Wear resistant solid lubricating coatings via compression molding and thermal spraying technologies

This work combines two industrially friendly processing methods in order to create wear resistant and solid-lubricating composite coatings potentially suitable for high load applications. Layered composite coatings were fabricated over wrought stainless steel 444 (SS444) by compression molding a mixture of solid lubricant polymer, polytetrafluoroethylene (PTFE, 80 wt%), and wear resistant polymer, polyimide (PI, 20 wt%), onto iron aluminide (Fe3Al) thermal spray coatings without the need of either primers or adhesives. The fabrication process consisted of three main steps: deposition of the Fe3Al thermal spray coating onto a SS444 substrate and transfer into a metal mold; transfer, compress, and sinter mixed polymeric powder onto the thermal spray coating; and finally, sample cooling to room temperature. This method takes advantage of the high surface roughness of thermal spray coatings, which increases mechanical adhesion of slippery PTFE to the underlying metallic material. Coatings were produced with and without a small amount of graphite (5 wt%) to analyze its impact on sliding and wear properties. Unlike current coating technologies, the thickness of the coatings presented herein can be easily and quickly tailored by varying the amount of polymer powder added to the mold prior to compression or by grinding after fabrication. We produced and analyzed coatings ~1.3 mm in total thickness that portray coefficient of frictions ~0.1, similar to pure PTFE. The calculated wear rates for both coatings with and without graphite are an order of magnitude lower than what has been previously reported for coatings of similar composition. The influence of graphite on wear properties was found to be minimal due to the high content of self-lubricating PTFE yet can act as a way to lower material costs and increase the coatings load capacity

Spin-dependent effective interactions for halo nuclei

We discuss the spin-dependence of the effective two-body interactions appropriate for three-body computations. The only reasonable choice seems to be the fine and hyperfine interactions known for atomic electrons interacting with the nucleus. One exception is the nucleon-nucleon interaction imposing a different type of symmetry. We use the two-neutron halo nucleus 11Li as illustration. We demonstrate that models with the wrong spin-dependence are basically without predictive power. The Pauli forbidden core and valence states must be consistently treated.Comment: TeX file, 6 pages, 3 postscript figure

Comparative analysis of cell death induction by Taurolidine in different malignant human cancer cell lines

<p>Abstract</p> <p>Background</p> <p>Taurolidine (TRD) represents an anti-infective substance with anti-neoplastic activity in many malignant cell lines. So far, the knowledge about the cell death inducing mechanisms and pathways activated by TRD is limited. The aim of this study was therefore, to perform a comparative analysis of cell death induction by TRD simultaneously in different malignant cell lines.</p> <p>Materials and methods</p> <p>Five different malignant cell lines (HT29/Colon, Chang Liver/Liver, HT1080/fibrosarcoma, AsPC-1/pancreas and BxPC-3/pancreas) were incubated with increasing concentrations of TRD (100 μM, 250 μM and 1000 μM) for 6 h and 24 h. Cell viability, apoptosis and necrosis were analyzed by FACS analysis (Propidiumiodide/AnnexinV staining). Additionally, cells were co-incubated with the caspase Inhibitor z-VAD, the radical scavenger N-Acetylcystein (NAC) and the Gluthation depleting agent BSO to examine the contribution of caspase activation and reactive oxygen species in TRD induced cell death.</p> <p>Results</p> <p>All cell lines were susceptible to TRD induced cell death without resistance toward this anti-neoplastic agent. However, the dose response effects were varying largely between different cell lines. The effect of NAC and BSO co-treatment were highly different among cell lines - suggesting a cell line specific involvement of ROS in TRD induced cell death. Furthermore, impact of z-VAD mediated inhibition of caspases was differing strongly among the cell lines.</p> <p>Conclusion</p> <p>This is the first study providing a simultaneous evaluation of the anti-neoplastic action of TRD across several malignant cell lines. The involvement of ROS and caspase activation was highly variable among the five cell lines, although all were susceptible to TRD induced cell death. Our results indicate, that TRD is likely to provide multifaceted cell death mechanisms leading to a cell line specific diversity.</p

Superdeformed rotational bands in Pu-240

The intermediate structure of the fission resonances has been observed in Pu-240. A resonance structure found around the excitation energy of 4.5 MeV was interpreted as a group of K-pi = 0(+) superdeformed rotational bands. The moments of inertia and level density distributions were also deduced for the individually observed band-heads

Nanostructure, osteopontin, and mechanical properties of calcitic avian eggshell

Avian (and formerly dinosaur) eggshells form a hard, protective biomineralized chamber for embryonic growth—an evolutionary strategy that has existed for hundreds of millions of years. We show in the calcitic chicken eggshell how the mineral and organic phases organize hierarchically across different length scales and how variation in nanostructure across the shell thicknessmodifies its hardness, elastic modulus, and dissolution properties.We also show that the nanostructure changes during egg incubation, weakening the shell for chick hatching. Nanostructure and increased hardness were reproduced in synthetic calcite crystals grown in the presence of the prominent eggshell protein osteopontin. These results demonstrate the contribution of nanostructure to avian eggshell formation, mechanical properties, and dissolution.This work was supported by a grant from the Canadian Institutes of Health Research (no. MOP-142330) and the Natural Sciences and Engineering Research Council of Canada (NSERC; no. RGPIN-2016-05031) to M.D.M., an NSERC (no. RGPIN-2016-04410) Discovery grant to M.T.H., a Spanish Government grant (CGL2015-64683-P) to A.B.R.-N., an Emmy Noether research grant from the German Research Foundation (no. WO1712/3-1) to S.E.W., and an NSF grant (NSF BMAT; no. 1507736) to J.J.G. M.D.M. is a member of the Fonds de Recherche Quebec–Sante Network for Oral and Bone Health Research and the McGill Centre for Bone and Periodontal Researc

DDoS Hide &amp; Seek:On the effectiveness of a booter services takedown

Booter services continue to provide popular DDoS-as-a-service platforms and enable anyone irrespective of their technical ability, to execute DDoS attacks with devastating impact. Since booters are a serious threat to Internet operations and can cause significant financial and reputational damage, they also draw the attention of law enforcement agencies and related counter activities. In this paper, we investigate booter-based DDoS attacks in the wild and the impact of an FBI takedown targeting 15 booter websites in December 2018 from the perspective of a major IXP and two ISPs. We study and compare attack properties of multiple booter services by launching Gbps-level attacks against our own infrastructure. To understand spatial and temporal trends of the DDoS traffic originating from booters we scrutinize 5 months, worth of inter-domain traffic. We observe that the takedown only leads to a temporary reduction in attack traffic. Additionally, one booter was found to quickly continue operation by using a new domain for its website

NASA Standing Review Board Handbook

No abstract availabl

Gene expression analysis of cell death induction by Taurolidine in different malignant cell lines

<p>Abstract</p> <p>Background</p> <p>The anti-infective agent Taurolidine (TRD) has been shown to have cell death inducing properties, but the mechanism of its action is largely unknown. The aim of this study was to identify potential common target genes modulated at the transcriptional level following TRD treatment in tumour cell lines originating from different cancer types.</p> <p>Methods</p> <p>Five different malignant cell lines (HT29, Chang Liver, HT1080, AsPC-1 and BxPC-3) were incubated with TRD (100 μM, 250 μM and 1000 μM). Proliferation after 8 h and cell viability after 24 h were analyzed by BrdU assay and FACS analysis, respectively. Gene expression analyses were carried out using the <it>Agilent </it>-microarray platform to indentify genes which displayed conjoint regulation following the addition of TRD in all cell lines. Candidate genes were subjected to <it>Ingenuity Pathways Analysis </it>and selected genes were validated by qRT-PCR and Western Blot.</p> <p>Results</p> <p>TRD 250 μM caused a significant inhibition of proliferation as well as apoptotic cell death in all cell lines. Among cell death associated genes with the strongest regulation in gene expression, we identified pro-apoptotic transcription factors (EGR1, ATF3) as well as genes involved in the ER stress response (PPP1R15A), in ubiquitination (TRAF6) and mitochondrial apoptotic pathways (PMAIP1).</p> <p>Conclusions</p> <p>This is the first conjoint analysis of potential target genes of TRD which was performed simultaneously in different malignant cell lines. The results indicate that TRD might be involved in different signal transduction pathways leading to apoptosis.</p