To Bear Arms (First prize, Peter Sears Prize in Poetry)

Winner of Peter Sears Poetry Priz

“Mes dernières volontés”: Testaments to the Life of Marie Couvent, a Former Slave in New Orleans

In her last will and testament recorded on November 12, 1832, Marie Justine Cirnaire, Veuve Couvent claimed a lasting legacy as a patron of African American education in New Orleans when she declared that a school be established on her property. It is little known, however, that Couvent, in fact, made two wills, the first dated twenty years earlier. Through a close reading of Couvent’s testaments, this article will explore the life of a woman who was born in Africa, enslaved in Saint-Domingue, and died a free and wealthy slave owner in New Orleans. As catalogs of material accumulation, acts of autobiography, and maps of social networks these wills suggest the ways Couvent and other former slaves created identities as free people through property ownership and personal relationships.Dans son testament enregistré le 12 novembre 1832, Marie Justine Cirnaire, veuve Couvent, s’attribuait durablement un rôle-clé dans le soutien à l’éducation des Afro-Américains à la Nouvelle-Orléans en émettant le vœu qu’une école soit établie pour eux sur sa propriété. Ce que l’on sait moins, c’est qu’elle écrivit en fait deux testaments, puisqu’un premier avait été enregistré 20 ans auparavant. À travers une analyse précise de ces deux testaments, cet article examine la vie d’une femme née en Afrique, réduite en esclavage à Saint-Domingue, et qui mourut libre, riche propriétaire d’esclave à la Nouvelle-Orléans. En tant que catalogues de ses biens matériels accumulés, mais aussi comme fragments d’autobiographie et cartographies de réseaux sociaux, ces testaments révèlent comment Mme Couvent et d’autres anciens esclaves se sont créé une identité de personnes libres grâce à la propriété et à leurs relations personnelles

The Life and Legacy of Marie Couvent: Social Networks, Property Ownership, and the Making of a Free People of Color Community in New Orleans.

This dissertation recovers the life of Marie Justine Sirnir Couvent and the Atlantic World she inhabited. Born in Africa around 1757, she was enslaved as a child and shipped to Saint-Domingue through the Bight of Benin in the 1760s. In the tumult of the Haitian Revolution, Couvent fled the island, along with tens of thousands of Saint-Domingue inhabitants. She resettled in New Orleans where she eventually died a free and wealthy slaveholder in 1837. Although illiterate, Couvent left property to establish a free black school in her will. L\u27Institution Catholique des Orphelins Indigents was founded on her land in 1847 and a school operated on the site for over 150 years. This unique example of free black philanthropy in New Orleans demonstrates how the city\u27s free people of color built a community through social ties, property, and collective institutions as the center of slavery shifted to the Deep South.;The dissertation traces both Couvent\u27s geographic movement from the Slave Coast through the French Caribbean to New Orleans and her social mobility from slave to free and from property to property owner. I argue that Couvent utilized social networks and property ownership to rebuild her life in New Orleans and participate in the development of a free people of color community. Couvent formed important social connections at all stages of her life that aided her survival of slavery and her relocation to Louisiana. Reconstructing her social networks in New Orleans reveals a shift from relationships centered on multiracial, Saint-Dominguan ties to a network dominated by free people of color, as Couvent became integrated into the city\u27s existing free black population. One way Couvent formed new relationships was through the acquisition and exchange of property. In addition to gaining economic security, Couvent bolstered her free status, created a family, and assisted in the creation of free black collective institutions through her property ownership. Taking into account her African birth and experience of enslavement in the Saint-Dominguan port city of Cap Francais, I analyze the different types of property Couvent owned separately to illustrate how property ownership facilitated as well as complicated the development of a free people of color community in New Orleans.;Her singular bequest and the remarkable endurance of the school have sustained Couvent\u27s legacy in New Orleans as a patron of African American education. A final chapter traces the history of the school(s) and the emphasis its administrators placed on education as a tool to challenge racial prejudice and combat inequality. Couvent remains within New Orleans\u27 public memory, but how she has been remembered varied over the twentieth century. The dissertation concludes with an analysis of the multiple interpretations of Couvent\u27s legacy

“Mes dernières volontés”: Testaments to the Life of Marie Couvent, a Former Slave in New Orleans

In her last will and testament recorded on November 12, 1832, Marie Justine Cirnaire, Veuve Couvent claimed a lasting legacy as a patron of African American education in New Orleans when she declared that a school be established on her property. It is little known, however, that Couvent, in fact, made two wills, the first dated twenty years earlier. Through a close reading of Couvent’s testaments, this article will explore the life of a woman who was born in Africa, enslaved in Saint-Domingue, and died a free and wealthy slave owner in New Orleans. As catalogs of material accumulation, acts of autobiography, and maps of social networks these wills suggest the ways Couvent and other former slaves created identities as free people through property ownership and personal relationships.Dans son testament enregistré le 12 novembre 1832, Marie Justine Cirnaire, veuve Couvent, s’attribuait durablement un rôle-clé dans le soutien à l’éducation des Afro-Américains à la Nouvelle-Orléans en émettant le vœu qu’une école soit établie pour eux sur sa propriété. Ce que l’on sait moins, c’est qu’elle écrivit en fait deux testaments, puisqu’un premier avait été enregistré 20 ans auparavant. À travers une analyse précise de ces deux testaments, cet article examine la vie d’une femme née en Afrique, réduite en esclavage à Saint-Domingue, et qui mourut libre, riche propriétaire d’esclave à la Nouvelle-Orléans. En tant que catalogues de ses biens matériels accumulés, mais aussi comme fragments d’autobiographie et cartographies de réseaux sociaux, ces testaments révèlent comment Mme Couvent et d’autres anciens esclaves se sont créé une identité de personnes libres grâce à la propriété et à leurs relations personnelles

Lumican is upregulated in osteoarthritis and contributes to TLR4-induced pro-inflammatory activation of cartilage degradation and macrophage polarization

Objective: Lumican (LUM) is a major extracellular matrix glycoprotein in adult articular cartilage and its expression is known to be upregulated upon cartilage degeneration. LUM is associated with the pathogen-associated molecular pattern (PAMP) activation of the TLR4 signalling cascade, with TLR4 being highly associated with inflammation in rheumatic diseases. However, the main role of the LUM structural molecule in osteoarthritis (OA) remains elusive. The aim of this study was, therefore, to understand the role of LUM during TLR4-mediated activation in OA. Methods: After measuring LUM levels in synovial fluid (SF) of OA patients and lipopolysaccharide (LPS)-induced TLR4 activation, the role of LUM in the expression of pro-inflammatory molecules and cartilage degradation was assessed in vitro and ex vivo in a cartilage explant model. Primary macrophage activation and polarization were studied upon LUM co-stimulation with LPS. Results: We demonstrate that LUM is not only significantly upregulated in SF from OA patients compared to healthy controls, but also that LUM increases lipopolysaccharide (LPS)-induced TLR4 activation. Furthermore, we show that a pathophysiological level of LUM augments the LPS-induced TLR4 activation and expression of downstream pro-inflammatory molecules, resulting in extensive cartilage degradation. LUM co-stimulation with LPS also provided a pro-inflammatory stimulus, upregulating primary macrophage activation and polarization towards the M1-like phenotype. Conclusions: These findings strongly support the role of LUM as a mediator of PAMP-induced TLR4 activation of inflammation, cartilage degradation, and macrophage polarization in the OA joint and potentially other rheumatic diseases. (C) 2019 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.Peer reviewe

Exercise capacity in patients with repaired Tetralogy of Fallot aged 6 to 63 years

OBJECTIVES: This study aimed to provide a perspective for the interpretation of exercise capacity (peakVO2) in patients with repaired Tetralogy of Fallot (patients with rTOF) by describing the course of peakVO2 from patients aged 6-63 years. METHODS: A retrospective study was performed between September 2001 and December 2016 in the German Heart Centre Munich, Germany, and in the University Medical Centre Groningen, the Netherlands. A total of 1175 cardiopulmonary exercise tests (CPETs) were collected from 586 patients with rTOF, 46% female. Maximal exertion was verified using a respiratory exchange ratio ≥1.00. PeakVO2 was modelled using time-dependent multilevel models for repeated measurements (n=889 in 300 patients), and compared with subject-specific reference values calculated by the models of Bongers et al and Mylius et al. RESULTS: The peakVO2 of patients with rTOF was reduced at all ages. At the age of 6, the peakVO2 was 614 mL/min (70% of predicted (95% CI 67 to 73)). The reduced increase in peakVO2 during adolescence resulted in a significant lower maximum peakVO2 of 1209 mL/min at 25 years (65% predicted, p<0.001). A linear decline after 25 years was observed in patients and references, although patients showed an accelerated decline, with a -0.24% point of predicted (95% CI 0.11 to 0.38) per year without differences between sexes (p=0.263). CONCLUSIONS: This study provides a context for peakVO2 across ages in patients with rTOF under contemporary treatment strategies. It showed that the reduction in peakVO2 originates from childhood and declines over time. Sex differences in patients with rTOF were similar to natural existing sex differences

Reduced Handgrip Strength in Congenital Heart Disease With Regard to the Shunt Procedure in Infancy

Objective: In many patients with congenital heart disease (CHD) arterial blood flow to the arms is inhibited due to shunt surgery in infancy. This study investigates the handgrip strength of patients with CHD in regard to previous shunt procedures.Patients and Methods: Handgrip was evaluated in 424 patients with various CHD (189 female, age 28.1 ± 13.4 years) including 63 with shunt procedures in infancy; and 123 controls (51 female, 35.6 ± 14.2 years) using a Jamar dynamometer adjusted for hand size. The best of three repetitions was recorded for each side and the right-to-left hand ratio was calculated. The 63 shunted patients were grouped considering the side of the shunt: 14 right, 35 central and 14 left.Results: Patients with CHD, especially shunts, had significantly lower handgrip strength in the dominant hand than controls (controls: 43.2 ± 14.8 kg, CHD: 36.8 ± 14.8 kg, left shunt: 33.6 ± 14.6 kg, central shunt: 30.7 ± 15.2 kg and right shunt 27.8 ± 13.6 kg; p &lt; 0.001). In controls the right hand was 8.3% stronger, comparable to patients with either no shunt or central shunt (controls: 8.3 ± 13.2%; no shunt: 7.9 ± 15.3%; central shunt: 9.5 ± 18.1% p = 0.820). In patients with a left shunt the right hand was 22.5 ± 17.8% stronger than the left (p = 0.027 compared to central) while in those with a right shunt the right hand was 2.3 ± 18.3% weaker (p = 0.049 compared to central).Conclusions: Shunt procedures in infancy cause reduced handgrip strength in adulthood and diminished handgrip strength of the ipsilateral site

Oxygen Availability in Respiratory Muscles During Exercise in Children Following Fontan Operation

Introduction: As survival of previously considered as lethal congenital heart disease forms is the case in our days, issues regarding quality of life including sport and daily activities emerge. In patients with Fontan circulation, there is no pump to propel blood into the pulmonary arteries since the systemic veins are directly connected to the pulmonary arteries. The complex hemodynamics of Fontan circulation include atrial function, peripheral muscle pump, integrity of the atrioventricular valve, absence of restrictive, or obstructive pulmonary lung function. Therefore, thoracic mechanics are of particular importance within the complex hemodynamics of Fontan circulation.Methods: To understand the physiology of respiratory muscles, the aim of this study was to examine the matching of auxiliary respiratory muscle oxygen delivery and utilization during incremental exercise in young male Fontan patients (n = 22, age = 12.04 ± 2.51) and healthy Controls (n = 10, age = 14.90 ± 2.23). All subjects underwent a cardiopulmonary exercise test (CPET) to exhaustion whereas respiratory muscle oxygenation was measured non-invasively using a near-infrared spectrometer (NIRS).Results: CPET revealed significantly lower peak power output, oxygen uptake and breath activity in Fontan patients. The onset of respiratory muscle deoxygenation was significantly earlier. The matching of local muscle perfusion to oxygen demand was significantly worse in Fontans between 50 and 90% V.O2peak.Findings: The results indicate that (a) there is high strain on respiratory muscles during incremental cycling exercise and (b) auxiliary respiratory muscles are worse perfused in patients who underwent a Fontan procedure compared to healthy Controls. This might be indicative of a more general skeletal muscle strain and worse perfusion in Fontan patients rather than a localized-limited to thoracic muscles phenomenon

Medical treatment of pulmonary hypertension in adults with congenital heart disease : updated and extended results from the International COMPERA-CHD Registry

Funding Information: The authors are indebted to the COMPERA investigators and their staff. We explicitly thank Dr. Claudia S. Copeland for the professional editing of the final draft of the manuscript. Funding: COMPERA is funded by unrestricted grants from Acceleron, Actelion Pharmaceuticals (Janssen), Bayer, OMT and GSK. These companies were not involved in data analysis or the writing of this manuscript. Funding Information: ICMJE uniform disclosure form (available at https:// dx.doi.org/10.21037/cdt-21-351). The series “Current Management Aspects in Adult Congenital Heart Disease (ACHD): Part IV” was commissioned by the editorial office without any funding or sponsorship. Dr. DH reports non-financial support from Actelion, Boehringer-Ingelheim, and Shire, outside the submitted work; Dr. DP reports personal fees from Actelion, Biogen, Aspen, Bayer, Boehringer Ingelheim, Daiichi Sankyo, and Sanofi, outside the submitted work; Dr. MD reports personal fees from Actelion, Bayer, GSK and MSD, outside the submitted work; Dr. HAG reports personal fees from Actelion, Bayer, Gilead, GSK, MSD, Pfizer and United Therapeutics, outside the submitted work; Dr. MG reports personal fees from Actelion, Bayer and GSK, outside the submitted work; Dr. MMH reports personal fees from Acceleron, Actelion, Bayer, MSD and Pfizer, outside the submitted work; Dr. CDV reports personal fees from Actelion, Bayer, GSK, MSD, Pfizer, and United Therapeutics, outside the submitted work; Dr. RE reports personal fees from Actelion, Boehringer Ingelheim, OMT, Bayer, and Berlin Chemie; grants from Actelion and Boehringer Ingelheim, outside the submitted work; Dr. MH reports grants and personal fees from Actelion, personal fees from Bayer, Berlin Chemie, Boehringer Ingelheim, GSK, Janssen, Novartis and MSD, outside the submitted work; Dr. MH reports personal fees from Acceleron, Actelion, AstraZeneca, Bayer, BERLIN CHEMIE, GSK, MSD, Novartis and OMT, outside the submitted work; Dr. HW reports personal fees from Action, Bayer, Biotest, Boehringer, GSK, Pfizer, and Roche, outside the submitted work; Dr. DS reports personal fees from Actelion, Bayer, and GSK, outside the submitted work; Dr. LS reports personal fees from Actelion, Bayer, and MSD, outside the submitted work; Dr. SU reports grants from Swiss National Science Foundation, Zurich Lung, Swiss Lung, and Orpha Swiss, grants and personal fees from Actelion SA/Johnson & Johnson, Switzerland, and MSD Switzerland, outside the submitted work; Dr. TJL reports personal fees from Actelion, Janssen-Cilag, BMS, MSD, and OMT GmbH, outside the submitted work; Dr. LB reports personal fees from Actelion, outside the submitted work; Dr. MC reports personal fees from Boehringer Ingelheim Pharma GmbH, Roche Pharma, and Boehringer Ingelheim, outside the submitted work; Dr. HW reports personal fees from Boehringer Ingelheim, and Roche, outside the submitted work. Dr. EG reports personal fees from Actelion, Janssen, Bayer, MSD, Bial, OrPha Swiss GmbH, OMT and Medscape, outside the submitted work; Dr. SR reports personal fees from Actelion, Bayer, GSK, Pfizer, Novartis, Gilead, MSD, and United Therapeutics, outside the submitted work. The authors have no other conflicts of interest to declare. Publisher Copyright: © Cardiovascular Diagnosis and Therapy. All rights reserved.Background: Pulmonary arterial hypertension (PAH) is common in congenital heart disease (CHD). Because clinical-trial data on PAH associated with CHD (PAH-CHD) remain limited, registry data on the long-term course are essential. This analysis aimed to update information from the COMPERA-CHD registry on management strategies based on real-world data. Methods: The prospective international pulmonary hypertension registry COMPERA has since 2007 enrolled more than 10,000 patients. COMPERA-CHD is a sub-registry for patients with PAH-CHD Results: A total of 769 patients with PAH-CHD from 62 specialized centers in 12 countries were included into COMPERA-CHD from January 2007 through September 2020. At the last follow-up in 09/2020, patients [mean age 45.3±16.8 years; 512 (66%) female] had either post-tricuspid shunts (n=359; 46.7%), pre-tricuspid shunts (n=249; 32.4%), complex CHD (n=132; 17.2%), congenital left heart or aortic valve or aortic disease (n=9; 1.3%), or miscellaneous CHD (n=20; 2.6%). The mean 6-minute walking distance was 369±121 m, and 28.2%, 56.0%, and 3.8% were in WHO functional class I/II, III or IV, respectively (12.0% unknown). Compared with the previously published COMPERA-CHD data, after 21 months of followup, the number of included PAH-CHD patients increased by 91 (13.4%). Within this group the number of Eisenmenger patients rose by 39 (16.3%), the number of “Non-Eisenmenger PAH” patients by 45 (26.9%). Currently, among the 674 patients from the PAH-CHD group with at least one follow-up, 450 (66.8%) received endothelin receptor antagonists (ERA), 416 (61.7%) PDE-5 inhibitors, 85 (12.6%) prostacyclin analogues, and 36 (5.3%) the sGC stimulator riociguat. While at first inclusion in the COMPERA-CHD registry, treatment was predominantly monotherapy (69.3%), this has shifted to favoring combination therapy in the current group (53%). For the first time, the nature, frequency, and treatment of significant comorbidities requiring supportive care and medication are described. Conclusions: Analyzing “real life data” from the international COMPERA-CHD registry, we present a comprehensive overview about current management modalities and treatment concepts in PAH-CHD. There was an trend towards more aggressive treatment strategies and combination therapies. In the future, particular attention must be directed to the “Non-Eisenmenger PAH” group and to patients with complex CHD, including Fontan patients.publishersversionPeer reviewe