What Drives Using Antibiotic without Prescriptions? A Qualitative Interview Study of University Students in United Arab Emirates

Bacterial resistance to antibiotics is considered as natural phenomenon that occurs over the time due to genetic changes. Bacterial resistance to antibiotics is significantly increasing in the UAE. Self-medication with antibiotics has been identified as a major factor for the development of antibiotic resistance, which is significantly increasing in the UAE.The purpose of this study was to explore the factors that contribute to the use of antibiotics without prescriptions among first year healthcare university students in UAE.Based on the findings of an earlier survey study, a qualitative interview study was designed to explore common themes related to student's knowledge, awareness, attitude, views, and perceptions. Data were analyzed thematically for the identification of themes and subthemes within the data through the use of coding.The interview study identified four main themes with multiple subthemes related to the use of antibiotics without a physician's prescription by first-year healthcare students. The thematic analysis of the interviews revealed four main themes; medication habits and practices; reasons for self-medication; access to antibiotics without a prescription and gaps in students' knowledge regarding antibiotic resistance.Healthcare students in UAE are influenced by several factors including parents and friends influence, successful previous experience and investment of time and money to visit a physician. Our sample of healthcare students has a misconception about the use of antibiotics. The current interview study identified six new reasons for using antibiotics without prescriptions as compared to our earlier survey study. There is a need of multifaceted strategies to decrease unnecessary antibiotic use in our population sample

Ontogenetic relationships between cranium and mandible in coyotes and hyenas

Developing animals must resolve the conflicting demands of survival and growth, ensuring that they can function as infants or juveniles while developing toward their adult form. In the case of the mammalian skull, the cranium and mandible must maintain functional integrity to meet the feeding needs of a juvenile even as the relationship between parts must change to meet the demands imposed on adults. We examine growth and development of the cranium and mandible, using a unique ontogenetic series of known-age coyotes ( Canis latrans ), analyzing ontogenetic changes in the shapes of each part, and the relationship between them, relative to key life-history events. Both cranial and mandibular development conform to general mammalian patterns, but each also exhibits temporally and spatially localized maturational transformations, yielding a complex relationship between growth and development of each part as well as complex patterns of synchronous growth and asynchronous development between parts. One major difference between cranium and mandible is that the cranium changes dramatically in both size and shape over ontogeny, whereas the mandible undergoes only modest shape change. Cranium and mandible are synchronous in growth, reaching adult size at the same life-history stage; growth and development are synchronous for the cranium but not for the mandible. This synchrony of growth between cranium and mandible, and asynchrony of mandibular development, is also characteristic of a highly specialized carnivore, the spotted hyena ( Crocuta crocuta ), but coyotes have a much less protracted development, being handicapped relative to adults for a much shorter time. Morphological development does not predict life-history events in these two carnivores, which is contrary to what has been reported for two rodent species. The changes seen in skull shape in successive life-history stages suggest that adult functional demands cannot be satisfied by the morphology characterizing earlier life-history stages. J. Morphol. 2011. © 2011 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/84382/1/10934_ftp.pd

High Resolution Imaging of Vascular Function in Zebrafish

Rationale: The role of the endothelium in the pathogenesis of cardiovascular disease is an emerging field of study, necessitating the development of appropriate model systems and methodologies to investigate the multifaceted nature of endothelial dysfunction including disturbed barrier function and impaired vascular reactivity. Objective: We aimed to develop and test an optimized high-speed imaging platform to obtain quantitative real-time measures of blood flow, vessel diameter and endothelial barrier function in order to assess vascular function in live vertebrate models. Methods and Results: We used a combination of cutting-edge optical imaging techniques, including high-speed, camera-based imaging (up to 1000 frames/second), and 3D confocal methods to collect real time metrics of vascular performance and assess the dynamic response to the thromboxane A2 (TXA2) analogue, U-46619 (1 μM), in transgenic zebrafish larvae. Data obtained in 3 and 5 day post-fertilization larvae show that these methods are capable of imaging blood flow in a large (1 mm) segment of the vessel of interest over many cardiac cycles, with sufficient speed and sensitivity such that the trajectories of individual erythrocytes can be resolved in real time. Further, we are able to map changes in the three dimensional sizes of vessels and assess barrier function by visualizing the continuity of the endothelial layer combined with measurements of extravasation of fluorescent microspheres. Conclusions: We propose that this system-based microscopic approach can be used to combine measures of physiologic function with molecular behavior in zebrafish models of human vascular disease. © 2012 Watkins et al

The potential of new tumor endothelium-specific markers for the development of antivascular therapy.

Angiogenesis is a hallmark of solid tumors, and disruption of tumor vasculature is an active anticancer therapy in some cases. Several proteins expressed on the surface of tumor endothelium have been identified during the last decade. However, due to the expression in both physiological and tumor angiogenesis, only a few targets have been developed for clinical therapeutics. By thorough SAGE analysis of mouse endothelial cells isolated from various normal resting tissues, regenerating liver, and liver-metastasized tumor, Seaman and colleagues in this issue of Cancer Cell have demonstrated organ-specific endothelial markers, physiological angiogenesis endothelial markers, and tumor endothelial markers and revealed striking differences between physiological and pathological angiogenesis

G-Quadruplex Dynamics Contribute To Regulation Of Mitochondrial Gene Expression

Single-stranded DNA or RNA sequences rich in guanine (G) can adopt non-canonical structures known as G-quadruplexes (G4). Mitochondrial DNA (mtDNA) sequences that are predicted to form G4 are enriched on the heavy-strand and have been associated with formation of deletion breakpoints. Increasing evidence supports the ability of mtDNA to form G4 in cancer cells; however, the functional roles of G4 structures in regulating mitochondrial nucleic acid homeostasis in non-cancerous cells remain unclear. Here, we demonstrate by live cell imaging that the G4-ligand RHPS4 localizes primarily to mitochondria at low doses. We find that low doses of RHPS4 do not induce a nuclear DNA damage response but do cause an acute inhibition of mitochondrial transcript elongation, leading to respiratory complex depletion. We also observe that RHPS4 interferes with mtDNA levels or synthesis both in cells and isolated mitochondria. Importantly, a mtDNA variant that increases G4 stability and anti-parallel G4-forming character shows a stronger respiratory defect in response to RHPS4, supporting the conclusion that mitochondrial sensitivity to RHPS4 is G4-mediated. Taken together, our results indicate a direct role for G4 perturbation in mitochondrial genome replication, transcription processivity, and respiratory function in normal cells

PDE limits of stochastic SIS epidemics on networks

Stochastic epidemic models on networks are inherently high-dimensional and the resulting exact models are intractable numerically even for modest network sizes. Mean-field models provide an alternative but can only capture average quantities, thus offering little or no information about variability in the outcome of the exact process. In this article, we conjecture and numerically demonstrate that it is possible to construct partial differential equation (PDE)-limits of the exact stochastic susceptible-infected-susceptible epidemics on Regular, Erdős–Rényi, Barabási–Albert networks and lattices. To do this, we first approximate the exact stochastic process at population level by a Birth-and-Death process (BD) (with a state space of O(N) rather than O(2N)⁠) whose coefficients are determined numerically from Gillespie simulations of the exact epidemic on explicit networks. We numerically demonstrate that the coefficients of the resulting BD process are density-dependent, a crucial condition for the existence of a PDE limit. Extensive numerical tests for Regular, Erdős–Rényi, Barabási–Albert networks and lattices show excellent agreement between the outcome of simulations and the numerical solution of the Fokker–Planck equations. Apart from a significant reduction in dimensionality, the PDE also provides the means to derive the epidemic outbreak threshold linking network and disease dynamics parameters, albeit in an implicit way. Perhaps more importantly, it enables the formulation and numerical evaluation of likelihoods for epidemic and network inference as illustrated in a fully worked out example

Fine structure in the off-resonance conductance of small Coulomb blockade systems

We show how a fine, multiple-peak structure can arise in the off-resonance, zero-bias conductance of Coulomb blockade systems. In order to understand how this effect comes about one must abandon the orthodox, mean-field understanding of the Coulomb blockade phenomenon and consider quantum fluctuations in the occupation of the single-particle electronic levels. We illustrate such an effect with a spinless Anderson-like model for multi-level systems and an equation-of-motion method for calculating Green's functions that combines two simple decoupling schemes.Comment: 5 pages, 3 figures, postscript file also available at http://www.pa.uky.edu/~palacios/papers/eom.ps One figure added. Discussion of results extende

Disruption of the Cr2 Locus Results in a Reduction in B-1a Cells and in an Impaired B Cell Response to T-Dependent Antigen

AbstractCovalent attachment of activated products of the third component of complement to antigen enhances its immunogenicity, but the mechanism is not clear. This effect is mediated by specific receptors, mCR1 (CD35) and mCR2 (CD21), expressed primarily on B cells and follicular dendritic cells in mice. To dissect the role of mCR1 and mCR2 in the humoral response, we have disrupted the Cr2 locus to generate mice deficient in both receptors. The deficient mice (Cr2−/−) were found to have a reduction in the CD5+ population of peritoneal B-1 cells, although their serum IgM levels were within the range of normal mice. Moreover, Cr2−/− mice had a severe defect in their humoral response to T-dependent antigens that was characterized by a reduction in serum antibody titers and in the number and size of germinal centers within splenic follicles. Reconstitution of the deficient mice with bone marrow from MHC-matched Cr2+/+ donors corrected the defect, demonstrating that the defect was due to B cells themselves. These results indicate an obligatory role of B cell complement receptors in responses of the B cells to protein antigens

The scientific foundations and associated injury risks of early soccer specialisation

Early specialisation is characterised by formal participation in a single sport at the exclusion of others. Limited data are available to support this approach in the development of soccer players who attain elite status later in life. Of growing concern is the associated increased risk of injury and suggestions that single sport specialisation is a risk factor independent of age, growth, biological maturation and training volumes In the United Kingdom, elite soccer organisations have recently adopted an early sport specialisation approach following the introduction of the Elite Player Performance Plan. A key tenet of this programme is increased opportunities for training through a marked rise in the specified on-pitch hours per week. The accumulation of high training hours may be less of a relevant marker for success, and the impact of such a significant increase in training volume for young athletes who are experiencing a range of growth and maturational processes is currently unknown. This critical commentary includes an evidence based discussion of the effectiveness of early sport specialisation and the potential injury risks associated with such programmes placing a specific focus on elite male youth soccer players. Available data indicate that modifications to the existing EPPP framework could enhance player development and reduce injury risk. Proposed alterations include reduced volume of soccer specific training at key stages of growth and maturation and guidelines for the provision of a greater variety of physical activities that are integrated within other programme components