1,727 research outputs found
Watch Out for the Beast: Fear Information and Attentional Bias in Children
Although valenced information about novel animals changes the implicit and explicit fear beliefs of children (Field & Lawson, 2003), how it might lead to anxiety is unknown. One possibility, based on cognitive models of anxiety, is that fear information creates attentional biases similar to those seen in anxiety disorders. Children between 7 and 9 years old were given positive information about 1 novel animal, negative information about another, and no information about the 3rd. A pictorial dot-probe task was used, immediately or with a 24-hr delay, to test for attentional biases to the different animals. The results replicated the finding that fear information changes children's fear beliefs. Regardless of whether there was a delay, children acquired an attentional bias in the left visual field toward the animal about which they held negative beliefs compared to the control animal. These results imply a possible way in which fear information might contribute to acquired fear
Facial expressions depicting compassionate and critical emotions: the development and validation of a new emotional face stimulus set
Attachment with altruistic others requires the ability to appropriately process affiliative and kind facial cues. Yet there is no stimulus set available to investigate such processes. Here, we developed a stimulus set depicting compassionate and critical facial expressions, and validated its effectiveness using well-established visual-probe methodology. In Study 1, 62 participants rated photographs of actors displaying compassionate/kind and critical faces on strength of emotion type. This produced a new stimulus set based on N = 31 actors, whose facial expressions were reliably distinguished as compassionate, critical and neutral. In Study 2, 70 participants completed a visual-probe task measuring attentional orientation to critical and compassionate/kind faces. This revealed that participants lower in self-criticism demonstrated enhanced attention to compassionate/kind faces whereas those higher in self-criticism showed no bias. To sum, the new stimulus set produced interpretable findings using visual-probe methodology and is the first to include higher order, complex positive affect displays
Mindfulness-based interventions for people diagnosed with a current episode of an anxiety or depressive disorder: a meta-analysis of randomised controlled trials
Objective
Mindfulness-based interventions (MBIs) can reduce risk of depressive relapse for people with a history of recurrent depression who are currently well. However, the cognitive, affective and motivational features of depression and anxiety might render MBIs ineffective for people experiencing current symptoms. This paper presents a meta-analysis of randomised controlled trials (RCTs) of MBIs where participants met diagnostic criteria for a current episode of an anxiety or depressive disorder.
Method
Post-intervention between-group Hedges g effect sizes were calculated using a random effects model. Moderator analyses of primary diagnosis, intervention type and control condition were conducted and publication bias was assessed.
Results
Twelve studies met inclusion criteria (n = 578). There were significant post-intervention between-group benefits of MBIs relative to control conditions on primary symptom severity (Hedges g = β0.59, 95% CI = β0.12 to β1.06). Effects were demonstrated for depressive symptom severity (Hedges g = β0.73, 95% CI = β0.09 to β1.36), but not for anxiety symptom severity (Hedges g = β0.55, 95% CI = 0.09 to β1.18), for RCTs with an inactive control (Hedges g = β1.03, 95% CI = β0.40 to β1.66), but not where there was an active control (Hedges g = 0.03, 95% CI = 0.54 to β0.48) and effects were found for MBCT (Hedges g = β0.39, 95% CI = β0.15 to β0.63) but not for MBSR (Hedges g = β0.75, 95% CI = 0.31 to β1.81).
Conclusions
This is the first meta-analysis of RCTs of MBIs where all studies included only participants who were diagnosed with a current episode of a depressive or anxiety disorder. Effects of MBIs on primary symptom severity were found for people with a current depressive disorder and it is recommended that MBIs might be considered as an intervention for this population
The Impact of Worry on Attention to Threat
Prior research has often linked anxiety to attentional vigilance for threat using the dot probe task, which presents probes in spatial locations that were or were not preceded by a putative threat stimulus. The present study investigated the impact of worry on threat vigilance by administering this task during a worry condition and during a mental arithmetic control condition to 56 undergraduate students scoring in the low normal range on a measure of chronic worry. The worry induction was associated with faster responses than arithmetic to probes in the attended location following threat words, indicating the combined influence of worry and threat in facilitating attention. Within the worry condition, responses to probes in the attended location were faster for trials containing threat words than for trials with only neutral words, whereas the converse pattern was observed for responses to probes in the unattended location. This connection between worry states and attentional capture by threat may be central to understanding the impact of hypervigilance on information processing in anxiety and its disorders
Activation of Muscarinic M1 Acetylcholine Receptors Induces Long-Term Potentiation in the Hippocampus
Muscarinic M1 acetylcholine receptors (M1Rs) are highly expressed in the hippocampus, and their inhibition or ablation disrupts the encoding of spatial memory. It has been hypothesized that the principal mechanism by which M1Rs influence spatial memory is by the regulation of hippocampal synaptic plasticity. Here, we use a combination of recently developed, well characterized, selective M1R agonists and M1R knock-out mice to define the roles of M1Rs in the regulation of hippocampal neuronal and synaptic function. We confirm that M1R activation increases input resistance and depolarizes hippocampal CA1 pyramidal neurons and show that this profoundly increases excitatory postsynaptic potential-spike coupling. Consistent with a critical role for M1Rs in synaptic plasticity, we now show that M1R activation produces a robust potentiation of glutamatergic synaptic transmission onto CA1 pyramidal neurons that has all the hallmarks of long-term potentiation (LTP): The potentiation requires NMDA receptor activity and bi-directionally occludes with synaptically induced LTP. Thus, we describe synergistic mechanisms by which acetylcholine acting through M1Rs excites CA1 pyramidal neurons and induces LTP, to profoundly increase activation of CA1 pyramidal neurons. These features are predicted to make a major contribution to the pro-cognitive effects of cholinergic transmission in rodents and humans
Coral Bleaching and Mortality in the Chagos Archipelago
The atolls and coral banks of the Chagos Archipelago (British Indian Ocean Territory) in the central
Indian Ocean were severely affected by the El NiΓ±o Southern Oscillation (ENSO) thermal event that
started in 2015 and which lasted for nearly two years. On these reefs, coral mortality reduced scleractinian
coral cover from 40%β50% to <10% and commonly to only about 5% in water less than 15 m depth. The
three-dimensional structure of the reefs was significantly reduced as a result, and the prolonged warming
almost eliminated soft corals. Most atolls of the archipelago are uninhabited, so any changes are driven by
broad environmental changes rather than by direct, local anthropogenic effects. Coral cover was first
measured in 1978, temperature loggers have recorded water temperature at various depths for the last 11
years, and the results of the recent warming event are placed in this context. Over this time, cover has
declined severely along with a general rise in water temperature of one-third of a degree Celsius on ocean
reefs and by more than one-half of a degree Celsius in lagoons. Major fluctuations of coral cover caused
by warm episodes have sometimes, but not always, coincided with ENSO events and have occurred on
top of the increasing trend in background temperatures. Juvenile coral populations have also recently
severely declined following the mortality of the adults. Estimates of calcification suggest a marked
reduction, from a state of vigorous reef growth that had not long recovered from the earlier severe
warming event of 1998, to a state of net erosion. Predictions suggest that recurrences of mass mortalities
will take place too frequently for any significant recovery of reef health in these atolls by the late 2020s
Risk Monitoring Tools in Bank Regulation and Supervision β Developments Since the Collapse of Barings Plc.
M1 muscarinic allosteric modulators slow prion neurodegeneration and restore memory loss
This is the final version of the article. Available from American Society for Clinical Investigation via the DOI in this record.The current frontline symptomatic treatment for Alzheimerβs disease (AD) is whole-body upregulation of cholinergic
transmission via inhibition of acetylcholinesterase. This approach leads to profound dose-related adverse effects. An
alternative strategy is to selectively target muscarinic acetylcholine receptors, particularly the M1 muscarinic acetylcholine
receptor (M1 mAChR), which was previously shown to have procognitive activity. However, developing M1 mAChRβselective orthosteric ligands has proven challenging. Here, we have shown that mouse prion disease shows many of the hallmarks
of human AD, including progressive terminal neurodegeneration and memory deficits due to a disruption of hippocampal
cholinergic innervation. The fact that we also show that muscarinic signaling is maintained in both AD and mouse prion
disease points to the latter as an excellent model for testing the efficacy of muscarinic pharmacological entities. The memory deficits we observed in mouse prion disease were completely restored by treatment with benzyl quinolone carboxylic acid (BQCA) and benzoquinazoline-12 (BQZ-12), two highly selective positive allosteric modulators (PAMs) of M1 mAChRs. Furthermore, prolonged exposure to BQCA markedly extended the lifespan of diseased mice. Thus, enhancing hippocampal muscarinic signaling using M1 mAChR PAMs restored memory loss and slowed the progression of mouse prion disease, indicating that this ligand type may have clinical benefit in diseases showing defective cholinergic transmission, such as AD.ABT, AC, and PMS received funding from a Wellcome Trust Collaborative
Award (201529/Z/16/Z). ABT, SJB, AJB, and TMH were
funded through a Medical Research Council programme leader
grant provided by the MRC Toxicology Unit. CCF, LMB, AJM, and
HES were funded by the Eli Lilly Company. JMB received funding
through a Lilly Research Award Program (LRAP) grant (Eli
Lilly). RP received funding from the Marie Curie grant βExtrabrainβ
(European Commission). AC is a senior principal research
fellow and PMS a principal research fellow of the National Health
and Medical Research Council of Australia. Tissue samples were
from Randy Woltjer at the Oregon Alzheimerβs Disease Center.
The Oregon Alzheimerβs Disease Center is supported by NIH grant P30AG008017
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