4,802 research outputs found

    Early Retirement and Inequality in Britain and Germany: How Important Is Health?

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    Both health and income inequalities have been shown to be much greater in Britain than in Germany. One of the main reasons seems to be the difference in the relative position of the retired, who, in Britain, are much more concentrated in the lower income groups. Inequality analysis reveals that while the distribution of health shocks is more concentrated among those on low incomes in Britain, early retirement is more concentrated among those on high incomes. In contrast, in Germany, both health shocks and early retirement are more concentrated among those with low incomes. We use comparable longitudinal data sets from Britain and Germany to estimate hazard models of the effect of health on early retirement. The hazard models show that health is a key determinant of the retirement hazard for both men and women in Britain and Germany. The size of the health effect appears large compared to the other variables. Designing financial incentives to encourage people to work for longer may not be sufficient as a policy tool if people are leaving the labour market involuntarily due to health problems.health, early retirement, hazard models

    Canard-like phenomena in piecewise-smooth Van der Pol systems

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    We show that a nonlinear, piecewise-smooth, planar dynamical system can exhibit canard phenomena. Canard solutions and explosion in nonlinear, piecewise-smooth systems can be qualitatively more similar to the phenomena in smooth systems than piecewise-linear systems, since the nonlinearity allows for canards to transition from small cycles to canards ``with heads." The canards are born of a bifurcation that occurs as the slow-nullcline coincides with the splitting manifold. However, there are conditions under which this bifurcation leads to a phenomenon called super-explosion, the instantaneous transition from a globally attracting periodic orbit to relaxations oscillations. Also, we demonstrate that the bifurcation---whether leading to canards or super-explosion---can be subcritical.Comment: 17 pages, 11 figure

    Statistical Models of Reconstructed Phase Spaces for Signal Classification

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    This paper introduces a novel approach to the analysis and classification of time series signals using statistical models of reconstructed phase spaces. With sufficient dimension, such reconstructed phase spaces are, with probability one, guaranteed to be topologically equivalent to the state dynamics of the generating system, and, therefore, may contain information that is absent in analysis and classification methods rooted in linear assumptions. Parametric and nonparametric distributions are introduced as statistical representations over the multidimensional reconstructed phase space, with classification accomplished through methods such as Bayes maximum likelihood and artificial neural networks (ANNs). The technique is demonstrated on heart arrhythmia classification and speech recognition. This new approach is shown to be a viable and effective alternative to traditional signal classification approaches, particularly for signals with strong nonlinear characteristics

    Wind tunnel balance

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    A flow-through balance is provided which includes a non-metric portion and a metric portion which form a fluid-conducting passage in fluid communication with an internal bore in the sting. The non-metric and metric portions of the balance are integrally connected together by a plurality of flexure beams such that the non-metric portion, the metric portion and the flexure beams form a one-piece construction which eliminates mechanical hysteresis between the non-metric and the metric portion. The system includes structures for preventing the effects of temperature, pressure and pressurized fluid from producing asymmetric loads on the flexure beams. A temperature sensor and a pressure sensor are located within the fluid-conducting passage of the balance. The system includes a longitudinal bellows member connected at two ends to one of the non-metric portion and the metric portion and at an intermediate portion thereof to the other of (1) and (2). A plurality of strain gages are mounted on the flexure beams to measure strain forces on the flexure beams. The flexure beams are disposed so as to enable symmetric forces on the flexure beams to cancel out so that only asymmetric forces are measured as deviations by the strain gages

    Effects of Flight on Gene Expression and Aging in the Honey Bee Brain and Flight Muscle

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    Honey bees move through a series of in-hive tasks (e.g., “nursing”) to outside tasks (e.g., “foraging”) that are coincident with physiological changes and higher levels of metabolic activity. Social context can cause worker bees to speed up or slow down this process, and foragers may revert back to their earlier in-hive tasks accompanied by reversion to earlier physiological states. To investigate the effects of flight, behavioral state and age on gene expression, we used whole-genome microarrays and real-time PCR. Brain tissue and flight muscle exhibited different patterns of expression during behavioral transitions, with expression patterns in the brain reflecting both age and behavior, and expression patterns in flight muscle being primarily determined by age. Our data suggest that the transition from behaviors requiring little to no flight (nursing) to those requiring prolonged flight bouts (foraging), rather than the amount of previous flight per se, has a major effect on gene expression. Following behavioral reversion there was a partial reversion in gene expression but some aspects of forager expression patterns, such as those for genes involved in immune function, remained. Combined with our real-time PCR data, these data suggest an epigenetic control and energy balance role in honey bee functional senescence

    Palmitoylation of Desmoglein 2 Is a Regulator of Assembly Dynamics and Protein Turnover.

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    Desmosomes are prominent adhesive junctions present between many epithelial cells as well as cardiomyocytes. The mechanisms controlling desmosome assembly and remodeling in epithelial and cardiac tissue are poorly understood. We recently identified protein palmitoylation as a mechanism regulating desmosome dynamics. In this study, we have focused on the palmitoylation of the desmosomal cadherin desmoglein-2 (Dsg2) and characterized the role that palmitoylation of Dsg2 plays in its localization and stability in cultured cells. We identified two cysteine residues in the juxtamembrane (intracellular anchor) domain of Dsg2 that, when mutated, eliminate its palmitoylation. These cysteine residues are conserved in all four desmoglein family members. Although mutant Dsg2 localizes to endogenous desmosomes, there is a significant delay in its incorporation into junctions, and the mutant is also present in a cytoplasmic pool. Triton X-100 solubility assays demonstrate that mutant Dsg2 is more soluble than wild-type protein. Interestingly, trafficking of the mutant Dsg2 to the cell surface was delayed, and a pool of the non-palmitoylated Dsg2 co-localized with lysosomal markers. Taken together, these data suggest that palmitoylation of Dsg2 regulates protein transport to the plasma membrane. Modulation of the palmitoylation status of desmosomal cadherins can affect desmosome dynamics

    Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia

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    BACKGROUND: Evidence from cachectic cancer patients and animal models of cancer cachexia supports the involvement of Forkhead box O (FoxO) transcription factors in driving cancer-induced skeletal muscle wasting. However, the genome-wide gene networks and associated biological processes regulated by FoxO during cancer cachexia are unknown. We hypothesize that FoxO is a central upstream regulator of diverse gene networks in skeletal muscle during cancer that may act coordinately to promote the wasting phenotype. METHODS: To inhibit endogenous FoxO DNA-binding, we transduced limb and diaphragm muscles of mice with AAV9 containing the cDNA for a dominant negative (d.n.) FoxO protein (or GFP control). The d.n.FoxO construct consists of only the FoxO3a DNA-binding domain that is highly homologous to that of FoxO1 and FoxO4, and which outcompetes and blocks endogenous FoxO DNA binding. Mice were subsequently inoculated with Colon-26 (C26) cells and muscles harvested 26 days later. RESULTS: Blocking FoxO prevented C26-induced muscle fiber atrophy of both locomotor muscles and the diaphragm and significantly spared force deficits. This sparing of muscle size and function was associated with the differential regulation of 543 transcripts (out of 2,093) which changed in response to C26. Bioinformatics analysis of upregulated gene transcripts that required FoxO revealed enrichment of the proteasome, AP-1 and IL-6 pathways, and included several atrophy-related transcription factors, including Stat3, Fos, and Cebpb. FoxO was also necessary for the cancer-induced downregulation of several gene transcripts that were enriched for extracellular matrix and sarcomere protein-encoding genes. We validated these findings in limb muscles and the diaphragm through qRT-PCR, and further demonstrate that FoxO1 and/or FoxO3a are sufficient to increase Stat3, Fos, Cebpb, and the C/EBPβ target gene, Ubr2. Analysis of the Cebpb proximal promoter revealed two bona fide FoxO binding elements, which we further establish are necessary for Cebpb promoter activation in response to IL-6, a predominant cytokine in the C26 cancer model. CONCLUSIONS: These findings provide new evidence that FoxO-dependent transcription is a central node controlling diverse gene networks in skeletal muscle during cancer cachexia, and identifies novel candidate genes and networks for further investigation as causative factors in cancer-induced wasting.R01 AR060217 - NIAMS NIH HHS; R01 AR060209 - NIAMS NIH HHS; T32 HD043730 - NICHD NIH HHS; R00 HL098453 - NHLBI NIH HHS; R00HL098453 - NHLBI NIH HHS; R01AR060209 - NIAMS NIH HHS; R01AR060217 - NIAMS NIH HH

    The genome and proteome of coliphage T1

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    AbstractThe genome of enterobacterial phage T1 has been sequenced, revealing that its 50.7-kb terminally redundant, circularly permuted sequence contains 48,836 bp of nonredundant nucleotides. Seventy-seven open reading frames (ORFs) were identified, with a high percentage of small genes located at the termini of the genomes displaying no homology to existing phage or prophage proteins. Of the genes showing homologs (47%), we identified those involved in host DNA degradation (three endonucleases) and T1 replication (DNA helicase, primase, and single-stranded DNA-binding proteins) and recombination (RecE and Erf homologs). While the tail genes showed homology to those from temperate coliphage N15, the capsid biosynthetic genes were unique. Phage proteins were resolved by 2D gel electrophoresis, and mass spectrometry was used to identify several of the spots including the major head, portal, and tail proteins, thus verifying the annotation
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