions in which eta_c decays are reconstructed in fifteen hadronic decay
channels. Consistent results are obtained in the two analyses. The averaged
results of the present measurements are M(h_c)=3525.28+-0.19 (stat)+-0.12(syst)
MeV, and B(psi(2S) -> pi0 h_c)xB(h_c -> gamma eta_c)= (4.19+-0.32+-0.45)x10^-4.
Using the 3PJ centroid mass, Delta M_hf(1P)= - M(h_c) =
+0.02+-0.19+-0.13 MeV.Comment: 9 pages, available through http://www.lns.cornell.edu/public/CLNS/,
submitted to PR
Precision Measurement of B(D+ -> mu+ nu) and the Pseudoscalar Decay Constant fD+
We measure the branching ratio of the purely leptonic decay of the D+ meson
with unprecedented precision as B(D+ -> mu+ nu) = (3.82 +/- 0.32 +/-
0.09)x10^(-4), using 818/pb of data taken on the psi(3770) resonance with the
CLEO-c detector at the CESR collider. We use this determination to derive a
value for the pseudoscalar decay constant fD+, combining with measurements of
the D+ lifetime and assuming |Vcd| = |Vus|. We find fD+ = (205.8 +/- 8.5 +/-
2.5) MeV. The decay rate asymmetry [B(D+ -> mu+ nu)-B(D- -> mu- nu)]/[B(D+ ->
mu+ nu)+B(D- -> mu- nu)] = 0.08 +/- 0.08, consistent with no CP violation. We
also set 90% confidence level upper limits on B(D+ -> tau+ nu) < 1.2x10^(-3)
and B(D+ -> e+ nu) < 8.8x10^(-6).Comment: 24 pages, 11 figures and 6 tables, v2 replaced some figure vertical
axis scales, v3 corrections from PRD revie
Measurement of the Absolute Branching Fraction of D_s^+ --> tau^+ nu_tau Decay
Using a sample of tagged D_s decays collected near the D^*_s D_s peak
production energy in e+e- collisions with the CLEO-c detector, we study the
leptonic decay D^+_s to tau^+ nu_tau via the decay channel tau^+ to e^+ nu_e
bar{nu}_tau. We measure B(D^+_s to tau^+ nu_tau) = (6.17 +- 0.71 +- 0.34) %,
where the first error is statistical and the second systematic. Combining this
result with our measurements of D^+_s to mu^+ nu_mu and D^+_s to tau^+ nu_tau
(via tau^+ to pi^+ bar{nu}_tau), we determine f_{D_s} = (274 +- 10 +- 5) MeV.Comment: 9 pages, postscript also available through
http://www.lns.cornell.edu/public/CLNS/2007/, revise
- …