Fuel containment, lightning protection and damage tolerance in large composite primary aircraft structures

The damage-tolerance characteristics of high strain-to-failure graphite fibers and toughened resins were evaluated. Test results show that conventional fuel tank sealing techniques are applicable to composite structures. Techniques were developed to prevent fuel leaks due to low-energy impact damage. For wing panels subjected to swept stroke lightning strikes, a surface protection of graphite/aluminum wire fabric and a fastener treatment proved effective in eliminating internal sparking and reducing structural damage. The technology features developed were incorporated and demonstrated in a test panel designed to meet the strength, stiffness, and damage tolerance requirements of a large commercial transport aircraft. The panel test results exceeded design requirements for all test conditions. Wing surfaces constructed with composites offer large weight savings if design allowable strains for compression can be increased from current levels

Composite transport wing technology development: Design development tests and advanced structural concepts

Numerous design concepts, materials, and manufacturing methods were investigated for the covers and spars of a transport box wing. Cover panels and spar segments were fabricated and tested to verify the structural integrity of design concepts and fabrication techniques. Compression tests on stiffened panels demonstrated the ability of graphite/epoxy wing upper cover designs to achieve a 35 percent weight savings compared to the aluminum baseline. The impact damage tolerance of the designs and materials used for these panels limits the allowable compression strain and therefore the maximum achievable weight savings. Bending and shear tests on various spar designs verified an average weight savings of 37 percent compared to the aluminum baseline. Impact damage to spar webs did not significantly degrade structural performance. Predictions of spar web shear instability correlated well with measured performance. The structural integrity of spars manufactured by filament winding equalled or exceeded those fabricated by hand lay-up. The information obtained will be applied to the design, fabrication, and test of a full-scale section of a wing box. When completed, the tests on the technology integration box beam will demonstrate the structural integrity of an advanced composite wing design which is 25 percent lighter than the metal baseline

Deferoxamine Preventable Hepatocellular Damage, Following Hemorrhagic Shock

To examine the role of iron in mediating hepatocellular damage during reperfusion after hemorrhagic shock, we studied five groups of n=4 or 5 dogs, bled to reduce mean arterial pressure to 35 mmHg (± 5mrnHg) for three hours and subsequently treated 20 minutes prior to reinfusion of shed blood with either 0.9% saline, 5 ml/kg; deferoxamine, 50 μg/kg in 0.9% saline; 6% pentastarch solution, 5 ml/kg; deferoxamine covalently bound to 6% pentastarch, 50 μg/kg; or iron loaded deferoxamine in 0.9% saline. Saturation of iron binding capacity increased during hemorrhagic shock and remained high in all but the def eroxamine pentastarch treated group. Serum iron levels were significantly lower in animals treated with saline or iron loaded deferoxamine. Serum alanine aminotransferase (ALT), a specific marker for hepatocellular injury in the dog, was measured as an indicator of hepatic reperfusion injury. During shock, ALT did not change significantly from the normal in any group. After reperfusion, however, ALT rose sharply in animals reperfused without iron chelators, from a mean baseline value of less than 36 U /L to a post-reperfusion plateau of 5509 ± 2260 U /L at four hours, a pattern suggesting hepatic reperfusion injury. Iron loaded deferoxamine control dogs, also showed a substantial rise in ALT activity to 6287 ± 2134 U/L four hours after reperfusion. However, dogs treated with free deferoxamine showed significantly smaller elevations in ALT to only 655 ± 139 U /L (P \u3c0.05). Histologic evaluation of liver sections showed significantly smaller areas of necrosis in both of the deferoxamine treated groups compared to other groups. These findings suggest that deferoxamine preventable reperfusion injury of the liver, perhaps involving the iron catalyzed Haber-Weiss reaction, may play a role in the pathophysiology of hemorrhagic shock

Scatchard Analysis of Methane Sulfinic Acid Production from Dimethyl Sulfoxide: A Method to Quantify Hydroxyl Radical Formation in Physiologic Systems

A major impediment to the confirmation of free radical mechanisms in pathogenesis is a lack of direct, chemical evidence that oxygen centered free radicals actually arise in living tissues in quantities sufficient to cause serious damage. This investigation was conducted to validate the use of dimethyl sulfoxide (DMSO) as a quantitative molecular probe for the generation of hydroxyl radicals (HO*) under physiologic conditions. Reaction of HO* with DMSO produces methane sulfinic acid (MSA) as a primary product, which can be detected by a simple colorimetric assay. To develop a method for estimating total HO* production, we studied two model systems: the superoxide driven Fenton reaction in vitro, using xanthine oxidase as the source of superoxide, and a computer model of Fenton chemistry. Measured MSA production both in vitro and in the computer model was a predictable function of the concentrations of DMSO and competing scavengers of HO*, according to the principle of competition kinetics. Both experimental results and model calculations showed that Scatchard analysis may be used to infer total HO* generation, despite the presence of scavengers other than DMSO, such as mannitol. Thus, methane sulfinic acid production from DMSO holds promise as an easily measured marker for HO* formation in biologic systems pretreated with DMSO, and Scatchard analysis of repeated experiments with varying DMSO concentrations can yield an estimate of total HO* generation

Tobramycin-Treated Pseudomonas aeruginosa PA14 Enhances Streptococcus constellatus 7155 Biofilm Formation in a Cystic Fibrosis Model System

Cystic fibrosis (CF) is a human genetic disorder which results in a lung environment that is highly conducive to chronic microbial infection. Over the past decade, deep-sequencing studies have demonstrated that the CF lung can harbor a highly diverse polymicrobial community. We expanded our existing in vitro model of Pseudomonas aeruginosa biofilm formation on CF-derived airway cells to include this broader set of CF airway colonizers to investigate their contributions to CF lung disease, particularly as they relate to the antibiotic response of the population. Using this system, we identified an interspecies interaction between P. aeruginosa, a bacterium associated with declining lung function and worsening disease, and Streptococcus constellatus, a bacterium correlated with the onset of pulmonary exacerbations in CF patients. The growth rate and cytotoxicity of S. constellatus 7155 and P. aeruginosa PA14 were unchanged when grown together as mixed biofilms in the absence of antibiotics. However, the addition of tobramycin, the frontline maintenance therapy antibiotic for individuals with CF, to a mixed biofilm of S. constellatus 7155 and P. aeruginosa PA14 resulted in enhanced S. constellatus biofilm formation. Through a candidate genetic approach, we showed that P. aeruginosa rhamnolipids were reduced upon tobramycin exposure, allowing for S. constellatus 7155 biofilm enhancement, and monorhamnolipids were sufficient to reduce S. constellatus 7155 biofilm viability in the absence of tobramycin. While the findings presented here are specific to a biofilm of S. constellatus 7155 and P. aeruginosa PA14, they highlight the potential of polymicrobial interactions to impact antibiotic tolerance in unanticipated ways

B -> K^* gamma from D -> K^* l nu

The B -> K^* gamma branching fraction is predicted using heavy quark spin symmetry at large recoil to relate the tensor and (axial-)vector form factors, using heavy quark flavor symmetry to relate the B decay form factors to the measured D -> K^* l nu form form factors, and extrapolating the semileptonic B decay form factors to large recoil assuming nearest pole dominance. This prediction agrees with data surprisingly well, and we comment on its implications for the extraction of |Vub| from B -> rho l nu.Comment: 10 page

Collective excitations of Bose-Einstein condensed gases at finite temperatures

We have applied the Popov version of the Hartree-Fock-Bogoliubov (HFB) approximation to calculate the finite-temperature excitation spectrum of a Bose-Einstein condensate (BEC) of $^{87}$Rb atoms. For lower values of the temperature, we find excellent agreement with recently-published experimental data for the JILA TOP trap. In contrast to recent comparison of the results of HFB--Popov theory with experimental condensate fractions and specific heats, there is disagreement of the theoretical and recent experimental results near the BEC phase transition temperature.Comment: 4 pages, Latex, with 4 figures. More info at http://amo.phy.gasou.edu/bec.htm

A perspective on physical reservoir computing with nanomagnetic devices

Neural networks have revolutionized the area of artificial intelligence and introduced transformative applications to almost every scientific field and industry. However, this success comes at a great price; the energy requirements for training advanced models are unsustainable. One promising way to address this pressing issue is by developing low-energy neuromorphic hardware that directly supports the algorithm's requirements. The intrinsic non-volatility, non-linearity, and memory of spintronic devices make them appealing candidates for neuromorphic devices. Here we focus on the reservoir computing paradigm, a recurrent network with a simple training algorithm suitable for computation with spintronic devices since they can provide the properties of non-linearity and memory. We review technologies and methods for developing neuromorphic spintronic devices and conclude with critical open issues to address before such devices become widely used

Intracellular Proton Conductance of the Hepatitis C Virus p7 Protein and Its Contribution to Infectious Virus Production

The hepatitis C virus (HCV) p7 protein is critical for virus production and an attractive antiviral target. p7 is an ion channel when reconstituted in artificial lipid bilayers, but channel function has not been demonstrated in vivo and it is unknown whether p7 channel activity plays a critical role in virus production. To evaluate the contribution of p7 to organelle pH regulation and virus production, we incorporated a fluorescent pH sensor within native, intracellular vesicles in the presence or absence of p7 expression. p7 increased proton (H+) conductance in vesicles and was able to rapidly equilibrate H+ gradients. This conductance was blocked by the viroporin inhibitors amantadine, rimantadine and hexamethylene amiloride. Fluorescence microscopy using pH indicators in live cells showed that both HCV infection and expression of p7 from replicon RNAs reduced the number of highly acidic (pH<5) vesicles and increased lysosomal pH from 4.5 to 6.0. These effects were not present in uninfected cells, sub-genomic replicon cells not expressing p7, or cells electroporated with viral RNA containing a channel-inactive p7 point mutation. The acidification inhibitor, bafilomycin A1, partially restored virus production to cells electroporated with viral RNA containing the channel inactive mutation, yet did not in cells containing p7-deleted RNA. Expression of influenza M2 protein also complemented the p7 mutant, confirming a requirement for H+ channel activity in virus production. Accordingly, exposure to acid pH rendered intracellular HCV particles non-infectious, whereas the infectivity of extracellular virions was acid stable and unaffected by incubation at low pH, further demonstrating a key requirement for p7-induced loss of acidification. We conclude that p7 functions as a H+ permeation pathway, acting to prevent acidification in otherwise acidic intracellular compartments. This loss of acidification is required for productive HCV infection, possibly through protecting nascent virus particles during an as yet uncharacterized maturation process