TESTING DECEPTION WITH A COMMERCIAL TOOL SIMULATING CYBERSPACE

Deception methods have been applied to the traditional domains of war (air, land, sea, and space). In the newest domain of cyber, deception can be studied to see how it can be best used. Cyberspace operations are an essential warfighting domain within the Department of Defense (DOD). Many training exercises and courses have been developed to aid leadership with planning and to execute cyberspace effects that support operations. However, only a few simulations train cyber operators about how to respond to cyberspace threats. This work tested a commercial product from Soar Technologies (Soar Tech) that simulates conflict in cyberspace. The Cyberspace Course of Action Tool (CCAT) is a decision-support tool that evaluates defensive deception in a wargame simulating a local-area network being attacked. Results showed that defensive deception methods of decoys and bait could be effective in cyberspace. This could help military cyber defenses since their digital infrastructure is threatened daily with cyberattacks.Marine Forces Cyberspace CommandChief Petty Officer, United States NavyChief Petty Officer, United States NavyApproved for public release. Distribution is unlimited

Rex E. Lee Conference on the Office of the Solicitor General of the United States: Panel for Former Solicitors General

I agree entirely that the chain of command is clear and that the Framers managed to make it all the way through all the articles of the Constitution without even conceiving of a solicitor general, let alone bothering to mention an attorney general. It is important nonetheless to distinguish between those things the solicitor general does pursuant to the longstanding notice-and-comment regulation, and the other things a solicitor general may do pursuant to his (and, someday, her!) statutory obligation to be of general assistance to the attorney general

Enhanced Tissue Integration During Cartilage RepairIn VitroCan Be Achieved by Inhibiting Chondrocyte Death at the Wound Edge

Objective: Experimental wounding of articular cartilage results in cell death at the lesion edge. The objective of this study was to investigate whether inhibition of this cell death results in enhanced integrative cartilage repair. Methods: Bovine articular cartilage discs (6mm) were incubated in media containing inhibitors of necrosis (Necrostatin-1, Nec-1) or apoptosis (Z-VAD-FMK, ZVF) before cutting a 3mm inner core. This core was left in situ to create disc/ring composites, cultured for up to 6 weeks with the inhibitors, and analyzed for cell death, sulfated glycosaminoglycan release, and tissue integration. Results: Creating the disc/ring composites resulted in a significant increase in necrosis. ZVF significantly reduced necrosis and apoptosis at the wound edge. Nec-1 reduced necrosis. Both inhibitors reduced the level of wound-induced sulfated glycosaminoglycan loss. Toluidine blue staining and electron microscopy of cartilage revealed significant integration of the wound edges in disc/ring composites treated with ZVF. Nec-1 improved integration, but to a lesser extent. Push-out testing revealed that ZVF increased adhesive strength compared to control composites. Conclusions: This study shows that treatment of articular cartilage with cell death inhibitors during wound repair increases the number of viable cells at the wound edge, prevents matrix loss, and results in a significant improvement in cartilage-cartilage integration

Investigations into the Influence of Chronic Colitis on Colonic Adenocarcinoma Cell Growth A Progress Report

Graduate Basi

Representative Missouri weeds and their control

Cover title.Include index

Peptide-Induced Lipid Flip-Flop in Asymmetric Liposomes Measured by Small Angle Neutron Scattering

© 2019 American Chemical Society. Despite the prevalence of lipid transbilayer asymmetry in natural plasma membranes, most biomimetic model membranes studied are symmetric. Recent advances have helped to overcome the difficulties in preparing asymmetric liposomes in vitro, allowing for the examination of a larger set of relevant biophysical questions. Here, we investigate the stability of asymmetric bilayers by measuring lipid flip-flop with time-resolved small-angle neutron scattering (SANS). Asymmetric large unilamellar vesicles with inner bilayer leaflets containing predominantly 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) and outer leaflets composed mainly of 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) displayed slow spontaneous flip-flop at 37 -C (half-time, t1/2 = 140 h). However, inclusion of peptides, namely, gramicidin, alamethicin, melittin, or pHLIP (i.e., pH-low insertion peptide), accelerated lipid flip-flop. For three of these peptides (i.e., pHLIP, alamethicin, and melittin), each of which was added externally to preformed asymmetric vesicles, we observed a completely scrambled bilayer in less than 2 h. Gramicidin, on the other hand, was preincorporated during the formation of the asymmetric liposomes and showed a time resolvable 8-fold increase in the rate of lipid asymmetry loss. These results point to a membrane surface-related (e.g., adsorption/insertion) event as the primary driver of lipid scrambling in the asymmetric model membranes of this study. We discuss the implications of membrane peptide binding, conformation, and insertion on lipid asymmetry

DUF2285 is a novel helix-turn-helix domain variant that orchestrates both activation and antiactivation of conjugative element transfer in proteobacteria.

Horizontal gene transfer is tightly regulated in bacteria. Often only a fraction of cells become donors even when regulation of horizontal transfer is coordinated at the cell population level by quorum sensing. Here, we reveal the widespread 'domain of unknown function' DUF2285 represents an 'extended-turn' variant of the helix-turn-helix domain that participates in both transcriptional activation and antiactivation to initiate or inhibit horizontal gene transfer. Transfer of the integrative and conjugative element ICEMlSymR7A is controlled by the DUF2285-containing transcriptional activator FseA. One side of the DUF2285 domain of FseA has a positively charged surface which is required for DNA binding, while the opposite side makes critical interdomain contacts with the N-terminal FseA DUF6499 domain. The QseM protein is an antiactivator of FseA and is composed of a DUF2285 domain with a negative surface charge. While QseM lacks the DUF6499 domain, it can bind the FseA DUF6499 domain and prevent transcriptional activation by FseA. DUF2285-domain proteins are encoded on mobile elements throughout the proteobacteria, suggesting regulation of gene transfer by DUF2285 domains is a widespread phenomenon. These findings provide a striking example of how antagonistic domain paralogues have evolved to provide robust molecular control over the initiation of horizontal gene transfer

The Lantern Vol. 46, No. 1, December 1979

• Visions in Chains • The Bean • Who Can We Watch Tonite? • Night Glider • The Hurricane • Crisp New Paper • Compassion • Loneliness • 301 • Ode to Man • Unsteady Hands • The Beachcomber • The Pounce • Graveyard Shift • Houston Refineries • Haiku • The End of the Game • A Rose • Ode to a Ziffle • To Carson McCullers • In the May Month • Ghostly Chanting • Travel Excerpts • Face in the Crowd • Waiting in an Airport • A Taste of Winter\u27s Embracehttps://digitalcommons.ursinus.edu/lantern/1115/thumbnail.jp

Alterations of immune response of non-small lung cancer with azacytidine

Innovative therapies are needed for advanced Non-Small Cell Lung Cancer (NSCLC). We have undertaken a genomics based, hypothesis driving, approach to query an emerging potential that epigenetic therapy may sensitize to immune checkpoint therapy targeting PD-L1/PD-1 interaction. NSCLC cell lines were treated with the DNA hypomethylating agent azacytidine (AZA - Vidaza) and genes and pathways altered were mapped by genome-wide expression and DNA methylation analyses. AZA-induced pathways were analyzed in The Cancer Genome Atlas (TCGA) project by mapping the derived gene signatures in hundreds of lung adeno (LUAD) and squamous cell carcinoma (LUSC) samples. AZA up-regulates genes and pathways related to both innate and adaptive immunity and genes related to immune evasion in a several NSCLC lines. DNA hypermethylation and low expression of IRF7, an interferon transcription factor, tracks with this signature particularly in LUSC. In concert with these events, AZA up-regulates PD-L1 transcripts and protein, a key ligand-mediator of immune tolerance. Analysis of TCGA samples demonstrates that a significant proportion of primary NSCLC have low expression of AZA-induced immune genes, including PD-L1. We hypothesize that epigenetic therapy combined with blockade of immune checkpoints - in particular the PD-1/PD-L1 pathway - may augment response of NSCLC by shifting the balance between immune activation and immune inhibition, particularly in a subset of NSCLC with low expression of these pathways. Our studies define a biomarker strategy for response in a recently initiated trial to examine the potential of epigenetic therapy to sensitize patients with NSCLC to PD-1 immune checkpoint blockade

Fading AGN candidates: AGN histories and outflow signatures

We consider the energy budgets and radiative history of eight fading active galactic nuclei (AGNs), identified from an energy shortfall between the requirements to ionize very extended (radius \u3e 10 kpc) ionized clouds and the luminosity of the nucleus as we view it directly. All show evidence of significant fading on timescales of ≈50,000 yr. We explore the use of minimum ionizing luminosity Qion derived from photoionization balance in the brightest pixels in Hα at each projected radius. Tests using presumably constant Palomar–Green QSOs, and one of our targets with detailed photoionization modeling, suggest that we can derive useful histories of individual AGNs, with the caveat that the minimum ionizing luminosity is always an underestimate and subject to uncertainties about fine structure in the ionized material. These consistency tests suggest that the degree of underestimation from the upper envelope of reconstructed Qion values is roughly constant for a given object and therefore does not prevent such derivation. The AGNs in our sample show a range of behaviors, with rapid drops and standstills; the common feature is a rapid drop in the last ≈2 × 104 yr before the direct view of the nucleus. The e-folding timescales for ionizing luminosity are mostly in the thousands of years, with a few episodes as short as 400 yr. In the limit of largely obscured AGNs, we find additional evidence for fading from the shortfall between even the lower limits from recombination balance and the maximum luminosities derived from far-infrared fluxes. We compare these long-term light curves, and the occurrence of these fading objects among all optically identified AGNs, to simulations of AGN accretion; the strongest variations over these timespans are seen in models with strong and local (parsec-scale) feedback. We present Gemini integral-field optical spectroscopy, which shows a very limited role for outflows in these ionized structures. While rings and loops of emission, morphologically suggestive of outflow, are common, their kinematic structure shows some to be in regular rotation. UGC 7342 exhibits local signatures of outflows \u3c300 km s−1, largely associated with very diffuse emission, and possibly entraining gas in one of the clouds seen in Hubble Space Telescope images. Only in the Teacup AGN do we see outflow signatures of the order of 1000 km s−1. In contrast to the extended emission regions around many radio-loud AGNs, the clouds around these fading AGNs consist largely of tidal debris being externally illuminated but not displaced by AGN outflows