Inverse scattering of 2d photonic structures by layer-stripping

Design and reconstruction of 2d and 3d photonic structures are usually carried out by forward simulations combined with optimization or intuition. Reconstruction by means of layer-stripping has been applied in seismic processing as well as in design and characterization of 1d photonic structures such as fiber Bragg gratings. Layer-stripping is based on causality, where the earliest scattered light is used to recover the structure layer-by-layer. Our set-up is a 2d layered nonmagnetic structure probed by plane polarized harmonic waves entering normal to the layers. It is assumed that the dielectric permittivity in each layer only varies orthogonal to the polarization. Based on obtained reflectance data covering a suitable frequency interval, time-localized pulse data are synthesized and applied to reconstruct the refractive index profile in the leftmost layer by identifying the local, time-domain Fresnel reflection at each point. Once the first layer is known, its impact on the reflectance data is stripped off, and the procedure repeated for the next layer. Through numerical simulations it will be demonstrated that it is possible to reconstruct structures consisting of several layers. The impact of evanescent modes and limited bandwidth is discussed

Numerical performance of layer stripping algorithms for two-dimensional inverse scattering problems

Numerical results of implementing a two-dimensional layer stripping algorithm to solve the two-dimensional Schrodinger equation inverse potential problem are presented and discussed. This is the first exact (all multiple scattering and diffraction effects are included) numerical solution of a multi-dimensional Schrodinger equation inverse potential problem, excluding optimization-based approaches. The results are as follows: (1) the layer stripping algorithm successfully reconstructed the potential from scattering data measured on a plane (as it would be in many applications); (2) the algorithm avoids multiple scattering errors present in Born approximation reconstructions; and (3) the algorithm is insensitive to small amounts of noise in the scattering data. Simplifications of layer stripping and invariant imbedding algorithms under the Born approximation are also discussed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49097/2/ip920412.pd

Site-Specific Labeling of Annexin V with F-18 for Apoptosis Imaging

Annexin V is useful in detecting apoptotic cells by binding to phosphatidylserine (PS) that is exposed on the outer surface of the cell membrane during apoptosis. In this study, we examined the labeling of annexin V-128, a mutated form of annexin V that has a single cysteine residue at the NH2 terminus, with the thiol-selective reagent 18F-labeling agent N-[4-[(4-[18F]fluorobenzylidene)aminooxy]butyl]maleimide ([18F]FBABM). We also examined the cell binding affinity of the 18F-labeled annexin V-128 ([18F]FAN-128). [18F]FBABM was synthesized in two-step, one-pot method modified from literature procedure. (Toyokuni et al., Bioconjugate Chem. 2003, 14, 1253−1259). The average yield of [18F]FBABM was 23 ± 4% (n = 4, decay-corrected) and the specific activity was ∼6000 Ci/mmol. The total synthesis time was ∼92 min. The critical improvement of this study was identifying and then developing a purification method to remove an impurity N-[4-[(4-dimethylaminobenzylidene)aminooxy]butyl]maleimide 4, whose presence dramatically decreased the yield of protein labeling. Conjugation of [18F]FBABM with the thiol-containing annexin V-128 gave [18F]FAN-128 in 37 ± 9% yield (n = 4, decay corrected). Erythrocyte binding assay of [18F]FAN-128 showed that this modification of annexin V-128 did not compromise its membrane binding affinity. Thus, an in vivo investigation of [18F]FAN-128 as an apoptosis imaging agent is warranted

Effects of Ethanol and NAP on Cerebellar Expression of the Neural Cell Adhesion Molecule L1

The neural cell adhesion molecule L1 is critical for brain development and plays a role in learning and memory in the adult. Ethanol inhibits L1-mediated cell adhesion and neurite outgrowth in cerebellar granule neurons (CGNs), and these actions might underlie the cerebellar dysmorphology of fetal alcohol spectrum disorders. The peptide NAP potently blocks ethanol inhibition of L1 adhesion and prevents ethanol teratogenesis. We used quantitative RT-PCR and Western blotting of extracts of cerebellar slices, CGNs, and astrocytes from postnatal day 7 (PD7) rats to investigate whether ethanol and NAP act in part by regulating the expression of L1. Treatment of cerebellar slices with 20 mM ethanol, 10−12 M NAP, or both for 4 hours, 24 hours, and 10 days did not significantly affect L1 mRNA and protein levels. Similar treatment for 4 or 24 hours did not regulate L1 expression in primary cultures of CGNs and astrocytes, the predominant cerebellar cell types. Because ethanol also damages the adult cerebellum, we studied the effects of chronic ethanol exposure in adult rats. One year of binge drinking did not alter L1 gene and protein expression in extracts from whole cerebellum. Thus, ethanol does not alter L1 expression in the developing or adult cerebellum; more likely, ethanol disrupts L1 function by modifying its conformation and signaling. Likewise, NAP antagonizes the actions of ethanol without altering L1 expression

Modulation of DNA synthesis by muscarinic cholinergic receptors

Acetylcholine muscarinic receptors are a family of five G-protein-coupled receptors widely distributed in the central nervous system and in peripheral organs. Activation of certain subtypes of muscarinic receptors (M1, M3, M5) has been found to modulate DNA synthesis in a number of cell types. In several cell types acetylcholine, by activating endogenous or transfected muscarinic receptors, can indeed elicit cell proliferation. In other cell types, however, or under different experimental conditions, activation of muscarinic receptors has no effect, or inhibits DNA synthesis. A large number of intracellular pathways are being investigated to define the mechanisms involved in these effects of muscarinic receptors; these include among others, phospholipase D, protein kinases C and mitogen-activated-protein kinases. The ability of acetylcholine to modulate DNA synthesis through muscarinic receptors may be relevant in the context of brain development and neoplastic growth

Modulation of DNA synthesis by muscarinic cholinergic receptors

Acetylcholine muscarinic receptors are a family of five G-protein-coupled receptors widely distributed in the central nervous system and in peripheral organs. Activation of certain subtypes of muscarinic receptors (M-1, M-3, M-5) has been found to modulate DNA synthesis in a number of cell types. In several cell types acetylcholine, by activating endogenous or transfected muscarinic receptors, can indeed elicit cell proliferation. In other cell types, however, or under different experimental conditions, activation of muscarinic receptors has no effect, or inhibits DNA synthesis. A large number of intracellular pathways are being investigated to define the mechanisms involved in these effects of muscarinic receptors; these include among others, phospholipase D, protein kinases C and mitogen-activated-protein kinases. The ability of acetylcholine to modulate DNA synthesis through muscarinic receptors may be relevant in the context of brain development and neoplastic growth