Effect of contrast on the perception of direction of a moving pattern

A series of experiments examining the effect of contrast on the perception of moving plaids was performed to test the hypothesis that the human visual system determines the direction of a moving plaid in a two-staged process: decomposition into component motion followed by application of the intersection-of-contraints rule. Although there is recent evidence that the first tenet of the hypothesis is correct, i.e., that plaid motion is initially decomposed into the motion of the individual grating components, the nature of the second-stage combination rule has not yet been established. It was found that when the gratings within the plaid are of different contrast the preceived direction is not predicted by the intersection-of-constraints rule. There is a strong (up to 20 deg) bias in the direction of the higher-constrast grating. A revised model, which incorporates a contrast-dependent weighting of perceived grating speed as observed for one-dimensional patterns, can quantitatively predict most of the results. The results are then discussed in the context of various models of human visual motion processing and of physiological responses of neurons in the primate visual system

Gravity Duals of Lifshitz-like Fixed Points

We find candidate macroscopic gravity duals for scale-invariant but non-Lorentz invariant fixed points, which do not have particle number as a conserved quantity. We compute two-point correlation functions which exhibit novel behavior relative to their AdS counterparts, and find holographic renormalization group flows to conformal field theories. Our theories are characterized by a dynamical critical exponent $z$, which governs the anisotropy between spatial and temporal scaling $t \to \lambda^z t$, $x \to \lambda x$; we focus on the case with $z=2$. Such theories describe multicritical points in certain magnetic materials and liquid crystals, and have been shown to arise at quantum critical points in toy models of the cuprate superconductors. This work can be considered a small step towards making useful dual descriptions of such critical points.Comment: 17 pages, harvmac; v2 comments about behavior of metric near r=0 added (thanks to S. Hartnoll and G. Horowitz

Alternative splicing of beta-tropomyosin pre-mRNA: cis-acting elements and cellular factors that block the use of a skeletal muscle exon in nonmuscle cells

The rat beta-tropomyosin (beta-TM) gene encodes both skeletal muscle beta-TM and fibroblast TM-1 by an alternative RNA-splicing mechanism. This gene contains 11 exons. Exons 1-5, 8, and 9 are common to all mRNAs expressed from the gene. Exons 6 and 11 are used in fibroblasts as well as smooth muscle cells, whereas exons 7 and 10 are used in skeletal muscle cells. In this study we have carried out an extensive mutational analysis to identify cis-acting elements that block the use of the skeletal muscle-specific exon 7 in nonmuscle cells. These studies localize the critical elements for regulated alternative splicing to sequences within exon 7 and the adjacent upstream intron. In addition, mutations that inactivate the 5'- or 3'-splice sites of exon 6 do not result in the use of the skeletal muscle-specific exon 7 in nonmuscle cells, suggesting that splice-site selection in vivo is not regulated by a simple cis-acting competition mechanism but, rather, by a mechanism that inhibits the use of exon 7 in certain cellular environments. In support of this hypothesis we have identified sequence-specific RNA-binding proteins in HeLa cell nuclear extracts using native gel electrophoresis and binding competition assays. Mutations in the pre-mRNA that result in the use of the skeletal muscle exon in vivo also disrupt the binding of these proteins to the RNA in vitro. We propose that the binding of these proteins to the pre-mRNA is involved in regulated alternative splicing and that this interaction is required for blocking the use of the skeletal muscle exon in nonmuscle cells

Phagocytes and the Lung

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72927/1/j.1749-6632.1997.tb46258.x.pd

Heart and Lung Transplantation in the United States, 1996–2005

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74833/1/j.1600-6143.2007.01783.x.pd

Being on the Juvenile Dermatomyositis Rollercoaster: a qualitative study

Objectives: Juvenile Dermatomyositis is a rare, potentially life-threatening condition with no known cure. There is no published literature capturinghow children and young people feel about their condition, from their perspective. This study was therefore unique in that it asked children and young people what is it like to live with Juvenile Dermatomyositis. Methods: Data wereobtained from fifteen young people with Juvenile Dermatomyositis, between eightand nineteen years of age from one Paediatric Rheumatology department using audio-recordedinterpretive phenomenology interviews. Data were analyzed phenomenologically, using a process that derives narratives from transcripts resulting in a collective composite of participants shared experiences, called a‘phenomenon’. Results:The overarching metaphor of a rollercoaster captures the phenomenon of living withJuvenile Dermatomyositisas a young person, with the ups and downs at different time points clearly described by those interviewed. The five themes plotted on the rollercoaster, began with confusion; followed by feeling different, being sick, steroidal and scared from the medications; uncertainty; and then ended with acceptance of the disease over time. Conclusion: Young people were able to talk about their experiences about having Juvenile Dermatomyositis. Our findings will aid clinicians in their practice by gaining a deeper understanding of what daily life is like and highlighting ways to enhance psychosocial functioning. Hopefully, this study and any further resulting studies,will raise understanding of Juvenile Dermatomyositis worldwide and will encourage health care professionals to better assess psychosocial needs in the future

Cardiorespiratory Fitness and Cancer in Women

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Heart and Lung Transplantation in the United States, 1997–2006

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73552/1/j.1600-6143.2008.02175.x.pd

Identification of two distinct intron elements involved in alternative splicing of beta-tropomyosin pre-mRNA

The rat beta-tropomyosin gene encodes two isoforms, termed skeletal muscle beta-tropomyosin and fibroblast last tropomyosim 1 (TM-1), via an alternative RNA processing mechanism. The gene contains 11 exons. Exons 1-5 and exons 8 and 9 are common to all mRNAs expressed from the gene. Exons 6 and 11 are used in fibroblasts, as well as smooth muscle, whereas exons 7 and 10 are used only in skeletal muscle. In the present studies we focused on the mutually exclusive internal alternative splice choice involving exon 6 (fibroblast-type splice) and exon 7 (skeletal muscle-type splice). We have identified two distinct elements in the intron, upstream of exon 7, involved in splice site selection. The first element is comprised of a polypyrimidine tract located 89-143 nucleotides upstream of the 3' splice site, which specifies the location of the lariat branchpoints used, 144-153 nucleotides upstream of exon 7. The 3' splice site AG dinucleotide has no role in selection of these branchpoints. The second element is comprised of intron sequences located between the polypyrimidine tract and the 3' splice site of exon 7. It contains an important determinant in alternative splice site selection, because deletion of these sequences results in the use of the skeletal muscle-specific exon in nonmuscle cells. We propose that the use of lariat branchpoints located far upstream from a 3' splice site may be a general feature of some alternatively excised introns, reflecting the presence of regulatory sequences located between the lariat branch site and the 3' splice site. The data also indicate that alternative splicing of the rat beta-tropomyosin gene is regulated by a somewhat different mechanism from that described for rat alpha-tropomyosin gene and the transformer-2 gene of Drosophila melanogaster