Paul M. Warburg: Founder of the United States Federal Reserve

The name Paul Moritz Warburg is synonymous with the founding of the Federal Reserve System. Over the years preceding the formation of the Federal Reserve, Warburg wrote many essays and gave many public addresses on banking reform. His reform ideas were modeled on the central banking systems of many European counties he dealt with through the family business M.M. Warburg

Benjamin Strong Jr.: The Common Monetary Thread

Benjamin Strong Jr. entered the banking industry after he graduated from public high school. Over the years he developed a deep knowledge of the banking history of the United States. Coupled with an intense interest in international affairs, he became a dominant force in U.S. monetary and banking affairs. In 1914 Strong was elected president of the Federal Reserve Bank of New York, where he served until his death in 1928

The Birth of the U.S. Federal Reserve

On November 16, 2014 the United States Federal Reserve celebrated the centennial of its organization. Its one hundred year legacy has left no doubt of its vast monetary control, its far-reaching geopolitical power, and its enigmatic secrecy. These defining features of the Fed remain a mirror of the men who created it. Wall Street barons and ambitious politicians vied for control over shaping the U.S. Federal Reserve to the specifications that suited the needs of both their country and themselves. This paper covers men like Senator Nelson Aldrich, J.P. Morgan, Jacob Schiff, and Paul M. Warburg, who were the undeniable masterminds of the structuring the Fed from inception to completion, and whose ambition molded them and other men like them into the most salient candidates for creating the only permanent central banking system in United States history

Cabbage and fermented vegetables : From death rate heterogeneity in countries to candidates for mitigation strategies of severe COVID-19

Large differences in COVID-19 death rates exist between countries and between regions of the same country. Some very low death rate countries such as Eastern Asia, Central Europe, or the Balkans have a common feature of eating large quantities of fermented foods. Although biases exist when examining ecological studies, fermented vegetables or cabbage have been associated with low death rates in European countries. SARS-CoV-2 binds to its receptor, the angiotensin-converting enzyme 2 (ACE2). As a result of SARS-CoV-2 binding, ACE2 downregulation enhances the angiotensin II receptor type 1 (AT(1)R) axis associated with oxidative stress. This leads to insulin resistance as well as lung and endothelial damage, two severe outcomes of COVID-19. The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is the most potent antioxidant in humans and can block in particular the AT(1)R axis. Cabbage contains precursors of sulforaphane, the most active natural activator of Nrf2. Fermented vegetables contain many lactobacilli, which are also potent Nrf2 activators. Three examples are: kimchi in Korea, westernized foods, and the slum paradox. It is proposed that fermented cabbage is a proof-of-concept of dietary manipulations that may enhance Nrf2-associated antioxidant effects, helpful in mitigating COVID-19 severity.Peer reviewe

Nrf2-interacting nutrients and COVID-19 : time for research to develop adaptation strategies

There are large between- and within-country variations in COVID-19 death rates. Some very low death rate settings such as Eastern Asia, Central Europe, the Balkans and Africa have a common feature of eating large quantities of fermented foods whose intake is associated with the activation of the Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) anti-oxidant transcription factor. There are many Nrf2-interacting nutrients (berberine, curcumin, epigallocatechin gallate, genistein, quercetin, resveratrol, sulforaphane) that all act similarly to reduce insulin resistance, endothelial damage, lung injury and cytokine storm. They also act on the same mechanisms (mTOR: Mammalian target of rapamycin, PPAR gamma:Peroxisome proliferator-activated receptor, NF kappa B: Nuclear factor kappa B, ERK: Extracellular signal-regulated kinases and eIF2 alpha:Elongation initiation factor 2 alpha). They may as a result be important in mitigating the severity of COVID-19, acting through the endoplasmic reticulum stress or ACE-Angiotensin-II-AT(1)R axis (AT(1)R) pathway. Many Nrf2-interacting nutrients are also interacting with TRPA1 and/or TRPV1. Interestingly, geographical areas with very low COVID-19 mortality are those with the lowest prevalence of obesity (Sub-Saharan Africa and Asia). It is tempting to propose that Nrf2-interacting foods and nutrients can re-balance insulin resistance and have a significant effect on COVID-19 severity. It is therefore possible that the intake of these foods may restore an optimal natural balance for the Nrf2 pathway and may be of interest in the mitigation of COVID-19 severity

Rhinosinusitis: Developing guidance for clinical trials

The Rhinosinusitis Initiative was developed by 5 national societies. The current guidance document is an expansion of the 2004 publication, "Rhinosinusitis: Establishing definitions for clinical research and patient care" and provides templates for clinical trials in antimicrobial, anti-inflammatory, and symptom-relieving therapies for the following: (1) acute presumed bacterial rhinosinusitis, (2) chronic rhinosinusitis (CRS) without nasal polyps, (3) CRS with nasal polyps, and (4) classic allergic fungal rhinosinusitis. In addition to the templates for clinical trials and proposed study designs, the Rhinosinusitis Initiative has developed 6 appendices, which address (1) health outcomes, (2) nasal endoscopy and staging of CRS, (3) rardiologic imaging, (4) microbiology, (5) laboratory measures, and (6) biostatistical methods. (C) 2006 American Academy of Otolaryngology-Head and Neck Surgery Foundation, Inc. All rights reserved

International consensus statement on allergy and rhinology : rhinosinusitis

Background: The body of knowledge regarding rhinosinusitis (RS) continues to expand, with rapid growth in number of publications, yet substantial variability in the quality of those presentations. In an effort to both consolidate and critically appraise this information, rhinologic experts from around the world have produced the International Consensus Statement on Allergy and Rhinology: Rhinosinusitis(ICAR:RS). Methods: Evidence-based reviews with recommendations(EBRRs) were developed for scores of topics, using previously reported methodology. Where existing evidence was insufficient for an EBRR, an evidence-based review (EBR)was produced. The sections were then synthesized and the entire manuscript was then reviewed by all authors for consensus. Results: The resulting ICAR:RS document addresses multiple topics in RS, including acute RS (ARS), chronic RS (CRS)with and without nasal polyps (CRSwNP and CRSsNP), re-current acute RS (RARS), acute exacerbation of CRS (AE-CRS), and pediatric RS. Conclusion: As a critical review of the RS literature, ICAR:RS provides a thorough review of pathophysiology and evidence-based recommendations for medical and surgical treatment. It also demonstrates the significant gaps in our understanding of the pathophysiology and optimal management of RS. Too often the foundation upon which these recommendations are based is comprised of lower-level evidence. It is our hope that this summary of the evidence in RS will point out where additional research efforts may be directed.188 page(s

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Isam Alobid, MD, PhD(1) , Nithin D. Adappa, MD(2) , Henry P. Barham, MD(3) , Thiago Bezerra, MD(4) , Nadieska Caballero, MD(5) , Eugene G. Chang, MD(6) , Gaurav Chawdhary, MD(7) , Philip Chen, MD(8) , John P. Dahl, MD, PhD(9) , Anthony Del Signore, MD(10) , Carrie Flanagan, MD(11) , Daniel N. Frank, PhD(12) , Kai Fruth, MD, PhD(13) , Anne Getz, MD(14) , Samuel Greig, MD(15) , Elisa A. Illing, MD(16) , David W. Jang, MD(17) , Yong Gi Jung, MD(18) , Sammy Khalili, MD, MSc(19) , Cristobal Langdon, MD(20) , Kent Lam, MD(21) , Stella Lee, MD(22) , Seth Lieberman, MD(23) , Patricia Loftus, MD(24) , Luis Macias-Valle, MD(25) , R. Peter Manes, MD(26) , Jill Mazza, MD(27) , Leandra Mfuna, MD(28) , David Morrissey, MD(29) , Sue Jean Mun, MD(30) , Jonathan B. Overdevest, MD, PhD(31) , Jayant M. Pinto, MD(32) , Jain Ravi, MD(33) , Douglas Reh, MD(34) , Peta L. Sacks, MD(35) , Michael H. Saste, MD(36) , John Schneider, MD, MA(37) , Ahmad R. Sedaghat, MD, PhD(38) , Zachary M. Soler, MD(39) , Neville Teo, MD(40) , Kota Wada, MD(41) , Kevin Welch, MD(42) , Troy D. Woodard, MD(43) , Alan Workman(44) , Yi Chen Zhao, MD(45) , David Zopf, MD(46) CONTRIBUTING AUTHOR AFFILIATIONS: (1) Universidad de Barcelona; (2) University of Pennsylvania; (3) Louisiana State University Health Sciences Center; (4) Universidade de São Paulo; (5) ENT Specialists of Illinois; (6) University of Arizona; (7) University of Oxford; (8) University of Texas; (9) University of Indiana; (10) Mount Sinai Beth Israel; (11) Emory University; (12) University of Colorado; (13) Wiesbaden, Germany; (14) University of Colorado; (15) University of Alberta; (16) University of Alabama at Birmingham; (17) Duke University; (18) Sungkyunkwan University; (19) University of Pennsylvania; (20) Universidad de Barcelona; (21) Northwestern University; (22) University of Pittsburgh; (23) New York University; (24) Emory University; (25) University of British Columbia; (26) Yale University School of Medicine; (27) Private Practice; (28) Department of Otolaryngology, Hôtel-Dieu Hospital, Centre de Recherche du Centre Hospitalier de l'Université de Montréal; (29) University of Adelaide; (30) Pusan National University; (31) University of California, San Francisco; (32) University of Chicago; (33) University of Auckland; (34) Johns Hopkins University; (35) University of New South Wales, Australia; (36) Stanford University; (37) Washington University; (38) Harvard Medical School; (39) Medical University of South Carolina; (40) Singapore General Hospital; (41) Taho University; (42) Northwestern University; (43) Cleveland Clinic Foundation; (44) University of Pennsylvania; (45) University of Adelaide; (46) University of Michigan.status: publishe

Differential Enzymatic Activity of Common Haplotypic Versions of the Human Acidic Mammalian Chitinase Protein*

Mouse models have shown the importance of acidic mammalian chitinase activity in settings of chitin exposure and allergic inflammation. However, little is known regarding genetic regulation of AMCase enzymatic activity in human allergic diseases. Resequencing the AMCase gene exons we identified 8 non-synonymous single nucleotide polymorphisms including three novel variants (A290G, G296A, G339T) near the gene area coding for the enzyme active site, all in linkage disequilibrium. AMCase protein isoforms, encoded by two gene-wide haplotypes, and differentiated by these three single nucleotide polymorphisms, were recombinantly expressed and purified. Biochemical analysis revealed the isoform encoded by the variant haplotype displayed a distinct pH profile exhibiting greater retention of chitinase activity at acidic and basic pH values. Determination of absolute kinetic activity found the variant isoform encoded by the variant haplotype was 4-, 2.5-, and 10-fold more active than the wild type AMCase isoform at pH 2.2, 4.6, and 7.0, respectively. Modeling of the AMCase isoforms revealed positional changes in amino acids critical for both pH specificity and substrate binding. Genetic association analyses of AMCase haplotypes for asthma revealed significant protective associations between the variant haplotype in several asthma cohorts. The structural, kinetic, and genetic data regarding the AMCase isoforms are consistent with the Th2-priming effects of environmental chitin and a role for AMCase in negatively regulating this stimulus

High evolutionary turnover of satellite families in Caenorhabditis

Background. The high density of tandem repeat sequences (satellites) in nematode genomes and the availability of genome sequences from several species in the group offer a unique opportunity to better understand the evolutionary dynamics and the functional role of these sequences. We take advantage of the previously developed SATFIND program to study the satellites in four Caenorhabditis species and investigate these questions./nMethods. The identification and comparison of satellites is carried out in three steps. First we find all the satellites present in each species with the SATFIND program. Each satellite is defined by its length, number of repeats, and repeat sequence. Only satellites with at least ten repeats are considered. In the second step we build satellite families with a newly developed alignment program. Satellite families are defined by a consensus sequence and the number of satellites in the family. Finally we compare the consensus sequence of satellite families in different species./nResults. We give a catalog of individual satellites in each species. We have also identified satellite families with a related sequence and compare them in different species. We analyze the turnover of satellites: they increased in size through duplications of fragments of 100-300 bases. It appears that in many cases they have undergone an explosive expansion. In C. elegans we have identified a subset of large satellites that have strong affinity for the centromere protein CENP-A. We have also compared our results with those obtained from other species, including one nematode and three mammals./nConclusions. Most satellite families found in Caenorhabditis are species-specific; in particular those with long repeats. A subset of these satellites may facilitate the formation of kinetochores in mitosis. Other satellite families in C. elegans are either related to Helitron transposons or to meiotic pairing centers.We are thankful to Dr. Lourdes Campos for valuable suggestions. Also to Messrs. W. Blevins and F. Acosta-Reyes for help in the preparation of the manuscript and figures. This work was funded by Ministerio de Economía y Competitividad (TIN2010-21062-C02-01, TIN2013-45732-C4-3-P, BFU2012-36820 and 2009–10380) with additional Feder funds