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Identifying characteristics of individuals at greatest risk for prolonged grief disorder (PGD) can improve its detection and elucidate the etiology of the disorder. The Safe Passage Study, a study of women at high risk for sudden infant death syndrome (SIDS), prospectively examined the psychosocial functioning of women while monitoring their healthy pregnancies. Mothers whose infants died of SIDS were followed in bereavement.
Pre-loss data were collected from 12 000 pregnant mothers and analyzed for their associations with grief symptoms and PGD in 50 mothers whose infants died from SIDS, from 2 to 48 months after their infant's death, focusing on pre-loss risk factors of anxiety, depression, alcohol use, maternal age, the presence of other living children in the home, and previous child loss.
The presence of any four risk factors significantly predicted PGD for 24 months post-loss (p < 0.003); 2–3 risk factors predicted PGD for 12 months (p = 0.02). PGD rates increased in the second post-loss year, converging in all groups to approximately 40% by 3 years. Pre-loss depressive symptoms were significantly associated with PGD. Higher alcohol intake and older maternal age were consistently positively associated with PGD. Predicted risk scores showed good discrimination between PGD and no PGD 6–24 months after loss (C-statistic = 0.83).
A combination of personal risk factors predicted PGD in 2 years of bereavement. There is a convergence of risk groups to high rates at 2–3 years, marked by increased PGD rates in mothers at low risk. The risk factors showed different effects on PGD.
Gamma-ray burst host galaxies are deficient in molecular gas, and show anomalous metal-poor regions close to GRB positions. Using recent Australia Telescope Compact Array (ATCA) Hi observations we show that they have substantial atomic gas reservoirs. This suggests that star formation in these galaxies may be fuelled by recent inflow of metal-poor atomic gas. While this process is debated, it can happen in low-metallicity gas near the onset of star formation because gas cooling (necessary for star formation) is faster than the Hi-to-H2 conversion.
The objective of this study was to compare the emergency department (ED) management and rate of admission of acute decompensated heart failure (ADHF) between two hospitals in Canada and the United States and to compare the outcomes of these patients.
This was a health records review of adults presenting with ADHF to two EDs in Canada and the United States between January 1 and April 30, 2010. Outcome measures were admission to the hospital, myocardial infarction (MI), and death or relapse rates to the ED. Data were analysed using descriptive, univariate and multivariate analyses.
In total, 394 cases were reviewed and 73 were excluded. Comparing 156 Canadian to 165 U.S. patients, respectively, mean age was 76.0 and 75.8 years; male sex was 54.5% and 52.1%. Canadian and U.S. ED treatments were noninvasive ventilation 7.7% v. 12.8% (p=0.13); IV diuretics 77.6% v. 36.0% (p<0.001); IV nitrates 4.5% v. 6.7% (p=0.39). There were significant differences in rate of admission (50.6% v. 95.2%, p<0.001) and length of stay in ED (6.7 v. 3.0 hours, p<0.001). Proportion of Canadian and U.S. patients who died within 30 days of the ED visit was 5.1% v. 9.7% (p=0.12); relapsed to the ED within 30 days was 20.8% v. 17.5% (p=0.5); and had MI within 30 days was 2.0% v. 1.9% (p=1.0).
The U.S. and Canadian centres saw ADHF patients with similar characteristics. Although the U.S. site had almost double the admission rate, the outcomes were similar between the sites, which question the necessity of routine admission for patients with ADHF.
In this paper we consider a class of stochastic processes based on binomial observations of continuous-time, Markovian population models. We derive the conditional probability mass function of the next binomial observation given a set of binomial observations. For this purpose, we first find the conditional probability mass function of the underlying continuous-time Markovian population model, given a set of binomial observations, by exploiting a conditional Bayes' theorem from filtering, and then use the law of total probability to find the former. This result paves the way for further study of the stochastic process introduced by the binomial observations. We utilize our results to show that binomial observations of the simple birth process are non-Markovian.
Prosocial emotions related to self-blame are important in guiding human altruistic decisions. These emotions are elevated in major depressive disorder (MDD), such that MDD has been associated with guilt-driven pathological hyper-altruism. However, the impact of such emotional impairments in MDD on different types of social decision-making is unknown.
In order to address this issue, we investigated different kinds of altruistic behaviour (interpersonal cooperation and fund allocation, altruistic punishment and charitable donation) in 33 healthy subjects, 35 patients in full remission (unmedicated) and 24 currently depressed patients (11 on medication) using behavioural-economical paradigms.
We show a significant main effect of clinical status on altruistic decisions (p = 0.04) and a significant interaction between clinical status and type of altruistic decisions (p = 0.03). More specifically, symptomatic patients defected significantly more in the Prisoner's Dilemma game (p < 0.05) and made significantly lower charitable donations, whether or not these incurred a personal cost (p < 0.05 and p < 0.01, respectively). Currently depressed patients also reported significantly higher guilt elicited by receiving unfair financial offers in the Ultimatum Game (p < 0.05).
Currently depressed individuals were less altruistic in both a charitable donation and an interpersonal cooperation task. Taken together, our results challenge the guilt-driven pathological hyper-altruism hypothesis in depression. There were also differences in both current and remitted patients in the relationship between altruistic behaviour and pathological self-blaming, suggesting an important role for these emotions in moral and social decision-making abnormalities in depression.
Typically, arguments for the neurobiological basis of reading disability/dyslexia are drawn from two large bodies of research – one on the brain and the other on the genome. This chapter first presents a discussion of the literature on the so-called reading brain – the brain as it is engaged in reading and reading-related processes (Wolf, 2007). After this, it turns to the genome, as variability in its structure and function is thought to form the substrate, through the brain and, perhaps, other organs of the human organism (e.g., the liver by means of metabolizing Omega 3 fish oil, as discussed in Lindmark & Clough, 2007), of the neurobiological foundation of reading.
This chapter necessarily makes reference to many technical terms (e.g., specific regions of the brain, biological processes) that are likely to be unfamiliar to the nonspecialist. In order to conform to space restrictions and to maintain narrative coherence and flow, descriptions and definitions of many of these have not been provided. Helpful information about these terms should be readily available both from Internet sources and publications referenced in this chapter.
In order to develop a causal model of RD (reading disability) that can inform intervention, it is necessary to develop a theory at the cognitive level of explanation.… Although some causes of RD have a genetic origin, and environmental factors play an important role, cognition mediates brain-behaviour relationships and at the present time, the cognitive level offers a necessary and sufficient level of explanation for the development of principled interventions. In short, we need to understand the cognitive difficulties that underpin reading problems, regardless of whether their origin is constitutional or environmental.
(Snowling & Hulme, 2011, p. 4)
This chapter examines the evidence concerning the nature and role of a number of cognitive processes that have been proposed as influential in dyslexia/reading disability (i.e., phonological awareness, rapid naming, short-term/working memory, low-level sensory auditory and visual processing, scotopic sensitivity, attentional factors, and motor processing). In each case the implications of the available research evidence for clinical and educational intervention will be considered. As this chapter demonstrates, this highly complex field is rendered additionally problematic by often contrasting and inconsistent research findings that have resulted in much debate and little consensus, beyond wide-spread agreement that reading disability appears to be explained by multiple deficits.
The phonological deficit hypothesis
For most of the past four decades, the phonological deficit hypothesis (Stanovich, 1988; Stanovich & Siegel, 1994) has been the dominant cognitive explanation (Vellutino et al., 2004). Studies of cognitive functioning in children with reading problems have consistently found three processes – phonological processing, short-term/working memory, and processing speed – that appear particularly significant when comparisons are made with typically achieving readers (Johnson et al., 2010). For each of these processes there appears to be a phonological component that is particularly important for reading. According to some theorists, the phonological deficit incorporates elements that map onto these three major dimensions: phonological awareness, verbal short-term memory, and slow retrieval of phonological information stored in long-term memory, as exemplified in rapid automatic naming tasks (Wagner & Torgesen, 1987). However, this grouping is controversial, and others argue that it is not helpful to conceive of verbal short-term/working memory and naming speed as core elements of phonology (Nicolson & Fawcett, 2008).
The Dyslexia Debate examines how we use the term 'dyslexia' and questions its efficacy as a diagnosis. While many believe that a diagnosis of dyslexia will shed light on a reader's struggles and help identify the best form of intervention, Julian G. Elliott and Elena L. Grigorenko show that it adds little value. In fact, our problematic interpretation of the term could prove to be a major disservice to many children with difficulties learning to read. This book outlines in detail the diverse ways in which reading problems have been conceptualized and operationalized. Elliott and Grigorenko consider the latest research in cognitive science, genetics, and neuroscience, and the limitations of these fields in terms of professional action. They then provide a more helpful, scientifically rigorous way to describe the various types of reading difficulties and discuss empirically supported forms of intervention.
The debate about how we should understand the concept of developmental dyslexia has sometimes become oversimplified to the point that the very existence of a biologically based reading disability has been questioned. Such a position is untenable, yet it is not always understood that criticism of the scientific rigor of a given label or construct does not necessarily imply that the problems it seeks to encompass are not real or meaningful. Thus, critical concerns expressed about the value of the dyslexia construct have been incorrectly understood or reframed by some as reflecting a perception that the term serves as an “excuse” for laziness, stupidity, or poor teaching. While there remain some commentators who certainly hold such views, the great majority of critiques in the academic literature (Elliott & Gibbs, 2008; Soler, 2010; Stanovich, 1994) have sought to provide a more nuanced perspective that eschews such notions.
In 2005, the dyslexia debate gained prominence in many countries as a result of widespread coverage given to a British television program, The Dyslexia Myth (http://topdocumentaryfilms.com/dyslexia-myth/). The main assertion of this program was that there were many myths surrounding the nature of dyslexia and its treatment. Existing practice, where only a limited proportion of struggling readers were identified as having dyslexia, typically on the basis of extensive cognitive assessments, was resulting in delays in intervention for some and no intervention for other candidates who also needed help. The program's message, largely reflecting the perspective of the response to intervention movement, was misperceived by some as stating that biologically based reading difficulties were a myth (see, for example, Nicolson  and a subsequent response to this by Elliott ). Surprisingly, this perception flew in the face of clear statements to the contrary that were offered throughout the program. What was actually being questioned were the rigor, utility, and added value of a clinical diagnosis of dyslexia, not the existence of the very real underlying problems that those with complex reading difficulties typically encounter. Rather than focusing on expensive assessments, often more accessible to children from socioeconomically advantaged families (Sternberg & Grigorenko, 1999b), and usually undertaken after long-term failure had been established, it was recommended that intervention should be conducted as early as possible with all those who were potentially at risk of reading difficulty, irrespective of etiology.