79 research outputs found
Alien Registration- Albert, Harmonia (Lewiston, Androscoggin County)
https://digitalmaine.com/alien_docs/29208/thumbnail.jp
Are negative index materials achievable with surface plasmon waveguides? A case study of three plasmonic geometries
We present a theoretical analysis of planar plasmonic waveguides
that support propagation of positive and negative index modes. Particular
attention is given to the modes sustained by metal-insulator-metal (MIM),
insulator-metal-insulator (IMI), and insulator-insulator-metal (IIM)
geometries at visible and near-infrared frequencies. We find that all three
plasmonic structures are characterized by negative indices over a finite
range of visible frequencies, with figures of merit approaching 20.
Moreover, using finite-difference time-domain simulations, we demonstrate
that visible-wavelength light propagating from free space into these
waveguides can exhibit negative refraction. Refractive index and figure-ofmerit
calculations are presented for Ag/GaP and Ag/Si3N_4 - based structures
with waveguide core dimensions ranging from 5 to 50 nm and excitation
wavelengths ranging from 350 nm to 850 nm. Our results provide the design
criteria for realization of broadband, visible-frequency negative index
materials and transformation-based optical elements for two-dimensional
guided waves. These geometries can serve as basic elements of threedimensional
negative-index metamaterials
The new "p-n junction": Plasmonics enables photonic access to the nanoworld
Since the development of the light microscope in the 16th century, optical device size and performance have been limited by diffraction. Optoelectronic devices of today are much bigger than the smallest electronic devices for this reason. Achieving control of light-material interactions for photonic device applications at the nanoscale requires structures that guide electromagnetic energy with subwavelength-scale mode confinement. By converting the optical mode into nonradiating surface plasmons, electromagnetic energy can be guided in structures with lateral dimensions of less than 10% of the free-space wavelength. A variety of methods-including electron-beam lithography and self-assembly-have been used to construct both particle and planar plasmon waveguides. Recent experimental studies have confirmed the strongly coupled collective plasmonic modes of metallic nanostructures. In plasmon waveguides consisting of closely spaced silver rods, electromagnetic energy transport over distances of 0.5 mu m has been observed. Moreover, numerical simulations suggest the possibility of multi-centimeter plasmon propagation in thin metallic stripes. Thus, there appears to be no fundamental scaling limit to the size and density of photonic devices, and ongoing work is aimed at identifying important device performance criteria in the subwavelength size regime. Ultimately, it may be possible to design an entire class of subwavelength-scale optoelectronic components (waveguides, sources, detectors, modulators) that could form the building blocks of an optical device technology-a technology scalable to molecular dimensions, with potential imaging, spectroscopy, and interconnection applications in computing, communications, and chemical/biological detection
Active plasmonic devices and optical metamaterials
We studied active near-infrared metamaterials based on phase transition of vanadium oxide thin films, asymmetrically coupled split-ring resonators for narrowing resonance line-widths , field effect modulation of plasmon propagation and 3D single layer, plasmonic negative-index metamaterials
Kinin B1 receptors contributes to acute pain following minor surgery in humans
<p>Abstract</p> <p>Background</p> <p>Kinins play an important role in regulation of pain and hyperalgesia after tissue injury and inflammation by activating two types of G-protein-coupled receptors, the kinin B<sub>1 </sub>and B<sub>2 </sub>receptors. It is generally accepted that the B<sub>2 </sub>receptor is constitutively expressed, whereas the B<sub>1 </sub>receptor is induced in response to inflammation. However, little is known about the regulatory effects of kinin receptors on the onset of acute inflammation and inflammatory pain in humans. The present study investigated the changes in gene expression of kinin receptors and the levels of their endogenous ligands at an early time point following tissue injury and their relation to clinical pain, as well as the effect of COX-inhibition on their expression levels.</p> <p>Results</p> <p>Tissue injury resulted in a significant up-regulation in the gene expression of B<sub>1 </sub>and B<sub>2 </sub>receptors at 3 hours post-surgery, the onset of acute inflammatory pain. Interestingly, the up-regulation in the gene expression of B<sub>1 </sub>and B<sub>2 </sub>receptors was positively correlated to pain intensity only after ketorolac treatment, signifying an interaction between prostaglandins and kinins in the inflammatory pain process. Further, the gene expression of both B<sub>1 </sub>and B<sub>2 </sub>receptors were correlated. Following tissue injury, B<sub>1 </sub>ligands des-Arg<sup>9</sup>-BK and des-Arg<sup>10</sup>-KD were significantly lower at the third hour compared to the first 2 hours in both the placebo and the ketorolac treatment groups but did not differ significantly between groups. Tissue injury also resulted in the down-regulation of TRPV1 gene expression at 3 hours post-surgery with no significant effect by ketorolac treatment. Interestingly, the change in gene expression of TRPV1 was correlated to the change in gene expression of B<sub>1 </sub>receptor but not B<sub>2 </sub>receptor.</p> <p>Conclusions</p> <p>These results provide evidence at the transcriptional level in a clinical model of tissue injury that up-regulation of kinin receptors are involved in the development of the early phase of inflammation and inflammatory pain. The up-regulation of B<sub>1 </sub>receptors may contribute to acute inflammatory pain through TRPV1 activation.</p
Secreted Bacterial Effectors and Host-Produced Eiger/TNF Drive Death in a Salmonella-Infected Fruit Fly
Death by infection is often as much due to the host's reaction as it is to the direct result of microbial action. Here we identify genes in both the host and microbe that are involved in the pathogenesis of infection and disease in Drosophila melanogaster challenged with Salmonella enterica serovartyphimurium (S. typhimurium). We demonstrate that wild-type S. typhimurium causes a lethal systemic infection when injected into the hemocoel of D. melanogaster. Deletion of the gene encoding the secreted bacterial effector Salmonella leucine-rich (PslrP) changes an acute and lethal infection to one that is persistent and less deadly. We propose a model in which Salmonella secreted effectors stimulate the fly and thus cause an immune response that is damaging both to the bacteria and, subsequently, to the host. In support of this model, we show that mutations in the fly gene eiger, a TNF homolog, delay the lethality of Salmonella infection. These results suggest that S. typhimurium-infected flies die from a condition that resembles TNF-induced metabolic collapse in vertebrates. This idea provides us with a new model to study shock-like biology in a genetically manipulable host. In addition, it allows us to study the difference in pathways followed by a microbe when producing an acute or persistent infection
Le Forum, Vol. 44 #3
https://digitalcommons.library.umaine.edu/francoamericain_forum/1105/thumbnail.jp
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