Edward Durell Stone. Dallo Stile Internazionale allo stile personale

Edward Durell Stone (1902-1978) was an American modernist who developed a unique signature style of ‘new romanticism’ during the middle phase of his career between 1954 and 1966.  The style was employed in several dozen major architectural projects and it coincided with his second marriage.  His first signature style project was the U.S. Embassy in New Delhi, and the most famous one is the John F. Kennedy Center for the Performing Arts in Washington D.C.  He achieved temporary global renown with his design for the U.S. Pavilion at the Brussels World’s Fair in 1958.  Sadly, his best projects are widely scattered and he has no significant signature style works in New York City, where he based his career.  His current obscurity is explained by the eccentric character of his signature style, his transition from personal design to corporate replication, and the abandonment of signature design principles after the breakdown of his second marriage.Edward Durell Stone (1902-1978) fu un architetto americano modernista, che successivamente sviluppò, durante la fase centrale della sua carriera, tra il 1954 e il 1966, uno stile personale, rappresentativo di un “nuovo romanticismo”. Questo personale stile è stato impiegato in diverse dozzine di importanti progetti e ha coinciso con il periodo del suo secondo matrimonio. Il primo progetto in cui Ed Stone utilizza questo personale stile è l’Ambasciata USA a New Delhi, ma il più famoso è il John F. Kennedy Center for the Performing Arts di Washington D.C.La sua fama internazionale è principalmente dovuta al suo progetto per il Padiglione USA alla Fiera mondiale di Bruxelles del 1958, purtroppo infatti, i suoi migliori progetti sono sparsi per il mondo e nessuna opera significativa è a New York, dove ha sede il suo studio d’architettura. La sua attuale oscurità è parzialmente dovuta dal suo carattere eccentrico e dal suo personalissimo stile, ma soprattutto è causato dal passaggio da una cifra stilistica riconoscibile e personale, all’anonimato della grande azienda di progettazione, soprattutto dall’abbandono dei principi del suo personale stile, dopo il naufragio del suo secondo matrimonio.

A Combined VLT and Gemini Study of the Atmosphere of the Directly-Imaged Planet, beta Pictoris b

We analyze new/archival VLT/NaCo and Gemini/NICI high-contrast imaging of the young, self-luminous planet $\beta$ Pictoris b in seven near-to-mid IR photometric filters, using advanced image processing methods to achieve high signal-to-noise, high precision measurements. While $\beta$ Pic b's near-IR colors mimick that of a standard, cloudy early-to-mid L dwarf, it is overluminous in the mid-infrared compared to the field L/T dwarf sequence. Few substellar/planet-mass objects -- i.e. $\kappa$ And b and 1RXJ 1609B -- match $\beta$ Pic b's $JHK_{s}L^\prime$ photometry, and its 3.1 $\mu m$ and 5 $\mu m$ photometry are particularly difficult to reproduce. Atmosphere models adopting cloud prescriptions and large ($\sim$ 60 $\mu m$) dust grains fail to reproduce the $\beta$ Pic b spectrum. However, models incorporating thick clouds similar to those found for HR 8799 bcde but also with small (a few microns) modal particle sizes yield fits consistent with the data within uncertainties. Assuming solar abundance models, thick clouds, and small dust particles ($$ = 4 $\mu m$) we derive atmosphere parameters of log(g) = 3.8 $\pm$ 0.2 and $T_{eff}$ = 1575--1650 $K$, an inferred mass of 7$^{+4}_{-3}$ $M_{J}$, and a luminosity of log(L/L$_{\odot}$) $\sim$ -3.80 $\pm$ 0.02. The best-estimated planet radius, $\approx$ 1.65 $\pm$ 0.06 $R_{J}$, is near the upper end of allowable planet radii for hot-start models given the host star's age and likely reflects challenges with constructing accurate atmospheric models. Alternatively, these radii are comfortably consistent with hot-start model predictions if $\beta$ Pic b is younger than $\approx$ 7 Myr, consistent with a late formation, well after its host star's birth $\sim$ 12$^{+8}_{-4}$ Myr ago.Comment: 24 pages, minor changes from previous version, Accepted for publication in Ap

A Combined Very Large Telescope and Gemini Study of the Atmosphere of the Directly Imaged Planet, Beta Pictoris b

We analyze new/archival VLT/NaCo and Gemini/NICI high-contrast imaging of the young, self-luminous planet Beta Pictoris b in seven near-to-mid IR photometric filters, using advanced image processing methods to achieve high signal-to-noise, high precision measurements. While Beta Pic b's near-IR colors mimic those of a standard, cloudy early-to-mid L dwarf, it is overluminous in the mid-infrared compared to the field L/T dwarf sequence. Few substellar/planet-mass objects-i.e., And b and 1RXJ 1609B-match Beta Pic b's JHKsL photometry and its 3.1 micron and 5 micron photometry are particularly difficult to reproduce. Atmosphere models adopting cloud prescriptions and large (approx. 60 micron)dust grains fail to reproduce the Beta Pic b spectrum. However, models incorporating thick clouds similar to those found forHR8799 bcde, but also with small (a fewmicrons) modal particle sizes, yield fits consistent with the data within the uncertainties. Assuming solar abundance models, thick clouds, and small dust particles (a = 4 micron), we derive atmosphere parameters of log(g) = 3.8 +/- 0.2 and Teff = 1575-1650 K, an inferred mass of 7+4 3 MJ, and a luminosity of log(L/L) approx. 3.80 +/- 0.02. The best-estimated planet radius, is approx. equal to 1.65 +/- 0.06 RJ, is near the upper end of allowable planet radii for hot-start models given the host star's age and likely reflects challenges constructing accurate atmospheric models. Alternatively, these radii are comfortably consistent with hot-start model predictions if Beta Pic b is younger than is approx. equal to 7 Myr, consistent with a late formation well after its host star's birth approx. 12+8 4 Myr ago

Rainfall infiltration and soil hydrological characteristics below ancient forest, planted forest, and grassland in a temperate northern climate

How rainfall infiltration rate and soil hydrological characteristics develop over time under forests of different ages in temperate regions is poorly understood. In this study, infiltration rate and soil hydrological characteristics were investigated under forests of different ages and under grassland. Soil hydraulic characteristics were measured at different scales under a 250-year-old grazed grassland (GL), 6-year-old (6yr) and 48-year-old (48yr) Scots pine (Pinus sylvestris) plantations, remnant 300-year-old individual Scots pine (OT) and a 4000-year-old Caledonian Forest (AF). In situ field-saturated hydraulic conductivity (Kfs) was measured, and visible root:soil area was estimated from soil pits. Macroporosity, pore structure and macropore connectivity were estimated from X-ray tomography of soil cores, and from water-release characteristics.At all scales, the median values for Kfs, root fraction, macroporosity and connectivity values tended to AF > OT > 48yr > GL > 6yr, indicating that infiltration rates and water storage increased with forest age. The remnant Caledonian Forest had a huge range of Kfs (12 to >4922 mm h−1), with maximum Kfs values 7 to 15 times larger than those of 48-year-old Scots pine plantation, suggesting that undisturbed old forests, with high rainfall and minimal evapotranspiration in winter, may act as important areas for water storage and sinks for storm rainfall to infiltrate and transport to deeper soil layers via preferential flow. The importance of the development of soil hydrological characteristics under different aged forests is discussed

Climate change, precipitation and impacts on an estuarine refuge from disease

© The Author(s), 2011. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in PLoS One 6 (2011): e18849, doi:10.1371/journal.pone.0018849.Oysters play important roles in estuarine ecosystems but have suffered recently due to overfishing, pollution, and habitat loss. A tradeoff between growth rate and disease prevalence as a function of salinity makes the estuarine salinity transition of special concern for oyster survival and restoration. Estuarine salinity varies with discharge, so increases or decreases in precipitation with climate change may shift regions of low salinity and disease refuge away from optimal oyster bottom habitat, negatively impacting reproduction and survival. Temperature is an additional factor for oyster survival, and recent temperature increases have increased vulnerability to disease in higher salinity regions. We examined growth, reproduction, and survival of oysters in the New York Harbor-Hudson River region, focusing on a low-salinity refuge in the estuary. Observations were during two years when rainfall was above average and comparable to projected future increases in precipitation in the region and a past period of about 15 years with high precipitation. We found a clear tradeoff between oyster growth and vulnerability to disease. Oysters survived well when exposed to intermediate salinities during two summers (2008, 2010) with moderate discharge conditions. However, increased precipitation and discharge in 2009 reduced salinities in the region with suitable benthic habitat, greatly increasing oyster mortality. To evaluate the estuarine conditions over longer periods, we applied a numerical model of the Hudson to simulate salinities over the past century. Model results suggest that much of the region with suitable benthic habitat that historically had been a low salinity refuge region may be vulnerable to higher mortality under projected increases in precipitation and discharge. Predicted increases in precipitation in the northeastern United States due to climate change may lower salinities past important thresholds for oyster survival in estuarine regions with appropriate substrate, potentially disrupting metapopulation dynamics and impeding oyster restoration efforts, especially in the Hudson estuary where a large basin constitutes an excellent refuge from disease.Funding was provided by the Hudson River Foundation, grant number 00607A, and the New York State Department of Environmental Conservation (MOU 2008)

Tourism and autism: Journeys of mixed emotions

There is an evolving tourism literature around psychological wellbeing, social exclusion and disability. This paper advances tourism knowledge into the terrain of psychological health and developmental complexities, and psychological distress. It draws on a phe-nomenological position to understand the lived experiences of mothers of children with developmental difficulties, in this case diagnosed with autism spectrum disorder (ASD). It discusses the emotional and everyday challenges of caring for a child diagnosed with ASD on holiday, discusses the perceived benefits holidays offer and outlines care-giving strategies adopted by mothers to manage their children’s tourism experiences. The paper discusses the uniqueness of the context of autism and problematizes popular discourses, which predominantly frame tourism as pleasurable settings of escape, stimulation, novelty and relaxation

Erratum to: Methods for evaluating medical tests and biomarkers

[This corrects the article DOI: 10.1186/s41512-016-0001-y.]

Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity

The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease