Modelling the evolution of distributions : an application to major league baseball

We develop Bayesian techniques for modelling the evolution of entire distributions over time and apply them to the distribution of team performance in Major League baseball for the period 1901-2000. Such models offer insight into many key issues (e.g. competitive balance) in a way that regression-based models cannot. The models involve discretizing the distribution and then modelling the evolution of the bins over time through transition probability matrices. We allow for these matrices to vary over time and across teams. We find that, with one exception, the transition probability matrices (and, hence, competitive balance) have been remarkably constant across time and over teams. The one exception is the Yankees, who have outperformed all other teams

Social reinforcement learning as a predictor of real-life experiences in individuals with high and low depressive symptomatology

Background: Several studies have reported diminished learning from non-social outcomes in depressed individuals. However, it is not clear how depression impacts learning from social feedback. Notably, mood disorders are commonly associated with deficits in social functioning, which raises the possibility that potential impairments in social learning may negatively affect real-life social experiences in depressed subjects. Methods: Ninety-two participants with high (HD; N=40) and low (LD; N=52) depression scores were recruited. Subjects performed a learning task, during which they received monetary outcomes or social feedback which they were told came from other people. Additionally, participants answered questions about their everyday social experiences. Computational models were fit to the data and model parameters were related to social experience measures. Results: HD subjects reported a reduced quality and quantity of social experiences compared to LD controls, including an increase in the amount of time spent in negative social situations. Moreover, HD participants showed lower learning rates than LD subjects in the social condition of the task. Interestingly, across all participants, reduced social learning rates predicted higher amounts of time spent in negative social situations, even when depression scores were controlled for. Conclusion: These findings indicate that deficits in social learning may affect the quality of everyday social experiences. Specifically, the impaired ability to use social feedback to appropriately update future actions, which was observed in HD subjects, may lead to suboptimal interpersonal behavior in real life. This, in turn, may evoke negative feedback from others, thus bringing about more unpleasant social encounters

Universal cloning of continuous quantum variables

The cloning of quantum variables with continuous spectra is analyzed. A universal - or Gaussian - quantum cloning machine is exhibited that copies equally well the states of two conjugate variables such as position and momentum. It also duplicates all coherent states with a fidelity of 2/3. More generally, the copies are shown to obey a no-cloning Heisenberg-like uncertainty relation.Comment: 4 pages, RevTex. Minor revisions, added explicit cloning transformation, added reference

Blunted neural response to anticipation, effort and consummation of reward and aversion in adolescents with depression symptomatology

Neural reward function has been proposed as a possible biomarker for depression. However how the neural response to reward and aversion might differ in young adolescents with current symptoms of depression is as yet unclear. 33 adolescents were recruited. 17 scoring low on the Mood and Feelings Questionnaire (MFQ) (Low Risk: LR) and 16 scoring high on the MFQ (High Risk: HR). Our fMRI task measured; anticipation (pleasant/unpleasant cue), effort (achieve a pleasant taste or avoid an unpleasant taste) and consummation (pleasant/unpleasant tastes) in Regions of Interest; ventral medial prefrontal cortex (vmPFC), pregenual cingulate cortex (pgACC), the insula and ventral striatum. We also examined whole brain group differences. In the ROI analysis we found reduced activity in the HR group in the pgACC during anticipation and reduced pgACC and vmPFC during effort and consummation. In the whole brain analysis we also found reduced activity in the HR group in the prefrontal cortex and the precuneus during anticipation. We found reduced activity in the hippocampus during the effort phase and in the anterior cingulate/frontal pole during consummation in the HR group. Increased anhedonia measures correlated with decreased pgACC activity during consummation in the HR group only. Our results are the first to show that adolescents with depression symptoms have blunted neural responses during the anticipation, effort and consummation of rewarding and aversive stimuli. This study suggests that interventions in young people at risk of depression, that can reverse blunted responses, might be beneficial as preventative strategies

From carewashing to radical care: the discursive explosions of care during Covid-19

Care, in all its permutations, is the buzzword of the moment, its meanings draining away in its constant evocation. Here, we briefly expand on older and newer meanings of care in the wake of Covid-19. These include the increasingly blurred boundaries between what has been traditionally understood as “care work” versus “essential work”; desperate attempts by corporations to promote themselves as ‘caring’; and the adoption of reactionary rather than progressive models of ‘care’ by populist leaders such as Trump, Johnson, and Bolsonaro. We then argue that we are in urgent need of a politics that recognises our mutual interdependence and vulnerability. Rejecting the extensive carelessness so evident today, our model of ‘universal care’ calls for inventive forms of collective care at every scale of life. We envisage a world in which genuine care is everywhere —from our most intimate ties to our relationship with the planet itself

The effect of induced sadness and moderate depression on attention networks

This study investigates how sadness and minor/moderate depression influences the three functions of attention: alerting, orienting, and executive control using the attention network test. The aim of the study is to investigate whether minor to moderate depression is more similar to sadness or clinical depression with regards to attentional processing. It was predicted that both induced sadness and minor to moderate depression will influence executive control by narrowing spatial attention and in turn this will lead to less interference from the flanker items (i.e., less effects of congruency) due to a focused attentional state. No differences were predicted for alerting or orienting functions. The results from the two experiments, the first inducing sadness (Experiment 1) and the second measuring subclinical depression (Experiment 2), show that, as expected, participants who are sad or minor to moderately depressed showed less flanker interference compared to participants who were neither sad nor depressed. This study provides strong evidence, that irrespective of its aetiology, sadness and minor/moderate depression have similar effects on spatial attention

Emergence of Anti-Cancer Drug Resistance: Exploring the Importance of the Microenvironmental Niche via a Spatial Model

Practically, all chemotherapeutic agents lead to drug resistance. Clinically, it is a challenge to determine whether resistance arises prior to, or as a result of, cancer therapy. Further, a number of different intracellular and microenvironmental factors have been correlated with the emergence of drug resistance. With the goal of better understanding drug resistance and its connection with the tumor microenvironment, we have developed a hybrid discrete-continuous mathematical model. In this model, cancer cells described through a particle-spring approach respond to dynamically changing oxygen and DNA damaging drug concentrations described through partial differential equations. We thoroughly explored the behavior of our self-calibrated model under the following common conditions: a fixed layout of the vasculature, an identical initial configuration of cancer cells, the same mechanism of drug action, and one mechanism of cellular response to the drug. We considered one set of simulations in which drug resistance existed prior to the start of treatment, and another set in which drug resistance is acquired in response to treatment. This allows us to compare how both kinds of resistance influence the spatial and temporal dynamics of the developing tumor, and its clonal diversity. We show that both pre-existing and acquired resistance can give rise to three biologically distinct parameter regimes: successful tumor eradication, reduced effectiveness of drug during the course of treatment (resistance), and complete treatment failure

The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity

53BP1 controls a specialized non-homologous end joining (NHEJ) pathway that is essential for adaptive immunity, yet oncogenic in BRCA1 mutant cancers. Intra-chromosomal DNA double-strand break (DSB) joining events during immunoglobulin class switch recombination (CSR) require 53BP1. However, in BRCA1 mutant cells, 53BP1 blocks homologous recombination (HR) and promotes toxic NHEJ, resulting in genomic instability. Here, we identify the protein dimerization hub—DYNLL1—as an organizer of multimeric 53BP1 complexes. DYNLL1 binding stimulates 53BP1 oligomerization, and promotes 53BP1’s recruitment to, and interaction with, DSB-associated chromatin. Consequently, DYNLL1 regulates 53BP1-dependent NHEJ: CSR is compromised upon deletion of Dynll1 or its transcriptional regulator Asciz, or by mutation of DYNLL1 binding motifs in 53BP1; furthermore, Brca1 mutant cells and tumours are rendered resistant to poly-ADP ribose polymerase (PARP) inhibitor treatments upon deletion of Dynll1 or Asciz. Thus, our results reveal a mechanism that regulates 53BP1-dependent NHEJ and the therapeutic response of BRCA1-deficient cancers