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Progress in Nonmetastatic Prostate Cancer Combined Analysis of Asthma Safety Trials of Long-Acting β2-Agonists Dupilumab Efficacy and Safety in Moderate-to-Severe Uncontrolled Asthma Metastasis-free Survival — A New End Point in Prostate Cancer Trials Efficacy and Safety of Dupilumab in Glucocorticoid-Dependent Severe Asthma Prophylaxis against Upper Gastrointestinal Bleeding in Hospitalized Patients Personhood and the Three Branches of Government Inhaled Corticosteroids and LABAs — Removal of the FDA’s Boxed Warning Making Neighborhood-Disadvantage Metrics Accessible — The Neighborhood Atlas Heat-Stable Carbetocin versus Oxytocin to Prevent Hemorrhage after Vaginal Birth Tongue Necrosis in Giant-Cell Arteritis Case 20-2018: A 64-Year-Old Man with Fever, Arthralgias, and Testicular Pain Enzalutamide in Men with Nonmetastatic, Castration-Resistant Prostate Cancer Firearm Injuries and Violence Prevention — The Potential Power of a Surgeon Gene... New Biologics for Asthma Accreditation of Clinical Research Sites — Moving Forward Adrenal Calcifications in an Infant What is the diagnosis?

Original Article

October 27, 2011 N Engl J Med 2011; 365:1597-1604 DOI: 10.1056/NEJMoa1105816

Abstract

After weight loss, changes in the circulating levels of several peripheral hormones involved in the homeostatic regulation of body weight occur. Whether these changes are transient or persist over time may be important for an understanding of the reasons behind the high rate of weight regain after diet-induced weight loss.

To test whether changes in reading skill were accompanied by measurable changes in white matter structure, we first examined MD and FA as a function of intervention time (hours) within the set of white matter tracts considered to be crucial for skilled reading Artsmith by Barse Art Smith by BARSE Turquoise DoubleDrop Earrings cA7SaCa
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and which showed significant relationships with pre-intervention reading skill in the current sample: the left AF, left ILF, and posterior CC. Intervention-driven tissue changes were evident within the AF and ILF but not within the CC: Specifically, mean diffusivity (MD) decreased as a function of intervention hours within the left AF ( F (1,77) = 8.46, p  = 0.0047, linear mixed effect model with a fixed effect of intervention time, in hours, and a random effect of subject) and the left ILF ( F (1,77) = 7.28, p  = 0.0086), but not within the CC ( F (1,77) = 2.37, p  = 0.13). Subject motion did not change over time (Supplementary Fig.) and including subject motion as a covariate in the model did not change the results: MD decreased as a function of intervention hours within the left AF ( F (1,76) = 10.48, p  = 0.0018) and the left ILF ( F (1,76) = 9.53, p  = 0.0028), but not within the CC ( F (1,76) = 2.11, p  = 0.15). The decline in MD was accompanied by a linear increase in fractional anisotropy (FA) in the left AF ( F (1,76) = 3.98, p  = 0.050, fixed effect of intervention hours and a random effect of subject, with subject motion included as a covariate, as above) and the left ILF ( F (1,76) = 8.82, p  = 0.0040) but not in the CC( F (1,76) = 0.24, p  = 0.62). Finally, since changes in white matter properties could theoretically follow a nonlinear trajectory, we tested a model that included a quadratic term for each tract and parameter. For MD in each tract, the linear model outperformed the nonlinear model (evaluated using Bayesian Information Criteria (BIC) , ), and no significant nonlinear effects were observed: AF linear: F (1,76) = 8.72, p  = 0.0041, AF quadratic: F (1,76) = 0.31, p  = 0.58, ILF linear: F (1,76) = 7.53, p  = 0.0076, ILF quadratic: F (1,76) = 0.33, p  = 0.57, CC linear: F (1,76) = 3.083, p  = 0.083, CC quadratic: F (1,76) = 3.90, p  = 0.052. In contrast, we observed significant quadratic effects in FA for the left AF only: AF linear: F (1,76) = 3.87, p  = 0.053, AF quadratic: F (1,76) = 7.77, p  = 0.0067, ILF linear: F (1,76) = 8.85, p  = 0.0039, ILF quadratic: F (1,76) = 3.20, p  = 0.078, CC linear: F (1,76) = 0.31, p  = 0.58, CC quadratic: F (1,76) = 2.047, p  = 0.16.

Like the reading outcomes reported above, intervention-driven changes in MD were specific to the intervention group, as indicated by a significant group (intervention vs. control) by time (days) interaction. As above, we substitute “days” for “intervention hours” to give a meaningful predictor for both the intervention and control subjects. In the left AF, we found a significant main effect of group ( F (1,125) = 7.047, p  = 0.009) but not of time ( F (1,125) = 1.033, p  = 0.31) and a significant group-by-time interaction ( F (1,125) = 4.97, p  = 0.028), consistent with a decrease in MD over time that was specific to the intervention subjects. Similarly, in the ILF, we saw a significant main effect of group ( F (1,125) = 10.29, p  = 0.0017) but not of time ( F (1,125) = 3.72, p  = 0.056) and a significant group-by-time interaction ( F (1,125) = 9.53, p  = 0.0025). In the CC, we saw a significant main effect of group ( F (1,125) = 6.69, p  = 0.011) but not of time ( F (1,125) = 0.90 p  = 0.34) and no significant group-by-time interaction ( F (1,125) = 0.027, p  = 0.87), consistent with the stability of MD values in this tract in all subjects. For FA, we observed a different pattern of results: In the AF, we saw no significant main effect of group (F(1,125) = 0.31, p  = 0.58) or time (F(1,125) = 0.055, p  = 0.82) and no significant group-by-time interaction (F(1,125) = 0.36, p  = 0.55). In the ILF, we saw no significant main effect of group ( F (1,125) = 0.0015, p  = 0.97) or time ( F (1,125) = 1.93, p  = 0.17) and no significant group-by-time interaction ( F (1,125) = 0.15, p  = 0.70). In the CC, we saw no significant main effect of group ( F (1,125) = 0.23, p  = 0.63) or time ( F (1,125) = 0.86, p  = 0.36) and no significant group-by-time interaction ( F (1,125) = 0.35, p  = 0.56). As shown in Supplementary Table, the group-by-time interaction approached significance for the quadratic term for FA in the left AF and ILF, but not for MD in the AF or ILF, or for either parameter in the CC.

Late Latin , from Latin
NEW! Time Traveler

First Known Use: 1612

in the meaning defined at sense 1a

Malthusian , anthropogenic , biomass , carbon footprint , crepuscular , niche , sere , symbiosis , taiga , tundra

Phrases Related to POPULATION

population

Definition of for English Language Learners

population

pop·u·la·tion \ ˌpä-pyə-ˈlā-shən \
1 : the whole number of people living in a country, city, or area
2 : a group of people or animals living in a certain place
The Latin word , meaning “people,” gives us the root popul . Words from the Latin have something to do with people. A popul is the group of people living in a particular place. Anything popul is common among or enjoyed by many people. A place that is popul has many people living in it.

population

pop·u·la·tion \ ˌpäp-yə-ˈlā-shən \
1 : the whole number of people or inhabitants in a country or region
2 a : a body of persons or individuals having a quality or characteristic in common
b ( 1 ) : the organisms inhabiting a particular locality
( 2 ) : a group of interbreeding organisms that represents the level of organization at which speciation begins
3 : a group of individual persons, objects, or items from which samples are taken for statistical measurement

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A growing number of brain imaging studies in humans, along with work in rodents and non-human primates, are beginning to define the brain circuits that mediate distinct aspects of mood and emotion under normal circumstances and in various pathological conditions that are indicative of low resilience. The field has identified several limbic regions in the forebrain, which are highly inter-connected and function as a series of integrated parallel circuits that regulate emotional states ( Novica Lapis lazuli dangle earrings Bihar Moons iAKh6Zfu
). In the sections that follow, we review how these various regions interact to mediate distinct emotional behaviours that are related to resilience. The neural regulation of endocrine and autonomic responses to stress, described in detail in REF. 70 , can be studied in humans by monitoring stress responses during functional imaging studies 71 .

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Figure 3
Neural circuitries of fear and reward

A simple schematic of the key limbic regions in the fear and reward circuitries. These regions are highly interconnected and function as a series of integrated parallel circuits that regulate emotional states. Each is heavily innervated by the brain's monoaminergic systems — noradrenaline (from the locus coeruleus (LC)), dopamine (from the ventral tegmental area (VTA)) and serotonin (from the raphe nuclei (not shown)) — which are thought to modulate the activity of these areas. a | Fear-inducing sensory information is relayed through the thalamus (Thal) to the amygdala (Amy). The amygdala is particularly important for conditioned aspects of learning and memory, as is best studied in fear models. The hippocampus (HP) has a crucial role in declarative memory, but it probably functions more broadly in regulating emotional, including fear, behaviour. b | The nucleus accumbens (NAc) is a key reward region that regulates an individual's responses to natural rewards and mediates the addicting actions of drugs of abuse. The prefrontal cortex (PFC) — which is composed of multiple regions (for example, the dorsolateral PFC, the medial PFC, the orbitofrontal cortex and the anterior cingulate cortex, among others) with distinct but overlapping functions — is sometimes also included in the limbic system and is essential to emotion regulation. PFC regions provide top-down control of emotional responses by acting on both the amygdala and the NAc ( a and b ). Several regions that are important for fear and reward learning are not shown in the respective circuits; for example, the NAc also regulates responses to fearful stimuli and the hippocampus also regulates responses to rewarding stimuli. The limbic regions depicted are also part of integrated circuits that mediate social responses and behaviour. The functional status of all of these circuits has important implications for resilience to stressful life events. Notably, alterations in one neurotransmitter, neuropeptide or hormone system will affect more than one circuit. Blue lines represent glutamatergic connections; green lines represent noradrenergic connections; red lines represent dopaminergic connections; the orange line represents a GABA (γ-aminobutyric acid)-ergic connection.

Neural circuitry of fear

Current models of the patho-physiology of PTSD, an example of conditions that are characterized by diminished resilience on exposure to a traumatic stressor, involve abnormal fear learning and an underlying dysfunction in the neural circuitry of fear, comprising the amygdala, the hippocampus and the ventromedial PFC (vmPFC) ( FIG. 3 ). Brain imaging studies in healthy participants have shown that acquisition of fear conditioning is centred in the amygdala, whereas extinction of fear memory involves both the vmPFC and the amygdala; activation in these structures, as well as the thickness of the vmPFC, has been associated with extinction success. A recent fmRI study examined the ability of physiological and neural fear responses to adapt flexibly to stimuli that changed from threatening to safe, and from safe to threatening. Both the initial fear response and the subsequent flexible shift were associated with activation of a network that includes the amygdala, the striatum and the vmPFC. In particular, the vmPFC seemed to mediate the shifting of fear to a different stimulus under stressful conditions. Findings from a recent study suggest that emotion regulation — a more advanced cognitive function — of conditioned fear might act through connections with more basic mechanisms of fear extinction, which humans share with other species.

The neural circuitry of fear is clearly important in resilience, but it has not been studied carefully in resilient individuals. It is possible that a well-functioning system in resilient individuals can prevent over-generalizing from specific conditioned stimuli, induce differential functioning of reconsolidation and extinction processes, or lead to an increased capacity for enhanced inhibition of amygdala responses by the medial PFC (mPFC) in stressful situations. Of note, preliminary findings suggest that treating patients with PTSD using cognitive behaviour therapy might have beneficial effects, by reducing amygdala activation and increasing rostral anterior cingulate cortex (ACC) activation during fear processing.

Much of our knowledge about the neural circuitry of fear comes from animal studies. The amygdala mediates the ability of cues that were associated with a fearful stimulus (for example, a footshock or a predator odour) to become aversive in their own right, as established in fear conditioning and related paradigms. The hippocampus mediates contextual and temporal aspects of fear conditioning. Reactivation of memories (that is, re-exposure to the cue or context) can lead to either reconsolidation (further strengthening of the memory) or extinction, with extinction generally requiring more intensive training. Conversely, conditioned inhibition of fear, in which animals are trained to feel protected from a threat in a certain environment, induces several antidepressant-like effects in mice. Animal studies have also made it possible to examine distinct functions of central, basolateral and medial amygdala nuclei.

Both amygdala- and hippocampus-dependent fear conditioning in animals have been related to long-term potentiation and other forms of synaptic plasticity. Accordingly, blockade of NMDA (-methyl- D -aspartate) glutamate receptors in the amygdala blocks cue-associated fear conditioning, and NMDA receptor blockade in the hippocampus blocks context-dependent fear conditioning. Consistent with the notion that extinction represents the formation of a new memory rather than the erasure of an existing memory, administration of D -cycloserine, an NMDA receptor partial agonist, can enhance extinction of fear conditioning in animal models and in patients with PTSD undergoing prolonged exposure therapy. Blockade of β-adrenergic receptors in the amygdala can also block cue-dependent fear conditioning, and β-adrenergic antagonists have been tested in patients exposed to trauma, with mixed results. In addition, fear conditioning and its extinction are regulated by activation of GRs in the hippocampus and perhaps in the amygdala, which suggests the possible use of glucocorticoids in the treatment of trauma. However, whether β-adrenergic and GR levels or functioning are different in resilient and non-resilient individuals has not yet been studied.

Neural circuitry of reward

Patients with major depressive disorder and PTSD have shown evidence of reward system dysfunction in fmRI studies, with reduced striatal activation during the performance of reward-related tasks. Altered activation of reward circuits in depressed adolescents was associated with self-reports of reduced positive affect in naturalistic settings. Differential reward system function has also been demonstrated in children of depressed versus never-depressed parents. Of note, there is evidence that inter-individual variability in neural responses to reward anticipation in healthy individuals is associated with the Val158met polymorphism.

Trait optimism, which is linked to resilience (as discussed above), might relate to reward circuit function. Sharot scanned participants who were imagining positive and negative future events. Optimism bias — the tendency to expect future events to be positive — was associated with higher activation in the amygdala and the rostral ACC when imagining positive events than when imagining negative events. The level of activation in the rostral ACC was positively correlated with dispositional optimism. Research on special forces soldiers showed that their reward-processing regions had higher reactivity than those of healthy civilian controls. Conversely, susceptibility to social-reward frustration in healthy males was associated with increased activation in prefrontal (top-down control) areas during performance of a monetary task.

Animal studies have greatly informed our understanding of the brain's reward circuitry and its possible importance for resilience. The best-established reward circuit is the mesolimbic dopamine system, which involves dopaminergic neurons of the VTA and their innervation of the nucleus accumbens and many other forebrain limbic regions ( FIG. 3 ). VTA dopamine neurons can be viewed as gauges of reward: they are activated in response to a reward (for example, food, sex or social interaction) or even the expectation of a reward, and are inhibited by an aversive stimulus or the absence of an expected reward. However, certain dopaminergic neurons are also activated by aversive stimuli, suggesting that they are more generally involved in mood regulation. Indeed, an increasing number of studies report the involvement of the VTA–nucleus accumbens circuit in depression and antidepressant responses in humans and rodents, although there is not yet a clear consensus on the role of dopamine function in resilience and vulnerability. A recent study in the social-defeat paradigm in mice (see Supplementary information S1 (box) ) has shown that increased activity of VTA dopamine neurons mediates vulnerability by increasing the activity-dependent release of BDNF onto nucleus accumbens neurons, and that resilient animals escape vulnerability in part by upregulating K channels in the VTA to prevent this increase in neuronal excitability and BDNF release ( FIG. 2 ).

Neural circuitry of emotion regulation

A greater capacity for emotion regulation has also been related to stress resilience, and studies of individuals with psychiatric disorders suggest that they have abnormalities in their emotion regulation systems. A neural model of emotion regulation consisting of ventral and dorsal systems has been described, with various patterns of abnormalities associated with a range of psychiatric disorders. Studies in mood and anxiety disorders have most consistently identified abnormalities in amygdala, hippocampus, subgenual ACC and PFC function.

In healthy individuals, differential amygdala reactivity to negative stimuli could represent an intermediate phenotype associated with vulnerability to anxiety and depressive disorders. Indeed, several studies have linked the short allele of and the Met158 allele of with higher anxiety levels, vulnerability to negative mood, increased amygdala reactivity to negative stimuli and altered functional coupling between the amygdala and the cortex. Furthermore, individual differences in cortico-limbic connectivity suggest that some people might have a genetic predisposition to inflexible emotion processing. As mentioned above, recent imaging studies have shown evidence that multiple gene interactions have an effect on limbic reactivity to unpleasant stimuli. In addition, studies of healthy children and young adults at high familial risk for depression have yielded evidence that their neural responses to emotional stimuli differed from those of controls at low familial risk for depression.

One mechanism of emotion regulation — cognitive reappraisal — has received particular attention. fMRI studies have shown increased activation in lateral and medial PFC regions and decreased amygdala activation during reappraisal, with increased activation in the lateral PFC associated with reappraisal success. It has thus been suggested that the PFC regulates the intensity of emotional responses by modulating the activation of the amygdala.

A recent fMRI study using mediation analysis demonstrated that the vlPFC acts on both the amygdala and the nucleus accumbens, resulting in opposite behavioural responses: the pathways through the amygdala and the nucleus accumbens were associated with reduced and increased reappraisal success, respectively. These findings are consistent with animal studies, which have established that the amygdala and the nucleus accumbens work in concert to regulate an individual's responses to both negative and positive emotional stimuli. Thus, variability in the functions of these two pathways might underlie individual differences in emotional response and emotion regulation in stressful contexts. Greater use of reappraisal in everyday life has also been linked to greater PFC and lower amygdala activation to negative stimuli, suggesting that there might be a central mechanism through which reappraisal could promote successful coping and reduce the risk of mood disorder onset.

A recent fMRI study found that resilient women with a history of sexual trauma were more successful at cognitively enhancing emotional responses to aversive pictures than women with PTSD after sexual trauma and healthy, non-traumatized controls. This increased capacity to enhance emotional responses was associated with increased PFC activation. These results highlight the complexity of emotion regulation systems and suggest that resilience could also be associated with the ability to sustain attention to unpleasant stimuli. Perhaps this increased attention is related to a more accurate or optimistic appraisal of the perceived threats.

Additional neural circuits relevant to social behaviour

The capacity for empathy enables individuals to generate appropriate emotional responses in social contexts and might be related to social competence, which is a characteristic of resilient individuals. Recent years have seen a surge of interest in the study of the so-called mirror neuron system, which comprises cortical neurons that fire similarly when an animal performs a task or observes another animal of the same species performing that task. It is proposed that this system, acting in conjunction with limbic brain regions, has a central role in understanding others' emotions and intentions. In humans, the vmPFC is activated both when people think about their own mental states and when they think about those of other people, and patients with lesions of this region have deficits in social emotions such as shame, guilt and empathy. Much future work is needed to understand possible links between the capacity for empathy, mirror neuron system function and resilience. Preliminary findings of greater activation in presumed mirror neuron and associated limbic areas during imitation of emotional faces in children with higher levels of empathy and interpersonal competence are promising. Of note, a recent study suggests that the neuropeptide oxytocin could improve a person's ability to infer the mental states of others.

The role of oxytocin in promoting social attachment in humans has recently received increased attention. A study in healthy men participating in a laboratory-based economic trust game showed that intranasal administration of oxytocin increased trust, and suggested involvement of the amygdala. Imaging studies have demonstrated that mutual cooperation induces activation in reward circuitry regions, which are modulated by oxytocin and vasopressin. Conversely, oxytocin reduced amygdala activation in response to fear-inducing visual stimuli and reduced connectivity between the amygdala and brainstem areas that mediate autonomic and behavioural fear responses. Oxytocin thus seems to facilitate social attachment by enhancing the reward value of social stimuli and reducing potential fear responses. In laboratory animals, central release of oxytocin and vasopressin regulates anxiety and social behaviour. In rodent species, oxytocin and vasopressin increase social recognition, pair bonding and affiliation.

Social contact promotes health and well-being. An fMRI study of married women demonstrated that holding hands with their husband attenuated neural responses to the threat of receiving a shock, a response that was proportional to the quality of their relationship. As discussed above, social competence and openness to social support are core characteristics of resilient individuals, and these qualities might help to modulate central responses to stress in these individuals. The effects of social contact on neural responses to threat, and the potential involvement of neuropeptides that promote social attachment, warrants direct investigation in resilient individuals.

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Stress resilience refers to an individual's capacity for successful adaptation to acute stress, trauma or more chronic forms of adversity. Although the range of complex mechanisms that lead to resilient phenotypes is far from being fully determined, a model of resilience has begun to emerge from the study of adaptive stress responses at multiple phenotypic levels. Beginning in development, an individual's genes and their inter action with environmental factors (and perhaps with stochastic epigenetic events) shape the neural circuitry and neuro chemical function that are expressed in an observable range of psychological strengths and behaviours characteristic of resilient individuals. Various genetic polymorphisms affect a person's limbic reactivity and prefrontal-limbic connectivity, influencing their initial responses to negative or traumatic events, as well their capacity for cognitive reappraisal of those events.

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