The classification of involuntary musical imagery: the case for earworms

Involuntary musical imagery (INMI) is the subject of much recent research interest. INMI covers a number of experience types such as musical obsessions and musical hallucinations. One type of experience has been called earworms, for which the literature provides a number of definitions. In this paper we consider the origins of the term earworm in the German language literature and compare that usage with the English language literature. We consider the published literature on earworms and conclude that there is merit in distinguishing between earworms and other types of types of involuntary musical imagery described in the scientific literature: e.g. musical hallucinations, musical obsessions. We also describe other experiences that can be considered under the term INMI. The aim of future research could be to ascertain similarities and differences between types of INMI with a view to refining the classification scheme proposed here.

Negative priming in free recall reconsidered

Recent investigations of the phenomenon of forgetting have been driven mostly by the development of a novel theoretical framework which places great emphasis on inhibitory control (Anderson, 2003; Anderson & Spellman, 1995; Bjork, 1989). Whereas traditional, interference-based theories consider forgetting to be a by-product of storing new information, the inhibitory framework postulates a specialized mechanism, or a group of mechanisms, that serves the function of ‘deactivating’ information which is currently irrelevant. This process of inhibiting currently irrelevant information is thought to have lasting consequences, affecting memory for the irrelevant information on subsequent tests. The active and functional perspective on forgetting embedded in the inhibitory framework opens new fields for examining the role of forgetting in cognitive functioning. Differences in the ability to inhibit irrelevant information have been postulated to play important roles in a range of clinical conditions (e.g., Soriano, Jiménez, Román, & Bajo, 2009; Storm & White, 2010) and the trajectory of cognitive development (e.g., Aslan & Bäuml, 2010) as well as contributing to individual differences in many other cognitive and social domains (Redick, Heitz, & Engle, 2007).

When enough is not enough: information overload and metacognitive decisions to stop studying information

People are often exposed to more information than they can actually remember. Despite this frequent form of information overload, little is known about how much information people choose to remember. Using a novel “stop” paradigm, the current research examined whether and how people choose to stop receiving new—possibly overwhelming—information with the intent to maximize memory performance. Participants were presented with a long list of items and were rewarded for the number of correctly remembered words in a following free recall test. Critically, participants in a stop condition were provided with the option to stop the presentation of the remaining words at any time during the list, whereas participants in a control condition were presented with all items. Across five experiments, we found that participants tended to stop the presentation of the items to maximize the number of recalled items, but this decision ironically led to decreased memory performance relative to the control group. This pattern was consistent even after controlling for possible confounding factors (e.g., task demands). The results indicated a general, false belief that we can remember a larger number of items if we restrict the quantity of learning materials. These findings suggest people have an incomplete understanding of how we remember excessive amounts of information.

Growth factor receptor-bound protein 2 contributes to (hem)immunoreceptor tyrosine-based activation motif-mediated signaling in platelets

Rationale: Platelets are anuclear cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity but may also cause pathological vessel occlusion. One major pathway of platelet activation is triggered by 2 receptors that signal through an (hem)immunoreceptor tyrosine-based activation motif (ITAM), the activating collagen receptor glycoprotein (GP) VI and the C-type lectin-like receptor 2 (CLEC-2). Growth factor receptor–bound protein 2 (Grb2) is a ubiquitously expressed adapter molecule involved in signaling processes of numerous receptors in different cell types, but its function in platelets and MKs is unknown. Objective: We tested the hypothesis that Grb2 is a crucial adapter protein in (hem)immunoreceptor tyrosine-based activation motif signaling in platelets. Methods and Results: Here, we show that genetic ablation of Grb2 in MKs and platelets did not interfere with MK differentiation or platelet production. However, Grb2-deficiency severely impaired glycoprotein VI–mediated platelet activation because of defective stabilization of the linker of activated T-cell (LAT) signalosome and activation of downstream signaling proteins that resulted in reduced adhesion, aggregation, and coagulant activity on collagen in vitro. Similarly, CLEC-2–mediated signaling was impaired in Grb2-deficient platelets, whereas the cells responded normally to stimulation of G protein–coupled receptors. In vivo, this selective (hem)immunoreceptor tyrosine-based activation motif signaling defect resulted in prolonged bleeding times but affected arterial thrombus formation only after concomitant treatment with acetylsalicylic acid, indicating that defective glycoprotein VI signaling in the absence of Grb2 can be compensated through thromboxane A2–induced G protein–coupled receptor signaling pathways. Conclusions: These results reveal an important contribution of Grb2 in (hem)immunoreceptor tyrosine-based activation motif signaling in platelets in hemostasis and thrombosis by stabilizing the LAT signalosome.

Don’t aim too high for your kids: parental over-aspiration undermines students’ learning in mathematics

Previous research has suggested that parents’ aspirations for their children’s academic attainment can have a positive influence on children’s actual academic performance. Possible negative effects of parental over-aspiration, however, have found little attention in the psychological literature. Employing a dual-change score model with longitudinal data from a representative sample of German schoolchildren and their parents (N = 3,530; grades 5 to 10), we showed that parental aspiration and children’s mathematical achievement were linked by positive reciprocal relations over time. Importantly, we also found that parental aspiration that exceeded their expectation (i.e., over-aspiration) had negative reciprocal relations with children’s mathematical achievement. These results were fairly robust after controlling for a variety of demographic and cognitive variables such as children’s gender, age, intelligence, school type, and family SES. The results were also replicated with an independent sample of US parents and their children. These findings suggest that unrealistically high parental aspiration can be detrimental for children’s achievement.

Ibrutinib inhibits platelet integrin αIIbβ3 outside-in signaling and thrombus stability but not adhesion to collagen

OBJECTIVE: Ibrutinib is an irreversible Bruton tyrosine kinase inhibitor approved for treatment of Waldenstrom macroglobulinemia, chronic lymphocytic leukemia, and mantle cell lymphoma that increases the risk of bleeding among patients. Platelets from ibrutinib-treated patients exhibit deficiencies in collagen-evoked signaling in suspension; however, the significance of this observation and how it relates to bleeding risk is unclear, as platelets encounter immobile collagen in vivo. We sought to clarify the effects of ibrutinib on platelet function to better understand the mechanism underlying bleeding risk. APPROACH AND RESULTS: By comparing signaling in suspension and during adhesion to immobilized ligands, we found that the collagen signaling deficiency caused by ibrutinib is milder during adhesion to immobilized collagen. We also found that platelets in whole blood treated with ibrutinib adhered to collagen under arterial shear but formed unstable thrombi, suggesting that the collagen signaling deficiency caused by ibrutinib may not be the predominant cause of bleeding in vivo. However, clot retraction and signaling evoked by platelet adhesion to immobilized fibrinogen were also inhibited by ibrutinib, indicating that integrin αIIbβ3 outside-in signaling is also effected in addition to GPVI signaling. When ibrutinib was combined with the P2Y12 inhibitor, cangrelor, thrombus formation under arterial shear was inhibited additively. CONCLUSIONS: These findings suggest that (1) ibrutinib causes GPVI and integrin αIIbβ3 platelet signaling deficiencies that result in formation of unstable thrombi and may contribute toward bleeding observed in vivo and (2) combining ibrutinib with P2Y12 antagonists, which also inhibit thrombus stability, may have a detrimental effect on hemostasis.

Endothelial cell-specific ROS production increases susceptibility to aortic dissection

Background—Increased production of reactive oxygen species (ROS) throughout the vascular wall is a feature of cardiovascular disease states, but therapeutic strategies remain limited by our incomplete understanding of the role and contribution of specific vascular cell ROS to disease pathogenesis. To investigate the specific role of endothelial cell (EC) ROS in the development of structural vascular disease, we generated a mouse model of endothelium-specific Nox2 overexpression and tested the susceptibility to aortic dissection after angiotensin II (Ang II) infusion. Methods and Results—A specific increase in endothelial ROS production in Nox2 transgenic mice was sufficient to cause Ang II–mediated aortic dissection, which was never observed in wild-type mice. Nox2 transgenic aortas had increased endothelial ROS production, endothelial vascular cell adhesion molecule-1 expression, matrix metalloproteinase activity, and CD45+ inflammatory cell infiltration. Conditioned media from Nox2 transgenic ECs induced greater Erk1/2 phosphorylation in vascular smooth muscle cells compared with wild-type controls through secreted cyclophilin A (CypA). Nox2 transgenic ECs (but not vascular smooth muscle cells) and aortas had greater secretion of CypA both at baseline and in response to Ang II stimulation. Knockdown of CypA in ECs abolished the increase in vascular smooth muscle cell Erk1/2 phosphorylation conferred by EC conditioned media, and preincubation with CypA augmented Ang II–induced vascular smooth muscle cell ROS production. Conclusions—These findings demonstrate a pivotal role for EC-derived ROS in the determination of the susceptibility of the aortic wall to Ang II–mediated aortic dissection. ROS-dependent CypA secretion by ECs is an important signaling mechanism through which EC ROS regulate susceptibility of structural components of the aortic wall to aortic dissection.

Inflame my heart (by p38-MAPK).

Although many studies have explored the stimuli which promote hypertrophic growth or death in cardiac myocytes and the signaling pathways which they activate, the mechanisms by which these pathways promote the pathophysiological responses are still obscure. The mitogen-activated protein kinase (MAPK) cascades (in which MAPKs are phosphorylated and activated by upstream MAPK kinases [MKKs] which are, in turn, phosphorylated and activated by MKK kinases [MKKKs]) were identified in the early- to mid-1990s as potentially key regulatory pathways in cardiac myocyte pathophysiology.1,2 The principal MAPKs investigated in cardiac myocytes are the extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNKs), and p38-MAPKs. ERK1/2 are potently activated by hypertrophic stimuli, whereas JNKs and p38-MAPKs are potently activated by cellular stresses (eg, oxidative stress). However, there is cross-talk such that JNKs and p38-MAPKs are activated by hypertrophic stimuli and ERK1/2 are activated by cellular stresses, and the contribution of each pathway to the overall cardiac myocyte response is not entirely clear. MAPKs phosphorylate a number of known transcription factors to alter their transactivating activities thus, presumably, influencing gene expression to elicit the cellular response.3 Nevertheless, the immediate consequences (ie, the transcription factors which are phosphorylated) and downstream consequences (ie, genes with altered expression) of MAPK signaling in the heart or specifically in cardiac myocytes are still largely unknown. To start to address this issue for the p38-MAPK pathway in the (rat) heart (Figure), Tenhunen et al4 directly injected adenoviruses encoding wild-type (WT) p38-MAPKα together …

The Cold War and its aftermath in the Americas: the search for a synthetic interpretation of U.S. policy

More than two decades have passed since the fall of the Berlin Wall and the transfer of the Cold War file from a daily preoccupation of policy makers to a more detached assessment by historians. Scholars of U.S.-Latin American relations are beginning to take advantage both of the distance in time and of newly opened archives to reflect on the four decades that, from the 1940s to the 1980s, divided the Americas, as they did much of the world. Others are seeking to understand U.S. policy and inter-American relations in the post-Cold War era, a period that not only lacks a clear definition but also still has no name. Still others have turned their gaze forward to offer policies in regard to the region for the new Obama administration. Numerous books and review essays have addressed these three subjects—the Cold War, the post-Cold War era, and current and future issues on the inter-American agenda. Few of these studies attempt, however, to connect the three subjects or to offer new and comprehensive theories to explain the course of U.S. policies from the beginning of the twentieth century until the present. Indeed, some works and policy makers continue to use the mind-sets of the Cold War as though that conflict were still being fought. With the benefit of newly opened archives, some scholars have nevertheless drawn insights from the depths of the Cold War that improve our understanding of U.S. policies and inter-American relations, but they do not address the question as to whether the United States has escaped the longer cycle of intervention followed by neglect that has characterized its relations with Latin America. Another question is whether U.S. policies differ markedly before, during, and after the Cold War. In what follows, we ask whether the books reviewed here provide any insights in this regard and whether they offer a compass for the future of inter-American relations. We also offer our own thoughts as to how their various perspectives could be synthesized to address these questions more comprehensively.

Meta-analysis to integrate effect sizes within a paper: Possible misuse and Type-1 error inflation

In recent years an increasing number of papers have employed meta-analysis to integrate effect sizes of researchers’ own series of studies within a single paper (“internal meta-analysis”). Although this approach has the obvious advantage of obtaining narrower confidence intervals, we show that it could inadvertently inflate false-positive rates if researchers are motivated to use internal meta-analysis in order to obtain a significant overall effect. Specifically, if one decides whether to stop or continue a further replication experiment depending on the significance of the results in an internal meta-analysis, false-positive rates would increase beyond the nominal level. We conducted a set of Monte-Carlo simulations to demonstrate our argument, and provided a literature review to gauge awareness and prevalence of this issue. Furthermore, we made several recommendations when using internal meta-analysis to make a judgment on statistical significance.

Followers are not followed: observed group interactions modulate subsequent social attention

We asked whether previous observations of group interactions modulate subsequent social attention episodes. Participants first completed a learning phase with two conditions. In the ‘leader’ condition one of three identities turned her gaze first, followed by the two other faces. In the ‘follower’ condition, one of the identities turned her gaze after the two other faces had first shifted their gaze. Thus, participants observed that some individuals were consistently ‘leaders’ and others ‘followers’ of others’ attention. In the test phase, the faces of ‘leaders’ and ‘followers’ were presented in a gaze cueing paradigm. Remarkably, the ‘followers’ did not elicit gaze cueing. Our data demonstrate that individuals who do not guide group attention in exploring the environment are ineffective social attention directors in later encounters. Thus, the role played in previous group social attention interactions modulates the relative weight assigned to others’ gaze: we ignore the gaze of group followers.

Are visual threats prioritized without awareness? A critical review and meta analysis involving 3 behavioral paradigms and 2696 observers

Given capacity limits, only a subset of stimuli 1 give rise to a conscious percept. Neurocognitive models suggest that humans have evolved mechanisms that operate without awareness and prioritize threatening stimuli over neutral stimuli in subsequent perception. In this meta analysis, we review evidence for this ‘standard hypothesis’ emanating from three widely used, but rather different experimental paradigms that have been used to manipulate awareness. We found a small pooled threat-bias effect in the masked visual probe paradigm, a medium effect in the binocular rivalry paradigm and highly inconsistent effects in the breaking continuous flash suppression paradigm. Substantial heterogeneity was explained by the stimulus type: the only threat stimuli that were robustly prioritized across all three paradigms were fearful faces. Meta regression revealed that anxiety may modulate threat biases, but only under specific presentation conditions. We also found that insufficiently rigorous awareness measures, inadequate control of response biases and low level confounds may undermine claims of genuine unconscious threat processing. Considering the data together, we suggest that uncritical acceptance of the standard hypothesis is premature: current behavioral evidence for threat-sensitive visual processing that operates without awareness is weak.

The “pain matrix” in pain-free individuals

Human functional imaging provides a correlative picture of brain activity during pain. A particular set of central nervous system structures (eg, the anterior cingulate cortex, thalamus, and insula) consistently respond to transient nociceptive stimuli causing pain. Activation of this so-called pain matrix or pain signature has been related to perceived pain intensity, both within and between individuals,1,2 and is now considered a candidate biomarker for pain in medicolegal settings and a tool for drug discovery. The pain-specific interpretation of such functional magnetic resonance imaging (fMRI) responses, although logically flawed,3,4 remains pervasive. For example, a 2015 review states that “the most likely interpretation of activity in the pain matrix seems to be pain.”4 Demonstrating the nonspecificity of the pain matrix requires ruling out the presence of pain when highly salient sensory stimuli are presented. In this study, we administered noxious mechanical stimuli to individuals with congenital insensitivity to pain and sampled their brain activity with fMRI. Loss-of-function SCN9A mutations in these individuals abolishes sensory neuron sodium channel Nav1.7 activity, resulting in pain insensitivity through an impaired peripheral drive that leaves tactile percepts fully intact.5 This allows complete experimental disambiguation of sensory responses and painful sensations

Breaking the double-edged sword of effort/trying hard: developmental equilibrium and Longitudinal relations among effort, achievement, and academic self-concept

Ever since the classic research of Nicholls (1976) and others, effort has been recognized as a double-edged sword: whilst it might enhance achievement, it undermines academic self-concept (ASC). However, there has not been a thorough evaluation of the longitudinal reciprocal effects of effort, ASC and achievement,in the context of modern self-concept theory and statistical methodology. Nor have there been developmental equilibrium tests of whether these effects are consistent across the potentially volatile early-to-middle adolescence. Hence, focusing on mathematics, we evaluate reciprocal effects models over the first four years of secondary school, relating effort, achievement (test scores and school grades), ASC, and ASCxEffort interactions for a representative sample of 3,421 German students (Mn age = 11.75 years at Wave 1). ASC, effort and achievement were positively correlated at each wave, and there was a clear pattern of positive reciprocal positive effects among ASC, test scores and school grades—each contributing to the other, after controlling for the prior effects of all others. There was an asymmetrical pattern of effects for effort that is consistent with the double-edged sword premise: prior school grades had positive effects on subsequent effort, but prior effort had non-significant or negative effects on subsequent grades and ASC. However, on the basis of a synergistic application of new theory and methodology, we predicted and found a significant ASC-by-effort interaction, such that prior effort had more positive effects on subsequent ASC and school grades when prior ASC was high—thus providing a key to breaking the double-edged sword.