Bloody Foundation? Ethical and Legal Implications of (Not) Removing the Equestrian Statue of Theodore Roosevelt at the American Museum of Natural History

On October 26, 2017, protestors calling themselves the Monument Removal Brigade (“MRB”) splashed red paint on the base of a statue of Theodore Roosevelt outside the American Museum of Natural History (“AMNH,” “Museum,” or “Natural History Museum”) in New York City as a form of public protest art. This 1939 sculpture by American artist James Earle Fraser (the “Equestrian Statue of Theodore Roosevelt” or “Equestrian Statue”) portrays the twenty-sixth president of the United States sitting upon a horse, flanked on either side by a standing African man and Native American man intended to represent their respective continents. On its anonymous blog, MRB called for the statue’s removal and claimed, “[t]he true damage lies with patriarchy, white supremacy, and settler-colonialism embodied by the statue.” The Mayoral Advisory Commission on City Art, Monuments, and Markers (the “Commission”) conducted a study of controversial monuments on public land in New York City and was unable to agree on an appropriate fate for the AMNH statue; for this reason, it has remained in place for the time being. In July of 2019, the AMNH opened a special exhibition entitled Addressing the Statue. This AMNH protest occurred within a larger national conversation about the place of public monuments, especially those commemorating leaders of the Confederacy. But the current debate often lacks scholarly rigor, with little consideration of the history, intention, or artistic merit of the monuments in question, or the federal, state, local, and administrative laws governing their removal or modification. This Article draws upon the disciplines of art history, museum studies, and the law to contextualize the AMNH Equestrian Statue and expand upon the Commission’s and AMNH’s analyses to develop a suggested framework for considering controversial monuments in the future

They Can’t Take that Away from Me: An Indemnification Solution to Unmerited VARA Claims

This Note argues that market participants should be indemnified against legally baseless revocations of attribution by living artists. Noland justifies her disavowals under the Visual Artists Rights Act of 1990 (“VARA”), the American answer to the French concept of droit moral or moral rights.8 Moral rights provide artists with control over the integrity and attribution of their art even after it has been sold. In a narrow set of circumstances, VARA permits a living artist to disavow her works if they have been modified so extensively as to be prejudicial to the artist’s reputation (excepting changes caused by aging or conservation).9 But there is a dearth of case law defining terms like modification, prejudice, and reputation. Even among Noland’s disavowals there is variation: she revoked authorship of the aluminum print Cowboys Milking because she perceived wear on its corners, and of the wooden building façade Log Cabin because conservators allegedly rebuilt the entire piece without permission.10 Noland is one of relatively few artists to bring lawsuits under VARA, and research for this Note has uncovered no cases of an owner or other stakeholder suing an artist for improperly invoking VARA. Even if a party were to sue Noland for abusing VARA and successfully obtain an injunction forcing her to legally affirm authorship of a work, this would likely not remedy the market damage caused by her public disavowal. No matter the conclusion of a court, collectors are unlikely to invest millions of dollars in art unsupported by its creator. Unfortunately, moral rights law in the United States has not yet addressed this situation. This Note proposes that the indemnification solutions contained in the droit moral provide a possible solution to the problems that result when an artist disavows her art without legal cause

The Education of the Accelerated Child

Nature has bestowed upon some of its children a gift so mysterious in its operations, so wonderful in its products and so tremendous in its influence that it baffles the most cultured and powerful minds in the attempt to analyze its workings. Even the possessor is unable to trace either -its origin or its mode of action. It is the common parent of invention and science of music and poetry and its chief distinction lies in the ability to penetrate farther into the field of truth than ordinary minds can do. To live in worlds that are unknown except to those divinely gifted, in other words possessing that peculiar quality of mind known as Genius. So subtle and impalpable is this faculty that although we are aware of its presence and can easily recognize it when it manifests itself yet we cannot tell exactly in what it consists. First, because no one unpossessed of creative imagination can study its operations within himself, while second, those who do possess this quality are seldom given to self analysis

Redox-dependent dimerization of p38 alpha mitogen-activated protein kinase with mitogen-activated protein kinase kinase 3

The kinase p38α MAPK (p38α) plays a pivotal role in many biological processes. p38α is activated by canonical upstream kinases that phosphorylate the activation region. The purpose of our study was to determine whether such activation may depend on redox-sensing cysteines within p38α. p38α was activated and formed a disulfide-bound heterodimer with MAP2K3 (MKK3) in rat cardiomyocytes and isolated hearts exposed to H2O2 This disulfide heterodimer was sensitive to reduction by mercaptoethanol and was enhanced by the thioredoxin-reductase inhibitor auranofin. We predicted that Cys-119 or Cys-162 of p38α, close to the known MKK3 docking domain, were relevant for these redox characteristics. The C119S mutation decreased whereas the C162S mutation increased the dimer formation, suggesting that these two Cys residues act as vicinal thiols, consistent with C119S/C162S being incapable of sensing H2O2 Similarly, disulfide heterodimer formation was abolished in H9C2 cells expressing both MKK3 and p38α C119S/C162S and subjected to simulated ischemia and reperfusion. However, the p38α C119S/C162S mutants did not exhibit appreciable alteration in activating dual phosphorylation. In contrast, the anti-inflammatory agent 10-nitro-oleic acid (NO2-OA), a component of the Mediterranean diet, reduced p38α activation and covalently modified Cys-119/Cys-162, probably obstructing MKK3 access. Moreover, NO2-OA reduced the dephosphorylation of p38α by hematopoietic tyrosine phosphatase (HePTP). Furthermore, steric obstruction of Cys-119/Cys-162 by NO2-OA pretreatment in Langendorff-perfused murine hearts prevented the p38-MKK3 disulfide dimer formation and attenuated H2O2-induced contractile dysfunction. Our findings suggest that cysteine residues within p38α act as redox sensors that can dynamically regulate the association between p38 and MKK3.</p

Multicenter cohort study, with a nested randomized comparison, to examine the cardiovascular impact of preterm preeclampsia

This study evaluated whether planned early delivery would ameliorate cardiovascular dysfunction six months postpartum, compared to usual care with expectant management, in women with late preterm preeclampsia. We conducted a mechanistic observational study in women with preterm preeclampsia between 34+0 and 36+6 weeks’ gestation, nested within a randomised controlled trial of planned early delivery versus expectant management (usual care), in 28 maternity hospitals in England and Wales. Women were followed up six months postpartum with cardiovascular assessments. The primary outcome was a composite of systolic and/or diastolic dysfunction (by 2009 and 2016 definitions of diastolic dysfunction). Between 27 April 2016 and 30 November 2018, 623 women were found to be eligible, of whom 420 (67%) were recruited. 133 women were randomised to planned delivery, 137 women were randomised to expectant management within the trial, while 150 women received expectant management outside of the trial. 321 (76.4%) completed their six month echocardiography assessment. 10% (31/321) had a left ventricular ejection fraction <55% whilst 71% (229/321) remained hypertensive. There were no differences in the primary outcome between the two randomised groups (planned delivery versus expectant management) using either the 2009 (RR 1.06; 95% CI 0.80, 1.40) or 2016 definitions (RR 0.78; 0.33, 1.86). In conclusion, we demonstrated that late preterm preeclampsia results in persistence of hypertension in the majority, and systolic LV dysfunction in 10%, of women six months postpartum. Planned early delivery does not affect these outcomes. Preeclampsia is not a self-limiting disease of pregnancy alone

Appearance of microvascular obstruction on high resolution first-pass perfusion, early and late gadolinium enhancement CMR in patients with acute myocardial infarction

<p>Abstract</p> <p>Background</p> <p>The presence and extent of microvascular obstruction (MO) after acute myocardial infarction can be measured by first-pass gadolinium-enhanced perfusion cardiovascular magnetic resonance (CMR) or after gadolinium injection with early or late enhancement (EGE/LGE) imaging. The volume of MO measured by these three methods may differ because contrast agent diffusion into the MO reduces its apparent extent over time. Theoretically, first-pass perfusion CMR should be the most accurate method to measure MO, but this technique has been limited by lower spatial resolution than EGE and LGE as well as incomplete cardiac coverage. These limitations of perfusion CMR can be overcome using spatio-temporal undersampling methods. The purpose of this study was to compare the extent of MO by high resolution first-pass <it>k-t </it>SENSE accelerated perfusion, EGE and LGE.</p> <p>Methods</p> <p>34 patients with acute ST elevation myocardial infarction, treated successfully with primary percutaneous coronary intervention (PPCI), underwent CMR within 72 hours of admission. <it>k-t </it>SENSE accelerated first-pass perfusion MR (7 fold acceleration, spatial resolution 1.5 mm × 1.5 mm × 10 mm, 8 slices acquired over 2 RR intervals, 0.1 mmol/kg Gd-DTPA), EGE (14 minutes after injection with a fixed TI of 440 ms) and LGE images (1012 minutes after injection, TI determined by a Look-Locker scout) were acquired. MO volume was determined for each technique by manual planimetry and summation of discs methodology.</p> <p>Results</p> <p><it>k-t </it>SENSE first-pass perfusion detected more cases of MO than EGE and LGE (22 vs. 20 vs. 14, respectively). The extent of MO imaged by first-pass perfusion (median mass 4.7 g, IQR 6.7) was greater than by EGE (median mass 2.3 g, IQR 7.1, p = 0.002) and LGE (median mass 0.2 g, IQR 2.4, p = 0.0003). The correlation coefficient between MO mass measured by first-pass perfusion and EGE was 0.91 (p < 0.001).</p> <p>Conclusion</p> <p>The extent of MO following acute myocardial infarction appears larger on high-resolution first-pass perfusion CMR than on EGE and LGE. Given the inevitable time delay between gadolinium administration and acquisition of either EGE or LGE images, high resolution first-pass perfusion imaging may be the most accurate method to quantify MO.</p

Biological variation of secretoneurin; a novel cardiovascular biomarker implicated in arrhythmogenesis

Background Secretoneurin is a novel prognostic biomarker that may predict mortality in heart failure and the occurrence of ventricular arrhythmias. This study reports the within subject variation (CVI), between subject variation (CVG), reference change values (RCV) and index of individuality (II) of secretoneurin. Methods Thirty healthy volunteers were included. Non-fasting samples were obtained between 8 and 10 am once a week for ten weeks. Secretoneurin was analyzed in duplicate using ELISA. No outliers were present according to Burnett and Reeds‘ criteria. Simple linear regression did not identify significant trends. Variance homogeneity in the analytical variance and CVI were tested using Cochrane’s and Bartlett’s tests and four participants were excluded. Calculation of CVI, CVG and RCV were done on ln transformed data as described by Fokkema, the II was calculated using retransformed data. Results The median age of the participants was 36 years and 53% were female. Non-fasting glucose, eGFR(CKD-EPI), cTnT and NT-proBNP concentrations were within the normal range. Median secretoneurin concentrations were 38 pmol/L (women) and 33 pmol/L (men), p-value < 0.001. CVI and CVG were 9.8% (CI 8.7% to 11.0%) and 20.0 (CI 15.4% to 28.0%), respectively. RCV were 38.7% (CI 35.5% to 42.7%) and −27.9 (CI −29.9 to −26.2) and the II were 0.60 (CI 0.42–0.78). No gender differences were present. Conclusion Secretoneurin has a fairly low CVI, CVG, RCV and II, indicating that it could be suitable as a diagnostic or prognostic biomarker and that delta values in serial samplings may be preferable for identifying clinical changes.publishedVersio

Planned delivery to improve postpartum cardiac function in women with preterm pre-eclampsia: the PHOEBE mechanisms of action study within the PHOENIX RCT

Background Women whose pregnancies are affected by hypertensive disorders of pregnancy, in particular preterm pre-eclampsia, are at increased risk of long-term cardiovascular morbidity and mortality. Objectives To investigate the hypothesis that prolongation of a pregnancy affected by preterm pre-eclampsia managed by expectant management compared with planned early delivery would result in worse cardiovascular function 6 months postpartum. Design A randomised controlled trial. Setting 28 maternity hospitals in England and Wales. Participants Women who were eligible for the Pre-eclampsia in HOspital: Early iNductIon or eXpectant management (PHOENIX) study were approached and recruited for the PHOEBE study. The PHOENIX (Pre-eclampsia in HOspital: Early iNductIon or eXpectant management) study was a parallel-group, non-masked, multicentre, randomised controlled trial that was carried out in 46 maternity units across England and Wales. This study compared planned early delivery with expectant management (usual care) with individual randomisation in women with late preterm pre-eclampsia who were 34 weeks’ gestation to less than 37 weeks’ gestation and having a singleton or dichorionic diamniotic twin pregnancy. Interventions Postpartum follow-up included medical history, blood pressure assessment and echocardiography. All women had blood sampling performed on at least two time points from recruitment to the 6-month follow-up for assessment of cardiac necrosis markers. Main outcome measures Primary outcome was a composite of systolic and/or diastolic dysfunction (originally by 2009 guidelines then updated by 2016 guidelines, with an amended definition of diastolic dysfunction). Analyses were by intention to treat, together with a per-protocol analysis for the primary and secondary outcomes. Results Between 27 April 2016 and 30 November 2018, 623 women were found to be eligible, of whom 420 (67%) were recruited across 28 maternity units in England and Wales. A total of 133 women were allocated to planned delivery, 137 women were allocated to expectant management and a further 150 received non-randomised expectant management within usual care. The mean time from enrolment to delivery was 2.5 (standard deviation 1.9) days in the planned delivery group compared with 6.8 (standard deviation 5.3) days in the expectant management group. There were no differences in the primary outcome between women in the planned delivery group and those in the expectant management group using either the 2009 (risk ratio 1.06, 95% confidence interval 0.80 to 1.40) or the 2016 definition (risk ratio 0.78, 95% confidence interval 0.33 to 1.86). Overall, 10% (31/321) of women had a left ventricular ejection fraction &lt; 55% and 71% of the cohort remained hypertensive at 6 months postpartum. No differences were observed between groups in cardiorespiratory outcomes prior to discharge from hospital or in systolic or diastolic blood pressure measurements. Variables associated with the primary outcome (2009 definition) at 6 months postpartum were maternal body mass index (adjusted odds ratio 1.33 per 5 kg/m2, 95% confidence interval 1.12 to 1.59 per 5 kg/m2) and maternal age (adjusted odds ratio 2.16, 95% confidence interval 1.44 to 3.22 per 10 years). Limitations include changing definitions regarding systolic and/or diastolic dysfunction. Conclusions Preterm pre-eclampsia results in persistence of hypertension in the majority of women with late preterm pre-eclampsia at 6 months postpartum and systolic dysfunction in 10%. Pre-eclampsia should not be considered a self-limiting disease of pregnancy alone. Future work Interventions aimed at reducing cardiovascular dysfunction. Trial registration Current Controlled Trials ISRCTN01879376. Funding This project was funded by the Efficacy and Mechanism Evaluation (EME) programme, a Medical Research Council and National Institute for Health Research (NIHR) partnership. This will be published in full in Efficacy and Mechanism Evaluation; Vol. 8, No. 12. See the NIHR Journals Library website for further project information