Vortex trapping and expulsion in thin-film YBCO strips

A scanning SQUID microscope was used to image vortex trapping as a function of the magnetic induction during cooling in thin-film YBCO strips for strip widths W from 2 to 50 um. We found that vortices were excluded from the strips when the induction Ba was below a critical induction Bc. We present a simple model for the vortex exclusion process which takes into account the vortex - antivortex pair production energy as well as the vortex Meissner and self-energies. This model predicts that the real density n of trapped vortices is given by n=(Ba-BK)/Phi0 with BK = 1.65Phi0/W^2 and Phi0 = h/2e the superconducting flux quantum. This prediction is in good agreement with our experiments on YBCO, as well as with previous experiments on thin-film strips of niobium. We also report on the positions of the trapped vortices. We found that at low densities the vortices were trapped in a single row near the centers of the strips, with the relative intervortex spacing distribution width decreasing as the vortex density increased, a sign of longitudinal ordering. The critical induction for two rows forming in the 35 um wide strip was (2.89 + 1.91-0.93)Bc, consistent with a numerical prediction

Self-aligned nanoscale SQUID on a tip

A nanometer-sized superconducting quantum interference device (nanoSQUID) is fabricated on the apex of a sharp quartz tip and integrated into a scanning SQUID microscope. A simple self-aligned fabrication method results in nanoSQUIDs with diameters down to 100 nm with no lithographic processing. An aluminum nanoSQUID with an effective area of 0.034 $\mu$m$^2$ displays flux sensitivity of 1.8$\cdot 10^{-6}$ $\Phi_0/\mathrm{Hz}^{1/2} and operates in fields as high as 0.6 T. With projected spin sensitivity of 65$\mu_B/\mathrm{Hz}^{1/2}$ and high bandwidth, the SQUID on a tip is a highly promising probe for nanoscale magnetic imaging and spectroscopy.Comment: 14 manuscript pages, 5 figure

Key mechanisms governing resolution of lung inflammation

Innate immunity normally provides excellent defence against invading microorganisms. Acute inflammation is a form of innate immune defence and represents one of the primary responses to injury, infection and irritation, largely mediated by granulocyte effector cells such as neutrophils and eosinophils. Failure to remove an inflammatory stimulus (often resulting in failed resolution of inflammation) can lead to chronic inflammation resulting in tissue injury caused by high numbers of infiltrating activated granulocytes. Successful resolution of inflammation is dependent upon the removal of these cells. Under normal physiological conditions, apoptosis (programmed cell death) precedes phagocytic recognition and clearance of these cells by, for example, macrophages, dendritic and epithelial cells (a process known as efferocytosis). Inflammation contributes to immune defence within the respiratory mucosa (responsible for gas exchange) because lung epithelia are continuously exposed to a multiplicity of airborne pathogens, allergens and foreign particles. Failure to resolve inflammation within the respiratory mucosa is a major contributor of numerous lung diseases. This review will summarise the major mechanisms regulating lung inflammation, including key cellular interplays such as apoptotic cell clearance by alveolar macrophages and macrophage/neutrophil/epithelial cell interactions. The different acute and chronic inflammatory disease states caused by dysregulated/impaired resolution of lung inflammation will be discussed. Furthermore, the resolution of lung inflammation during neutrophil/eosinophil-dominant lung injury or enhanced resolution driven via pharmacological manipulation will also be considered

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570