2,058 research outputs found

    Quenching of lamellar ordering in an n-alkane embedded in nanopores

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    We present an X-ray diffraction study of the normale alkane nonadecane C_{19}H_{40} embedded in nanoporous Vycor glass. The confined molecular crystal accomplishes a close-packed structure by alignment of the rod-like molecules parallel to the pore axis while sacrificing one basic principle known from the bulk state, i.e. the lamellar ordering of the molecules. Despite this disorder, the phase transitions observed in the confined solid mimic the phase behavior of the 3D unconfined crystal, though enriched by the appearance of a true rotator phase known only from longer alkane chains.Comment: 7 pages, 3 figure

    Microdamage repair and remodeling requires mechanical loading

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    Bone remodeling is necessary to avoid microdamage accumulation, which could lead to whole-bone failure. Previous studies have shown that this bone-repair mechanism is triggered by osteocyte apoptosis. Through the use of a rodent hindlimb suspension model and tibial four-point bending model, the effects of disuse on microdamage remodeling was examined. At day 0, male rats were assigned to one of three groups: weight bearing (WB), hindlimb suspension (HS), or hindlimb suspension with daily intermittent weight bearing following damage-inducing loading (HW). Within each group, the rats were further divided into subgroups corresponding to three sacrifice time points [day 14 (WB and HS only), day 18, or day 35]. At day 14, animals were anesthetized, and their left tibiae underwent cyclic four-point bending to produce fatigue-induced microdamage. At sacrifice, the tibiae were examined using 3D micro-computed tomography (µCT), flow cytometry, and histologic and immunohistochemical stains. The results indicate that only the WB and HW groups had a significant increase in intracortical TRAP-positive resorption pits following damage induction, which was paralleled by a significant decrease in microdamage over time in combination with a shift in the osteoclast lineage owing to a decrease in monocytes. These results demonstrate that osteocyte apoptosis may be insufficient for repair of microdamage without the stimulation provided through physiologic loading. In addition, this potentially could have clinical implications for the current therapeutic paradigm for treating stress fractures, where extended non-weight bearing is employed. © 2010 American Society for Bone and Mineral ResearchPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71374/1/91016_ftp.pd

    Downregulation of HLA Class I Renders Inflammatory Neutrophils More Susceptible to NK Cell-Induced Apoptosis

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    Neutrophils are potent effector cells and contain a battery of harmful substances and degrading enzymes. A silent neutrophil death, i.e., apoptosis, is therefore of importance to avoid damage to the surrounding tissue and to enable termination of the acute inflammatory process. There is a pile of evidence supporting the role for pro-inflammatory cytokines in extending the life-span of neutrophils, but relatively few studies have been devoted to mechanisms actively driving apoptosis induction in neutrophils. We have previously demonstrated that natural killer (NK) cells can promote apoptosis in healthy neutrophils. In this study, we set out to investigate how neutrophil sensitivity to NK cell-mediated cytotoxicity is regulated under inflammatory conditions. Using in vitro-activated neutrophils and a human skin chamber model that allowed collection of in vivo-transmigrated neutrophils, we performed a comprehensive characterization of neutrophil expression of ligands to NK cell receptors. These studies revealed a dramatic downregulation of HLA class I molecules in inflammatory neutrophils, which was associated with an enhanced susceptibility to NK cell cytotoxicity. Collectively, our data shed light on the complex regulation of interactions between NK cells and neutrophils during an inflammatory response and provide further support for a role of NK cells in the resolution phase of inflammation

    Time Reversal Violation from the entangled B0-antiB0 system

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    We discuss the concepts and methodology to implement an experiment probing directly Time Reversal (T) non-invariance, without any experimental connection to CP violation, by the exchange of "in" and "out" states. The idea relies on the B0-antiB0 entanglement and decay time information available at B factories. The flavor or CP tag of the state of the still living neutral meson by the first decay of its orthogonal partner overcomes the problem of irreversibility for unstable systems, which prevents direct tests of T with incoherent particle states. T violation in the time evolution between the two decays means experimentally a difference between the intensities for the time-ordered (l^+ X, J/psi K_S) and (J/psi K_L, l^- X) decays, and three other independent asymmetries. The proposed strategy has been applied to simulated data samples of similar size and features to those currently available, from which we estimate the significance of the expected discovery to reach many standard deviations.Comment: 17 pages, 2 figures, 6 table

    Probing scalar particle and unparticle couplings in e+ e- -> t tbar with transversely polarized beams

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    In searching for indications of new physics scalar particle and unparticle couplings in e^+ e^- \to t\bar t, we consider the role of transversely polarized initial beams at e^+ e^- colliders. By using a general relativistic spin density matrix formalism for describing the particles spin states, we find analytical expressions for the squared amplitude of the process with t or \bar t polarization measured, including the anomalous coupling contributions. Thanks to the transversely polarized initial beams these contributions are first order anomalous coupling corrections to the Standard Model (SM) contributions. We present and analyse the main features of the SM and anomalous coupling contributions. We show how differences between SM and anomalous coupling contributions provide means to search for anomalous coupling manifestations at future e^+ e^- linear colliders.Comment: 28 pages in LaTeX, including 7 encapsulated PostScript figures, published versio

    Sputum microbiome profiling in COPD: beyond singular pathogen detection.

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    Culture-independent microbial sequencing techniques have revealed that the respiratory tract harbours a complex microbiome not detectable by conventional culturing methods. The contribution of the microbiome to chronic obstructive pulmonary disease (COPD) pathobiology and the potential for microbiome-based clinical biomarkers in COPD are still in the early phases of investigation. Sputum is an easily obtainable sample and has provided a wealth of information on COPD pathobiology, and thus has been a preferred sample type for microbiome studies. Although the sputum microbiome likely reflects the respiratory microbiome only in part, there is increasing evidence that microbial community structure and diversity are associated with disease severity and clinical outcomes, both in stable COPD and during the exacerbations. Current evidence has been limited to mainly cross-sectional studies using 16S rRNA gene sequencing, attempting to answer the question 'who is there?' Longitudinal studies using standardised protocols are needed to answer outstanding questions including differences between sputum sampling techniques. Further, with advancing technologies, microbiome studies are shifting beyond the examination of the 16S rRNA gene, to include whole metagenome and metatranscriptome sequencing, as well as metabolome characterisation. Despite being technically more challenging, whole-genome profiling and metabolomics can address the questions 'what can they do?' and 'what are they doing?' This review provides an overview of the basic principles of high-throughput microbiome sequencing techniques, current literature on sputum microbiome profiling in COPD, and a discussion of the associated limitations and future perspectives

    Behavior therapy for pediatric trichotillomania: Exploring the effects of age on treatment outcome

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    <p>Abstract</p> <p>Background</p> <p>A randomized controlled trial examining the efficacy of behavior therapy for pediatric trichotillomania was recently completed with 24 participants ranging in age from 7 - 17. The broad age range raised a question about whether young children, older children, and adolescents would respond similarly to intervention. In particular, it is unclear whether the younger children have the cognitive capacity to understand concepts like "urges" and whether they are able to introspect enough to be able to benefit from awareness training, which is a key aspect of behavior therapy for trichotillomania.</p> <p>Methods</p> <p>Participants were randomly assigned to receive either behavior therapy (N = 12) or minimal attention control (N = 12), which was included to control for repeated assessments and the passage of time. Primary outcome measures were the independent evaluator-rated NIMH-Trichotillomania Severity Scale, a semi-structured interview often used in trichotillomania treatment trials, and a post-treatment clinical global impression improvement rating (CGI-I).</p> <p>Results</p> <p>The correlation between age and change in symptom severity for all patients treated in the trial was small and not statistically significant. A 2 (group: behavioral therapy, minimal attention control) × 2 (time: week 0, 8) × 2 (children < 9 yrs., children > 10) ANOVA with independent evaluator-rated symptom severity scores as the continuous dependent variable also detected no main effects for age or for any interactions involving age. In light of the small sample size, the mean symptom severity scores at weeks 0 and 8 for younger and older patients randomized to behavioral therapy were also plotted. Visual inspection of these data indicated that although the groups appeared to have started at similar levels of severity for children ≤ 9 vs. children ≥ 10; the week 8 data show that the three younger children did at least as well as if not slightly better than the nine older children and adolescents.</p> <p>Conclusions</p> <p>Behavior therapy for pediatric trichotillomania appears to be efficacious even in young children. The developmental and clinical implications of these findings will be discussed.</p> <p>Trial Registration</p> <p>Clinicaltrials.gov NCT00043563.</p

    Genetic differences in the frequency of the hinge variants of porcine IgA is breed dependent

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    The distribution of the IgAa and IgAb alleles of porcine IgA in over 160 randomly-selected animals revealed an abundance of heterozygotes but only two b/b homozygotes. Since the IgAb allotype is a splice site mutant lacking two-thirds of the hinge, this study tests the hypothesis that pigs with this genotype may be at a selective disadvantage while heterozygous individuals may be at some advantage. This hypothesis was tested by collecting data on 374 animals of known breed and often parentage. We show here that when breed was not considered, young animals of known parentage had genotypic frequencies identical to that expected for Mendelian alleles but that a/b heterozygotes were overrepresented in adults. However, when analyzed with regard to breed, a very strong association between breed and the frequency of the IgAa and IgAb alleles was discovered. Meishan and NIH minipigs were homozygous for IgA while heterozygotes predominated in Berkshire, Chester White, Durocs, Hampshire and Landrace. Animals homozygous for IgAb were best represented in the White Cross line. We show here that this very strong breed dependency of IgA allotypy in swine can produce a sample bias that can explain why only two b/b homozygotes (1.3%) were found in the 160 randomly-selected samples since the original samples came from primarily Landrace and Yorkshire animals. The expected frequency of b/b homozygotes in these breeds would be \u3c3%. Thus, the data presented here reject the hypothesis that swine homozygous for a trait that results in loss of two-thirds of the IgA hinge, are selected against and that heterozygotes are positively selected. Rather, the study shows that IgAa and IgAb appear to be simple, breed-dependent allotypic markers
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