492 research outputs found
Structural issues affecting mixed methods studies in health research: a qualitative study
<p>Abstract</p> <p>Background</p> <p>Health researchers undertake studies which combine qualitative and quantitative methods. Little attention has been paid to the structural issues affecting this mixed methods approach. We explored the facilitators and barriers to undertaking mixed methods studies in health research.</p> <p>Methods</p> <p>Face-to-face semi-structured interviews with 20 researchers experienced in mixed methods research in health in the United Kingdom.</p> <p>Results</p> <p>Structural facilitators for undertaking mixed methods studies included a perception that funding bodies promoted this approach, and the multidisciplinary constituency of some university departments. Structural barriers to exploiting the potential of these studies included a lack of education and training in mixed methods research, and a lack of templates for reporting mixed methods articles in peer-reviewed journals. The 'hierarchy of evidence' relating to effectiveness studies in health care research, with the randomised controlled trial as the gold standard, appeared to pervade the health research infrastructure. Thus integration of data and findings from qualitative and quantitative components of mixed methods studies, and dissemination of integrated outputs, tended to occur through serendipity and effort, further highlighting the presence of structural constraints. Researchers are agents who may also support current structures - journal reviewers and editors, and directors of postgraduate training courses - and thus have the ability to improve the structural support for exploiting the potential of mixed methods research.</p> <p>Conclusion</p> <p>The environment for health research in the UK appears to be conducive to mixed methods research but not to exploiting the potential of this approach. Structural change, as well as change in researcher behaviour, will be necessary if researchers are to fully exploit the potential of using mixed methods research.</p
Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity
Lung epithelial cells exhibit a high degree of plasticity. Alterations to lung epithelial cell function are critically involved in several chronic lung diseases such as pulmonary fibrosis. Pulmonary fibrosis is characterized by repetitive injury and subsequent impaired repair of epithelial cells, which leads to aberrant growth factor activation and fibroblast accumulation. Increased proliferation and hyper- and metaplasia of epithelial cells upon injury have also been observed in pulmonary fibrosis; this epithelial cell activation might represent the basis for lung cancer development. Indeed, several studies have provided histopathological evidence of an increased incidence of lung cancer in pulmonary fibrosis. The mechanisms involved in the development of cancer in pulmonary fibrosis, however, remain poorly understood. This review highlights recently uncovered molecular mechanisms shared between lung cancer and fibrosis, which extend the current evidence of a common trait of cancer and fibrosis, as provided by histopathological observations. Copyright (C) 2011 S. Karger AG, Base
Lorentz violation, Gravity, Dissipation and Holography
We reconsider Lorentz Violation (LV) at the fundamental level. We show that
Lorentz Violation is intimately connected with gravity and that LV couplings in
QFT must always be fields in a gravitational sector. Diffeomorphism invariance
must be intact and the LV couplings transform as tensors under coordinate/frame
changes. Therefore searching for LV is one of the most sensitive ways of
looking for new physics, either new interactions or modifications of known
ones. Energy dissipation/Cerenkov radiation is shown to be a generic feature of
LV in QFT. A general computation is done in strongly coupled theories with
gravity duals. It is shown that in scale invariant regimes, the energy
dissipation rate depends non-triviallly on two characteristic exponents, the
Lifshitz exponent and the hyperscaling violation exponent.Comment: LateX, 51 pages, 9 figures. (v2) References and comments added.
Misprints correcte
Interfacial Tension of the Lipid Membrane Formed from Phosphatidylcholine–Decanoic Acid and Phosphatidylcholine–Decylamine Systems
Interfacial tension has been determined for phosphatidylcholine (PC)–decanoic acid (DA) and PC–decylamine (DE) membranes. PC (lecithin), DA and DE were used in the experiments; the interfacial tension values of the pure components are 1.62 × 10−3, −2.38 × 10−2 and −3.88 × 10−2 N/m (hypothetical values for DA and DE), respectively. The 1:1 complexes were formed during formation of PC–DA and PC–DE membranes. The following parameters describing the complexes were determined: the surface concentrations of the lipid membranes formed from these complexes, \documentclass[12pt]{minimal}
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Cigarette smoking among school-going adolescents in Lithuania: Results from the 2005 Global Youth Tobacco Survey
<p>Abstract</p> <p>Background</p> <p>The majority of people who suffer morbidity due to smoking may have initiated smoking during adolescent period. The aim of this study is to determine the prevalence and associated factors for cigarette smoking among school-going adolescents in Lithuania.</p> <p>Findings</p> <p>Data from the Global Youth Tobacco Survey (GYTS) 2005 were used to conduct this study. Data were analyzed using SUDAAN software 9.03. Comparisons for categorical variables were done using the Pearson's Chi-square test. The cut of point for statistical significance was set at 5% level. Logistic regression analyses were conducted to determine factors associated with the outcome. Unadjusted odds ratios (OR) and adjusted odds ratios (AOR) together with their 95% confidence intervals (CI) are reported.</p> <p>Of the 1822 respondents, 35.8% males and 27.1% females reported being current cigarette smokers (p < 0.001). Having friends who smoke cigarettes was associated with smoking after controlling for age, gender, parental smoking status, and perception of risks of smoking (AOR = 3.76; 95% CI [2.33, 6.90] for some friends using tobacco; and AOR = 17.18; 95% CI [10.46, 28.21] for most or all friends using tobacco). Male gender and having one or both parents who smoke cigarettes were associated with smoking (AOR = 1.31; 95% CI [1.03, 1.66]) and AOR = 1.76; 95% CI [1.37, 2.27]) respectively).</p> <p>Conclusions</p> <p>There is a high prevalence of cigarette smoking among Lithuanian adolescents. Male adolescents and adolescents who have friends or parents who smoke should be the main target for tobacco control in Lithuania.</p
Methylation-Dependent Binding of the Epstein-Barr Virus BZLF1 Protein to Viral Promoters
The switch between latent and lytic Epstein-Barr virus (EBV) infection is mediated by the viral immediate-early (IE) protein, BZLF1 (Z). Z, a homologue of c-jun that binds to AP1-like motifs (ZREs), induces expression of the BRLF1 (R) and BRRF1 (Na) viral proteins, which cooperatively activate transcription of the Z promoter and thereby establish a positive autoregulatory loop. A unique feature of Z is its ability to preferentially bind to, and activate, the methylated form of the BRLF1 promoter (Rp). To date, however, Rp is the only EBV promoter known to be regulated in this unusual manner. We now demonstrate that the promoter driving transcription of the early BRRF1 gene (Nap) has two CpG-containing ZREs (ACGCTCA and TCGCCCG) that are only bound by Z in the methylated state. Both Nap ZREs are highly methylated in cells with latent EBV infection. Z efficiently activates the methylated, but not unmethylated, form of Nap in reporter gene assays, and both ZREs are required. Z serine residue 186, which was previously shown to be required for Z binding to methylated ZREs in Rp, but not for Z binding to the AP1 site, is required for Z binding to methylated Nap ZREs. The Z(S186A) mutant cannot activate methylated Nap in reporter gene assays and does not induce Na expression in cells with latent EBV infection. Molecular modeling studies of Z bound to the methylated Nap ZREs help to explain why methylation is required for Z binding, and the role of the Z Ser186 residue. Methylation-dependent Z binding to critical viral promoters may enhance lytic reactivation in latently infected cells, where the viral genome is heavily methylated. Conversely, since the incoming viral genome is initially unmethylated, methylation-dependent Z activation may also help the virus to establish latency following infection
Clostridium perfringens epsilon toxin increases the small intestinal permeability in mice and rats
Epsilon toxin is a potent neurotoxin produced by Clostridium perfringens types B and D, an anaerobic bacterium that causes enterotoxaemia in ruminants. In the affected animal, it causes oedema of the lungs and brain by damaging the endothelial cells, inducing physiological and morphological changes. Although it is believed to compromise the intestinal barrier, thus entering the gut vasculature, little is known about the mechanism underlying this process. This study characterizes the effects of epsilon toxin on fluid transport and bioelectrical parameters in the small intestine of mice and rats. The enteropooling and the intestinal loop tests, together with the single-pass perfusion assay and in vitro and ex vivo analysis in Ussing's chamber, were all used in combination with histological and ultrastructural analysis of mice and rat small intestine, challenged with or without C. perfringens epsilon toxin. Luminal epsilon toxin induced a time and concentration dependent intestinal fluid accumulation and fall of the transepithelial resistance. Although no evident histological changes were observed, opening of the mucosa tight junction in combination with apoptotic changes in the lamina propria were seen with transmission electron microscopy. These results indicate that C. perfringens epsilon toxin alters the intestinal permeability, predominantly by opening the mucosa tight junction, increasing its permeability to macromolecules, and inducing further degenerative changes in the lamina propria of the bowel. © 2009 Goldstein et al
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