U.S. Infrastructure: 1929-2023

This paper examines the history of U.S. infrastructure since 1929 and in the process reports an interesting fact about the U.S. economy. Infrastructure stock as a percent of GDP began a steady decline around 1970, and the government budget deficit became positive and large at roughly the same time. The infrastructure pattern in other countries does not mirror that in the United States, so the United States appears to be a special case. The overall results suggest that the United States became less future oriented beginning around 1970, an increase in the social discount rate. This change has persisted. This is the interesting fact. The paper contains speculation on possible causes

Policy Note | Weekly Fed Report Still Drives Discount Window Stigma

As banking regulators work to destigmatize the Federal Reserve’s discount window—and fervently so since the 2023 banking crisis—they’ve pointed to several potentially fruitful policy routes. These have included supervisory improvements, regulatory changes, and operational enhancements by both the banks and the Fed. Left off the menu so far have been changes to the Fed’s weekly publications that reveal up-to-date discount window borrowing data by regional geography. Reforms following the Global Financial Crisis of 2007–2009 have made mandatory the disclosure of discount window borrowers on a two-year lag—higher transparency than previously when no disclosure was required. However, bigger banks, such as those that failed or otherwise came under severe market pressure in the Banking Crisis of 2023, remain at risk of their borrowing being disclosed on a weekly basis, despite Fed changes in its reporting in 2020 that were intended to address this risk. This article shows how these weekly Fed balance sheet publications, as structured, still reveal any individual large bank’s discount window borrowing in a particular geography. The pursuant risk of the market’s discovery of such discount window borrowing has further stigmatized discount window use, undermining policymakers’ other destigmatization efforts to encourage its use when appropriate

YPFS Lessons Learned Oral History Project: An Interview with Ádám Banai

The Yale Program on Financial Stability (YPFS) interviewed Ádám Banai regarding his time as an analyst and director of the National Bank of Hungary (Magyar Nemzeti Bank, or MNB) during the Global Financial Crisis (GFC) and in the subsequent era to date

A Hero\u27s Journey: Experiences Using A Therapeutic Comicbook In A Children’s Psychiatric Inpatient Unit

Children’s mental health care has been on the decline since the start of the century. The COVID-19 pandemic further unearthed this significant worsening of mental health in children with heightened levels of anxiety, depression, loneliness, anger, and fatigue leading to an increase in the number of emergency room visits and inpatient hospitalizations. Art and narrative-based interventions are known to improve patient outcomes and are a crucial component of pediatric inpatient psychiatric care. We discuss the process of adoption of a novel therapeutic comic book that was developed for children admitted to the hospital in a psychiatric inpatient unit at Yale-New Haven Hospital. A Hero’s Journey, a 38-page zine, is a short booklet that was created to demystify the experience of hospitalization, provide scaffolding for skill-building, and promote interaction and socialization. The zine was administered to patients and subsequently, 19 interviews were done with healthcare providers. Using qualitative research methods, a thematic analysis was performed. Three main domains were identified. The main domains of themes were: 1) Implementing or rolling-out of the zine: what worked and what did not work during the process of rollout; 2) Optimizing: the zine was appropriate in length and content for the patient population at hand; 3) Anticipating: the zine has potential areas for growth and development. The zine is a wonderful resource. Yet its implementation faced many challenges including staffing shortages and time constraints. Some ways to overcome these are having a champion for the zine, educating each user on the content, using individual pages of the zine instead of the whole booklet, and exploring avenues for personalization

Somatic Mutations In Aging, Paroxysmal Nocturnal Hemoglobinuria, And Myeloid Neoplasms

Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal blood disorder frequently associated with bone marrow failure that in rare instances can progress to leukemia. PNH clones of varying sizes occasionally present even in patients with hematologic malignancies and no known history of classical PNH, particularly in myelodysplastic neoplasms (MDS). Curiously, somatic driver mutations considered to be pathogenic and likely pathogenic in myeloid leukemias can be found in phenotypically normal, elderly individuals, as well as those with clonal disorders such as PNH, clonal hematopoiesis of indeterminate potential (CHIP), and age-related clonal hematopoiesis (ARCH). These mutations may be the critical link between PNH and the development of cancer. We suspect that PNH clones, derived from mutations in PIGA, may reflect a disordered bone marrow prone to additional genetic hits involved in tumorigenesis. It is uncertain, however, whether leukemic cells directly arise from PNH+ progenitors with additional genetic variants or if they are in fact distinct populations. Moreover, the specific driver mutations that underlie both PNH and myeloid neoplasms remains an area of active investigation. Our study aims to characterize the prevalence of myeloid neoplasm-associated somatic mutations in older adults and in patients who develop myeloid malignancies (MN+ patients), stratified by whether they also harbor PNH clones. We retrospectively examined the initial genetic evaluation by next-generation sequencing (NGS) of 197 individuals at Yale-New Haven Hospital and elicited the most common driver mutations and their association with age and PNH clonal presence. We demonstrated that pathogenic and likely pathogenic somatic mutations increased with age (average age of patients with one or more mutations was 69.8 years compared to 58.0 years in those with no mutations of interest, p\u3c 0.0001). Variants in SF3B1 (average age= 74.4 years, p= 0.0015), TP53 (average age= 72.8 years, p= 0.0057), SRSF2 (average age= 72.4 years, p= 0.0024), DNMT3A (average age= 71.9 years, p= 0.0059), TET2 (average age= 70.8 years, p= 0.0032), ASXL1 (average age= 70 years, p= 0.0052), and U2AF1 (average age= 69.7 years, p= 0.0082) were most commonly present in adults who were significantly older than those with no relevant mutations. Those with a diagnosis of a myeloid neoplasm were drastically more likely to harbor driver mutations (81.1% with at least one variant of interest vs. 23.5% among those without a myeloid neoplasm, p\u3c 0.0001), and had a greater number of mutations on average (1.95 vs. 0.38 mutations per patient, p\u3c 0.0001). Interestingly, MN+ patients who had a PNH clone ≥0.01% were significantly more likely to possess a neoplasm-associated mutation than those with no PNH clones (91.9% vs. 60.6%, p= 0.0005), indicating that the presence of PNH clones augments the odds of possessing cancer-related genetic lesions as early as the time of the initial evaluation. Specifically, patients who were both MN+ and PNH+ were more likely than their PNH- counterparts to have one or two pathogenic and likely pathogenic variants (58.1% vs. 27.3%), though they were equally likely to possess three or more mutations (33.9% vs. 33.3%). Furthermore, among all patients in the cohort ≥70 years, PNH presence significantly increased the overall likelihood of discovering relevant gene variants (78.9% vs. 48.7%, ?2 p= 0.0027). Among all patients, PNH clone presence was correlated with mutations in SF3B1 (85.7% of cases with SF3B1 variants had PNH clones compared 56.8% of cases with no mutations had PNH clones, Fisher’s exact test, p= 0.0402), and to a lesser degree, with RUNX1 (83.3% PNH+ cases, p= 0.0686) and DNMT3A (80.0% PNH+ cases, p= 0.0914). Finally, we qualitatively described that mutations in ASXL1, TET2, and SRSF2 tended to occur together; there were also concomitant mutations in TET2 with EZH2 and in SF3B1 with RUNX1. Therefore, we recommend early genetic screening of all elderly patients ≥70 years who present with PNH clones of any size in the peripheral blood as these patients have a higher likelihood of harboring pathogenic and likely pathogenic driver mutations. We demonstrated that certain neoplasm-associated mutations are common in elderly patients, while others correlated with PNH clone presence, and that some variants tend to co-occur. Future studies should address the molecular mechanisms of these lesions in leukemogenesis. The observation that PNH clone presence is significantly correlated with somatic mutations in MN+ disease suggests an important relationship between PNH clones and cancer, either as direct tumor precursor populations or as an incidental consequence of high genetic mutability in a vulnerable bone marrow