983 resultados para Not ludic way of playing


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Full activation of T cells requires signaling through the T-cell antigen receptor (TCR) and additional surface molecules interacting with ligands on the antigen-presenting cell. TCR recognition of agonist ligands in the absence of accessory signals frequently results in the induction of a state of unresponsiveness termed anergy. However, even in the presence of costimulation, anergy can be induced by TCR partial agonists. The unique pattern of early receptor-induced tyrosine phosphorylation events induced by partial agonists has led to the hypothesis that altered TCR signaling is directly responsible for the development of anergy. Here we show that anergy induction is neither correlated with nor irreversibly determined by the pattern of early TCR-induced phosphorylation. Rather, it appears to result from the absence of downstream events related to interleukin 2 receptor occupancy and/or cell division. This implies that the anergic state can be manipulated independently of the precise pattern of early biochemical changes following TCR occupancy, a finding with implications for understanding the induction of self-tolerance and the use of partial agonist ligands in the treatment of autoimmune diseases.

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Current theories of sexual differentiation maintain that ovarian estrogen prevents masculine development of the copulatory system in birds, whereas estrogen derived from testicular androgens promotes masculine sexual differentiation of neuroanatomy and sexual behavior in mammals. Paradoxically, some data suggest that the neural song system in zebra finches follows the mammalian pattern with estrogenic metabolites of testicular secretions causing masculine development. To test whether the removal of estrogen from males during early development would prevent the development of masculine song systems, zebra finches were treated embryonically with an inhibitor of estrogen synthesis. In addition, this treatment in genetic female zebra finches induced both functional ovarian and testicular tissue to develop, thus allowing the assessment of the direct effects of testicular secretions on song system development. In males, the inhibition of estrogen synthesis before hatching had a small but significant effect in demasculinizing one aspect of the neural song system. In treated females, the song systems remained morphologically feminine. These results suggest that masculinization of the song system is not determined solely by testicular androgens or their estrogenic metabolites.

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A constitutively active fragment of rat MEK kinase 1 (MEKK1) consisting of only its catalytic domain (MEKK-C) expressed in bacteria quantitatively activates recombinant mitogen-activated protein (MAP) kinase/extracellular signal-regulated protein kinase (ERK) kinases 1 and 2 (MEK1 and MEK2) in vitro. Activation of MEK1 by MEKK-C is accompanied by phosphorylation of S218 and S222, which are also phosphorylated by the protein kinases c-Mos and Raf-1. MEKK1 has been implicated in regulation of a parallel but distinct cascade that leads to phosphorylation of N-terminal sites on c-Jun; thus, its role in the MAP kinase pathway has been questioned. However, in addition to its capacity to phosphorylate MEK1 in vitro, MEKK-C interacts with MEK1 in the two-hybrid system, and expression of mouse MEKK1 or MEKK-C in mammalian cells causes constitutive activation of both MEK1 and MEK2. Neither cotransfected nor endogenous ERK2 is highly activated by MEKK1 compared to its stimulation by epidermal growth factor in spite of significant activation of endogenous MEK. Thus, other as yet undefined mechanisms may be involved in determining information flow through the MAP kinase and related pathways.

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It has previously been shown that mRNA encoding the arginine vasopressin (AVP) precursor is targeted to axons of rat magnocellular neurons of the hypothalamo-neurohypophyseal tract. In the homozygous Brattle-boro rat, which has a G nucleotide deletion in the coding region of the AVP gene, no such targeting is observed although the gene is transcribed. RNase protection and heteroduplex analyses demonstrate that, in heterozygous animals, which express both alleles of the AVP gene, the wild-type but not the mutant transcript is subject to axonal compartmentation. In contrast, wild-type and mutant AVP mRNAs are present in dendrites. These data suggest the existence of different mechanisms for mRNA targeting to the two subcellular compartments. Axonal mRNA localization appears to take place after protein synthesis; the mutant transcript is not available for axonal targeting because it lacks a stop codon preventing its release from ribosomes. Dendritic compartmentation, on the other hand, is likely to precede translation and, thus, would be unable to discriminate between the two mRNAs.

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The missense mutation Lys-296-->Glu (K296E) in the rhodopsin gene produces an opsin with no chromophore binding site and therefore is not activated by light. Nevertheless, the mutant opsin constitutively activates transducin in vitro and causes photoreceptor degeneration in vivo, possibly by continuously activating the phototransduction cascade, analogous to constant exposure to environmental light. We studied the K296E mutation in eight lines of transgenic mice. Each line developed photoreceptor degeneration with the rate of degeneration increasing monotonically as the ratio of mutant:wild-type opsin mRNA increased. At no time in the course of degeneration was there endogenous light adaptation in the retina as measured by the electroretinogram. The mutant opsin was found to be invariably phosphorylated and stably bound to arrestin. Light-independent activation of transducin was demonstrated only after the removal of arrestin and dephosphorylation of K296E opsin. Thus, K296E opsin in vivo does not activate the phototransduction cascade because it is shut off by photoreceptor inactivation mechanisms. Our data show that the K296E mutation does not cause photoreceptor degeneration by continuous activation of phototransduction.

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Research on the psychological impact of women's fashion has focused on fashion's negative influence over how women think and feel about themselves. Several studies have examined the relationship between fashion and women's self-appraisals (Martin & Gentry, 1997; Pinhas, Toner, Ali, Garfinkel, & Stuckless, 1999; Tiggemann, Polivy, & Hargreaves, 2009), although few investigations have explored the range of viewpoints that arise when women interact with their own personal style or with other forms of fashion media. This paper presents a narrative review of what has been written about fashion in clinical research. I briefly discuss why this is an important topic and why fashion has psychological meaning. Cognitive behavioral therapy (CBT) is considered in the exploration of fashion's impact on conjuring unproductive and productive schemas (Beck, 1976; Wright, Basco, & Thase, 2006). This discussion includes a presentation of interviews with female consultants, hypothetical examples, my own accounts, and feminist perspectives. While emphasizing the potential biases of women's interactions with fashion, I discuss matters of gender performance and reflections on clinical work. The purpose of this article is to present a pro-social defense of fashion. I do this by acquiring personal chronicles, applying those findings to the current body of research, and adding to the continued investigation of why women's fashion is still important in a postfeminist world.

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v. 1. Ad astra. The skaith of Guillardun. Amy Robsart. Nature Poems, Love poems. Sacred poems. Lyrics from three dramas. Historical and political poems. Miscellaneous poems.--v.2 David and Bathshua. Donna Marina. Undine.

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Mode of access: Internet.