87,080 research outputs found
Sad-Loser Lottery
No full textWe consider lotteries with reimbursements. It turns out that without loss of generality it is enough analyze lotteries where the winner gets her expenses reimbursed. We find that such a lottery (Sad-Loser) has multiple pure-strategy equilibria. We describe all equilibria and discuss their properties. In particular, we find (1) a sufficient condition for the net total spending to be higher in the Sad-Loser lottery than in the standard lottery, (2) that the Exclusion Principle holds.
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Identifying a common cause of the loser cell status in Drosophila melanogaster.
No full textCell competition is the process whereby less fit cells termed “losers” are selectively eliminated from a tissue by their fitter neighbors – or “ winners.” This sacrifice of aberrant cells is thought to have evolved at the advent of multicellularity to enforce cell co-operativity and ensure the fitness of the host organism. Accumulating evidence over the last 40 years has suggested key roles for cell competition during development, adult tissue homeostasis and at the onset and during the progression of diseases including cancer. However, if we are to exploit competition in the treatment of human pathologies and in tissue regeneration, we still have a lot to learn about the underlying mechanisms that ultimately instruct the elimination of loser cells.
The main goal of this work was to identify the key molecular events that are responsible for initiating the loser status of Minute heterozygous cells. As many Minute mutations affect ribosomal genes, it has long been assumed that the loser status is closely linked to their associated slow growth phenotype, which occurs a consequence of reduced protein synthesis. Surprisingly, I have found that the loser status is independent of rates of translation. Instead, the activity of a single transcription factor, Nrf2, that typically co-ordinates an oxidative stress response, is sufficient to instruct the elimination of cells by their neighbors. Given the importance of Nrf2, I have sought to identify events occurring both upstream and downstream of the pathway in the loser context. Here, I have shown how multiple loser cell types are suffering from an underlying proteotoxic stress, as a result of an imbalance in proteostasis and their accumulation of toxic protein aggregates. In addition, I have developed a screening strategy to identify key molecules downstream of Nrf2 that could be involved in loser cell recognition. These findings not only provide new insights into the mechanisms of cell competition, but broaden the implications of the process to age-related diseases including those that result in neurodegeneration
Heterozygosity at Gr64 loci exacerbates competitive <i>RpS3</i><sup><i>+/-</i></sup> loser cell elimination.
No full text(A–G) Representative images of wing discs containing RpS3+/- loser cells (green) competing against wild-type winners (unlabelled) and stained for cleaved-Dcp1 (red). RpS3+/- clones were generated in a wild-type background (A) or in wing discs heterozygous for any one of the Gr64 genes a through f (mutations used were Gr64aGAL4, Gr64bLEXA, Gr64cLEXA, Gr64d1, Gr64eLEXA, and Gr64fLEXA) (B–G). (H) Quantification of the percentage of cells undergoing apoptosis at loser clone borders in wing discs of genotypes as shown in (A–G). Statistics reflect multiple logistic regression across 3 replicates (details provided in Materials and methods). (I) Quantification of loser cell growth in wing discs of the genotypes shown in (A–G), as measured by the percent loser clone coverage of the pouch. Statistics reflect Student t test with FDR p-correction. ncontrol = 16, nGr64aGAL4 = 15, nGr64bLEXA = 15, nGr64cLEXA = 11, nGr64d[1] = 12, nGr64eLEXA = 9, nGr64fLEXA = 8. For all quantifications, the horizontal line indicates the mean. Scale bars correspond to 50 μm. Numerical data can be found in the “Fig 2” sheet of S1 Data. FDR, false discovery rate; Gr64, Gustatory Receptor 64; Rp, ribosome protein.</p
Variations on the Author
No full text“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Live imaging of the GSC niche following transplantation of fluorescently labeled winner and loser GSCs.
No full textGSCs from each winner and loser pair were isolated by FACS and labeled with cell tracker dyes (winner GSCs (WG, labeled green); loser GSCs (LG, labeled red)) and co-injected into a subclone of the loser genotype. 24 h later the newly developing GSC niche was imaged (A-I). The dotted white line is superimposed on the epidermis, the evagination is the newly developing zooid, and the niche is between the white line and the developing zooid viscera (see S1 Fig). Representative images of the three types of phenotypes observed in this experiment are shown (A-C; D-F; G-I), and described in detail in the text. Superimposed images of light and both fluorescent channels are shown in panels A, D, and G. J. Labeled cells were observed in ca. 70% of the GSC niches visualized, shown is the quantification of the number of winner vs loser GSCs observed (n = 9). Winner GSCs had a slight advantage versus loser GSCs (1.9X; p<0.02).</p
Proteotoxic stress is a driver of the loser status and of cell competition
No full textCell competition allows winner cells to eliminate less fit loser cells in tissues. In Minute cell competition, cells with a heterozygous mutation in ribosome genes, such as RpS3+/− cells, are eliminated by wild-type cells. How cells are primed as losers is partially understood and it has been proposed that reduced translation underpins the loser status of ribosome mutant, or Minute, cells. Here, using Drosophila, we show that reduced translation does not cause cell competition. Instead, we identify proteotoxic stress as the underlying cause of the loser status for Minute competition and competition induced by mahjong, an unrelated loser gene. RpS3+/− cells exhibit reduced autophagic and proteasomal flux, accumulate protein aggregates and can be rescued from competition by improving their proteostasis. Conversely, inducing proteotoxic stress is sufficient to turn otherwise wild-type cells into losers. Thus, we propose that tissues may preserve their health through a proteostasis-based mechanism of cell competition and cell selection
Field-induced delocalization and Zener breakdown in semiconductor superlattices
No full textWe investigate the energy spectrum and the electron dynamics of a band in a semiconductor superlattice as a function of the electric field. Linear optical spectroscopy shows that, for high fields, the well-known localization of the Bloch states is followed by a field-induced delocalization, associated with Zener breakdown. Using time-resolved measurements, we observe Bloch oscillations in a regime where they are damped by Zener breakdown
Why do winners keep winning? Androgen mediation of winner but not loser effects in cichlid fish
No full textAnimal conflicts are influenced by social experience such that a previous winning experience increases the probability of winning the next agonistic interaction, whereas a previous losing experience has the opposite effect. Since androgens respond to social interactions, increasing in winners and decreasing in losers, we hypothesized that socially induced transient changes in androgen levels could be a causal mediator of
winner/loser effects. To test this hypothesis, we staged fights between dyads of size-matched males of the Mozambique tilapia (Oreochromis mossambicus). After the first contest, winners were treated with the antiandrogen cyproterone acetate and losers were supplemented with 11-ketotestosterone. Two hours after the end of the first fight, two contests were staged simultaneously between the winner of the first fight and a
naive male and between the loser of first fight and another naive male. The majority (88%) of control winners also won the second interaction, whereas the majority of control losers (87%) lost their second fight, thus confirming the presence of winner/loser effects in this species. As predicted, the success of anti-androgen-treated winners in the second fight decreased significantly to chance levels (44%), but the success of androgenized losers (19%) did not show a significant increase. In summary, the treatment with anti-androgen blocks the winner effect, whereas androgen administration fails to reverse the loser effect, suggesting an involvement of androgens on the winner but not on the loser effect
An investigation of anomalies at Istanbul Securities Exchange : winner-loser effect
No full textCataloged from PDF version of article.Includes bibliographical references (leaves 27-28).In this study , the presence of winner -1 oser effect
in Istanbul Stock Exchange is investigated. Tests are
done for the period of January .1988 - December 1992.
Past performance is used to form the " Winner " and
"Loser" portfolios pri or to the lest period. Duration for past performance measure ments change from 1 month to 48 months.Test periods change from 3 months to 36 months.
The results show that, in the first month of the
test period, loser portfolio outperforms the winner
p o r t f o l i o . This ef f ect is e m p h a s i z e d if the first mont h
of the lest period is January.
The above results carry similarities with the
empirical results obtained from slock markets of USA
and Japan.Sayın, Gürka
Xrp1 and Irbp18 trigger a feed-forward loop of proteotoxic stress to induce the loser status
No full textCell competition induces the elimination of less-fit “loser” cells by fitter “winner” cells. In Drosophila, cells heterozygous mutant in ribosome genes, Rp/+, known as Minutes, are outcompeted by wild-type cells. Rp/+ cells display proteotoxic stress and the oxidative stress response, which drive the loser status. Minute cell competition also requires the transcription factors Irbp18 and Xrp1, but how these contribute to the loser status is partially understood. Here we provide evidence that initial proteotoxic stress in RpS3/+ cells is Xrp1-independent. However, Xrp1 is sufficient to induce proteotoxic stress in otherwise wild-type cells and is necessary for the high levels of proteotoxic stress found in RpS3/+ cells. Surprisingly, Xrp1 is also induced downstream of proteotoxic stress, and is required for the competitive elimination of cells suffering from proteotoxic stress or overexpressing Nrf2. Our data suggests that a feed-forward loop between Xrp1, proteotoxic stress, and Nrf2 drives Minute cells to become losers
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