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Politics, markets, and Mexico's \London debt,\ 1823-1887
In 1823 and 1824, the newly independent government of Mexico entered the international capital market, raising two loans in London totaling ¹6.4 million. Intended to cover a variety of expenses, the loans fell into default by 1827 and remained in default until 1887. THis case study explores how the loan process worked in Mexico in the early nineteenth century, when foreign lending was still a novelty, and he unexpected ways in which international debt could influence politics and policy. The history of the loans, the efforts of successive governments in Mexico to resume repayment, and the efforts of the foreign lenders to recover their investment became one of the most significant, persistent, and contentious, if largely misunderstood, issues in the political and financial history of nineteenth-century Mexico. The loans themselves became entangled in partisan politics in Mexico and abroad, especially in Great Britain and France, and were a fertile source of speculation for a wide range of legitimate--and not-so-legitimate--international financiers, including Baring Brothers and the House of Lizardi.
Book
White House warns of default danger
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.
Streaming Video
Catecholaminergic Modulation of Large‐Scale Network Dynamics Is Tied to the Reconfiguration of Corticostriatal Connectivity
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.
Journal Article
American default : the untold story of FDR, the Supreme Court, and the battle over gold
The untold story of how FDR did the unthinkable to save the American economy.
BOOK
Psilocybin desynchronizes the human brain
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
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. 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.
Journal Article
Development of the default-mode network during childhood and adolescence: A longitudinal resting-state fMRI study
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.
Journal Article
Nicotinic receptor modulation of the default mode network
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.
Journal Article
Credit Ratings and Credit Risk: Is One Measure Enough?
This paper investigates the information in corporate credit ratings. If ratings are to be informative indicators of credit risk, they must reflect what a risk-averse investor cares about: both raw default probability and systematic risk. We find that ratings are relatively inaccurate measures of raw default probability—they are dominated as predictors of failure by a simple model based on publicly available financial information. However, ratings do contain relevant information since they are related to a measure of exposure to common (and undiversifiable) variation in default probability (“failure beta”). Systematic risk is shown to be related to joint default probabilities in the context of the Merton [Merton RC (1974) On the pricing of corporate debt: The risk structure of interest rates.
J. Finance
29(2):449–470] model. Empirically, it is related to credit default swap spreads and risk premia. Given the multidimensional nature of credit risk, it is not possible for one measure to capture all the relevant information.
This paper was accepted by Gustavo Manso, finance
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Journal Article