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Active emulsions and liquid crystalline shells are intriguing and experimentally realisable types of topological matter. Here we numerically study the morphology and spatiotemporal dynamics of a double emulsion, where one or two passive small droplets are embedded in a larger active droplet. We find activity introduces a variety of rich and nontrivial nonequilibrium states in the system. First, a double emulsion with a single active droplet becomes self-motile, and there is a transition between translational and rotational motion: both of these regimes remain defect-free, hence topologically trivial. Second, a pair of particles nucleate one or more disclination loops, with conformational dynamics resembling a rotor or chaotic oscillator, accessed by tuning activity. In the first state a single, topologically charged, disclination loop powers the rotation. In the latter state, this disclination stretches and writhes in 3D, continuously undergoing recombination to yield an example of an active living polymer. These emulsions can be self-assembled in the lab, and provide a pathway to form flow and topological patterns in active matter in a controlled way, as opposed to bulk systems that typically yield active turbulence. Active emulsions and liquid crystalline shells offer a unique framework for exploring topological matter due to their complex morphologies and dynamic properties. Here the authors report how activity generates diverse nonequilibrium states, from defect-free motile states to complex topologically active configurations, providing insights into controlled flow and topology in active systems. [ABSTRACT FROM AUTHOR]

Objectives: Posterior fossa decompression is currently an operative treatment of choice for Chiari Malformation I (CM1). However, there is controversy surrounding the possible benefits of employing intraoperative neuromonitoring (INM) for this type of procedure. In addition to presenting our single-center experience on the use of INM, we analyze the cost associated with INM in Chiari Malformation (CM) decompression surgery using the Healthcare Cost and Utilization Project (HCUP) database and discuss the legal implications of somatosensory evoked potentials (SSEP) monitoring during decompression for CM1. Methods: We conducted a retrospective review of all patients undergoing CM1 decompression with SSEP neuromonitoring from 2011 to 2018. We collected patient characteristics, hospital charges, and surgical cost data from the HCUP database for patients undergoing CM decompression. Finally, we performed a review within the Thompson Reuters Westlaw Edge database for reported litigation involving INM for CM decompression. Results: None of the 110 patients submitted to surgery for CM1 at our institution had any significant SSEP changes intraoperatively or developed post-operative neurological deterioration. There were higher mean total hospital charges and surgical costs associated with INM ($31,272) for patients who received INM compared to patients who did not receive INM ($24,112). A careful review of the Westlaw database with multiple-word search strategies revealed no reported medical malpractice claims regarding the absence of SSEP neuromonitoring in a CM decompression procedure. Conclusion: Using data collected at our institution and the HCUP national database, we showed that intraoperative neuromonitoring did not affect surgical planning and decision-making or post operative care, while adding unnecessary costs to CM decompression procedures. The absence of reported malpractice claims targeting the lack of neuromonitoring in CM cases suggests that SSEP neuromonitoring during CM may be unnecessary. We propose that neuromonitoring should not be used for routine CM decompression. [ABSTRACT FROM AUTHOR]

DIII-D research is being accelerated by leveraging high performance computing (HPC) and data resources available through the National Energy Research Scientific Computing Center (NERSC) Superfacility initiative. As part of this initiative, a high-resolution, fully automated, whole discharge kinetic equilibrium reconstruction workflow was developed that runs at the NERSC for most DIII-D shots in under 20 min. This has eliminated a long-standing research barrier and opened the door to more sophisticated analyses, including plasma transport and stability. These capabilities would benefit from being automated and executed within the larger Department of Energy Advanced Scientific Computing Research program's Integrated Research Infrastructure (IRI) framework. The goal of IRI is to empower researchers to meld DOE's world-class research tools, infrastructure, and user facilities seamlessly and securely in novel ways to radically accelerate discovery and innovation. For transport, we are looking at producing flux matched profiles and also using particle tracing to predict fast ion heat deposition from neutral beam injection before a shot takes place. Our starting point for evaluating plasma stability focuses on the pedestal limits that must be navigated to achieve better confinement. This information is meant to help operators run more effective experiments, so it needs to be available rapidly inside the DIII-D control room. So far this has been achieved by ensuring the data is available with existing tools, but as more novel results are produced new visualization tools must be developed. In addition, all of the high-quality data we have generated has been collected into databases that can unlock even deeper insights. This has already been leveraged for model and code validation studies as well as for developing AI/ML surrogates. The workflows developed for this project are intended to serve as prototypes that can be replicated on other experiments and can be run to provide timely and essential information for ITER, as well as next stage fusion power plants. [ABSTRACT FROM AUTHOR]

Context: In Australia's Murray–Darling Basin, the invasive common carp (Cyprinus carpio) poses a significant ecological threat. Efforts to manage their population include the potential use of cyprinid herpesvirus (CyHV-3) as a biological control agent. The environmental benefits of carp elimination could be substantial in the long term; our knowledge of the immediate ecological consequences resulting from large-scale fish die-offs remains limited. Aim: This study sought to investigate the effect of a large-scale fish-mortality event on water quality. Methods: Experiments of an increasing scale (bucket, mesocosm and whole wetland) were conducted to assess how decomposing carp carcasses alter dissolved oxygen and nutrient concentrations in water. Key results: In mesocosms, dead carp decayed more rapidly at 18 than 12°C, yielding oxygen demands of 1.022 ± 0.029 and 0.496 ± 0.239 mg kg−1 min−1 respectively. This carp decay released phosphorus, yielding 2121.1 ± 140.4 mg kg−1. In the wetland experiment, carp addition of 2400 kg ha−1 resulted in anoxic conditions over the following 2 weeks. The release of dissolved organic carbon and lipids led to a peak biological oxygen demand of 95.3 mg L−1. Conclusions: Carp decomposition considerably contributes to biological oxygen demand and algal growth through nutrient enrichment and is strongly influenced by carp density. Implications: The finding highlights key factors to consider before using biocontrol agents causing mass carp mortality, including hypoxia, anoxia and increased risk of harmful algal blooms. Investigations into the decomposition of common carp across three experiments of an increasing scale (bucket, mesocosm, wetland) showed a considerable release of phosphorus, with faster decomposition rates in warm conditions. The addition of 2400 kg ha−1 of carp induced anoxia in the wetland, underscoring essential considerations deploying biocontrol agents (e.g. cyprinid herpesvirus, CyHV-3) causing mass carp mortality. [ABSTRACT FROM AUTHOR]

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Acute respiratory distress syndrome is characterized by non-cardiogenic pulmonary edema, decreased pulmonary compliance, and abnormalities in gas exchange, especially hypoxemia. Patients with acute respiratory distress syndrome (ARDS) who receive support with venovenous (V-V) extracorporeal membrane oxygenation (ECMO) usually have severe lung disease. Many patients with ARDS have associated pulmonary vascular injury which can result in elevated pulmonary vascular resistance and right heart dysfunction. Since V-V ECMO relies upon preserved cardiac function, right heart failure has important implications for patient evaluation, management, and outcomes. Worsening right heart function complicates ARDS and disease processes. Given the increasing use of ECMO to support patients with ARDS, an understanding of right ventricular-ECMO and cardiopulmonary interactions is essential for the clinician. A narrative review of the manifestations of right heart dysfunction, as well as diagnosis and management strategies for the patient with ARDS on ECMO, is provided.

The Omicron BA.1 variant of SARS-CoV-2 escapes convalescent sera and monoclonal antibodies that are effective against earlier strains of the virus. This immune evasion is largely a consequence of mutations in the BA.1 receptor binding domain (RBD), the major antigenic target of SARS-CoV-2. Previous studies have identified several key RBD mutations leading to escape from most antibodies. However, little is known about how these escape mutations interact with each other and with other mutations in the RBD. Here, we systematically map these interactions by measuring the binding affinity of all possible combinations of these 15 RBD mutations (215=32,768 genotypes) to 4 monoclonal antibodies (LY-CoV016, LY-CoV555, REGN10987, and S309) with distinct epitopes. We find that BA.1 can lose affinity to diverse antibodies by acquiring a few large-effect mutations and can reduce affinity to others through several small-effect mutations. However, our results also reveal alternative pathways to antibody escape that does not include every large-effect mutation. Moreover, epistatic interactions are shown to constrain affinity decline in S309 but only modestly shape the affinity landscapes of other antibodies. Together with previous work on the ACE2 affinity landscape, our results suggest that the escape of each antibody is mediated by distinct groups of mutations, whose deleterious effects on ACE2 affinity are compensated by another distinct group of mutations (most notably Q498R and N501Y).

Older adults often suffer an accidental fall when navigating challenging surfaces during common locomotor tasks, such as walking and ascending stairs. This study examined the effect of slick and uneven surfaces on lower limb joint work in older and younger adults while walking and ascending stairs. Fifteen young (18–25 years) and 12 older (>65 years) adults had stance phase positive limb and joint work quantified during walking and stair ascent tasks on a normal, slick, and uneven surface, which was then submitted to a two-way mixed model ANOVA for analysis. The stair ascent required greater limb, and hip, knee, and ankle work than walking (all p < 0.001), with participants producing greater hip and knee work during both the walk and stair ascent (both p < 0.001). Surface, but not age, impacted positive limb work. Participants increased limb (p < 0.001), hip (p = 0.010), and knee (p < 0.001) positive work when walking over the challenging surfaces, and increased hip (p = 0.015), knee (p < 0.001), and ankle (p = 0.010) work when ascending stairs with challenging surfaces. Traversing a challenging surface during both walking and stair ascent tasks required greater work production from the large proximal hip and knee musculature, which may increase the likelihood of an accidental fall in older adults.

SARS-CoV-2 continues to acquire mutations in the spike receptor-binding domain (RBD) that impact ACE2 receptor binding, folding stability, and antibody recognition. Deep mutational scanning prospectively characterizes the impacts of mutations on these biochemical properties, enabling rapid assessment of new mutations seen during viral surveillance. However, the effects of mutations can change as the virus evolves, requiring updated deep mutational scans. We determined the impacts of all single amino acid mutations in the Omicron BA.1 and BA.2 RBDs on ACE2-binding affinity, RBD folding, and escape from binding by the LY-CoV1404 (bebtelovimab) monoclonal antibody. The effects of some mutations in Omicron RBDs differ from those measured in the ancestral Wuhan-Hu-1 background. These epistatic shifts largely resemble those previously seen in the Alpha variant due to the convergent epistatically modifying N501Y substitution. However, Omicron variants show additional lineage-specific shifts, including examples of the epistatic phenomenon of entrenchment that causes the Q498R and N501Y substitutions present in Omicron to be more favorable in that background than in earlier viral strains. In contrast, the Omicron substitution Q493R exhibits no sign of entrenchment, with the derived state, R493, being as unfavorable for ACE2 binding in Omicron RBDs as in Wuhan-Hu-1. Likely for this reason, the R493Q reversion has occurred in Omicron sub-variants including BA.4/BA.5 and BA.2.75, where the affinity buffer from R493Q reversion may potentiate concurrent antigenic change. Consistent with prior studies, we find that Omicron RBDs have reduced expression, and identify candidate stabilizing mutations that ameliorate this deficit. Last, our maps highlight a broadening of the sites of escape from LY-CoV1404 antibody binding in BA.1 and BA.2 compared to the ancestral Wuhan-Hu-1 background. These BA.1 and BA.2 deep mutational scanning datasets identify shifts in the RBD mutational landscape and inform ongoing efforts in viral surveillance.

Abstract Quantitative genetic theory proposes that phenotypic evolution is shaped by G, the matrix of genetic variances and covariances among traits. In species with separate sexes, the evolution of sexual dimorphism is also shaped by B, the matrix of between‐sex genetic variances and covariances. Despite considerable focus on estimating these matrices, their underlying biological mechanisms are largely speculative. We experimentally tested the hypothesis that G and B are structured by hormonal pleiotropy, which occurs when one hormone influences multiple phenotypes. Using juvenile brown anole lizards (Anolis sagrei) bred in a paternal half‐sibling design, we elevated the steroid hormone testosterone with slow‐release implants while administering empty implants to siblings as a control. We quantified the effects of this manipulation on the genetic architecture of a suite of sexually dimorphic traits, including body size (males are larger than females) and the area, hue, saturation, and brightness of the dewlap (a colorful ornament that is larger in males than in females). Testosterone masculinized females by increasing body size and dewlap area, hue, and saturation, while reducing dewlap brightness. Control females and males differed significantly in G, but treatment of females with testosterone rendered G statistically indistinguishable from males. Whereas B was characterized by low between‐sex genetic correlations when estimated between control females and males, these same correlations increased significantly when estimated between testosterone females and either control or testosterone males. The full G matrix (including B) for testosterone females and either control or testosterone males was significantly less permissive of sexually dimorphic evolution than was G estimated between control females and males, suggesting that natural sex differences in testosterone help decouple genetic variance between the sexes. Our results confirm that hormonal pleiotropy structures genetic covariance, implying that hormones play an important yet overlooked role in mediating evolutionary responses to selection.

Emerging SARS-CoV-2 mutants may escape neutralization by antibodies. Here, the authors use deep mutational scanning to identify mutations in the RBD that escape human monoclonal antibodies or convalescent plasmas.