FLYING DIRTY: EVTOL CASEVAC ON THE CONTAMINATED BATTLEFIELD

The American military’s reliance on manned airpower on the modern battlefield invites a critical vulnerability for great power adversaries to target with chemical, biological, radiological, and nuclear (CBRN) weapons. Modern efforts to increase combat effectiveness are incremental improvements to decades-old technology that fail to fundamentally change how the Joint Force fights in a contaminated environment. Ongoing military adoption of emerging commercial aviation technology could be readily leveraged to shore up this critical vulnerability. By presenting three articles intended to address distinct aspects of this capability, this capstone aims to demonstrate that unmanned electric vertical takeoff and landing (eVTOL) aircraft can remove the aircrews from a dangerous and dirty task, preserving manned combat power for the broader war effort. However, the military must overcome both technical and cultural barriers for adoption to be successful. These barriers can be overcome by establishing and leveraging advocacy networks and tying innovative solutions to operational challenges. To ignore the promise that these future technologies present will risk remaining vulnerable to a credible threat in a future great power conflict.Lieutenant Commander, United States NavyMaster Sergeant, United States Air ForceSenior Master Sergeant, United States Air ForceApproved for public release. Distribution is unlimited

Limits on Superconductivity-Related Magnetization in Sr2_2RuO4_4 and PrOs4_4Sb12_{12} from Scanning SQUID Microscopy

We present scanning SQUID microscopy data on the superconductors Sr2RuO4 (Tc = 1.5 K) and PrOs$_4$Sb$_{12}$ (Tc = 1.8 K). In both of these materials, superconductivity-related time-reversal symmetry-breaking fields have been observed by muon spin rotation; our aim was to visualize the structure of these fields. However in neither Sr$_2$RuO$_4$ nor PrOs$_4$Sb$_{12}$ do we observe spontaneous superconductivity-related magnetization. In Sr$_2$RuO$_4$, many experimental results have been interpreted on the basis of a $px \pm ipy$ superconducting order parameter. This order parameter is expected to give spontaneous magnetic induction at sample edges and order parameter domain walls. Supposing large domains, our data restrict domain wall and edge fields to no more than ~0.1% and ~0.2% of the expected magnitude, respectively. Alternatively, if the magnetization is of the expected order, the typical domain size is limited to ~30 nm for random domains, or ~500 nm for periodic domains.Comment: 8 pages, 7 figures. Submitted to Phys. Rev.

The Synergistic Action of Melittin and Phospholipase A2 with Lipid Membranes: Development of Linear Dichroism for Membrane-Insertion Kinetics

Here we present data on the kinetics of insertion of melittin, a peptide from bee venom, into lipid membranes of different composition. Another component of bee venom is the enzyme phospholipase A2 (PLA₂). We have examined the interaction of melittin and PLA₂ with liposomes both separately and combined and demonstrate that they work synergistically to disrupt the membranes. A dramatic difference in the action of melittin and PLA₂ is observed when the composition of the membrane is altered. Temperature also has a large effect on the kinetics of insertion and membrane disruption. We use a combination of techniques to measure liposome size (dynamic light scattering), peptide secondary structure (circular dichroism spectroscopy), peptide orientation relative to the membrane (linear dichroism spectroscopy) and enzymatic digestion of the lipids (mass spectrometry)

On the degrees of freedom of a semi-Riemannian metric

A semi-Riemannian metric in a n-manifold has n(n-1)/2 degrees of freedom, i.e. as many as the number of components of a differential 2-form. We prove that any semi-Riemannian metric can be obtained as a deformation of a constant curvature metric, this deformation being parametrized by a 2-for

Deconvoluting lung evolution: from phenotypes to gene regulatory networks

Speakers in this symposium presented examples of respiratory regulation that broadly illustrate principles of evolution from whole organ to genes. The swim bladder and lungs of aquatic and terrestrial organisms arose independently from a common primordial "respiratory pharynx” but not from each other. Pathways of lung evolution are similar between crocodiles and birds but a low compliance of mammalian lung may have driven the development of the diaphragm to permit lung inflation during inspiration. To meet the high oxygen demands of flight, bird lungs have evolved separate gas exchange and pump components to achieve unidirectional ventilation and minimize dead space. The process of "screening” (removal of oxygen from inspired air prior to entering the terminal units) reduces effective alveolar oxygen tension and potentially explains why nonathletic large mammals possess greater pulmonary diffusing capacities than required by their oxygen consumption. The "primitive” central admixture of oxygenated and deoxygenated blood in the incompletely divided reptilian heart is actually co-regulated with other autonomic cardiopulmonary responses to provide flexible control of arterial oxygen tension independent of ventilation as well as a unique mechanism for adjusting metabolic rate. Some of the most ancient oxygen-sensing molecules, i.e., hypoxia-inducible factor-1alpha and erythropoietin, are up-regulated during mammalian lung development and growth under apparently normoxic conditions, suggesting functional evolution. Normal alveolarization requires pleiotropic growth factors acting via highly conserved cell-cell signal transduction, e.g., parathyroid hormone-related protein transducing at least partly through the Wingless/int pathway. The latter regulates morphogenesis from nematode to mammal. If there is commonality among these diverse respiratory processes, it is that all levels of organization, from molecular signaling to structure to function, co-evolve progressively, and optimize an existing gas-exchange framewor

Acceleration predicts energy expenditure in a fat, flightless, diving bird

Funding The project was supported logistically by the French Polar Institute and funded by the PEW fellowship to Y.R.-C., the WWF-UK, and the Zone Atelier Antarctique et Terres Australes from the CNRS. D.M.W. received funding from the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska‐Curie Individual Fellowship Grant Agreement No. 748026.Peer reviewedPublisher PD

Deconvoluting lung evolution: from phenotypes to gene regulatory networks

Speakers in this symposium presented examples of respiratory regulation that broadly illustrate principles of evolution from whole organ to genes. The swim bladder and lungs of aquatic and terrestrial organisms arose independently from a common primordial “respiratory pharynx” but not from each other. Pathways of lung evolution are similar between crocodiles and birds but a low compliance of mammalian lung may have driven the development of the diaphragm to permit lung inflation during inspiration. To meet the high oxygen demands of flight, bird lungs have evolved separate gas exchange and pump components to achieve unidirectional ventilation and minimize dead space. The process of “screening” (removal of oxygen from inspired air prior to entering the terminal units) reduces effective alveolar oxygen tension and potentially explains why nonathletic large mammals possess greater pulmonary diffusing capacities than required by their oxygen consumption. The “primitive” central admixture of oxygenated and deoxygenated blood in the incompletely divided reptilian heart is actually co-regulated with other autonomic cardiopulmonary responses to provide flexible control of arterial oxygen tension independent of ventilation as well as a unique mechanism for adjusting metabolic rate. Some of the most ancient oxygen-sensing molecules, i.e., hypoxia-inducible factor-1alpha and erythropoietin, are up-regulated during mammalian lung development and growth under apparently normoxic conditions, suggesting functional evolution. Normal alveolarization requires pleiotropic growth factors acting via highly conserved cell–cell signal transduction, e.g., parathyroid hormone-related protein transducing at least partly through the Wingless/int pathway. The latter regulates morphogenesis from nematode to mammal. If there is commonality among these diverse respiratory processes, it is that all levels of organization, from molecular signaling to structure to function, co-evolve progressively, and optimize an existing gas-exchange framework

The spectrum of resistance in SR/CR mice: the critical role of chemoattraction in the cancer/leukocyte interaction

<p>Abstract</p> <p>Background</p> <p>Spontaneous regression/complete resistance (SR/CR) mice are a unique colony of mice that possess an inheritable, natural cancer resistance mediated primarily by innate cellular immunity. This resistance is effective against sarcoma 180 (S180) at exceptionally high doses and these mice remain healthy.</p> <p>Methods</p> <p>In this study, we challenged SR/CR mice with additional lethal transplantable mouse cancer cell lines to determine their resistance spectrum. The ability of these transplantable cancer cell lines to induce leukocyte infiltration was quantified and the percentage of different populations of responding immune cells was determined using flow cytometry.</p> <p>Results</p> <p>In comparison to wild type (WT) mice, SR/CR mice showed significantly higher resistance to all cancer cell lines tested. However, SR/CR mice were more sensitive to MethA sarcoma (MethA), B16 melanoma (B16), LL/2 lung carcinoma (LL/2) and J774 lymphoma (J774) than to sarcoma 180 (S180) and EL-4 lymphoma (EL-4). Further mechanistic studies revealed that this lower resistance to MethA and LL/2 was due to the inability of these cancer cells to attract SR/CR leukocytes, leading to tumor cell escape from resistance mechanism. This escape mechanism was overcome by co-injection with S180, which could attract SR/CR leukocytes allowing the mice to resist higher doses of MethA and LL/2. S180-induced cell-free ascites fluid (CFAF) co-injection recapitulated the results obtained with live S180 cells, suggesting that this chemoattraction by cancer cells is mediated by diffusible molecules. We also tested for the first time whether SR/CR mice were able to resist additional cancer cell lines prior to S180 exposure. We found that SR/CR mice had an innate resistance against EL-4 and J774.</p> <p>Conclusions</p> <p>Our results suggest that the cancer resistance in SR/CR mice is based on at least two separate processes: leukocyte migration/infiltration to the site of cancer cells and recognition of common surface properties on cancer cells. The infiltration of SR/CR leukocytes was based on both the innate ability of leukocytes to respond to chemotactic signals produced by cancer cells and on whether cancer cells produced these chemotactic signals. We found that some cancer cells could escape from SR/CR resistance because they did not induce infiltration of SR/CR leukocytes. However, if infiltration of leukocytes was induced by co-injection with chemotactic factors, these same cancer cells could be effectively recognized and killed by SR/CR leukocytes.</p