Mott Children's Health Center Eatfit Summer Camp II

The purpose of this study was to design an evaulation tool for EatFit Summer Camp II held at Mott Children's Health Center. This camp is in need of a formal evaluation tool to be utilized by participants thirteen to sixteen years of age. The variables that will be concentrated on are self-efficacy and environment. The final MCHC questionnaire is comprised from questions from three existing evaluation tools. Two of the tools were utilized by children/adolescents. The other questionnaire was utilized by adults; however, questions regarding environment are relevant to population being serviced.Master'sSchool of Health Professions and Studies: Health EducationUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/117736/1/Polacek.pd

The convergence of haemodynamics, genomics, and endothelial structure in studies of the focal origin of atherosclerosis

The completion of the Human Genome Project and ongoing sequencing of mouse, rat and other genomes has led to an explosion of genetics-related technologies that are finding their way into all areas of biological research; the field of biorheology is no exception. Here we outline how two disparate modern molecular techniques, microarray analyses of gene expression and real-time spatial imaging of living cell structures, are being utilized in studies of endothelial mechanotransduction associated with controlled shear stress in vitro and haemodynamics in vivo. We emphasize the value of such techniques as components of an integrated understanding of vascular rheology. In mechanotransduction, a systems approach is recommended that encompasses fluid dynamics, cell biomechanics, live cell imaging, and the biochemical, cell biology and molecular biology methods that now encompass genomics. Microarrays are a useful and powerful tool for such integration by identifying simultaneous changes in the expression of many genes associated with interconnecting mechanoresponsive cellular pathways

Detection of myxoma viruses encoding a defective M135R gene from clinical cases of myxomatosis; possible implications for the role of the M135R protein as a virulence factor

<p>Abstract</p> <p>Background</p> <p>Myxoma virus is a member of the <it>Poxviridae </it>and causes disease in European rabbits. Laboratory confirmation of the clinical disease, which occurs in the autumn of most years in Denmark, has been achieved previously using antigen ELISA and electron microscopy.</p> <p>Results</p> <p>An unusually large number of clinically suspected cases of myxomatosis were observed in Denmark during 2007. Myxoma virus DNA was detected, using a new real time PCR assay which targets the M029L gene, in over 70% of the clinical samples submitted for laboratory confirmation. Unexpectedly, further analysis revealed that a high proportion of these viral DNA preparations contained a frame-shift mutation within the M135R gene that has previously been identified as a virulence factor. This frame-shift mutation results in expression of a greatly truncated product. The same frame-shift mutation has also been found recently within an avirulent strain of myxoma virus (6918). However, three other frame-shift mutations found in this strain (in the genes M009L, M036L and M148R) were not shared with the Danish viruses but a single nucleotide deletion in the M138R/M139R intergenic region was a common feature.</p> <p>Conclusions</p> <p>It appears that expression of the full-length myxoma virus M135R protein is not required for virulence in rabbits. Hence, the frame-shift mutation in the M135R gene in the nonpathogenic 6918 virus strain is not sufficient to explain the attenuation of this myxoma virus but one/some of the other frame-shift mutations alone or in conjunction with one/some of the thirty two amino acid substitutions must also contribute. The real time PCR assay for myxoma virus is a useful diagnostic tool for laboratory confirmation of suspected cases of myxomatosis.</p

Laser calibration of the ATLAS Tile Calorimeter during LHC Run 2

This article reports the laser calibration of the hadronic Tile Calorimeter of the ATLAS experiment in the LHC Run 2 data campaign. The upgraded Laser II calibration system is described. The system was commissioned during the first LHC Long Shutdown, exhibiting a stability better than 0.8% for the laser light monitoring. The methods employed to derive the detector calibration factors with data from the laser calibration runs are also detailed. These allowed to correct for the response fluctuations of the 9852 photomultiplier tubes of the Tile Calorimeter with a total uncertainty of 0.5% plus a luminosity-dependent sub-dominant term. Finally, we report the regular monitoring and performance studies using laser events in both standalone runs and during proton collisions. These studies include channel timing and quality inspection, and photomultiplier linearity and response dependence on anode current

The Puromycin Route to Assess Stereo- and Regiochemical Constraints on Peptide Bond Formation in Eukaryotic Ribosomes

We synthesized a series of puromycin analogues to probe the chemical specificity of the ribosome in an intact eukaryotic translation system. These studies reveal that both d-enantiomers and β-amino acid analogues can be incorporated into protein, and provide a quantitative means to rank natural and unnatural residues. Modeling of a d-amino acid analogue into the 50S ribosomal subunit indicates that steric clash may provide part of the chiral discrimination. The data presented provide one metric of the chiral and regiospecificity of mammalian ribosomes

Strong LP formulations for scheduling splittable jobs on unrelated machines

International audienceA natural extension of the makespan minimization problem on unrelated machines is to allow jobs to be partially processed by different machines while incurring an arbitrary setup time. In this paper we present increasingly stronger LP-relaxations for this problem and their implications on the approximability of the problem. First we show that the straightforward LP, extending the approach for the original problem, has an integrality gap of 3 and yields an approximation algorithm of the same factor. By applying a lift-and-project procedure, we are able to improve both the integrality gap and the implied approximation factor to 1+ϕ1+ϕ , where ϕϕ is the golden ratio. Since this bound remains tight for the seemingly stronger machine configuration LP, we propose a new job configuration LP that is based on an infinite continuum of fractional assignments of each job to the machines. We prove that this LP has a finite representation and can be solved in polynomial time up to any accuracy. Interestingly, we show that our problem cannot be approximated within a factor better than ee−1≈1.582(unless =)ee−1≈1.582(unless P=NP) , which is larger than the inapproximability bound of 1.5 for the original problem

Could increased axial wall stress be responsible for the development of atheroma in the proximal segment of myocardial bridges?

<p>Abstract</p> <p>Background</p> <p>A recent model describing the mechanical interaction between a stenosis and the vessel wall has shown that axial wall stress can considerably increase in the region immediately proximal to the stenosis during the (forward) flow phases, so that abnormal biological processes and wall damages are likely to be induced in that region. Our objective was to examine what this model predicts when applied to myocardial bridges.</p> <p>Method</p> <p>The model was adapted to the hemodynamic particularities of myocardial bridges and used to estimate by means of a numerical example the cyclic increase in axial wall stress in the vessel segment proximal to the bridge. The consistence of the results with reported observations on the presence of atheroma in the proximal, tunneled, and distal vessel segments of bridged coronary arteries was also examined.</p> <p>Results</p> <p>1) Axial wall stress can markedly increase in the entrance region of the bridge during the cardiac cycle. 2) This is consistent with reported observations showing that this region is particularly prone to atherosclerosis.</p> <p>Conclusion</p> <p>The proposed mechanical explanation of atherosclerosis in bridged coronary arteries indicates that angioplasty and other similar interventions will not stop the development of atherosclerosis at the bridge entrance and in the proximal epicardial segment if the decrease of the lumen of the tunneled segment during systole is not considerably reduced.</p

Down-Regulation of the Interferon Signaling Pathway in T Lymphocytes from Patients with Metastatic Melanoma

BACKGROUND: Dysfunction of the immune system has been documented in many types of cancers. The precise nature and molecular basis of immune dysfunction in the cancer state are not well defined. METHODS AND FINDINGS: To gain insights into the molecular mechanisms of immune dysfunction in cancer, gene expression profiles of pure sorted peripheral blood lymphocytes from 12 patients with melanoma were compared to 12 healthy controls. Of 25 significantly altered genes in T cells and B cells from melanoma patients, 17 are interferon (IFN)-stimulated genes. These microarray findings were further confirmed by quantitative PCR and functional responses to IFNs. The median percentage of lymphocytes that phosphorylate STAT1 in response to interferon-α was significantly reduced (Δ = 16.8%; 95% confidence interval, 0.98% to 33.35%) in melanoma patients (n = 9) compared to healthy controls (n = 9) in Phosflow analysis. The Phosflow results also identified two subgroups of patients with melanoma: IFN-responsive (33%) and low-IFN-response (66%). The defect in IFN signaling in the melanoma patient group as a whole was partially overcome at the level of expression of IFN-stimulated genes by prolonged stimulation with the high concentration of IFN-α that is achievable only in IFN therapy used in melanoma. The lowest responders to IFN-α in the Phosflow assay also showed the lowest gene expression in response to IFN-α. Finally, T cells from low-IFN-response patients exhibited functional abnormalities, including decreased expression of activation markers CD69, CD25, and CD71; T(H)1 cytokines interleukin-2, IFN-γ, and tumor necrosis factor α, and reduced survival following stimulation with anti-CD3/CD28 antibodies compared to controls. CONCLUSIONS: Defects in interferon signaling represent novel, dominant mechanisms of immune dysfunction in cancer. These findings may be used to design therapies to counteract immune dysfunction in melanoma and to improve cancer immunotherapy

Upscaling of methane exchange in a boreal forest using soil chamber measurements and high-resolution LiDAR elevation data

Forest soils are generally considered to be net sinks of methane (CH4), but CH4 fluxes vary spatially depending on soil conditions. Measuring CH4 exchange with chambers, which are commonly used for this purpose, might not result in representative fluxes at site scale. Appropriate methods for upscaling CH4 fluxes from point measurements to site scale are therefore needed. At the boreal forest research site, Norunda, chamber measurements of soils and vegetation indicate that the site is a net sink of CH4, while tower gradient measurements indicate that the site is a net source of CH4. We investigated the discrepancy between chamber and tower gradient measurements by upscaling soil CH4 exchange to a 100 ha area based on an empirical model derived from chamber measurements of CH4 exchange and measurements of soil moisture, soil temperature and water table depth. A digital elevation model (DEM) derived from high-resolution airborne Light Detection and Ranging (LiDAR) data was used to generate gridded water table depth and soil moisture data of the study area as input data for the upscaling. Despite the simplistic approach, modeled fluxes were significantly correlated to four out of five chambers with R>0.68. The upscaling resulted in a net soil sink of CH4 of -10 mu mol m(-2) h(-1), averaged over the entire study area and time period June-September, 2010). Our findings suggest that additional contributions from CH4 soil sources outside the upscaling study area and possibly CH4 emissions from vegetation could explain the net emissions measured by tower gradient measurements. (C) 2015 Elsevier B.V. All rights reserved