Designing the Machine Age in America: Streamlining in the 20th Century

Streamlining, the major U.S. commercial design style of the 1930s, was promoted by industrial designers who sought to eliminate sales resistance just as aerodynamic streamlining was intended to eliminate wind resistance. Popularized in 1934 by two passenger trains, the Union Pacific railroads M-10,000 and the Burlington railroads Zephyr, the style was introduced into the automotive market through the Chrysler Airflow and was quickly incorporated into non-vehicular consumer products. While 1930s streamlining expressed a cultural desire for stability and stasis during the Great Depression, the postwar variant, exemplified by the sharply angled, flaring automotive tailfin, expressed a popular faith in limitless technological progress. The architect Eero Saarinen, who had learned streamlining in the industrial design office of Norman Bel Geddes in the late 1930s, brought postwar streamlining to full expression in such projects as the TWA terminal in New York and Dulles airport in northern Virginia. During the 1990s a nostalgic retro mode of streamlining appeared in such products as the New Beetle automobile, the first Apple iMac computer, and the Smart car

Youve Been with the Professors: Influence, Appropriation, and the Cultural Interpretation of Bob Dylan

Sean Wilentz, Bob Dylan in America. New York: Doubleday, 2010. 390 pp., 99 b..w illus., index. Greil Marcus, Bob Dylan: Writings 1968-2010. New York: PublicAffairs, 2010. xx, 483 pp, 14 b&w illus., index.American Studies as a discipline, at least as practiced in the United States, has sometimes attracted criticism that it encourages narcissistic navel-gazing by a culture whose socioeconomic base is affluent enough to afford that luxury. This complaint is especially prevalent in attacks on scholars who direct their attention to popular examples of the products of mass culture. A former colleague of mine, or example, often aimed sarcastic barbs at people who write about their record collections. At the least, he believed, such unprofessional scholars are too lazy to look beyond narrow personal interests; at worst, they project their own guilty pleasures onto the larger culture in a solipsistic gesture motivated by self-justification. Although my colleagues opinion reflected a bitter, ultimately dismissive attitude toward recent scholarship on contemporary mass culture, there is indeed a gray area where celebrity worship, fanboy obsession, and personal desire to claim cultural capital may blur traditional notions of scholarships neutral objectivity. Attempts to overcome such attacks often seek to prove by applying audience or reception theory that popular culture products do have substantive impact on the lives of those who consume them. That defense may appear questionable not only because reception is notoriously difficult to measure but also because critical theorys densely-worded, jargon-laden arguments may seem like self-serving obfuscation to readers already inclined to be skeptical of serious claims for popular or mass culture

Systematic Blueshift of Line Profiles in the Type IIn Supernova 2010jl: Evidence for Post-Shock Dust Formation?

Type IIn SNe show spectral evidence for strong interaction between their blast wave and dense circumstellar material (CSM) around the progenitor star. SN2010jl was the brightest core-collapse SN in 2010, and it was a Type IIn explosion with strong CSM interaction. Andrews et al. recently reported evidence for an IR excess in SN2010jl, indicating either new dust formation or the heating of CSM dust in an IR echo. Here we report multi-epoch spectra of SN2010jl that reveal the tell-tale signature of new dust formation: emission-line profiles becoming systematically more blueshifted as the red side of the line is blocked by increasing extinction. The effect is seen clearly in the intermediate-width (400--4000 km/s) component of H$\alpha$ beginning roughly 30d after explosion. Moreover, we present near-IR spectra demonstrating that the asymmetry in the hydrogen-line profiles is wavelength dependent, appearing more pronounced at shorter wavelengths. This evidence suggests that new dust grains had formed quickly in the post-shock shell of SN 2010jl arising from CSM interaction. Since the observed dust temperature has been attributed to an IR echo and not to new dust, either (1) IR excess emission at $\lambda < 5 \mu$m is not a particularly sensitive tracer of new dust formation in SNe, or (2) some assumptions about expected dust temperatures might require further study. Lastly, we discuss one possible mechanism other than dust that might lead to increasingly blueshifted line profiles in SNeIIn, although the wavelength dependence of the asymmetry argues against this hypothesis in the case of SN2010jl.Comment: 6 pages, 4 figures, submitted to A

Hepatic accumulation of intestinal cholesterol is decreased and fecal cholesterol excretion is increased in mice fed a high-fat diet supplemented with milk phospholipids

<p>Abstract</p> <p>Background</p> <p>Milk phospholipids (PLs) reduce liver lipid levels when given as a dietary supplement to mice fed a high-fat diet. We have speculated that this might be due to reduced intestinal cholesterol uptake.</p> <p>Methods</p> <p>Mice were given a high-fat diet for 3 or 5 weeks that had no added PL or that were supplemented with 1.2% by wt PL from cow's milk. Two milk PL preparations were investigated: a) a PL-rich dairy milk extract (PLRDME), and b) a commercially-available milk PL concentrate (PC-700). Intestinal cholesterol uptake was assessed by measuring fecal and hepatic radioactivity after intragastric administration of [¹⁴C]cholesterol and [³H]sitostanol. Fecal and hepatic lipids were measured enzymatically and by ESI-MS/MS.</p> <p>Results</p> <p>Both PL preparations led to significant decreases in total liver cholesterol and triglyceride (-20% to -60%, <it>P </it>< 0.05). Hepatic accumulation of intragastrically-administered [¹⁴C]cholesterol was significantly less (-30% to -60%, <it>P </it>< 0.05) and fecal excretion of [¹⁴C]cholesterol and unlabeled cholesterol was significantly higher in PL-supplemented mice (+15% to +30%, <it>P </it>< 0.05). Liver cholesterol and triglyceride levels were positively correlated with hepatic accumulation of intragastrically-administered [¹⁴C]cholesterol (<it>P </it>< 0.001) and negatively correlated with fecal excretion of [¹⁴C]cholesterol (<it>P </it>< 0.05). Increased PL and ceramide levels in the diet of mice supplemented with milk PL were associated with significantly higher levels of fecal PL and ceramide excretion, but reduced levels of hepatic PL and ceramide, specifically, phosphatidylcholine (-21%, <it>P </it>< 0.05) and monohexosylceramide (-33%, <it>P </it>< 0.01).</p> <p>Conclusion</p> <p>These results indicate that milk PL extracts reduce hepatic accumulation of intestinal cholesterol and increase fecal cholesterol excretion when given to mice fed a high-fat diet.</p

A Spitzer Survey for Dust in Type IIn Supernovae

Recent observations suggest that Type IIn supernovae (SNe IIn) may exhibit late-time (>100 days) infrared (IR) emission from warm dust more than other types of core-collapse SNe. Mid-IR observations, which span the peak of the thermal spectral energy distribution, provide useful constraints on the properties of the dust and, ultimately, the circumstellar environment, explosion mechanism, and progenitor system. Due to the low SN IIn rate (<10% of all core-collapse SNe), few IR observations exist for this subclass. The handful of isolated studies, however, show late-time IR emission from warm dust that, in some cases, extends for five or six years post-discovery. While previous Spitzer/IRAC surveys have searched for dust in SNe, none have targeted the Type IIn subclass. This article presents results from a warm Spitzer/IRAC survey of the positions of all 68 known SNe IIn within a distance of 250 Mpc between 1999 and 2008 that have remained unobserved by Spitzer more than 100 days post-discovery. The detection of late-time emission from ten targets (~15%) nearly doubles the database of existing mid-IR observations of SNe IIn. Although optical spectra show evidence for new dust formation in some cases, the data show that in most cases the likely origin of the mid-IR emission is pre-existing dust, which is continuously heated by optical emission generated by ongoing circumstellar interaction between the forward shock and circumstellar medium. Furthermore, an emerging trend suggests that these SNe decline at ~1000--2000 days post-discovery once the forward shock overruns the dust shell. The mass-loss rates associated with these dust shells are consistent with luminous blue variable (LBV) progenitors.Comment: Accepted for publication to ApJ, 17 pages, 10 figures, 10 table

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

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 hospitalization2,3,4 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

Transatlantic Refractions: Ambivalence and Cultural Hybridity in the Euro-American Road Movie

This article analyses a variety of ways in which the “road movie” has been reinterpreted by modern European directors (German Wim Wenders, Finn Aki Kaurismäki) or American director Jim Jarmusch with his pronounced European sensibilities. Despite the ubiquity of American popular culture in many of these movies, the films themselves are far from representing a simple “colonization” on the part of American culture. The ambivalent view of the United States adopted by these men has helped transform a typically “American” genre into a new demonstration of transatlantic cultural hybridity