18 research outputs found
Nanoelectromechanical coupling in fullerene peapods probed via resonant electrical transport experiments
Fullerene peapods, that is carbon nanotubes encapsulating fullerene
molecules, can offer enhanced functionality with respect to empty nanotubes.
However, the present incomplete understanding of how a nanotube is affected by
entrapped fullerenes is an obstacle for peapods to reach their full potential
in nanoscale electronic applications. Here, we investigate the effect of C60
fullerenes on electron transport via peapod quantum dots. Compared to empty
nanotubes, we find an abnormal temperature dependence of Coulomb blockade
oscillations, indicating the presence of a nanoelectromechanical coupling
between electronic states of the nanotube and mechanical vibrations of the
fullerenes. This provides a method to detect the C60 presence and to probe the
interplay between electrical and mechanical excitations in peapods, which thus
emerge as a new class of nanoelectromechanical systems.Comment: 7 pages, 3 figures. Published in Nature Communications. Free online
access to the published version until Sept 30th, 2010, see
http://www.nature.com/ncomms/journal/v1/n4/abs/ncomms1034.htm
On the frequentist coverage of Bayesian credible intervals for lower bounded means
For estimating a lower bounded location or mean parameter for a symmetric and
logconcave density, we investigate the frequentist performance of the
Bayesian HPD credible set associated with priors which are
truncations of flat priors onto the restricted parameter space. Various new
properties are obtained. Namely, we identify precisely where the minimum
coverage is obtained and we show that this minimum coverage is bounded between
and ; with
the lower bound improving (for ) on the
previously established ([9]; [8]) lower bound .
Several illustrative examples are given.Comment: Published in at http://dx.doi.org/10.1214/08-EJS292 the Electronic
Journal of Statistics (http://www.i-journals.org/ejs/) by the Institute of
Mathematical Statistics (http://www.imstat.org
Autoimmune and autoinflammatory mechanisms in uveitis
The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders
The hospital microbiome project: Meeting report for the 1st hospital microbiome project, Chicago, USA, January 15<sup>th</sup>, 2013
Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema
<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p