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The White House warns of default danger as President Biden and House Republicans inch closer to a deal on raising the debt ceiling. Bharat Ramamurti, the Deputy Director of the National Economic Council, speaks with The Washington Post’s Libby Casey.

Throughout history, rich and poor countries alike have been lending, borrowing, crashing--and recovering--their way through an extraordinary range of financial crises. Each time, the experts have chimed, \"this time is different\"--claiming that the old rules of valuation no longer apply and that the new situation bears little similarity to past disasters. With this breakthrough study, leading economists Carmen Reinhart and Kenneth Rogoff definitively prove them wrong. Covering sixty-six countries across five continents, This Time Is Different presents a comprehensive look at the varieties of financial crises, and guides us through eight astonishing centuries of government defaults, banking panics, and inflationary spikes--from medieval currency debasements to today's subprime catastrophe. Carmen Reinhart and Kenneth Rogoff, leading economists whose work has been influential in the policy debate concerning the current financial crisis, provocatively argue that financial combustions are universal rites of passage for emerging and established market nations. The authors draw important lessons from history to show us how much--or how little--we have learned.

Large‐scale brain network function is critical for healthy cognition, yet links between such network function, neurochemistry, and smaller‐scale neurocircuitry are unclear. Here, we evaluated 59 healthy individuals using resting‐state fMRI to determine how network‐level temporal dynamics were impacted by two well‐characterized pharmacotherapies targeting catecholamines: methylphenidate (20 mg) and haloperidol (2 mg)—administered via randomized, double‐blind, placebo‐controlled design. Network temporal dynamic changes were tested for links with drug‐induced alterations in complex corticostriatal connections as this circuit is a primary site of action for both drugs. Methylphenidate increased time in the default mode network state (DMN p < 0.001) and dorsal attention network state (DAN p < 0.001) and reduced time in the frontoparietal network state (p < 0.01). Haloperidol increased time in a sensory motor‐DMN state (p < 0.01). The magnitude of change in network dynamics induced by methylphenidate vs. placebo correlated with the magnitude of methylphenidate‐induced rearrangement of complex corticostriatal connectivity (R = 0.32, p = 0.014). Haloperidol did not alter complex corticostriatal connectivity. Methylphenidate enhanced time in network states involved in internal and external attention (DMN and DAN, respectively), aligning with methylphenidate's established role in attention. Methylphenidate also significantly changed complex corticostriatal connectivity by altering the relative strength between multiple corticostriatal connections, indicating that methylphenidate may shift which corticostriatal connections are prioritized relative to others. Findings show that these corticostriatal circuit changes are linked with large‐scale network temporal dynamics. Collectively, these findings provide a deeper understanding of large‐scale network function, set a stage for mechanistic understanding of network engagement, and provide useful information to guide medication use based on network‐level effects. Trial Registration: Registry name: ClinicalTrials.gov; URL: Brain Networks and Addiction Susceptibility—Full Text View—ClinicalTrials.gov; URL Plain text: https://classic.clinicaltrials.gov/ct2/show/NCT01924468; Identifier: NCT01924468 At rest, the dopamine/norepinephrine agonist, methylphenidate, enhances time spent in external and internal attentional neurobiological states (DAN and DMN, respectively), suggesting the brain is primed to respond to different attentional demands. Large‐scale network dynamics relate to drug‐induced changes in complex corticostriatal connectivity, revealing direct links between circuit‐level and network‐level effects.

A single dose of psilocybin, a psychedelic that acutely causes distortions of space–time perception and ego dissolution, produces rapid and persistent therapeutic effects in human clinical trials 1 – 4 . In animal models, psilocybin induces neuroplasticity in cortex and hippocampus 5 – 8 . It remains unclear how human brain network changes relate to subjective and lasting effects of psychedelics. Here we tracked individual-specific brain changes with longitudinal precision functional mapping (roughly 18 magnetic resonance imaging visits per participant). Healthy adults were tracked before, during and for 3 weeks after high-dose psilocybin (25 mg) and methylphenidate (40 mg), and brought back for an additional psilocybin dose 6–12 months later. Psilocybin massively disrupted functional connectivity (FC) in cortex and subcortex, acutely causing more than threefold greater change than methylphenidate. These FC changes were driven by brain desynchronization across spatial scales (areal, global), which dissolved network distinctions by reducing correlations within and anticorrelations between networks. Psilocybin-driven FC changes were strongest in the default mode network, which is connected to the anterior hippocampus and is thought to create our sense of space, time and self. Individual differences in FC changes were strongly linked to the subjective psychedelic experience. Performing a perceptual task reduced psilocybin-driven FC changes. Psilocybin caused persistent decrease in FC between the anterior hippocampus and default mode network, lasting for weeks. Persistent reduction of hippocampal-default mode network connectivity may represent a neuroanatomical and mechanistic correlate of the proplasticity and therapeutic effects of psychedelics. Healthy adults were tracked before, during and after high doses of psilocybin and methylphenidate to assess how psychedelics can change human brain networks, and psilocybin was found to massively disrupt functional connectivity in cortex and subcortex with some changes persisting for weeks.

The default-mode network (DMN) is a set of functionally connected regions that play crucial roles in internal cognitive processing. Previous resting-state fMRI studies have demonstrated that the intrinsic functional organization of the DMN undergoes remarkable reconfigurations during childhood and adolescence. However, these studies have mainly focused on cross-sectional designs with small sample sizes, limiting the consistency and interpretations of the findings. Here, we used a large sample of longitudinal resting-state fMRI data comprising 305 typically developing children (6–12 years of age at baseline, 491 scans in total) and graph theoretical approaches to delineate the developmental trajectories of the functional architecture of the DMN. For each child, the DMN was constructed according to a prior parcellation with 32 brain nodes. We showed that the overall connectivity increased in strength from childhood to adolescence and became spatially similar to that in the young adult group (N = 61, 18–28 years of age). These increases were primarily located in the midline structures. Global and local network efficiency in the DMN also increased with age, indicating an enhanced capability in parallel information communication within the brain system. Based on the divergent developmental rates of nodal centrality, we identified three subclusters within the DMN, with the fastest rates in the cluster mainly comprising the anterior medial prefrontal cortex and posterior cingulate cortex. Together, our findings highlight the developmental patterns of the functional architecture in the DMN from childhood to adolescence, which has implications for the understanding of network mechanisms underlying the cognitive development of individuals.

Adolescence is a time of rapid neurodevelopment and the endocannabinoid system is particularly prone to change during this time. Cannabis is a commonly used drug with a particularly high prevalence of use among adolescents. The two predominant phytocannabinoids are Delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), which affect the endocannabinoid system. It is unknown whether this period of rapid development makes adolescents more or less vulnerable to the effects of cannabis on brain-network connectivity, and whether CBD may attenuate the effects of THC. Using fMRI, we explored the impact of vaporized cannabis (placebo, THC: 8 mg/75 kg, THC + CBD: 8 mg/75 kg THC & 24 mg/75 kg CBD) on resting-state networks in groups of semi-regular cannabis users (usage frequency between 0.5 and 3 days/week), consisting of 22 adolescents (16–17 years) and 24 young adults (26–29 years) matched for cannabis use frequency. Cannabis caused reductions in within-network connectivity in the default mode (F[2,88] = 3.97, P = 0.022, η² = 0.018), executive control (F[2,88] = 18.62, P < 0.001, η² = 0.123), salience (F[2,88] = 12.12, P < 0.001, η² = 0.076), hippocampal (F[2,88] = 14.65, P < 0.001, η² = 0.087), and limbic striatal (F[2,88] = 16.19, P < 0.001, η² = 0.102) networks compared to placebo. Whole-brain analysis showed cannabis significantly disrupted functional connectivity with cortical regions and the executive control, salience, hippocampal, and limbic striatal networks compared to placebo. CBD did not counteract THC’s effects and further reduced connectivity both within networks and the whole brain. While age-related differences were observed, there were no interactions between age group and cannabis treatment in any brain network. Overall, these results challenge the assumption that CBD can make cannabis safer, as CBD did not attenuate THC effects (and in some cases potentiated them); furthermore, they show that cannabis causes similar disruption to resting-state connectivity in the adolescent and adult brain.

RationalePrevious neuroimaging studies of cognition involving nicotinic acetylcholine receptor (nAChR) agonist administration have repeatedly found enhanced task-induced deactivation of regions of the default mode network (DMN), a group of brain systems that is more active at rest and mediates task-independent thought processes. This effect may be related to pro-cognitive nAChR agonist effectsObjectivesThe present study sought to test whether nAChR modulation of the DMN is bi-directional, i.e., whether a nAChR antagonist would reduce task-induced deactivation.MethodsEighteen healthy non-smokers underwent functional magnetic resonance imaging while performing a letter N-back task. Scans were performed after nicotine administration (7 mg/24 h, transdermally), after administration of the nAChR antagonist mecamylamine (7.5 mg, p.o.), and after double placebo, in counterbalanced sequence. Blood-oxygen-level-dependent (BOLD) signal was analyzed within ventromedial prefrontal cortex (vmPFC) and posterior cingulate cortex (PCC) regions of interest—central hubs of the DMN in which consistent nAChR agonist–induced changes had previously been identified.ResultsNicotine enhanced hit rate in both the 0-back and 2-back condition, while mecamylamine slowed reaction time in the 2-back condition. Mecamylamine reduced task-induced deactivation of vmPFC and PCC. Nicotine had no significant effects on the BOLD signal.ConclusionsThe finding that nAChR tone reduction by mecamylamine weakened task-induced DMN deactivation indicates that a constant tone of nAChR activation helps regulate DMN activity in healthy individuals. This suggests that low nAChR tone may play a causal role in DMN dysregulation seen in conditions such as mild cognitive impairment or Alzheimer’s disease.

We use survey data to measure households' propensity to default on mortgages even if they can afford to pay them (strategic default) when the value of the mortgage exceeds the value of the house. The willingness to default increases in both the absolute and the relative size of the home-equity shortfall. Our evidence suggests that this willingness is affected by both pecuniary and non-pecuniary factors, such as views about fairness and morality. We also find that exposure to other people who strategically defaulted increases the propensity to default strategically because it conveys information about the probability of being sued.

This paper builds a model of a sovereign borrower that has access to credit from private sector creditors and an IFI. Private sector creditors and the IFI offer different debt contracts that are modelled based on the institutional frameworks of these two types of debt. We analyze the decisions of a sovereign on how to allocate its borrowing needs between these two types of creditors, and when to default on its debt to the private sector creditor. The numerical analysis shows that, consistent with the data; the model predicts countercyclical IFI debt along with procyclical commercial debt flows, also matching other features of the data such as frequency of IFI borrowing and mean IFI debt stock.

The effects of prolonged infrasound (IS) exposure on brain function and behavior are largely unknown, with only one prior study investigating functional connectivity (FC) changes. In a long-term randomized-controlled trial, 38 participants were exposed to inaudible airborne IS (6 Hz, 80–90 dB) or sham devices for four weeks (8 h/night). We assessed FC changes in resting-state networks (auditory, default mode (DMN), sensorimotor (SMN), and executive control (ECN)), and explored IS ‘sensitivity’ as a predictor of identified significant FC changes. We also examined correlations between somatic symptoms and FC. IS exposure led to decreased FC in the right precuneus (DMN) and increased FC in the Vermis IV and V (SMN). In the ECN, we observed increased FC in the right frontal middle gyrus (BA8) and the right inferior parietal lobe, and decreased FC in another region of the right frontal middle gyrus. Changes in the ECN (right inferior parietal lobe) were negatively associated with self-reported annoyance from IS/low-frequency noise. A significant negative association was found between FC changes in the DMN (right precuneus) and somatic symptoms. Our study is the first to investigate prolonged IS exposure effects on brain FC, revealing changes in the vDMN, SMN, and ECN, but not in the auditory network. Future studies should assess annoyance and sensitivity markers, fine-grained measures of somatic symptoms, and stratify samples by sensitivity to uncover individual differences in response to IS.